PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
27665006-10	2017	The CY-induced increases in malondialdehyde (MDA) content and decreases in total antioxidant capacity (T-AOC), glutathione, vitamin C, and alpha-tocopherol levels, and total superoxide dismutase and glutathione peroxidase activities in both serum and the liver were attenuated by vitamin E (P < 0.05).	Cyclophosphamide	4-6	probable phospholipid hydroperoxide glutathione peroxidase	Glycine max	199-221
28427156-5	2017	Furthermore, NSG mice xenografted with DLEU1 knockdown BL cells had significantly shortened survival (p < 0.05 and p < 0.005), whereas those xenografted with DLEU1 overexpressing BL cells had significantly improved survival (p < 0.05 and p < 0.0001), following treatment with rituximab and/or cyclophosphamide.	Cyclophosphamide	305-321	deleted in lymphocytic leukemia 1	Homo sapiens	39-44
28428632-0	2017	Cyclophosphamide-induced HCN1 channel upregulation in interstitial Cajal-like cells leads to bladder hyperactivity in mice.	Cyclophosphamide	0-16	hyperpolarization activated cyclic nucleotide gated potassium channel 1	Mus musculus	25-29
28412730-8	2017	High expression of treRNA was independently prognostic for shorter progression free survival in patients receiving fludarabine plus cyclophosphamide.	Cyclophosphamide	132-148	translation regulatory long non-coding RNA 1	Homo sapiens	19-25
28445949-6	2017	These cells survived longer following treatment with a combination of cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP).	Cyclophosphamide	70-86	DNA damage inducible transcript 3	Homo sapiens	129-133
28291124-2	2017	MYC, a transcriptional factor and oncoprotein, is overexpressed in a fraction of DLBCL and indicates poor prognosis and aggressive clinical course when treated with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP).	Cyclophosphamide	180-196	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	0-3
28131632-0	2017	CD56-enriched donor cell infusion after post-transplantation cyclophosphamide for haploidentical transplantation of advanced myeloid malignancies is associated with prompt reconstitution of mature natural killer cells and regulatory T cells with reduced incidence of acute graft versus host disease: A pilot study.	Cyclophosphamide	61-77	neural cell adhesion molecule 1	Homo sapiens	0-4
28131632-1	2017	We conducted a pilot study on the feasibility of CD56-enriched donor cell infusion after post-transplantation cyclophosphamide (PTCy) for 10 patients with advanced myeloid malignancies undergoing haploidentical peripheral blood stem cell transplantation with cyclosporine alone as graft-versus-host disease (GVHD) prophylaxis and compared the outcome and immune reconstitution with a control group of 20 patients undergoing the same without CD56-enriched donor cell infusion.	Cyclophosphamide	110-126	neural cell adhesion molecule 1	Homo sapiens	49-53
28216407-3	2017	Previously we identified MDR-dependent cytoprotection from cyclophosphamide in mouse and human oocytes by use of MDR inhibitors.	Cyclophosphamide	59-75	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	25-28
27454143-7	2017	In the present study, the role of oral cyclophosphamide (100 mg per day for 15 consecutive days, every 30 for a total of six cycles) associated with anti-CD20 monoclonal antibody has been evaluated in 30 newly diagnosed SMZL patients, not fit for splenectomy or more toxic chemotherapic regimens.	Cyclophosphamide	39-55	keratin 20	Homo sapiens	154-158
28064347-9	2017	Finally, the combination of doxorubicin and cyclophosphamide significantly reduced hippocampal alpha7 nAChR mRNA expression.	Cyclophosphamide	44-60	cholinergic receptor nicotinic beta 1 subunit	Rattus norvegicus	102-107
28064347-10	2017	These results suggest that nicotine inhibits doxorubicin and cyclophosphamide-induced cognitive impairment via alpha7 nAChR and alpha4beta2 nAChR, and also enhances hippocampal neurogenesis.	Cyclophosphamide	61-77	cholinergic receptor nicotinic beta 1 subunit	Rattus norvegicus	118-123
28064347-10	2017	These results suggest that nicotine inhibits doxorubicin and cyclophosphamide-induced cognitive impairment via alpha7 nAChR and alpha4beta2 nAChR, and also enhances hippocampal neurogenesis.	Cyclophosphamide	61-77	cholinergic receptor nicotinic beta 1 subunit	Rattus norvegicus	140-145
28216407-3	2017	Previously we identified MDR-dependent cytoprotection from cyclophosphamide in mouse and human oocytes by use of MDR inhibitors.	Cyclophosphamide	59-75	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	113-116
28216407-4	2017	Here we use genetic deletions in MDR1a/b/BCRP of mice to test MDR function in ovarian somatic cells and find that mdr1a/b/bcrp-/- mice had significantly increased sensitivity to cyclophosphamide.	Cyclophosphamide	178-194	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	33-38
28216407-4	2017	Here we use genetic deletions in MDR1a/b/BCRP of mice to test MDR function in ovarian somatic cells and find that mdr1a/b/bcrp-/- mice had significantly increased sensitivity to cyclophosphamide.	Cyclophosphamide	178-194	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	33-36
28216407-4	2017	Here we use genetic deletions in MDR1a/b/BCRP of mice to test MDR function in ovarian somatic cells and find that mdr1a/b/bcrp-/- mice had significantly increased sensitivity to cyclophosphamide.	Cyclophosphamide	178-194	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	114-119
28216407-4	2017	Here we use genetic deletions in MDR1a/b/BCRP of mice to test MDR function in ovarian somatic cells and find that mdr1a/b/bcrp-/- mice had significantly increased sensitivity to cyclophosphamide.	Cyclophosphamide	178-194	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	122-126
28559645-7	2017	TREATMENT AND OUTCOME: The patient had a good initial response to a CHOP scheme (cyclophosphamide, doxorubicin, vincristine and prednisone) with filgrastim.	Cyclophosphamide	81-97	DNA damage inducible transcript 3	Homo sapiens	68-72
28087538-7	2017	Consistent with these findings, during cyclophosphamide-induced myeloablation or specific monocyte depletion, BCAP-/- mice replenished circulating monocytes and neutrophils earlier than WT mice.	Cyclophosphamide	39-55	phosphoinositide-3-kinase adaptor protein 1	Mus musculus	110-114
28300840-0	2017	Ganetespib synergizes with cyclophosphamide to improve survival of mice with autochthonous tumors in a mutant p53-dependent manner.	Cyclophosphamide	27-43	transformation related protein 53, pseudogene	Mus musculus	110-113
28087538-8	2017	During myeloid replenishment after cyclophosphamide-induced myeloablation, BCAP-/- mice had increased LSK proliferation and increased numbers of LSK and GMP cells compared with WT mice.	Cyclophosphamide	35-51	phosphoinositide-3-kinase adaptor protein 1	Mus musculus	75-79
28270133-1	2017	BACKGROUND: We previously showed that 1-methylnicotinamide (1-MNA) and its analog 1,4-dimethylpyridine (1,4-DMP) could inhibit the formation of lung metastases and enhance the efficacy of cyclophosphamide-based chemotherapy in the model of spontaneously metastasizing 4T1 mouse mammary gland tumors.	Cyclophosphamide	188-204	dentin matrix protein 1	Mus musculus	108-111
27928587-1	2017	Cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP)/CHOP-like chemotherapy has been mostly applied to patients with untreated peripheral T cell lymphoma (PTCL).	Cyclophosphamide	0-16	DNA damage inducible transcript 3	Homo sapiens	62-66
28035725-0	2017	Cyclophosphamide promotes breast cancer cell migration through CXCR4 and matrix metalloproteinases.	Cyclophosphamide	0-16	C-X-C motif chemokine receptor 4	Homo sapiens	63-68
28035725-3	2017	In this study, we investigate the effect of cyclophosphamide on cancer cell migration and its correlation to chemokine (C-X-C motif) receptor 4 (CXCR4), a biomarker for cancer metastasis.	Cyclophosphamide	44-60	C-X-C motif chemokine receptor 4	Homo sapiens	109-143
28035725-3	2017	In this study, we investigate the effect of cyclophosphamide on cancer cell migration and its correlation to chemokine (C-X-C motif) receptor 4 (CXCR4), a biomarker for cancer metastasis.	Cyclophosphamide	44-60	C-X-C motif chemokine receptor 4	Homo sapiens	145-150
28035725-5	2017	We found that the migration ability of MDA-MB-231 cells was enhanced with increasing concentrations of cyclophosphamide, which induced the cell-surface expression of CXCR4, but had no effect on the overall amount of CXCR4.	Cyclophosphamide	103-119	C-X-C motif chemokine receptor 4	Homo sapiens	166-171
28035725-7	2017	Studies on the mRNA expression profile of matrix metalloproteinases (MMPs) in MDA-MB-231 cells further indicate that MMP9 and MMP13 may be involved in the action of cyclophosphamide.	Cyclophosphamide	165-181	matrix metallopeptidase 9	Homo sapiens	117-121
28035725-7	2017	Studies on the mRNA expression profile of matrix metalloproteinases (MMPs) in MDA-MB-231 cells further indicate that MMP9 and MMP13 may be involved in the action of cyclophosphamide.	Cyclophosphamide	165-181	matrix metallopeptidase 13	Homo sapiens	126-131
28035725-8	2017	The protein expression of both MMP9 and MMP13 was increased in the presence of cyclophosphamide.	Cyclophosphamide	79-95	matrix metallopeptidase 9	Homo sapiens	31-35
28035725-8	2017	The protein expression of both MMP9 and MMP13 was increased in the presence of cyclophosphamide.	Cyclophosphamide	79-95	matrix metallopeptidase 13	Homo sapiens	40-45
28008595-8	2017	In the CY group, we observed increased BAX, BCLW, CFLIPL and CIAP1 and decreased BIK and BID gene expressions after transplantation.	Cyclophosphamide	7-9	CASP8 and FADD like apoptosis regulator	Homo sapiens	50-56
28008595-8	2017	In the CY group, we observed increased BAX, BCLW, CFLIPL and CIAP1 and decreased BIK and BID gene expressions after transplantation.	Cyclophosphamide	7-9	BCL2 associated X, apoptosis regulator	Homo sapiens	39-42
28008595-8	2017	In the CY group, we observed increased BAX, BCLW, CFLIPL and CIAP1 and decreased BIK and BID gene expressions after transplantation.	Cyclophosphamide	7-9	BCL2 like 2	Homo sapiens	44-48
28008595-8	2017	In the CY group, we observed increased BAX, BCLW, CFLIPL and CIAP1 and decreased BIK and BID gene expressions after transplantation.	Cyclophosphamide	7-9	baculoviral IAP repeat containing 2	Homo sapiens	61-66
28008595-8	2017	In the CY group, we observed increased BAX, BCLW, CFLIPL and CIAP1 and decreased BIK and BID gene expressions after transplantation.	Cyclophosphamide	7-9	BCL2 interacting killer	Homo sapiens	81-84
28008595-8	2017	In the CY group, we observed increased BAX, BCLW, CFLIPL and CIAP1 and decreased BIK and BID gene expressions after transplantation.	Cyclophosphamide	7-9	BH3 interacting domain death agonist	Homo sapiens	89-92
26968188-3	2017	The principal objective of this study was to determine whether the tumors" microenvironment expressions of CD11c and FOXP3 are predictive of clinical outcomes in diffuse large B-cell lymphoma (DLBCL) patients receiving treatment with rituximab, cyclophosphamide, anthracycline, vincristine, and prednisone (R-CHOP) combination chemotherapy.	Cyclophosphamide	245-261	integrin subunit alpha X	Homo sapiens	107-112
28132769-3	2017	Intravenous administration of cyclophosphamide (37.5 mg/kg body weight) resulted in immunosuppresion induction, as significant drops were observed in blood leukocytes and lymphocyte subset counts (CD2+, CD4+, CD8+, CD19+), lasting 3-10 days after its administration.	Cyclophosphamide	30-46	CD2 molecule	Homo sapiens	197-200
28132769-3	2017	Intravenous administration of cyclophosphamide (37.5 mg/kg body weight) resulted in immunosuppresion induction, as significant drops were observed in blood leukocytes and lymphocyte subset counts (CD2+, CD4+, CD8+, CD19+), lasting 3-10 days after its administration.	Cyclophosphamide	30-46	CD4 molecule	Homo sapiens	203-206
28132769-3	2017	Intravenous administration of cyclophosphamide (37.5 mg/kg body weight) resulted in immunosuppresion induction, as significant drops were observed in blood leukocytes and lymphocyte subset counts (CD2+, CD4+, CD8+, CD19+), lasting 3-10 days after its administration.	Cyclophosphamide	30-46	CD8a molecule	Homo sapiens	209-212
27729272-0	2017	Cyclophosphamide promotes the proliferation inhibition of mouse ovarian granulosa cells and premature ovarian failure by activating the lncRNA-Meg3-p53-p66Shc pathway.	Cyclophosphamide	0-16	maternally expressed 3	Mus musculus	143-147
28246585-6	2017	Doses of the chemotherapeutics [cisplatin (Cis), cyclophosphamide (CTX), doxorubicin (Dox) and paclitaxel (PTX)] to effectively reduce cell viability were calculated.	Cyclophosphamide	49-65	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	67-70
27988429-1	2017	OBJECTIVE: To compare the efficacy and safety of calcineurin inhibitors (CNIs) with cyclophosphamide (CTX) in the treatment of idiopathic membranous nephropathy (IMN).	Cyclophosphamide	84-100	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	102-105
27888016-8	2017	Furthermore, cyclophosphamide prevented the surge of IL-1beta, GVHD aggravation, and sudden death associated with prolonged administration of ixazomib after HSCT.	Cyclophosphamide	13-29	interleukin 1 beta	Mus musculus	53-61
28011377-0	2017	Possible involvement of Nrf2 and PPARgamma up-regulation in the protective effect of umbelliferone against cyclophosphamide-induced hepatotoxicity.	Cyclophosphamide	107-123	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	33-42
27816715-1	2017	A few recent studies investigated the prognostic impact of CD30 expression in diffuse large B-cell lymphoma (DLBCL) patients treated with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone.	Cyclophosphamide	149-165	TNF receptor superfamily member 8	Homo sapiens	59-63
28004985-0	2017	Cyclophosphamide enhances anti-tumor effects of a fibroblast activation protein alpha-based DNA vaccine in tumor-bearing mice with murine breast carcinoma.	Cyclophosphamide	0-16	fibroblast activation protein	Mus musculus	50-85
28004985-5	2017	This study evaluated the efficacy of a previously unreported CY combination strategy to enhance the limited anti-tumor effect of a DNA vaccine targeting FAPalpha.	Cyclophosphamide	61-63	fibroblast activation protein	Mus musculus	153-161
28004985-6	2017	The results suggested CY administration could promote the percentage of splenic CD8+ T cells and decrease the proportion of CD4 + CD25 + Foxp3+ Tregs in spleen.	Cyclophosphamide	22-24	CD4 antigen	Mus musculus	124-127
28004985-6	2017	The results suggested CY administration could promote the percentage of splenic CD8+ T cells and decrease the proportion of CD4 + CD25 + Foxp3+ Tregs in spleen.	Cyclophosphamide	22-24	interleukin 2 receptor, alpha chain	Mus musculus	130-134
28004985-6	2017	The results suggested CY administration could promote the percentage of splenic CD8+ T cells and decrease the proportion of CD4 + CD25 + Foxp3+ Tregs in spleen.	Cyclophosphamide	22-24	forkhead box P3	Mus musculus	137-142
28167568-17	2017	The Oncologist 2017;22:139-143Implications for Practice: This is the first study describing the role of doxorubicin and cyclophosphamide followed by paclitaxel and dual anti-HER2 therapy with trastuzumab and pertuzumab (ACTHP) in patients with early stage HER2-positive breast cancer.	Cyclophosphamide	120-136	erb-b2 receptor tyrosine kinase 2	Homo sapiens	256-260
28286727-2	2017	In cyclophosphamide-induced anemic rats, the treatment of combined flavonoids, or EPO, improved the levels of red blood cells, white blood cells, hemoglobin, and hematocrit.	Cyclophosphamide	3-19	erythropoietin	Rattus norvegicus	82-85
27729272-0	2017	Cyclophosphamide promotes the proliferation inhibition of mouse ovarian granulosa cells and premature ovarian failure by activating the lncRNA-Meg3-p53-p66Shc pathway.	Cyclophosphamide	0-16	transformation related protein 53, pseudogene	Mus musculus	148-151
27729272-0	2017	Cyclophosphamide promotes the proliferation inhibition of mouse ovarian granulosa cells and premature ovarian failure by activating the lncRNA-Meg3-p53-p66Shc pathway.	Cyclophosphamide	0-16	src homology 2 domain-containing transforming protein C1	Mus musculus	152-158
27729272-3	2017	The expressions of p53, p66Shc and p16 were significantly higher in OGCs of the cyclophosphamide treatment group.	Cyclophosphamide	80-96	transformation related protein 53, pseudogene	Mus musculus	19-22
27729272-3	2017	The expressions of p53, p66Shc and p16 were significantly higher in OGCs of the cyclophosphamide treatment group.	Cyclophosphamide	80-96	src homology 2 domain-containing transforming protein C1	Mus musculus	24-30
27729272-3	2017	The expressions of p53, p66Shc and p16 were significantly higher in OGCs of the cyclophosphamide treatment group.	Cyclophosphamide	80-96	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	35-38
27729272-6	2017	And, the expression of p53, p66Shc, p16 and cleaved caspase-3 in the OGCs of the cyclophosphamide treatment group significant increases.	Cyclophosphamide	81-97	transformation related protein 53, pseudogene	Mus musculus	23-26
27729272-6	2017	And, the expression of p53, p66Shc, p16 and cleaved caspase-3 in the OGCs of the cyclophosphamide treatment group significant increases.	Cyclophosphamide	81-97	src homology 2 domain-containing transforming protein C1	Mus musculus	28-34
27729272-6	2017	And, the expression of p53, p66Shc, p16 and cleaved caspase-3 in the OGCs of the cyclophosphamide treatment group significant increases.	Cyclophosphamide	81-97	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	36-39
27729272-7	2017	The Northern blot showed that the intensity of the lncRNA-Meg3 hybridization signal of the OGCs in the cyclophosphamide treatment group was significantly higher than that in the control group.	Cyclophosphamide	103-119	maternally expressed 3	Mus musculus	58-62
27729272-8	2017	ChIP results confirmed the significant increase in the obtained p66Shc promoter DNA fragment, which was enriched on p53 protein, in the OGCs treated with cyclophosphamide.	Cyclophosphamide	154-170	src homology 2 domain-containing transforming protein C1	Mus musculus	64-70
27729272-8	2017	ChIP results confirmed the significant increase in the obtained p66Shc promoter DNA fragment, which was enriched on p53 protein, in the OGCs treated with cyclophosphamide.	Cyclophosphamide	154-170	transformation related protein 53, pseudogene	Mus musculus	116-119
27729272-9	2017	When cyclophosphamide treatment was conducted after siRNA-Meg3 was used, the expression of endogenous lncRNA-Meg3, p53, p66Shc, p16 and cleaved caspase-3 was significantly lower than that in the siRNA-Mock control group.	Cyclophosphamide	5-21	maternally expressed 3	Mus musculus	58-62
27729272-9	2017	When cyclophosphamide treatment was conducted after siRNA-Meg3 was used, the expression of endogenous lncRNA-Meg3, p53, p66Shc, p16 and cleaved caspase-3 was significantly lower than that in the siRNA-Mock control group.	Cyclophosphamide	5-21	maternally expressed 3	Mus musculus	109-113
27729272-9	2017	When cyclophosphamide treatment was conducted after siRNA-Meg3 was used, the expression of endogenous lncRNA-Meg3, p53, p66Shc, p16 and cleaved caspase-3 was significantly lower than that in the siRNA-Mock control group.	Cyclophosphamide	5-21	transformation related protein 53, pseudogene	Mus musculus	115-118
27729272-9	2017	When cyclophosphamide treatment was conducted after siRNA-Meg3 was used, the expression of endogenous lncRNA-Meg3, p53, p66Shc, p16 and cleaved caspase-3 was significantly lower than that in the siRNA-Mock control group.	Cyclophosphamide	5-21	src homology 2 domain-containing transforming protein C1	Mus musculus	120-126
27729272-9	2017	When cyclophosphamide treatment was conducted after siRNA-Meg3 was used, the expression of endogenous lncRNA-Meg3, p53, p66Shc, p16 and cleaved caspase-3 was significantly lower than that in the siRNA-Mock control group.	Cyclophosphamide	5-21	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	128-131
27729272-10	2017	In summary, cyclophosphamide promotes the proliferation inhibition of mouse OGCs and premature ovarian failure by activating the lncRNA-Meg3-p53-p66Shc pathway.	Cyclophosphamide	12-28	maternally expressed 3	Mus musculus	136-140
27729272-10	2017	In summary, cyclophosphamide promotes the proliferation inhibition of mouse OGCs and premature ovarian failure by activating the lncRNA-Meg3-p53-p66Shc pathway.	Cyclophosphamide	12-28	transformation related protein 53, pseudogene	Mus musculus	141-144
27729272-10	2017	In summary, cyclophosphamide promotes the proliferation inhibition of mouse OGCs and premature ovarian failure by activating the lncRNA-Meg3-p53-p66Shc pathway.	Cyclophosphamide	12-28	src homology 2 domain-containing transforming protein C1	Mus musculus	145-151
27482943-0	2017	The Pharmacogenomic Association of Fcgamma Receptors and Cytochrome P450 Enzymes With Response to Rituximab or Cyclophosphamide Treatment in Antineutrophil Cytoplasmic Antibody-Associated Vasculitis.	Cyclophosphamide	111-127	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	57-72
28698872-1	2017	Cyclophosphamide- (CYP-) induced cystitis in the rat is a well-known model of bladder inflammation that leads to an overactive bladder, a process that appears to involve enhanced nitric oxide (NO) production.	Cyclophosphamide	0-16	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	19-22
26754092-0	2017	Docetaxel and cyclophosphamide as neoadjuvant chemotherapy in HER2-negative primary breast cancer.	Cyclophosphamide	14-30	erb-b2 receptor tyrosine kinase 2	Homo sapiens	62-66
26754092-1	2017	BACKGROUND: Docetaxel plus cyclophosphamide (TC) has recently been established as a standard adjuvant chemotherapy regimen for HER2-negative (HER2-) operable breast cancer.	Cyclophosphamide	27-43	erb-b2 receptor tyrosine kinase 2	Homo sapiens	127-131
26754092-1	2017	BACKGROUND: Docetaxel plus cyclophosphamide (TC) has recently been established as a standard adjuvant chemotherapy regimen for HER2-negative (HER2-) operable breast cancer.	Cyclophosphamide	27-43	erb-b2 receptor tyrosine kinase 2	Homo sapiens	142-146
27283030-4	2017	The patient was diagnosed with PEL-LL and treated with six cycles of rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP), which resulted in a complete remission.	Cyclophosphamide	84-100	DNA damage inducible transcript 3	Homo sapiens	148-152
27940354-0	2017	Pharmacogenetic association of MBL2 and CD95 polymorphisms with grade 3 infection following adjuvant therapy for breast cancer with doxorubicin and cyclophosphamide.	Cyclophosphamide	148-164	mannose binding lectin 2	Homo sapiens	31-35
29358974-5	2017	The level of the cytokine IL-10 in sera of cyclophosphamide-induced mice was decreased after pretreatments of polysaccharides.	Cyclophosphamide	43-59	interleukin 10	Mus musculus	26-31
27769927-6	2017	Additionally, all four LRP fractions exhibited protective effects against Cy-induced immunosuppression in mice by improving immune organs as well as stimulating the release of major cytokines TNF-alpha and INF-gamma.	Cyclophosphamide	74-76	low density lipoprotein receptor-related protein 1	Mus musculus	23-26
28626187-0	2017	Efficacy of Intravenous Cyclophosphamide Pulse Therapy for P-Glycoprotein-expressing B Cell-associated Active True Renal Lupus Vasculitis in Lupus Nephritis.	Cyclophosphamide	24-40	ATP binding cassette subfamily B member 1	Homo sapiens	59-73
29279550-7	2017	Patients with ALK-positive ALCL are usually treated with anthracycline-based regimens, such as combination cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) or CHOEP (CHOP plus etoposide), which provide a favorable prognosis, except in patients with multiple International Prognostic Index factors.	Cyclophosphamide	107-123	ALK receptor tyrosine kinase	Homo sapiens	14-17
29081796-2	2017	Examples of CYP2B6"s impacts include its linkage to mortality during cyclophosphamide therapy and its role in determining hepatotoxicity and CNS toxicity during efavirenz therapy for HIV infection.	Cyclophosphamide	69-85	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	12-18
27416845-9	2017	Our patient was prescribed methylprednisolone (MP) and cyclophosphamide (CTX).	Cyclophosphamide	55-71	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	73-76
27940354-0	2017	Pharmacogenetic association of MBL2 and CD95 polymorphisms with grade 3 infection following adjuvant therapy for breast cancer with doxorubicin and cyclophosphamide.	Cyclophosphamide	148-164	Fas cell surface death receptor	Homo sapiens	40-44
28381691-5	2017	Recombinant FVIIa was effective for management of his bleeding; in addition, FVIII inhibitor reduction and FVIII:C recovery, in parallel with improvement of the skin lesions, were achieved by administering prednisolone and cyclophosphamide.	Cyclophosphamide	223-239	coagulation factor VIII	Homo sapiens	77-82
28381691-5	2017	Recombinant FVIIa was effective for management of his bleeding; in addition, FVIII inhibitor reduction and FVIII:C recovery, in parallel with improvement of the skin lesions, were achieved by administering prednisolone and cyclophosphamide.	Cyclophosphamide	223-239	coagulation factor VIII	Homo sapiens	107-112
28978846-6	2017	From recent prospective trials, conventional R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone) regimen, which is the current standard regimen for DLBCL, has been acknowledged as a well-established regimen for DLBCL.	Cyclophosphamide	64-80	DNA damage inducible transcript 3	Homo sapiens	47-51
30263469-6	2016	Oral administration of WGE for 28 days recovered cyclophosphamide (CY)-induced suppression of the immune system in mice via the MKK4-JNK pathway.	Cyclophosphamide	49-65	mitogen-activated protein kinase kinase 4	Mus musculus	128-132
30263469-6	2016	Oral administration of WGE for 28 days recovered cyclophosphamide (CY)-induced suppression of the immune system in mice via the MKK4-JNK pathway.	Cyclophosphamide	49-65	mitogen-activated protein kinase 8	Mus musculus	133-136
30263469-6	2016	Oral administration of WGE for 28 days recovered cyclophosphamide (CY)-induced suppression of the immune system in mice via the MKK4-JNK pathway.	Cyclophosphamide	67-69	mitogen-activated protein kinase kinase 4	Mus musculus	128-132
30263469-6	2016	Oral administration of WGE for 28 days recovered cyclophosphamide (CY)-induced suppression of the immune system in mice via the MKK4-JNK pathway.	Cyclophosphamide	67-69	mitogen-activated protein kinase 8	Mus musculus	133-136
28032863-9	2016	Notably, TERT-positive LCLs treated with BIBR in combination with fludarabine or cyclophosphamide showed a significant increase in the number of apoptotic cells with respect to those treated with chemotherapeutic agents alone.	Cyclophosphamide	81-97	telomerase reverse transcriptase	Homo sapiens	9-13
27995963-8	2016	Histone deacetylase (HDAC) inhibitor, suberoylanilide hydroxamic acid (SAHA), restored Ogg1 expression in cells treated with acrolein and mice treated with cyclophosphamide superior to the standard of care, mesna or nicotinamide-induced DNA demethylation.	Cyclophosphamide	156-172	8-oxoguanine DNA-glycosylase 1	Mus musculus	87-91
27991432-5	2016	The concommitant use of omeprazole/esomeprazole, therefore, could have critical clinical relevance in individualizing medications metabolized primarily by CYP2C19 such as PPI, clopidogrel, phenytoin, cyclophosphamide, thalidomide, citalopram, clonazepam, diazepam, proguanil, tivantinib etc.	Cyclophosphamide	200-216	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	155-162
27997541-8	2016	Furthermore, we identified the satiety-signaling neuropeptide Allatostatin A (AstA) as a key mediator that conveys inhibitory input onto PAM-gamma3.	Cyclophosphamide	78-82	Allatostatin A	Drosophila melanogaster	62-76
27924862-7	2016	Furthermore, both cyclophosphamide and ASC treatment significantly decreased the ratio of Th1/Th2 compared with the saline-treatment.	Cyclophosphamide	18-34	negative elongation factor complex member C/D, Th1l	Mus musculus	90-93
27737889-2	2016	It is well documented that ABC-DLBCL cases have a significantly poorer survival response than GCB-DLBCLs in both the CHOP (cyclophosphamide, vincristine, doxorubicin, and prednisone) and the rituximab (R)-CHOP eras.	Cyclophosphamide	123-139	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	27-30
28101033-2	2016	Here, we present the case of a 33-year-old female patient with extensive metastatic ER+/PR+/HER2- mucinous adenocarcinoma of the breast, who was started on doxorubicin/cyclophosphamide therapy after progressing on paclitaxel and ovarian suppressor goserelin with aromatase inhibitor exemestane.	Cyclophosphamide	168-184	erb-b2 receptor tyrosine kinase 2	Homo sapiens	92-96
27924862-7	2016	Furthermore, both cyclophosphamide and ASC treatment significantly decreased the ratio of Th1/Th2 compared with the saline-treatment.	Cyclophosphamide	18-34	heart and neural crest derivatives expressed 2	Mus musculus	94-97
27924862-10	2016	Thus, treatment with cyclophosphamide or ASC can change miRNAs and decrease miR-96-5p and miR-182-5p expression, as well as decreasing the CD138 proportion and the Th1/Th2 ratio, which might be involved in the therapeutic mechanism.	Cyclophosphamide	21-37	microRNA 182	Mus musculus	90-97
27924862-10	2016	Thus, treatment with cyclophosphamide or ASC can change miRNAs and decrease miR-96-5p and miR-182-5p expression, as well as decreasing the CD138 proportion and the Th1/Th2 ratio, which might be involved in the therapeutic mechanism.	Cyclophosphamide	21-37	syndecan 1	Mus musculus	139-144
27924862-10	2016	Thus, treatment with cyclophosphamide or ASC can change miRNAs and decrease miR-96-5p and miR-182-5p expression, as well as decreasing the CD138 proportion and the Th1/Th2 ratio, which might be involved in the therapeutic mechanism.	Cyclophosphamide	21-37	negative elongation factor complex member C/D, Th1l	Mus musculus	164-167
27924862-10	2016	Thus, treatment with cyclophosphamide or ASC can change miRNAs and decrease miR-96-5p and miR-182-5p expression, as well as decreasing the CD138 proportion and the Th1/Th2 ratio, which might be involved in the therapeutic mechanism.	Cyclophosphamide	21-37	heart and neural crest derivatives expressed 2	Mus musculus	168-171
27572525-3	2016	METHOD OF STUDY: This study aims to investigate the effect of LBP on spermatogenesis of rats with impaired reproduction system induced by cyclophosphamide.	Cyclophosphamide	138-154	lipopolysaccharide binding protein	Rattus norvegicus	62-65
27333332-8	2016	Patients with MPO-ANCA-positive GPA frequently had limited disease without severe organ involvement, had a high prevalence of subglottic stenosis, and had less need for aggressive immunosuppressive therapy (cyclophosphamide/rituximab).	Cyclophosphamide	207-223	myeloperoxidase	Homo sapiens	14-17
27234646-0	2016	Cyclophosphamide-induced Down-Regulation of Uroplakin II in the Mouse Urinary Bladder Epithelium is Prevented by S-Allyl Cysteine.	Cyclophosphamide	0-16	uroplakin 2	Mus musculus	44-56
27856111-10	2016	All the above results together proposed that, DMSE sensitized tumor cells to cyclophosphamide therapy through ROS-induced p53 activation and mitochondria-mediated caspase dependent apoptosis.	Cyclophosphamide	77-93	transformation related protein 53, pseudogene	Mus musculus	122-125
27545090-0	2016	Improvement of anti-tumor immunity of fibroblast activation protein alpha based vaccines by combination with cyclophosphamide in a murine model of breast cancer.	Cyclophosphamide	109-125	fibroblast activation protein	Mus musculus	38-73
27545090-7	2016	Furthermore, CAFs, stromal factors and immunosuppressive factors such as IL-10 and Tregs were also markedly decreased by the CY combination.	Cyclophosphamide	125-127	interleukin 10	Mus musculus	73-78
28174484-1	2016	OBJECTIVE: A previous study demonstrated that non-anthracycline-containing docetaxel plus cyclophosphamide (TC) regimen was inferior to docetaxel, anthracycline and cyclophosphamide (TAC) in neoadjuvant treatment of triple-negative breast cancer (TNBC) and human epidermal growth factor receptor-2-(HER2)-positive breast cancer in a short-term follow-up.	Cyclophosphamide	90-106	erb-b2 receptor tyrosine kinase 2	Homo sapiens	263-297
28174484-1	2016	OBJECTIVE: A previous study demonstrated that non-anthracycline-containing docetaxel plus cyclophosphamide (TC) regimen was inferior to docetaxel, anthracycline and cyclophosphamide (TAC) in neoadjuvant treatment of triple-negative breast cancer (TNBC) and human epidermal growth factor receptor-2-(HER2)-positive breast cancer in a short-term follow-up.	Cyclophosphamide	90-106	erb-b2 receptor tyrosine kinase 2	Homo sapiens	299-303
27812954-6	2016	Targeting mTORC1 over-activation with N-acetylcysteine, rapamycin, and rapalogs provides an opportunity to supplant current therapies with severe side effect profiles such as prednisone or cyclophosphamide.	Cyclophosphamide	189-205	CREB regulated transcription coactivator 1	Mus musculus	10-16
28154512-11	2016	In the additive genetic model results for each IL10 polymorphism, the rs1800871 and rs1800872 polymorphisms represented a marginal association with OS (p = 0.09 and p = 0.06) and PFS (p = 0.05 and p = 0.08) in B-cell lymphoma patients treated with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP).	Cyclophosphamide	263-279	interleukin 10	Homo sapiens	47-51
27709450-1	2016	The study was aimed to explore the efficacy and safety of allo-HSCT with high-dose cyclophosphamide-induced immune tolerance for SAA.	Cyclophosphamide	83-99	serum amyloid A1 cluster	Homo sapiens	129-132
27709450-11	2016	Reduced-intensity allo-HSCT with high-dose cyclophosphamide-induced immune tolerance treatment is effective for SAA and can be the key technology extensively used in clinic, but its efficacy needs to be confirmed further with prospective randomized study with increased sample size.	Cyclophosphamide	43-59	serum amyloid A1 cluster	Homo sapiens	112-115
27640002-9	2016	There was a significant difference of WBC nadir in favor of the cyclophosphamide regimen with 2.5 g/m2 (0.8 vs. 0.3 Gpt/L, p = 0.021), and neutropenic fever was more often observed in patients who received 4 g/m2 cyclophosphamide (34 vs. 15 %, p = 0.078).	Cyclophosphamide	64-80	glutamic--pyruvic transaminase	Homo sapiens	116-119
28030899-8	2016	In univariate analysis, the rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) regimen resulted in a better PFS than the cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) regimen (88.9% vs. 50.0%; p = 0.053).	Cyclophosphamide	39-55	DNA damage inducible transcript 3	Homo sapiens	209-213
28024499-1	2016	OBJECTIVE: To investigate the efficacy and safety of haploidentical allo-HSCT in combination of reduced intensity preconditioning combined with cyclophosphamid (CTX)-induced immune tolerance after transplanitation for treatment of severe aplastic anemia (SAA).	Cyclophosphamide	144-159	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	161-164
28123833-3	2016	The protein expression of PAR2 was amplified in rats with cystitis by inducing it with systemic administration of cyclophosphamide (CYP) as compared with control rats.	Cyclophosphamide	114-130	F2R like trypsin receptor 1	Rattus norvegicus	26-30
27633142-0	2016	Activation of Nrf2-ARE signaling mitigates cyclophosphamide-induced myelosuppression.	Cyclophosphamide	43-59	nuclear factor, erythroid derived 2, like 2	Mus musculus	14-18
27633142-4	2016	Single dosage of cyclophosphamide induced significantly severer acute myelosuppression in Nrf2-/- mice than in wild type mice.	Cyclophosphamide	17-33	nuclear factor, erythroid derived 2, like 2	Mus musculus	90-94
27633142-5	2016	Furthermore, Nrf2-/- mice exhibited greater loss of peripheral blood nucleated cells and recovered slower from myelosuppression nadir upon multiple consecutive dosages of cyclophosphamide than wild type mice did.	Cyclophosphamide	171-187	nuclear factor, erythroid derived 2, like 2	Mus musculus	13-17
27633142-7	2016	More importantly, activation of Nrf2 signaling by CDDO-Me significantly alleviated cyclophosphamide-induced myelosuppression, while this alleviation was diminished in Nrf2-/- mice.	Cyclophosphamide	83-99	nuclear factor, erythroid derived 2, like 2	Mus musculus	32-36
27633142-8	2016	In conclusion, the present study shows that Nrf2 plays a protective role in cyclophosphamide-induced myelosuppression and activation of Nrf2 is a promising strategy to prevent or treat chemotherapy-induced myelosuppression.	Cyclophosphamide	76-92	nuclear factor, erythroid derived 2, like 2	Mus musculus	44-48
27680685-0	2016	CCR2 Influences T Regulatory Cell Migration to Tumors and Serves as a Biomarker of Cyclophosphamide Sensitivity.	Cyclophosphamide	83-99	C-C motif chemokine receptor 2	Homo sapiens	0-4
27680685-5	2016	Notably, in mouse models, low-dose cyclophosphamide treatment preferentially depleted CCR2+ Treg, enhancing priming of tumor-specific CD8+ T cells.	Cyclophosphamide	35-51	chemokine (C-C motif) receptor 2	Mus musculus	86-90
27680685-7	2016	Our results define a novel subset of CCR2+ Treg involved in tumoral immune escape, and they offer evidence that this Treg subset may be preferentially eradicated by low-dose cyclophosphamide treatment.	Cyclophosphamide	174-190	C-C motif chemokine receptor 2	Homo sapiens	37-41
27852964-9	2016	We found that glial fibrillary acidic protein rather than OX42/Iba1 or P-P38 was significantly increased in the spinal cord of cyclophosphamide-induced cystitis.	Cyclophosphamide	127-143	allograft inflammatory factor 1	Rattus norvegicus	63-67
27852964-11	2016	Furthermore, we found that spinal IL-1beta was dramatically increased in cyclophosphamide-induced cystitis, and activated astrocytes were the only source of IL-1beta release, which contributed to allodynia in cystitis rats.	Cyclophosphamide	73-89	interleukin 1 beta	Rattus norvegicus	34-42
27852964-12	2016	Besides, spinal P-NR1 was statistically increased in cyclophosphamide-induced cystitis and only localized in IL-1RI positive neurons in spinal dorsal horn.	Cyclophosphamide	53-69	glutamate ionotropic receptor NMDA type subunit 1	Rattus norvegicus	18-21
27061017-5	2016	After C57BL/6 mice were treated with intermediate- and high-dose (25/50 mg/kg) cyclophosphamide (CTX) for 10 days, the body-weight, changes in thymus and spleen, number of white blood cells (WBCs), red blood cells (RBCs), and platelets (PLTs) and changes in bone marrow in the mice were systematically evaluated at the next 2, 7 and 14 days.	Cyclophosphamide	79-95	V-set and immunoglobulin domain containing 2	Mus musculus	97-100
27802299-5	2016	The data of the present study showed that treatment of male mice with cyclophosphamide (2.5 mg/Kg BW) as repeated dose for 28 consecutive days was found to induce hepatotoxicity through the elevation in the activities of AST, ALT, and ALP.	Cyclophosphamide	70-86	glutamic pyruvic transaminase, soluble	Mus musculus	226-229
27521770-1	2016	OBJECTIVE: To assess fertility counseling and preservation practices among children, adolescents, and young adults with rheumatic diseases undergoing cyclophosphamide (CTX) treatment.	Cyclophosphamide	150-166	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	168-171
27802299-5	2016	The data of the present study showed that treatment of male mice with cyclophosphamide (2.5 mg/Kg BW) as repeated dose for 28 consecutive days was found to induce hepatotoxicity through the elevation in the activities of AST, ALT, and ALP.	Cyclophosphamide	70-86	alopecia, recessive	Mus musculus	235-238
27780878-3	2016	RESULTS: The expression of p-mTOR, mTOR-mediated phosphorylation of p70 ribosomal S6 protein kinase 1 (p-S6K1), 4 E-binding protein 4 (p-4 E-BP1), as well as phosphatidylinositide 3-kinase (p-PI3K) pathway were amplified in cyclophosphamide rats as compared with control rats.	Cyclophosphamide	224-240	mechanistic target of rapamycin kinase	Rattus norvegicus	35-39
27280953-5	2016	And additionally, PCs-1 and PCs-2 were also found to reverse the surface particle size and roughness decrease of peritoneal macrophages isolated from cyclophosphamide induced immunosuppressive mice, suggesting the activation effects of PCs-1 and PCs-2 on immunosuppressive macrophages.	Cyclophosphamide	150-166	polar cataract and small eyes 1	Mus musculus	18-23
27280953-5	2016	And additionally, PCs-1 and PCs-2 were also found to reverse the surface particle size and roughness decrease of peritoneal macrophages isolated from cyclophosphamide induced immunosuppressive mice, suggesting the activation effects of PCs-1 and PCs-2 on immunosuppressive macrophages.	Cyclophosphamide	150-166	dominant cataract 4	Mus musculus	28-33
27760335-3	2016	(2016) identified two bacterial species potentiating the anti-tumor effect of cyclophosphamide that are kept in check by the sensor NOD2.	Cyclophosphamide	78-94	nucleotide binding oligomerization domain containing 2	Homo sapiens	132-136
27602952-3	2016	The CEBPA gene sequence was analyzed in 118 ovarian cancer patients (44 platinum/cyclophosphamide (PC)-treated and 74 taxane/platinum (TP)-treated), both in tumors and blood samples, and in blood from 236 healthy women, using PCR-Sanger sequencing and Real-Time quantitative PCR (qPCR)-based genotyping methods, respectively.	Cyclophosphamide	81-97	CCAAT enhancer binding protein alpha	Homo sapiens	4-9
27980738-2	2016	Clinicians should be aware of this differential diagnosis because CD8+ T-cell lymphoma prognosis can be remarkably favorable upon oral treatment with cyclophosphamide.	Cyclophosphamide	150-166	CD8a molecule	Homo sapiens	66-69
27470289-0	2016	Improved Outcome of Refractory/Relapsed Acute Myeloid Leukemia after Post-Transplantation Cyclophosphamide-Based Haploidentical Transplantation with Myeloablative Conditioning and Early Prophylactic Granulocyte Colony-Stimulating Factor-Mobilized Donor Lymphocyte Infusions.	Cyclophosphamide	90-106	colony stimulating factor 3	Homo sapiens	199-236
27780878-6	2016	Inhibition of either mTOR or PI3K blunted the enhanced spinal substance P and calcitonin gene-related peptide in cyclophosphamide rats.	Cyclophosphamide	113-129	mechanistic target of rapamycin kinase	Rattus norvegicus	21-25
27780878-7	2016	CONCLUSIONS: The data for the first time revealed specific signaling pathways leading to cyclophosphamide-induced bladder hyperactivity and pain, including the activation of mTOR and PI3K.	Cyclophosphamide	89-105	mechanistic target of rapamycin kinase	Rattus norvegicus	174-178
27084027-1	2016	Rituximab is a chimeric anti-CD20 monoclonal antibody that is used as an immunosuppressive agent in cyclophosphamide refractory lupus nephritis to induce remission.	Cyclophosphamide	100-116	keratin 20	Homo sapiens	29-33
27562137-0	2016	The metronomic therapy with prednisone, etoposide, and cyclophosphamide reduces the serum levels of VEGF and circulating endothelial cells and improves response rates and progression-free survival in patients with relapsed or refractory non-Hodgkin"s lymphoma.	Cyclophosphamide	55-71	vascular endothelial growth factor A	Homo sapiens	100-104
27562137-10	2016	CONCLUSION: Metronomic chemotherapy with prednisone, etoposide, and cyclophosphamide resulted in higher ORR and DCR, fewer adverse effects, and longer PFS in patients with relapsed or refractory NHL, with significant reduction in serum CECs and VEGF levels.	Cyclophosphamide	68-84	vascular endothelial growth factor A	Homo sapiens	245-249
27689358-3	2016	We show that specific thermogenetic activation of peptidergic Allatostatin A (AstA)-expressing PLP neurons and enteroendocrine cells reduces feeding and promotes sleep in the fruit fly Drosophila.	Cyclophosphamide	78-82	Allatostatin A	Drosophila melanogaster	62-76
27689358-3	2016	We show that specific thermogenetic activation of peptidergic Allatostatin A (AstA)-expressing PLP neurons and enteroendocrine cells reduces feeding and promotes sleep in the fruit fly Drosophila.	Cyclophosphamide	78-82	Pericentrin-like protein	Drosophila melanogaster	95-98
27381428-9	2016	Similar treatment of HoCl3 with 1a or 1b and K2COT as three-component reactions in a 1 : 1 : 1 molar ratio afforded the solvated half-sandwich complexes (COT)Ho(c-C3H5-C[triple bond, length as m-dash]C-C(NR)2)(THF) (13: R = (i)Pr; 14: R = Cy).	Cyclophosphamide	239-241	mitogen-activated protein kinase kinase kinase 8	Homo sapiens	47-50
27494852-8	2016	Finally, by analyzing overall and progression-free survival in DLBCL patients that underwent rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone chemotherapy, low levels of PATZ1 were significantly associated to a worst outcome and demonstrated an independent prognostic factor in multivariate analysis, including known prognostic factors of DLBCL, IPI score and cell of origin (GCB/non-GCB).	Cyclophosphamide	108-124	POZ/BTB and AT hook containing zinc finger 1	Homo sapiens	195-200
27605551-3	2016	Patients who received Cy/Flu lymphodepletion had increased CAR-T cell expansion and persistence, and higher response rates [50% complete remission (CR), 72% overall response rate (ORR)] than patients who received Cy-based lymphodepletion without Flu (8% CR, 50% ORR).	Cyclophosphamide	22-24	nuclear receptor subfamily 1 group I member 3	Homo sapiens	59-62
27486759-5	2016	The complete eradication of a significant number of tumor lesions occurred only in mice receiving cyclophosphamide shortly before immunotherapy, and was associated with increased serum anti HER-2/p185 antibodies and tumor leukocyte infiltration.	Cyclophosphamide	98-114	cullin 7	Mus musculus	196-200
27609734-10	2016	Steroids and cyclophosphamide were added to suppress the fVIII inhibitors.	Cyclophosphamide	13-29	coagulation factor VIII	Homo sapiens	57-62
27605551-5	2016	Cy/Flu minimized the effects of an immune response to the murine single-chain variable fragment component of the CAR, which limited CAR-T cell expansion and clinical efficacy in patients who received Cy-based lymphodepletion without Flu.	Cyclophosphamide	0-2	nuclear receptor subfamily 1, group I, member 3	Mus musculus	113-116
27605551-5	2016	Cy/Flu minimized the effects of an immune response to the murine single-chain variable fragment component of the CAR, which limited CAR-T cell expansion and clinical efficacy in patients who received Cy-based lymphodepletion without Flu.	Cyclophosphamide	0-2	nuclear receptor subfamily 1, group I, member 3	Mus musculus	132-135
27605551-5	2016	Cy/Flu minimized the effects of an immune response to the murine single-chain variable fragment component of the CAR, which limited CAR-T cell expansion and clinical efficacy in patients who received Cy-based lymphodepletion without Flu.	Cyclophosphamide	200-202	nuclear receptor subfamily 1, group I, member 3	Mus musculus	113-116
27605551-5	2016	Cy/Flu minimized the effects of an immune response to the murine single-chain variable fragment component of the CAR, which limited CAR-T cell expansion and clinical efficacy in patients who received Cy-based lymphodepletion without Flu.	Cyclophosphamide	200-202	nuclear receptor subfamily 1, group I, member 3	Mus musculus	132-135
26590598-0	2016	Cyclophosphamide-responsive Lgi1-related limbic encephalitis with basal ganglia hypermetabolism.	Cyclophosphamide	0-16	leucine rich glioma inactivated 1	Homo sapiens	28-32
27709010-5	2016	CYP2B6 has been demonstrated to play a role in the metabolism of 2%-10% of clinically used drugs including widely used antineoplastic agents cyclophosphamide and ifosfamide, anesthetics propofol and ketamine, synthetic opioids pethidine and methadone, and the antiretrovirals nevirapine and efavirenz, among others.	Cyclophosphamide	141-157	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	0-6
27382104-1	2016	PURPOSE: Utility of combined-modality therapy for patients with limited-stage diffuse large B-cell lymphoma (DLBCL) was shown in the Southwest Oncology Group (SWOG) S8736 study, where three cycles of CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisone) plus radiotherapy (CHOP3RT) improved 5-year progression-free (PFS) and overall survival (OS) compared with eight cycles of CHOP (CHOP8).	Cyclophosphamide	206-222	DNA damage inducible transcript 3	Homo sapiens	200-204
27486759-5	2016	The complete eradication of a significant number of tumor lesions occurred only in mice receiving cyclophosphamide shortly before immunotherapy, and was associated with increased serum anti HER-2/p185 antibodies and tumor leukocyte infiltration.	Cyclophosphamide	98-114	erb-b2 receptor tyrosine kinase 2	Mus musculus	190-195
27795636-4	2016	Allograft biopsy revealed crescentic IgAN, which was successfully treated with intravenous steroids and cyclophosphamide.	Cyclophosphamide	104-120	IGAN1	Homo sapiens	37-41
27485835-6	2016	The present study used a cyclophosphamide-induced mouse model of POF.	Cyclophosphamide	25-41	POF1B actin binding protein	Homo sapiens	65-68
27485835-12	2016	Therefore, telocytes may serve as a potential novel marker of POF induced by cyclophosphamide.	Cyclophosphamide	77-93	POF1B actin binding protein	Homo sapiens	62-65
27515027-5	2016	In LLC tumors, where CPA/6d treatment is shown to be anti-angiogenic, CPA/6d suppressed VEGFA target genes and down regulated cell adhesion and leukocyte transendothelial migration genes.	Cyclophosphamide	21-24	vascular endothelial growth factor A	Mus musculus	88-93
27498213-7	2016	However, heterologous vaccination in combination with a low-dose of cyclophosphamide (CY), which was reported to reduce IL-10 production and promote a shift from immunosuppression to immunopotentiation, resulted in enhanced effects in terms of numbers of effector T cells and tumor growth inhibition rates, compared to the CY alone or DNA alone group.	Cyclophosphamide	86-88	interleukin 10	Mus musculus	120-125
27498213-0	2016	Enhancement of fibroblast activation protein alpha-based vaccines and adenovirus boost immunity by cyclophosphamide through inhibiting IL-10 expression in 4T1 tumor bearing mice.	Cyclophosphamide	99-115	interleukin 10	Mus musculus	135-140
27498213-7	2016	However, heterologous vaccination in combination with a low-dose of cyclophosphamide (CY), which was reported to reduce IL-10 production and promote a shift from immunosuppression to immunopotentiation, resulted in enhanced effects in terms of numbers of effector T cells and tumor growth inhibition rates, compared to the CY alone or DNA alone group.	Cyclophosphamide	68-84	interleukin 10	Mus musculus	120-125
27259880-1	2016	We have determined if cyclophosphamide (CYP)-induced cystitis produces additional changes in growth factor/receptors expression in the urinary bladder (urothelium, detrusor) and lumbosacral (L6-S1) dorsal root ganglia (DRG) in a transgenic mouse model with chronic urothelial overexpression of NGF (NGF-OE).	Cyclophosphamide	22-38	nerve growth factor	Mus musculus	294-297
27071778-5	2016	Both genetic and pharmacological CXCR4 inhibition significantly reduced B-ALL cell migration to CXCL12 gradients and beneath BMSC, and restored drug sensitivity to dexamethasone, vincristine and cyclophosphamide.	Cyclophosphamide	195-211	chemokine (C-X-C motif) receptor 4	Mus musculus	33-38
27259880-1	2016	We have determined if cyclophosphamide (CYP)-induced cystitis produces additional changes in growth factor/receptors expression in the urinary bladder (urothelium, detrusor) and lumbosacral (L6-S1) dorsal root ganglia (DRG) in a transgenic mouse model with chronic urothelial overexpression of NGF (NGF-OE).	Cyclophosphamide	22-38	nerve growth factor	Mus musculus	299-305
27468286-9	2016	Moreover, adoptive CD11b(+) myeloid cell transfer rescued cyclophosphamide immunosuppressed mice from lethal A. fumigatus infection but not cortisone and cyclophosphamide immunosuppressed mice.	Cyclophosphamide	58-74	integrin subunit alpha M	Homo sapiens	19-24
27184798-7	2016	In early TNBC, combined HIF1alpha and CAIX protein expression may serve as an unfavorable prognostic indicator particularly in patients treated with cyclophosphamide-based chemotherapy or radiotherapy as well as those with basal phenotype of breast cancer.	Cyclophosphamide	149-165	hypoxia inducible factor 1 subunit alpha	Homo sapiens	24-33
27184798-7	2016	In early TNBC, combined HIF1alpha and CAIX protein expression may serve as an unfavorable prognostic indicator particularly in patients treated with cyclophosphamide-based chemotherapy or radiotherapy as well as those with basal phenotype of breast cancer.	Cyclophosphamide	149-165	carbonic anhydrase 9	Homo sapiens	38-42
27400751-4	2016	RESULTS: We found from Cox hazard models, logrank test and Wilcoxon test that osteopontin exon 4 was associated with a favorable response to tamoxifen, but a poor response to chemotherapy with CMF (cyclophosphamide, methotrexate, fluorouracil).	Cyclophosphamide	198-214	secreted phosphoprotein 1	Homo sapiens	78-89
27388155-0	2016	CYP2B6rs2279343 Is Associated with Improved Survival of Pediatric Rhabdomyosarcoma Treated with Cyclophosphamide.	Cyclophosphamide	96-112	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	0-6
27388155-3	2016	CYP2B6 is a highly polymorphic drug metabolizing enzyme involved in CPA bioactivation.	Cyclophosphamide	68-71	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	0-6
27388155-5	2016	METHODS: We genotyped CYP2B6SNPs rs2279343, rs3745274, and rs3211371 by restriction fragment polymorphism (RFLP) after PCR amplification in a cohort of 73 pediatric RMS patients treated with CPA-based first line treatment.	Cyclophosphamide	191-194	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	22-28
27388155-10	2016	CONCLUSION: Our results demonstrated that CYP2B6 rs2279343 may predict EFS in RMS patients and warrants future studies to clarify the pharmacogenetics of CPA in pediatrics.	Cyclophosphamide	154-157	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	42-48
27310207-4	2016	Punicalagin also attenuated the histopathological liver tissue damage, and decreased cyclooxygenase-2 expression in liver of rats received cyclophosphamide in a dose-dependent manner.	Cyclophosphamide	139-155	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	85-101
27512188-8	2016	This was restricted to Dsg1 for the azathioprine group and both Dsg3 and Dsg1 levels for the cyclophosphamide group.	Cyclophosphamide	93-109	desmoglein 1	Homo sapiens	73-77
27347041-5	2016	In the present study, a mouse model of POF was generated using cyclophosphamide.	Cyclophosphamide	63-79	POF1B actin binding protein	Homo sapiens	39-42
27362808-4	2016	Here we show a strong correlation between miR-205 expression and chemosensitivtiy to TAC (docetaxol, doxorubicin plus cyclophosphamide), a widely-used neoadjuvant chemotherapy (NAC) regimen, for breast cancer patients.	Cyclophosphamide	118-134	microRNA 205	Homo sapiens	42-49
26526985-5	2016	We report the case of a patient who began with clinical manifestations of tuberous sclerosis complex (TSC) 30 years after the onset of SLE with severe renal disease (tipe IV nephritis) who improved after treatment with iv pulses of cyclophosphamide.	Cyclophosphamide	232-248	TSC complex subunit 1	Homo sapiens	102-105
27006168-13	2016	Furthermore, blocking aberrant TGF-beta signalling in cyclophosphamide-induced cystitis with TbetaR-1 inhibition decreased afferent nerve hyperexcitability with a concomitant decrease in urothelial ATP release.	Cyclophosphamide	54-70	transforming growth factor beta 1	Homo sapiens	31-39
27315798-0	2016	Intrathecal administration of TRPA1 antagonists attenuate cyclophosphamide-induced cystitis in rats with hyper-reflexia micturition.	Cyclophosphamide	58-74	transient receptor potential cation channel, subfamily A, member 1	Rattus norvegicus	30-35
27356598-2	2016	In this review, we present different treatment methods (e.g. cyclophosphamide, rituximab, plasma exchange) used for remission induction and maintenance in renal AAV.	Cyclophosphamide	61-77	adeno-associated virus integration site 1	Homo sapiens	161-164
27382316-0	2016	Expression of CD40 is a positive prognostic factor of diffuse large B-cell lymphoma treated with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone).	Cyclophosphamide	116-132	CD40 molecule	Homo sapiens	14-18
27382316-1	2016	OBJECTIVES: The objective of this study was to investigate the expression level of CD40 and its role in the prognosis of patients with diffuse large B-cell lymphoma (DLBCL) who were treated with rituximab-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone).	Cyclophosphamide	222-238	CD40 molecule	Homo sapiens	83-87
26621483-8	2016	CONCLUSIONS: Patients with PR3-AAV respond better to RTX than to CYC/AZA.	Cyclophosphamide	65-68	proteinase 3	Homo sapiens	27-30
27462230-10	2016	Two years after, the patient suffered a relapse and underwent 6 cycles of CHOP-R (cyclophosphamide, hydroxydaunomycin, oncovin, prednisone, and rituximab), achieving partial remission.	Cyclophosphamide	82-98	DNA damage inducible transcript 3	Homo sapiens	74-78
27489498-1	2016	Cyclophosphamide (CYP) induced hemorrhagic cystitis is a dose-limiting side effect involving increased oxidative stress, inflammatory cytokines and suppressed activity of nuclear factor related erythroid 2-related factor (Nrf2).	Cyclophosphamide	0-16	nuclear factor, erythroid derived 2, like 2	Mus musculus	222-226
26980576-0	2016	Response to Intravenous Cyclophosphamide Treatment for Lupus Nephritis Associated with Polymorphisms in the FCGR2B-FCRLA Locus.	Cyclophosphamide	24-40	Fc gamma receptor IIb	Homo sapiens	108-114
25964071-11	2016	Patients who received cyclophosphamide or steroids showed a significant increase in plasma Ang-1 level.	Cyclophosphamide	22-38	angiopoietin 1	Homo sapiens	91-96
27183627-3	2016	We report that cell surface IL-15 expression is upregulated during lymphopenia induced by total body irradiation (TBI), cyclophosphamide, or Thy1 Ab-mediated T cell depletion, as well as in RAG(-/-) mice; interestingly, the cellular profile of surface IL-15 expression is distinct in each model.	Cyclophosphamide	120-136	interleukin 15	Mus musculus	28-33
26426431-8	2016	Increased infiltration of PD-1(+) cells was associated with prolonged progression-free survival (P = 0.005) and overall survival (P = 0.026) in DLBCL patients treated with rituximab-cyclophosphamide, doxorubicin, vincristine, prednisone (R-CHOP), whereas PD-L1 expression had no prognostic significance.	Cyclophosphamide	182-198	programmed cell death 1	Homo sapiens	26-30
26980576-0	2016	Response to Intravenous Cyclophosphamide Treatment for Lupus Nephritis Associated with Polymorphisms in the FCGR2B-FCRLA Locus.	Cyclophosphamide	24-40	Fc receptor like A	Homo sapiens	115-120
26980576-5	2016	RESULTS: Genetic polymorphisms in the Fcgamma receptor gene (FCGR) cluster at human chromosome 1q23, previously associated with lupus nephritis susceptibility, were associated with the response to CYC treatment for lupus nephritis.	Cyclophosphamide	197-200	Fc gamma receptor Ia	Homo sapiens	38-54
26980576-5	2016	RESULTS: Genetic polymorphisms in the Fcgamma receptor gene (FCGR) cluster at human chromosome 1q23, previously associated with lupus nephritis susceptibility, were associated with the response to CYC treatment for lupus nephritis.	Cyclophosphamide	197-200	Fc gamma receptor IIa	Homo sapiens	61-65
27129176-1	2016	Cyclophosphamide, doxorubicin, vincristine, and prednisolone plus rituximab (R-CHOP) is the standard treatment for patients with diffuse large B cell lymphoma (DLBCL).	Cyclophosphamide	0-16	DNA damage inducible transcript 3	Homo sapiens	79-83
27113739-0	2016	Neo-adjuvant doxorubicin and cyclophosphamide followed by paclitaxel in triple-negative breast cancer among BRCA1 mutation carriers and non-carriers.	Cyclophosphamide	29-45	BRCA1 DNA repair associated	Homo sapiens	108-113
27190631-4	2016	METHODS: MUK Five is a phase II open label, randomised, controlled, parallel group, multi-centre trial that will compare the activity of carfilzomib, cyclophosphamide and dexamethasone (CCD) with that of CVD, given over an equivalent treatment period (24 weeks), in participants with multiple myeloma at first relapse, or refractory to no more than 1 line of treatment.	Cyclophosphamide	150-166	mitogen-activated protein kinase kinase kinase 12	Homo sapiens	9-12
26864346-0	2016	Comparison of Doctors" and Breast Cancer Patients" Perceptions of Docetaxel, Epirubicin, and Cyclophosphamide (TEC) Toxicity.	Cyclophosphamide	93-109	tec protein tyrosine kinase	Homo sapiens	111-114
26864346-2	2016	The aim this study was to compare the perceptions of nonhematologic toxicities after administration of a docetaxel, epirubicin, and cyclophosphamide (TEC) regimen between breast cancer patients and oncologists.	Cyclophosphamide	132-148	tec protein tyrosine kinase	Homo sapiens	150-153
26990931-1	2016	BACKGROUND: Chemoimmunotherapy containing rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP) is the standard treatment for diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	53-69	DNA damage inducible transcript 3	Homo sapiens	117-121
26895351-8	2016	CONCLUSION: PE-EPS stimulated the IFN-gamma-primed macrophages and primary splenocytes to induce immune responses and improved the cyclophosphamide-induced immunosuppression in mice.	Cyclophosphamide	131-147	interferon gamma	Mus musculus	34-43
26905436-6	2016	After cyclophosphamide injection, we demonstrated a significant decrease in bladder reduced glutathione (39%) and catalase (55.4%) levels and a significant increase of nitric oxide (5.6 folds), tumor necrosis factor-alpha (3.3 folds), vascular endothelial growth factor (2 folds) and intercellular adhesion molecule-1 (8 folds) bladder contents when compared to those in normal control rats.	Cyclophosphamide	6-22	catalase	Rattus norvegicus	114-122
26905436-6	2016	After cyclophosphamide injection, we demonstrated a significant decrease in bladder reduced glutathione (39%) and catalase (55.4%) levels and a significant increase of nitric oxide (5.6 folds), tumor necrosis factor-alpha (3.3 folds), vascular endothelial growth factor (2 folds) and intercellular adhesion molecule-1 (8 folds) bladder contents when compared to those in normal control rats.	Cyclophosphamide	6-22	tumor necrosis factor	Rattus norvegicus	194-221
26905436-6	2016	After cyclophosphamide injection, we demonstrated a significant decrease in bladder reduced glutathione (39%) and catalase (55.4%) levels and a significant increase of nitric oxide (5.6 folds), tumor necrosis factor-alpha (3.3 folds), vascular endothelial growth factor (2 folds) and intercellular adhesion molecule-1 (8 folds) bladder contents when compared to those in normal control rats.	Cyclophosphamide	6-22	intercellular adhesion molecule 1	Rattus norvegicus	235-317
30133214-1	2016	Objective: To investigate the protective effect and mechanism of Wuzi Yanzong prescription on apoptosis in germ cell of adult male mice induced by cyclophosphamide( CTX).	Cyclophosphamide	147-163	V-set and immunoglobulin domain containing 2	Mus musculus	165-168
26842876-6	2016	Treatment of preexisting CSCs with a genotoxic drug combination (5-fluorouracil, doxorubicin, and cyclophosphamide) generated an NFkappaB-IL6-dependent inflammatory environment that imparted stemness to nonstem cancer cells, induced multidrug resistance, and enhanced the migration potential of CSCs.	Cyclophosphamide	98-114	nuclear factor kappa B subunit 1	Homo sapiens	129-137
27023359-2	2016	This study was undertaken to investigate the onset of menopause and the incidence of primary ovarian insufficiency in women with antineutrophil cytoplasmic antibody-associated vasculitis (AAV), especially after treatment with orally administered cyclophosphamide.	Cyclophosphamide	246-262	adeno-associated virus integration site 1	Homo sapiens	188-191
27023359-3	2016	METHODS: We retrospectively studied the onset of menopause and the influence of cyclophosphamide in women diagnosed as having AAV in our center between 1970 and 2012.	Cyclophosphamide	80-96	adeno-associated virus integration site 1	Homo sapiens	126-129
27023359-11	2016	CONCLUSION: Earlier menopause and primary ovarian insufficiency frequently develop after oral cyclophosphamide therapy in premenopausal women with AAV.	Cyclophosphamide	94-110	adeno-associated virus integration site 1	Homo sapiens	147-150
26960952-4	2016	The patient was then treated with 8 cycles of R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) therapy, which resulted in histological and functional improvement of her salivary glands.	Cyclophosphamide	65-81	DNA damage inducible transcript 3	Homo sapiens	48-52
26726942-1	2016	Cyclophosphamide plus G-CSF (C+G-CSF) is one of the most widely used stem cell (SC) mobilization regimens for patients with multiple myeloma (MM).	Cyclophosphamide	0-16	colony stimulating factor 3	Homo sapiens	29-36
26621134-14	2016	For the binary logistic regression model, CYC cumulative dosage of more than 10 g was the only independent risk factor of POF (hazard ratio 17.0, 95% CI 1.96-147.72, p = 0.01).	Cyclophosphamide	42-45	POF1B actin binding protein	Homo sapiens	122-125
27073670-1	2016	The cyclophosphamide, doxorubicin, vincristine and prednisolone (CHOP) regimen is considered to be a standard treatment for non-Hodgkin"s lymphoma (NHL).	Cyclophosphamide	4-20	DNA damage inducible transcript 3	Homo sapiens	65-69
26972092-8	2016	In case of monoclonal cryoglobulinemia associated with a plasma-cell clone (IgG or IgA), the treatment is based on the combination of bortezomib, cyclophosphamide and dexamethasone.	Cyclophosphamide	146-162	immunoglobulin heavy variable 4-38-2-like	Homo sapiens	83-86
26586169-1	2016	We describe two cases of polyneuropathy, organomegaly, endocrinopathy, monoclonal protein, and skin changes (POEMS) syndrome patients with deteriorated extravascular volume overload without increased levels of vascular endothelial growth factor after the administration of cyclophosphamide + granulocyte colony-stimulating factor for stem cell mobilization.	Cyclophosphamide	273-289	colony stimulating factor 3	Homo sapiens	292-329
27010488-3	2016	High Mobility Group Box-1 (HMGB1), a chromatin-binding protein, mediates bladder pain (but not inflammation) in an experimental model (cyclophosphamide) of cystitis.	Cyclophosphamide	135-151	high mobility group box 1	Mus musculus	0-25
26764356-2	2016	We hypothesized that high-dose cyclophosphamide given after G-CSF-mobilized blood cell transplantation would reduce the cumulative 1-year incidence of chronic GVHD to 15% or less.	Cyclophosphamide	31-47	colony stimulating factor 3	Homo sapiens	60-65
23718870-9	2016	The response rate to oral cyclophosphamide was 44% with 10 of the 23 patients achieving a partial response (PR) based on GCIG (CA125) criteria.	Cyclophosphamide	26-42	mucin 16, cell surface associated	Homo sapiens	127-132
26959744-0	2016	Combination of metronomic cyclophosphamide and dietary intervention inhibits neuroblastoma growth in a CD1-nu mouse model.	Cyclophosphamide	26-42	CD1 antigen complex	Mus musculus	103-106
27002825-0	2016	Glutathione S Transferases Polymorphisms Are Independent Prognostic Factors in Lupus Nephritis Treated with Cyclophosphamide.	Cyclophosphamide	108-124	glutathione S-transferase kappa 1	Homo sapiens	0-26
27002825-1	2016	OBJECTIVE: To investigate association between genetic polymorphisms of GST, CYP and renal outcome or occurrence of adverse drug reactions (ADRs) in lupus nephritis (LN) treated with cyclophosphamide (CYC).	Cyclophosphamide	182-198	glutathione S-transferase kappa 1	Homo sapiens	71-74
27002825-1	2016	OBJECTIVE: To investigate association between genetic polymorphisms of GST, CYP and renal outcome or occurrence of adverse drug reactions (ADRs) in lupus nephritis (LN) treated with cyclophosphamide (CYC).	Cyclophosphamide	200-203	glutathione S-transferase kappa 1	Homo sapiens	71-74
26437056-1	2016	The most common means of mobilizing autologous stem cells is G-CSF alone or combined with cyclophosphamide (CY) to obtain sufficient CD34+ cells for one to two transplants.	Cyclophosphamide	108-110	CD34 molecule	Homo sapiens	133-137
25008867-6	2016	CONCLUSION: Among Japanese women who received epirubicin and cyclophosphamide as perioperative chemotherapy for early breast cancer, those with the A/A genotype of the GSTP1 polymorphism (rs1695) were more likely to have FN.	Cyclophosphamide	61-77	glutathione S-transferase pi 1	Homo sapiens	168-173
27010488-3	2016	High Mobility Group Box-1 (HMGB1), a chromatin-binding protein, mediates bladder pain (but not inflammation) in an experimental model (cyclophosphamide) of cystitis.	Cyclophosphamide	135-151	high mobility group box 1	Mus musculus	27-32
26013248-0	2016	Cyclophosphamide Treatment for Acquired Factor VIII Inhibitor in a Patient with AIDS-Associated Progressive Multifocal Leukoencephalopathy.	Cyclophosphamide	0-16	coagulation factor VIII	Homo sapiens	40-51
26915059-1	2016	In this study, we investigated the effects of the drugs, palonosetron hydrochloride, bevacizumab and cyclophosphamide, on human serum paraoxonase-I (hPON1) enzyme activity in in vitro conditions.	Cyclophosphamide	101-117	paraoxonase 1	Homo sapiens	149-154
27064666-1	2016	PURPOSE: Doxorubicin/cyclophosphamide followed by docetaxel chemotherapy (AC-D) is an intermediate risk factor (incidence of 10%-20%) for febrile neutropenia (FN) in breast cancer.	Cyclophosphamide	21-37	ACD shelterin complex subunit and telomerase recruitment factor	Homo sapiens	74-78
26836029-5	2016	In vivo immunomodulatory activity of RPS-2 was evaluated in normal and cyclophosphamide-induced immunosuppressed mice.	Cyclophosphamide	71-87	ribosomal protein S2	Mus musculus	37-42
26894931-1	2016	AIM: Correlation of outcomes of cyclophosphamide (CP) therapy in antineutrophil cytoplasmic antibody-associated vasculitis with genotype polymorphisms in prodrug activating cytochrome P450 enzyme genes CYP2C9 and CYP2C19.	Cyclophosphamide	32-48	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	202-208
26500140-5	2016	In R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone)-treated DLBCL patients (n=150), reduced HLA-DRA (<90% frequency) expression correlated with inferior overall survival (P=0.0003) and progression-free survival (P=0.0012) and with non-GCB subtype stratified by the Hans, Choi or Visco-Young algorithms (all P<0.01).	Cyclophosphamide	22-38	major histocompatibility complex, class II, DR alpha	Homo sapiens	121-128
26823489-1	2016	The constitutive androstane receptor (CAR and NR1i3) is a key regulator of CYP2B6, the enzyme predominantly responsible for the biotransformation of cyclophosphamide (CPA) to its pharmacologically active metabolite, 4-hydroxycyclophosphamide (4-OH-CPA).	Cyclophosphamide	149-165	nuclear receptor subfamily 1 group I member 3	Homo sapiens	38-41
26823489-1	2016	The constitutive androstane receptor (CAR and NR1i3) is a key regulator of CYP2B6, the enzyme predominantly responsible for the biotransformation of cyclophosphamide (CPA) to its pharmacologically active metabolite, 4-hydroxycyclophosphamide (4-OH-CPA).	Cyclophosphamide	149-165	nuclear receptor subfamily 1 group I member 3	Homo sapiens	46-51
26823489-1	2016	The constitutive androstane receptor (CAR and NR1i3) is a key regulator of CYP2B6, the enzyme predominantly responsible for the biotransformation of cyclophosphamide (CPA) to its pharmacologically active metabolite, 4-hydroxycyclophosphamide (4-OH-CPA).	Cyclophosphamide	149-165	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	75-81
26823489-1	2016	The constitutive androstane receptor (CAR and NR1i3) is a key regulator of CYP2B6, the enzyme predominantly responsible for the biotransformation of cyclophosphamide (CPA) to its pharmacologically active metabolite, 4-hydroxycyclophosphamide (4-OH-CPA).	Cyclophosphamide	167-170	nuclear receptor subfamily 1 group I member 3	Homo sapiens	38-41
26823489-1	2016	The constitutive androstane receptor (CAR and NR1i3) is a key regulator of CYP2B6, the enzyme predominantly responsible for the biotransformation of cyclophosphamide (CPA) to its pharmacologically active metabolite, 4-hydroxycyclophosphamide (4-OH-CPA).	Cyclophosphamide	167-170	nuclear receptor subfamily 1 group I member 3	Homo sapiens	46-51
26823489-1	2016	The constitutive androstane receptor (CAR and NR1i3) is a key regulator of CYP2B6, the enzyme predominantly responsible for the biotransformation of cyclophosphamide (CPA) to its pharmacologically active metabolite, 4-hydroxycyclophosphamide (4-OH-CPA).	Cyclophosphamide	167-170	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	75-81
26823489-2	2016	Previous studies from our laboratory illustrated that CAR activation increases the formation of 4-OH-CPA; however, CPA is rarely used clinically outside of combination therapies.	Cyclophosphamide	101-104	nuclear receptor subfamily 1 group I member 3	Homo sapiens	54-57
26823489-3	2016	Here, we hypothesize that including a selective human CAR activator with the CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisone) regimen can improve the efficacy without exacerbating off-target toxicity of this regimen in non-Hodgkin lymphoma treatment.	Cyclophosphamide	83-99	nuclear receptor subfamily 1 group I member 3	Homo sapiens	54-57
26894931-1	2016	AIM: Correlation of outcomes of cyclophosphamide (CP) therapy in antineutrophil cytoplasmic antibody-associated vasculitis with genotype polymorphisms in prodrug activating cytochrome P450 enzyme genes CYP2C9 and CYP2C19.	Cyclophosphamide	32-48	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	213-220
26894931-8	2016	CONCLUSION: Patients with variant CYP2C9 are at increased risk for cyclophosphamide-induced leukopenia but may have a better chance to respond to treatment.	Cyclophosphamide	67-83	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	34-40
27471610-3	2016	Here, we investigated the possible contribution of FPR1 to the efficacy of a combination of mitoxantrone (MTX) and cyclophosphamide (CTX) for the treatment of hormone-induced breast cancer.	Cyclophosphamide	115-131	formyl peptide receptor 1	Homo sapiens	51-55
28352766-9	2016	After the case was treated by cyclophosphamide pirarubicin vindesine dexamethasone (CHOP) chemotherapy for six courses, her clinical symptoms were partially alleviated, while CT showed progression disease.	Cyclophosphamide	30-46	DNA damage inducible transcript 3	Homo sapiens	84-88
26874859-4	2016	Bcl-2 dependent xenografts derived from aggressive human NB tumors are cured with a combination of cyclophosphamide and ABT-737, a Bcl-2/Bcl-XL/Bcl-w small molecule antagonist.	Cyclophosphamide	99-115	BCL2 like 1	Homo sapiens	137-143
26822718-2	2016	It is well-known that cyclophosphamide (CTX) applied at high dose often damages the immune system by inhibiting immune cell proliferation.	Cyclophosphamide	22-38	V-set and immunoglobulin domain containing 2	Mus musculus	40-43
26692166-7	2016	Furthermore, both XPA and FANCD2 deficient cells were sensitized to PM treatment as compared to that of wild type cells, suggesting that Fanconi anemia and nucleotide excision repair pathways are involved in the removal of cyclophosphamide-induced DNA damage.	Cyclophosphamide	223-239	XPA, DNA damage recognition and repair factor	Homo sapiens	18-21
26692166-7	2016	Furthermore, both XPA and FANCD2 deficient cells were sensitized to PM treatment as compared to that of wild type cells, suggesting that Fanconi anemia and nucleotide excision repair pathways are involved in the removal of cyclophosphamide-induced DNA damage.	Cyclophosphamide	223-239	FA complementation group D2	Homo sapiens	26-32
26874859-4	2016	Bcl-2 dependent xenografts derived from aggressive human NB tumors are cured with a combination of cyclophosphamide and ABT-737, a Bcl-2/Bcl-XL/Bcl-w small molecule antagonist.	Cyclophosphamide	99-115	BCL2 apoptosis regulator	Homo sapiens	0-5
26874859-4	2016	Bcl-2 dependent xenografts derived from aggressive human NB tumors are cured with a combination of cyclophosphamide and ABT-737, a Bcl-2/Bcl-XL/Bcl-w small molecule antagonist.	Cyclophosphamide	99-115	BCL2 apoptosis regulator	Homo sapiens	131-136
26456622-0	2016	Genetic markers in CYP2C19 and CYP2B6 for prediction of cyclophosphamide"s 4-hydroxylation, efficacy and side effects in Chinese patients with systemic lupus erythematosus.	Cyclophosphamide	56-72	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	19-26
26456622-0	2016	Genetic markers in CYP2C19 and CYP2B6 for prediction of cyclophosphamide"s 4-hydroxylation, efficacy and side effects in Chinese patients with systemic lupus erythematosus.	Cyclophosphamide	56-72	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	31-37
26721701-1	2016	BACKGROUND: Preclinical results showing therapeutic effect and low toxicity of metronomic chemotherapy with cyclophosphamide (Cy) + celecoxib (Cel) for mammary tumors encouraged its translation to the clinic for treating advanced breast cancer patients (ABCP).	Cyclophosphamide	108-124	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	254-258
26721701-1	2016	BACKGROUND: Preclinical results showing therapeutic effect and low toxicity of metronomic chemotherapy with cyclophosphamide (Cy) + celecoxib (Cel) for mammary tumors encouraged its translation to the clinic for treating advanced breast cancer patients (ABCP).	Cyclophosphamide	126-128	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	254-258
26492934-0	2016	Fludarabine, cyclophosphamide, and rituximab treatment achieves long-term disease-free survival in IGHV-mutated chronic lymphocytic leukemia.	Cyclophosphamide	13-29	immunoglobulin heavy variable 3-69-1 (pseudogene)	Homo sapiens	99-103
26915059-0	2016	In vitro inhibitory effects of palonosetron hydrochloride, bevacizumab and cyclophosphamide on purified paraoxonase-I (hPON1) from human serum.	Cyclophosphamide	75-91	paraoxonase 1	Homo sapiens	119-124
26573232-0	2016	A genome-wide association study identifies WT1 variant with better response to 5-fluorouracil, pirarubicin and cyclophosphamide neoadjuvant chemotherapy in breast cancer patients.	Cyclophosphamide	111-127	WT1 transcription factor	Homo sapiens	43-46
26806558-0	2016	AMPK Suppresses Connexin43 Expression in the Bladder and Ameliorates Voiding Dysfunction in Cyclophosphamide-induced Mouse Cystitis.	Cyclophosphamide	92-108	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	0-4
26806558-7	2016	In vivo administration of the AMPK agonist AICAR attenuated cyclophosphamide-initiated bladder oxidation, inflammation, Cx43 expression and voiding dysfunction.	Cyclophosphamide	60-76	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	30-34
26806558-7	2016	In vivo administration of the AMPK agonist AICAR attenuated cyclophosphamide-initiated bladder oxidation, inflammation, Cx43 expression and voiding dysfunction.	Cyclophosphamide	60-76	gap junction protein, alpha 1	Mus musculus	120-124
26806558-8	2016	Further analysis comparing the responses of the wild-type (Cx43(+/+)) and heterozygous (Cx43(+/-)) Cx43 mice to cyclophosphamide revealed that the Cx43(+/-) mice retained a relatively normal micturition pattern compared to the Cx43(+/+) mice.	Cyclophosphamide	112-128	gap junction protein, alpha 1	Mus musculus	88-92
26806558-8	2016	Further analysis comparing the responses of the wild-type (Cx43(+/+)) and heterozygous (Cx43(+/-)) Cx43 mice to cyclophosphamide revealed that the Cx43(+/-) mice retained a relatively normal micturition pattern compared to the Cx43(+/+) mice.	Cyclophosphamide	112-128	gap junction protein, alpha 1	Mus musculus	88-92
26806558-8	2016	Further analysis comparing the responses of the wild-type (Cx43(+/+)) and heterozygous (Cx43(+/-)) Cx43 mice to cyclophosphamide revealed that the Cx43(+/-) mice retained a relatively normal micturition pattern compared to the Cx43(+/+) mice.	Cyclophosphamide	112-128	gap junction protein, alpha 1	Mus musculus	88-92
26806558-8	2016	Further analysis comparing the responses of the wild-type (Cx43(+/+)) and heterozygous (Cx43(+/-)) Cx43 mice to cyclophosphamide revealed that the Cx43(+/-) mice retained a relatively normal micturition pattern compared to the Cx43(+/+) mice.	Cyclophosphamide	112-128	gap junction protein, alpha 1	Mus musculus	88-92
26848281-1	2016	BACKGROUND: Conditioning regimens including total body irradiation (TBI) or cyclophosphamide can mobilize high-mobility group box 1 (HMGB1) to peripheral blood.	Cyclophosphamide	76-92	high mobility group box 1	Homo sapiens	106-131
26848281-1	2016	BACKGROUND: Conditioning regimens including total body irradiation (TBI) or cyclophosphamide can mobilize high-mobility group box 1 (HMGB1) to peripheral blood.	Cyclophosphamide	76-92	high mobility group box 1	Homo sapiens	133-138
26848281-7	2016	Additionally, levels of HMGB1 at day 0 were significantly increased in TBI+ patients and cyclophosphamide/TBI patients.	Cyclophosphamide	89-105	high mobility group box 1	Homo sapiens	24-29
26238069-0	2016	TP53 mutations are associated with higher rates of pathologic complete response to anthracycline/cyclophosphamide-based neoadjuvant chemotherapy in operable primary breast cancer.	Cyclophosphamide	97-113	tumor protein p53	Homo sapiens	0-4
26238069-7	2016	Our results suggested that patients with TP53 mutations are more likely to respond to anthracycline/ cyclophosphamide-based neoadjuvant chemotherapy and have a favorable survival.	Cyclophosphamide	101-117	tumor protein p53	Homo sapiens	41-45
26874859-4	2016	Bcl-2 dependent xenografts derived from aggressive human NB tumors are cured with a combination of cyclophosphamide and ABT-737, a Bcl-2/Bcl-XL/Bcl-w small molecule antagonist.	Cyclophosphamide	99-115	BCL2 like 2	Homo sapiens	144-149
26874859-16	2016	In contrast, Bcl-2 dependent xenografts responded to ABT-199 alone and had sustained complete remission (CR) to the ABT-199/cyclophosphamide combination, with one recurrent tumor maintaining Bcl-2 dependence and obtaining a second CR after a second course of therapy.	Cyclophosphamide	124-140	BCL2 apoptosis regulator	Homo sapiens	13-18
26834485-7	2016	CONCLUSION: It is generally believed that the regimen consisting of cyclophosphamide, hydroxydaunorubicin (doxorubicin), vincristine, and prednisolone (CHOP) is also applicable to ALCL.	Cyclophosphamide	68-84	DNA damage inducible transcript 3	Homo sapiens	152-156
24675549-1	2016	This article describes the first reported case of dramatic lymphocytosis flare after initiation of R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) therapy for an indolent lymphoma.	Cyclophosphamide	118-134	DNA damage inducible transcript 3	Homo sapiens	101-105
26449391-1	2016	BACKGROUND: To establish the role of antiemetic therapy with neurokinin-1 (NK1) receptor antagonists (RAs) in nonanthracycline and cyclophosphamide (AC)-based moderately emetogenic chemotherapy (MEC) regimens, this study evaluated single-dose intravenous (i.v.)	Cyclophosphamide	131-147	tachykinin receptor 1	Homo sapiens	61-88
27039799-1	2016	BACKGROUND: A combination of rituximab to cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is one of the most effective front-line therapies to treat B-cell non-Hodgkin"s lymphoma (NHL).	Cyclophosphamide	42-58	DNA damage inducible transcript 3	Homo sapiens	104-108
27034868-10	2016	The patient was initiated on cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy, demonstrating a striking response.	Cyclophosphamide	29-45	DNA damage inducible transcript 3	Homo sapiens	89-93
28936387-7	2016	Oral or intravenous cyclophosphamide and high-dose glucocorticoids are considered to be standard of care for induction of remission in AAV patients with generalised disease.	Cyclophosphamide	20-36	adeno-associated virus integration site 1	Homo sapiens	135-138
26545405-9	2016	Separate analyses indicated the significant relationship was only in ER-positive disease (P = 0.002) and the subgroup treated with doxorubicin/cyclophosphamide (P = 0.005).	Cyclophosphamide	143-159	estrogen receptor 1	Homo sapiens	69-71
27641484-0	2016	Haploidentical related donor hematopoietic stem cell transplantation with post-transplantation cyclophosphamide for DOCK8 deficiency.	Cyclophosphamide	95-111	dedicator of cytokinesis 8	Homo sapiens	116-121
25820250-0	2016	A novel method for assessing bladder-related pain reveals the involvement of nerve growth factor in pain associated with cyclophosphamide-induced chronic cystitis in mice.	Cyclophosphamide	121-137	nerve growth factor	Mus musculus	77-96
26710934-4	2016	We found that cyclophosphamide significantly enhanced long-term expression of the transgenic human CFTR and the reporter gene LacZ by reducing host immune responses.	Cyclophosphamide	14-30	CF transmembrane conductance regulator	Homo sapiens	99-103
26875970-3	2016	All of these symptoms were ameliorated and the level of PR3-ANCA declined following treatment with prednisolone and cyclophosphamide.	Cyclophosphamide	116-132	proteinase 3	Homo sapiens	56-59
26716793-10	2016	The cerebellar and cerebral catalase (CAT), superoxide dismutase and glutathione-S-transferase (GST) activities were significantly (p < .05) reduced in CPA treated group.	Cyclophosphamide	155-158	hematopoietic prostaglandin D synthase	Rattus norvegicus	69-94
26077666-7	2016	Survival of the patients treated with cyclophosphamide-/doxorubicin-/vincristine-/prednisone-based chemotherapy demonstrated that the prognosis of diffuse large B cell patients was unfavorable in the mRNA-positive group compared with the negative group, and that AID expression levels were correlated with the poor prognosis.	Cyclophosphamide	38-54	activation induced cytidine deaminase	Homo sapiens	263-266
27334858-6	2016	A substantial high yield of CD34(+) cells was achieved when patients were treated with a dose-modified IVE regimen, compared with that during the previous regimen (two with the ifosfamide, carboplatin, and etoposide [ICE] regimen, one with high-dose cyclophosphamide and one with the original IVE regimen).	Cyclophosphamide	250-266	CD34 molecule	Homo sapiens	28-32
26716793-10	2016	The cerebellar and cerebral catalase (CAT), superoxide dismutase and glutathione-S-transferase (GST) activities were significantly (p < .05) reduced in CPA treated group.	Cyclophosphamide	155-158	hematopoietic prostaglandin D synthase	Rattus norvegicus	96-99
26986862-11	2016	We describe a case of therapy-related T/myeloid mixed phenotype acute leukemia following rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone R-CHOP chemotherapy for primary cutaneous diffuse large B-cell lymphoma DLBCL.	Cyclophosphamide	100-116	DNA damage inducible transcript 3	Homo sapiens	161-165
26466512-5	2016	However, AMH concentrations of the CY group at 72 hours were significantly lower than those of the control group (p = 0.015).	Cyclophosphamide	35-37	anti-Mullerian hormone	Rattus norvegicus	9-12
26466512-6	2016	AMH concentrations of the CY + NAC group at 72 hours were also significantly lower than those of the NAC group (p = 0.002) and the control group (p = 0.002).	Cyclophosphamide	26-28	anti-Mullerian hormone	Rattus norvegicus	0-3
26466512-7	2016	The AMH levels of CY and CY + NAC groups at 72 hours were significantly lower than those at 24 hours.	Cyclophosphamide	18-20	anti-Mullerian hormone	Rattus norvegicus	4-7
26466512-7	2016	The AMH levels of CY and CY + NAC groups at 72 hours were significantly lower than those at 24 hours.	Cyclophosphamide	25-27	anti-Mullerian hormone	Rattus norvegicus	4-7
28074115-0	2016	Gamma-Glutamylcysteine Ethyl Ester Protects against Cyclophosphamide-Induced Liver Injury and Hematologic Alterations via Upregulation of PPARgamma and Attenuation of Oxidative Stress, Inflammation, and Apoptosis.	Cyclophosphamide	52-68	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	138-147
29693342-5	2016	Conclusions: The study confirmed the proximal tubulardysfunction in rats with both cyclophosphamide- andifosfamide-induced cystitis, which was reflected by anincreased urinary KIM-1 excretion.	Cyclophosphamide	83-99	hepatitis A virus cellular receptor 1	Rattus norvegicus	176-181
26986862-5	2016	We present a patient with T/myeloid mixed-phenotype acute leukemia secondary to rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone R-CHOP chemotherapy for primary cutaneous diffuse large B-cell lymphoma.	Cyclophosphamide	91-107	DNA damage inducible transcript 3	Homo sapiens	152-156
26397389-0	2015	Benzyl butyl phthalate increases the chemoresistance to doxorubicin/cyclophosphamide by increasing breast cancer-associated dendritic cell-derived CXCL1/GROalpha and S100A8/A9.	Cyclophosphamide	68-84	chemokine (C-X-C motif) ligand 1	Mus musculus	147-152
26397389-0	2015	Benzyl butyl phthalate increases the chemoresistance to doxorubicin/cyclophosphamide by increasing breast cancer-associated dendritic cell-derived CXCL1/GROalpha and S100A8/A9.	Cyclophosphamide	68-84	S100 calcium binding protein A8 (calgranulin A)	Mus musculus	166-172
26397389-4	2015	Specific knockdown analysis revealed that S100A9 is the major factor responsible for the chemoresistance of doxorubicin/cyclophosphamide induced by BBP-stimulated TADCs in breast cancer.	Cyclophosphamide	120-136	S100 calcium binding protein A9 (calgranulin B)	Mus musculus	42-48
26398662-0	2015	Combined expression of aldehyde dehydrogenase 1A1 and beta-catenin is associated with lymph node metastasis and poor survival in breast cancer patients following cyclophosphamide treatment.	Cyclophosphamide	162-178	catenin beta 1	Homo sapiens	54-66
26398662-9	2015	ALDH1A1(high) expression or beta-catenin(c) expression alone was associated with lymph node metastasis, and worse clinical outcome in breast cancer patients, especially in patients receiving cyclophosphamide treatment.	Cyclophosphamide	191-207	aldehyde dehydrogenase 1 family member A1	Homo sapiens	0-7
26398662-9	2015	ALDH1A1(high) expression or beta-catenin(c) expression alone was associated with lymph node metastasis, and worse clinical outcome in breast cancer patients, especially in patients receiving cyclophosphamide treatment.	Cyclophosphamide	191-207	aldehyde dehydrogenase 1 family member A1	Homo sapiens	8-12
26398662-10	2015	Combined expression of ALDH1A1(high) and beta-catenin(c) was associated with lymph node metastasis, poor outcome, and resistance to cyclophosphamide treatment.	Cyclophosphamide	132-148	aldehyde dehydrogenase 1 family member A1	Homo sapiens	23-36
26398662-10	2015	Combined expression of ALDH1A1(high) and beta-catenin(c) was associated with lymph node metastasis, poor outcome, and resistance to cyclophosphamide treatment.	Cyclophosphamide	132-148	catenin beta 1	Homo sapiens	41-53
26481550-9	2015	Cyclophosphamide impaired weight gain, decreased blood cell count parameters and total protein concentration, and increased the GGTP activity.	Cyclophosphamide	0-16	gamma-glutamyltransferase 1	Rattus norvegicus	128-132
26581448-11	2015	Subsequent cyclophosphamide therapy successfully controlled IP, paralleled with the declining pattern of IL-18 and KL-6 levels.	Cyclophosphamide	11-27	mucin 1, cell surface associated	Homo sapiens	115-119
26884983-9	2015	In addition, LRGP3 treatment restored the levels of interleukin-2 (IL-2), IL-6 and tumor necrosis factor-alpha (TNF-alpha) in the serum of Cy-treated mice.	Cyclophosphamide	139-141	tumor necrosis factor	Mus musculus	83-110
26884983-9	2015	In addition, LRGP3 treatment restored the levels of interleukin-2 (IL-2), IL-6 and tumor necrosis factor-alpha (TNF-alpha) in the serum of Cy-treated mice.	Cyclophosphamide	139-141	tumor necrosis factor	Mus musculus	112-121
26885107-1	2015	The present study aimed to evaluate the efficacy and safety of combination of cyclophosphamide (CTX) and mycophenolate mofetil (MMF) as induction treatment in Chinese patients with class IV lupus nephritis (LN).	Cyclophosphamide	78-94	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	96-99
26544874-0	2015	Cytochrome P450 Oxidoreductase Influences CYP2B6 Activity in Cyclophosphamide Bioactivation.	Cyclophosphamide	61-77	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	42-48
26544874-2	2015	Cyclophosphamide is a prodrug activated mainly by cytochrome P450 2B6 (CYP2B6) in the liver.	Cyclophosphamide	0-16	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	50-69
26544874-2	2015	Cyclophosphamide is a prodrug activated mainly by cytochrome P450 2B6 (CYP2B6) in the liver.	Cyclophosphamide	0-16	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	71-77
26544874-4	2015	MATERIALS AND METHODS: Hydroxylation of cyclophosphamide was investigated in vitro using three microsomal batches of CYP2B6*1 with different ratios of POR/CYP expression levels.	Cyclophosphamide	40-56	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	117-123
26544874-4	2015	MATERIALS AND METHODS: Hydroxylation of cyclophosphamide was investigated in vitro using three microsomal batches of CYP2B6*1 with different ratios of POR/CYP expression levels.	Cyclophosphamide	40-56	cytochrome p450 oxidoreductase	Homo sapiens	151-154
26544874-4	2015	MATERIALS AND METHODS: Hydroxylation of cyclophosphamide was investigated in vitro using three microsomal batches of CYP2B6*1 with different ratios of POR/CYP expression levels.	Cyclophosphamide	40-56	peptidylprolyl isomerase G	Homo sapiens	117-120
26544874-10	2015	RESULTS: A strong correlation between the in vitro intrinsic clearance of cyclophosphamide and the POR/CYP ratio was found.	Cyclophosphamide	74-90	cytochrome p450 oxidoreductase	Homo sapiens	99-102
26544874-10	2015	RESULTS: A strong correlation between the in vitro intrinsic clearance of cyclophosphamide and the POR/CYP ratio was found.	Cyclophosphamide	74-90	peptidylprolyl isomerase G	Homo sapiens	103-106
26544874-12	2015	In patients, the average expression of the POR gene in blood was significantly (P <0.001) up-regulated after cyclophosphamide infusion, with high inter-individual variations and significant correlation with the concentration ratio of the active metabolite 4-hydroxy-cyclophosphamide/cyclophosphamide.	Cyclophosphamide	112-128	cytochrome p450 oxidoreductase	Homo sapiens	43-46
26544874-12	2015	In patients, the average expression of the POR gene in blood was significantly (P <0.001) up-regulated after cyclophosphamide infusion, with high inter-individual variations and significant correlation with the concentration ratio of the active metabolite 4-hydroxy-cyclophosphamide/cyclophosphamide.	Cyclophosphamide	269-285	cytochrome p450 oxidoreductase	Homo sapiens	43-46
26544874-14	2015	CONCLUSIONS: This investigation shows for the first time that POR besides CYP2B6 can influence cyclophosphamide metabolism.	Cyclophosphamide	95-111	cytochrome p450 oxidoreductase	Homo sapiens	62-65
26544874-14	2015	CONCLUSIONS: This investigation shows for the first time that POR besides CYP2B6 can influence cyclophosphamide metabolism.	Cyclophosphamide	95-111	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	74-80
26544874-15	2015	Our results indicate that not only CYPs are important, but also POR expression and/or activity may influence cyclophosphamide bioactivation, affecting therapeutic efficacy and treatment related toxicity and hence on clinical outcome.	Cyclophosphamide	109-125	cytochrome p450 oxidoreductase	Homo sapiens	64-67
26544874-16	2015	Thus, both POR and CYP genotype and expression levels may have to be taken into account when personalizing treatment schedules to achieve optimal therapeutic drug plasma concentrations of cyclophosphamide.	Cyclophosphamide	188-204	cytochrome p450 oxidoreductase	Homo sapiens	11-14
26544874-16	2015	Thus, both POR and CYP genotype and expression levels may have to be taken into account when personalizing treatment schedules to achieve optimal therapeutic drug plasma concentrations of cyclophosphamide.	Cyclophosphamide	188-204	peptidylprolyl isomerase G	Homo sapiens	19-22
25382543-0	2015	Strontium fructose 1, 6-diphosphate alleviate cyclophosphamide-induced oligozoospermia by improving antioxidant and inhibiting testicular apoptosis via FAS/FASL pathway.	Cyclophosphamide	46-62	Fas ligand	Rattus norvegicus	156-160
26823793-2	2015	This study was undertaken to investigate the efficacy and safety of adding regulatory T cell inhibitor cyclophosphamide to pemetrexed therapy for the second-line treatment of NSCLC with wild-type epidermal growth factor receptor (EGFR).	Cyclophosphamide	103-119	epidermal growth factor receptor	Homo sapiens	196-228
26823793-2	2015	This study was undertaken to investigate the efficacy and safety of adding regulatory T cell inhibitor cyclophosphamide to pemetrexed therapy for the second-line treatment of NSCLC with wild-type epidermal growth factor receptor (EGFR).	Cyclophosphamide	103-119	epidermal growth factor receptor	Homo sapiens	230-234
26823793-9	2015	The present study showed that pemetrexed in combination with low-dose cyclophosphamide may be a better treatment approach than pemetrexed monotherapy when considering second-line treatment for wild-type EGFR NSCLC.	Cyclophosphamide	70-86	epidermal growth factor receptor	Homo sapiens	203-207
26055221-4	2015	A reduced-intensity regimen using fludarabine and low-dose cyclophosphamide might be effective for patients with LIG4, NHEJ1, and NBS1 defects, although more data are needed to confirm these findings and characterize late effects.	Cyclophosphamide	59-75	DNA ligase 4	Homo sapiens	113-117
26055221-4	2015	A reduced-intensity regimen using fludarabine and low-dose cyclophosphamide might be effective for patients with LIG4, NHEJ1, and NBS1 defects, although more data are needed to confirm these findings and characterize late effects.	Cyclophosphamide	59-75	non-homologous end joining factor 1	Homo sapiens	119-124
26762567-10	2016	CONCLUSIONS: The combination treatment of colon cancer with endostatin and a chemotherapeutic agent, cyclophosphamide proves to be an efficient therapeutic strategy to inhibit the rapid vasculature formation confirmed by the differential expression of notch signaling components.	Cyclophosphamide	101-117	collagen, type XVIII, alpha 1	Mus musculus	60-70
27863757-3	2016	Combining other treatments to granulocyte-colony stimulating factor, such as cyclophosphamide, could overcome the mobilization limitation.	Cyclophosphamide	77-93	colony stimulating factor 3	Homo sapiens	30-67
27863757-4	2016	The objective of this study was to assess the number of CD34+ cells mobilized using granulocyte-colony stimulating factor with and without cyclophosphamide after induction with cyclophosphamide, thalidomide and dexamethasone.	Cyclophosphamide	177-193	CD34 molecule	Homo sapiens	56-60
26667243-7	2015	CONCLUSIONS: >=32-years-old women, AMH <3.32 ng/mL and AFC <13 follicles determined significantly higher risk of amenorrhea or oligomenorrhea after CTX with cyclophosphamide.	Cyclophosphamide	166-182	anti-Mullerian hormone	Homo sapiens	38-41
26681005-1	2015	CYP2B6 is a highly polymorphic isoenzyme involved in the metabolism of many drugs including cyclophosphamide, bupropion, and efavirenz.	Cyclophosphamide	92-108	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	0-6
26341140-2	2015	We have previously shown that low HIP1R protein expression was associated with poorer survival in diffuse large B-cell lymphoma (DLBCL) patients from Denmark treated with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone).	Cyclophosphamide	190-206	huntingtin interacting protein 1 related	Homo sapiens	34-39
26809312-3	2015	The Japanese man was diagnosed with diffuse large B-cell lymphoma, and underwent chemotherapy treatment with THP-COP (cyclophosphamide, pirarubicin, vincristine, and prednisolone).	Cyclophosphamide	118-134	caspase recruitment domain family member 16	Homo sapiens	113-116
26884853-8	2015	We concluded that CD30 may be useful as a prognostic marker in rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) treated DLBCLs, indicating favorable outcomes in a Chinese population.	Cyclophosphamide	74-90	TNF receptor superfamily member 8	Homo sapiens	18-22
26490556-3	2015	We have shown the presence of one PRR (NLRP3) in the urothelia and its central role in the inflammatory response to cyclophosphamide.	Cyclophosphamide	116-132	NLR family, pyrin domain containing 3	Rattus norvegicus	39-44
26153045-6	2015	In our study, the cellularity and weight of the spleen were significantly reduced after Rg1 treatment in CY-treated mice.	Cyclophosphamide	105-107	protein phosphatase 1, regulatory subunit 3A	Mus musculus	88-91
26153045-8	2015	Unexpectedly, the proliferation activity of c-Kit(+) HSPCs was only up-regulated in the spleen, but not in the bone marrow, after Rg1 treatment in CY-treated mice.	Cyclophosphamide	147-149	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	44-49
26153045-8	2015	Unexpectedly, the proliferation activity of c-Kit(+) HSPCs was only up-regulated in the spleen, but not in the bone marrow, after Rg1 treatment in CY-treated mice.	Cyclophosphamide	147-149	protein phosphatase 1, regulatory subunit 3A	Mus musculus	130-133
26153045-10	2015	Interestingly, the effects of Rg1 on the elevation of HSPCs in bone marrow and in the peripheral blood were suppressed in CY-treated splenectomized mice.	Cyclophosphamide	122-124	protein phosphatase 1, regulatory subunit 3A	Mus musculus	30-33
26939331-0	2015	[Effects of acupuncture-moxibustion on contents of IL-12 and TNF-alpha in spleen of cyclophosphamide- induced cancer-bearing mice].	Cyclophosphamide	84-100	tumor necrosis factor	Mus musculus	61-70
26057360-0	2015	Doxorubicin and cyclophosphamide treatment produces anxiety-like behavior and spatial cognition impairment in rats: Possible involvement of hippocampal neurogenesis via brain-derived neurotrophic factor and cyclin D1 regulation.	Cyclophosphamide	16-32	brain-derived neurotrophic factor	Rattus norvegicus	169-202
26057360-0	2015	Doxorubicin and cyclophosphamide treatment produces anxiety-like behavior and spatial cognition impairment in rats: Possible involvement of hippocampal neurogenesis via brain-derived neurotrophic factor and cyclin D1 regulation.	Cyclophosphamide	16-32	cyclin D1	Rattus norvegicus	207-216
26057360-10	2015	These results suggest that the co-administration of doxorubicin and cyclophosphamide induces psychological and cognitive impairment, in addition to negatively affecting hippocampal neurogenesis, which may be related to hippocampal cyclin D1 levels, but not hippocampal BDNF levels.	Cyclophosphamide	68-84	cyclin D1	Rattus norvegicus	231-240
26057360-10	2015	These results suggest that the co-administration of doxorubicin and cyclophosphamide induces psychological and cognitive impairment, in addition to negatively affecting hippocampal neurogenesis, which may be related to hippocampal cyclin D1 levels, but not hippocampal BDNF levels.	Cyclophosphamide	68-84	brain-derived neurotrophic factor	Rattus norvegicus	269-273
26099816-0	2015	Doxorubicin and cyclophosphamide induce cognitive dysfunction and activate the ERK and AKT signaling pathways.	Cyclophosphamide	16-32	Eph receptor B1	Rattus norvegicus	79-82
26099816-0	2015	Doxorubicin and cyclophosphamide induce cognitive dysfunction and activate the ERK and AKT signaling pathways.	Cyclophosphamide	16-32	AKT serine/threonine kinase 1	Rattus norvegicus	87-90
26222310-1	2015	Pulsed low-dose cyclophosphamide (CTX) therapy has become a very effective approach in improving the clinical outcomes of lupus nephritis (LN) patients.	Cyclophosphamide	16-32	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	34-37
26413271-4	2015	We report here a 16-year-old male with the vasculitic form of IgAN who failed to respond to aggressive conventional therapy including high-dose steroids, cyclophosphamide and plasma exchange and who was treated with four weekly doses of 900 mg eculizumab followed by a single dose of 1200 mg.	Cyclophosphamide	154-170	IGAN1	Homo sapiens	62-66
26669198-1	2015	OBJECTIVE: To observe the effect of acupuncture and moxibustion intervention on the contents of serum IL-7 and IL-18 and white blood cell counts in cyclophosphamide (CTX)-induced hypofunction of immunity in tumor-bearing mice, so as to explore its mechanism underlying improvement of immune suppression caused by chemotherapy.	Cyclophosphamide	148-164	V-set and immunoglobulin domain containing 2	Mus musculus	166-169
26664382-6	2015	Paclitaxel, doxorubicin, carboplatin and endoxan alone or in combination were added at the beginning of culture and after 6 days, Alamar blue test was used for showing action on cell proliferation why caspase- 3 activity assays for verifying action on apoptosis.	Cyclophosphamide	41-48	caspase 3	Homo sapiens	201-211
25601761-0	2015	Cytochrome P450 2J2, a new key enzyme in cyclophosphamide bioactivation and a potential biomarker for hematological malignancies.	Cyclophosphamide	41-57	cytochrome P450 family 2 subfamily J member 2	Homo sapiens	0-19
25601761-1	2015	The role of cytochrome P450 2J2 (CYP2J2) in cyclophosphamide (Cy) bioactivation was investigated in patients, cells and microsomes.	Cyclophosphamide	44-60	cytochrome P450 family 2 subfamily J member 2	Homo sapiens	12-31
25601761-1	2015	The role of cytochrome P450 2J2 (CYP2J2) in cyclophosphamide (Cy) bioactivation was investigated in patients, cells and microsomes.	Cyclophosphamide	44-60	cytochrome P450 family 2 subfamily J member 2	Homo sapiens	33-39
25601761-1	2015	The role of cytochrome P450 2J2 (CYP2J2) in cyclophosphamide (Cy) bioactivation was investigated in patients, cells and microsomes.	Cyclophosphamide	62-64	cytochrome P450 family 2 subfamily J member 2	Homo sapiens	12-31
25601761-1	2015	The role of cytochrome P450 2J2 (CYP2J2) in cyclophosphamide (Cy) bioactivation was investigated in patients, cells and microsomes.	Cyclophosphamide	62-64	cytochrome P450 family 2 subfamily J member 2	Homo sapiens	33-39
25601761-4	2015	Cy bioactivation was significantly correlated to CYP2J2 expression.	Cyclophosphamide	0-2	cytochrome P450 family 2 subfamily J member 2	Homo sapiens	49-55
25601761-5	2015	Studies in HL-60 cells expressing CYP2J2 showed reduced cell viability when incubated with Cy (half maximal inhibitory concentration=3.6 mM).	Cyclophosphamide	91-93	cytochrome P450 family 2 subfamily J member 2	Homo sapiens	34-40
25601761-6	2015	Inhibition of CYP2J2 using telmisartan reduced Cy bioactivation by 50% and improved cell survival.	Cyclophosphamide	47-49	cytochrome P450 family 2 subfamily J member 2	Homo sapiens	14-20
25601761-8	2015	This is the first study demonstrating that CYP2J2 is equally important to CYP2B6 in Cy metabolism.	Cyclophosphamide	84-86	cytochrome P450 family 2 subfamily J member 2	Homo sapiens	43-49
25601761-8	2015	This is the first study demonstrating that CYP2J2 is equally important to CYP2B6 in Cy metabolism.	Cyclophosphamide	84-86	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	74-80
26458444-2	2015	The current standard therapy for DLBCL is R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) therapy, which allows many patients to achieve disease cure.	Cyclophosphamide	61-77	DNA damage inducible transcript 3	Homo sapiens	44-48
26116901-0	2015	High-dose cyclophosphamide induces specific tumor immunity with concomitant recruitment of LAMP1/CD107a-expressing CD4-positive T cells into tumor sites.	Cyclophosphamide	10-26	lysosomal-associated membrane protein 1	Mus musculus	91-96
26315113-1	2015	Treatment with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) has greatly improved clinical outcomes in patients with diffuse large B-cell lymphoma (DLBCL) compared with CHOP.	Cyclophosphamide	30-46	DNA damage inducible transcript 3	Homo sapiens	92-96
26315113-1	2015	Treatment with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) has greatly improved clinical outcomes in patients with diffuse large B-cell lymphoma (DLBCL) compared with CHOP.	Cyclophosphamide	30-46	DNA damage inducible transcript 3	Homo sapiens	206-210
26116901-0	2015	High-dose cyclophosphamide induces specific tumor immunity with concomitant recruitment of LAMP1/CD107a-expressing CD4-positive T cells into tumor sites.	Cyclophosphamide	10-26	lysosomal-associated membrane protein 1	Mus musculus	97-103
26116901-0	2015	High-dose cyclophosphamide induces specific tumor immunity with concomitant recruitment of LAMP1/CD107a-expressing CD4-positive T cells into tumor sites.	Cyclophosphamide	10-26	CD4 antigen	Mus musculus	115-118
26116901-1	2015	Cancer chemotherapy regimens, particularly those employing high-dose cytotoxic drugs such as cyclophosphamide (CTX), have been considered to be immune suppressive.	Cyclophosphamide	93-109	V-set and immunoglobulin domain containing 2	Mus musculus	111-114
26109089-0	2015	Cyclophosphamide-induced vasopressin-independent activation of aquaporin-2 in the rat kidney.	Cyclophosphamide	0-16	arginine vasopressin	Rattus norvegicus	25-36
26370464-1	2015	BACKGROUND: The regimen of cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) is an efficient treatment of non-Hodgkin"s lymphoma (NHL).	Cyclophosphamide	27-43	DNA damage inducible transcript 3	Homo sapiens	89-93
26109089-0	2015	Cyclophosphamide-induced vasopressin-independent activation of aquaporin-2 in the rat kidney.	Cyclophosphamide	0-16	aquaporin 2	Rattus norvegicus	63-74
26109089-3	2015	In cyclophosphamide-treated rats, significant increases in renal expression of aquaporin-2 (AQP2) and Na-K-2Cl cotransporter type 2 (NKCC2) were shown by immunoblot analysis and immunohistochemistry.	Cyclophosphamide	3-19	aquaporin 2	Rattus norvegicus	79-90
26109089-3	2015	In cyclophosphamide-treated rats, significant increases in renal expression of aquaporin-2 (AQP2) and Na-K-2Cl cotransporter type 2 (NKCC2) were shown by immunoblot analysis and immunohistochemistry.	Cyclophosphamide	3-19	aquaporin 2	Rattus norvegicus	92-96
26109089-3	2015	In cyclophosphamide-treated rats, significant increases in renal expression of aquaporin-2 (AQP2) and Na-K-2Cl cotransporter type 2 (NKCC2) were shown by immunoblot analysis and immunohistochemistry.	Cyclophosphamide	3-19	solute carrier family 12 member 1	Rattus norvegicus	102-131
26109089-3	2015	In cyclophosphamide-treated rats, significant increases in renal expression of aquaporin-2 (AQP2) and Na-K-2Cl cotransporter type 2 (NKCC2) were shown by immunoblot analysis and immunohistochemistry.	Cyclophosphamide	3-19	solute carrier family 12 member 1	Rattus norvegicus	133-138
26109089-8	2015	We demonstrated that, in the rat kidney, cyclophosphamide may activate V2R and induce upregulation of AQP2 in the absence of vasopressin stimulation, suggesting the possibility of drug-induced nephrogenic syndrome of inappropriate antidiuresis (NSIAD).	Cyclophosphamide	41-57	aquaporin 2	Rattus norvegicus	102-106
26620897-0	2015	Increased Expression of Neuregulin 1 and erbB2 Tyrosine Kinase in the Bladder of Rats With Cyclophosphamide-Induced Interstitial Cystitis.	Cyclophosphamide	91-107	neuregulin 1	Rattus norvegicus	24-36
25985920-4	2015	The TBI >= 8 Gy + Ara-C/G-CSF + CY regimen showed significantly higher incidence of neutrophil engraftment (hazard ratio, 1.52; 95% confidence interval [CI], 1.10 to 2.08; P = .009) and lower overall mortality (hazard ratio, .46; 95% CI, .26 to .82; P = .008) rates compared with those without a G-CSF regimen.	Cyclophosphamide	35-37	colony stimulating factor 3	Homo sapiens	299-304
26243621-3	2015	We investigated the therapeutic potential of IDO inhibitor 1-methyl-D-tryptophan (D-1MT) with cyclophosphamide (CY) in a mouse model of lymphoma.	Cyclophosphamide	94-110	indoleamine 2,3-dioxygenase 1	Mus musculus	45-48
26620897-0	2015	Increased Expression of Neuregulin 1 and erbB2 Tyrosine Kinase in the Bladder of Rats With Cyclophosphamide-Induced Interstitial Cystitis.	Cyclophosphamide	91-107	erb-b2 receptor tyrosine kinase 2	Rattus norvegicus	41-46
26620897-1	2015	PURPOSE: The aim of this study was to evaluate changes in expressions of neuregulin (NRG)1 and erbB2 tyrosine kinase (ErbB2) in bladders of rats with cyclophosphamide (CYP)-induced interstitial cystitis (IC).	Cyclophosphamide	150-166	neuregulin 1	Rattus norvegicus	73-90
26620897-1	2015	PURPOSE: The aim of this study was to evaluate changes in expressions of neuregulin (NRG)1 and erbB2 tyrosine kinase (ErbB2) in bladders of rats with cyclophosphamide (CYP)-induced interstitial cystitis (IC).	Cyclophosphamide	150-166	erb-b2 receptor tyrosine kinase 2	Rattus norvegicus	95-100
26620897-1	2015	PURPOSE: The aim of this study was to evaluate changes in expressions of neuregulin (NRG)1 and erbB2 tyrosine kinase (ErbB2) in bladders of rats with cyclophosphamide (CYP)-induced interstitial cystitis (IC).	Cyclophosphamide	150-166	erb-b2 receptor tyrosine kinase 2	Rattus norvegicus	118-123
26620897-1	2015	PURPOSE: The aim of this study was to evaluate changes in expressions of neuregulin (NRG)1 and erbB2 tyrosine kinase (ErbB2) in bladders of rats with cyclophosphamide (CYP)-induced interstitial cystitis (IC).	Cyclophosphamide	168-171	neuregulin 1	Rattus norvegicus	73-90
26620897-1	2015	PURPOSE: The aim of this study was to evaluate changes in expressions of neuregulin (NRG)1 and erbB2 tyrosine kinase (ErbB2) in bladders of rats with cyclophosphamide (CYP)-induced interstitial cystitis (IC).	Cyclophosphamide	168-171	erb-b2 receptor tyrosine kinase 2	Rattus norvegicus	95-100
26620897-1	2015	PURPOSE: The aim of this study was to evaluate changes in expressions of neuregulin (NRG)1 and erbB2 tyrosine kinase (ErbB2) in bladders of rats with cyclophosphamide (CYP)-induced interstitial cystitis (IC).	Cyclophosphamide	168-171	erb-b2 receptor tyrosine kinase 2	Rattus norvegicus	118-123
25666327-4	2015	We present a 52-year-old male with lymphoma who was treated with R-CHOP (R: Rituximab; C: Cyclophosphamide; H: Doxorubicin; O: Vincristine; P: Prednisone).	Cyclophosphamide	90-106	DNA damage inducible transcript 3	Homo sapiens	67-71
26272322-4	2015	Urinary excretion of MIF (ng/mg of urinary creatinine) was measured both pre- and post-treatment with combined steroids and cyclophosphamide.	Cyclophosphamide	124-140	macrophage migration inhibitory factor	Homo sapiens	21-24
26162690-0	2015	Cyclophosphamide-Mediated Tumor Priming for Enhanced Delivery and Antitumor Activity of HER2-Targeted Liposomal Doxorubicin (MM-302).	Cyclophosphamide	0-16	erb-b2 receptor tyrosine kinase 2	Homo sapiens	88-92
26030368-5	2015	Although highly homologous, CY and the archetypal cyclophilin A (CyPA) present distinct catalytic and CsA-binding activities owing to unique structural features between these cylophilins.	Cyclophosphamide	28-30	peptidylprolyl isomerase A	Homo sapiens	65-69
26030368-9	2015	This study unravels chemical probes for multimodal regulation of CY of Ranbp2 and its substrates, and this regulation likely results in the allosterism stemming from the interconversion of conformational substates of cyclophilins.	Cyclophosphamide	65-67	RAN binding protein 2	Homo sapiens	71-77
26030368-10	2015	The results also demonstrate the feasibility of CY in drug discovery against disease-relevant substrates controlled by Ranbp2, and they open new opportunities for therapeutic interventions.	Cyclophosphamide	48-50	RAN binding protein 2	Homo sapiens	119-125
26135617-6	2015	Notably, therapy with rituximab, cyclophosphamide and fludarabine resulted in a significant reduction in the number of non-classical CD14+CD16++ monocytes and soluble form of CD163 but upregulation of membrane-associated monocyte CD163.	Cyclophosphamide	33-49	CD14 molecule	Homo sapiens	133-137
26135617-6	2015	Notably, therapy with rituximab, cyclophosphamide and fludarabine resulted in a significant reduction in the number of non-classical CD14+CD16++ monocytes and soluble form of CD163 but upregulation of membrane-associated monocyte CD163.	Cyclophosphamide	33-49	Fc gamma receptor IIIa	Homo sapiens	138-142
26135617-6	2015	Notably, therapy with rituximab, cyclophosphamide and fludarabine resulted in a significant reduction in the number of non-classical CD14+CD16++ monocytes and soluble form of CD163 but upregulation of membrane-associated monocyte CD163.	Cyclophosphamide	33-49	CD163 molecule	Homo sapiens	175-180
26135617-6	2015	Notably, therapy with rituximab, cyclophosphamide and fludarabine resulted in a significant reduction in the number of non-classical CD14+CD16++ monocytes and soluble form of CD163 but upregulation of membrane-associated monocyte CD163.	Cyclophosphamide	33-49	CD163 molecule	Homo sapiens	230-235
26376594-2	2015	We present a 64-year-old man who was treated with R-CHOP (rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisolone) chemoimmunotherapy for mantle cell lymphoma and developed purulent meningitis, probably caused by Leuconostoc sp.	Cyclophosphamide	73-89	DNA damage inducible transcript 3	Homo sapiens	52-56
25940712-8	2015	Finally, we found that fludarabine and cyclophosphamide, frequently used before CART administration, downregulated IDO expression in lymphoma cells and improved the antitumor activity of CD19-CART in vivo.	Cyclophosphamide	39-55	indoleamine 2,3-dioxygenase 1	Homo sapiens	115-118
26232259-8	2015	In contrast, treatment with cyclophosphamide significantly increased numbers of crypt micronuclei and qualitatively increased gamma-H2AX immunostaining.	Cyclophosphamide	28-44	H2A.X variant histone	Mus musculus	126-136
26151598-8	2015	Pirt expression is decreased in the bladder of cyclophosphamide (CYP)-treated mice, a commonly used model of bladder overactivity.	Cyclophosphamide	47-63	phosphoinositide-interacting regulator of transient receptor potential channels	Mus musculus	0-4
25869285-7	2015	Anthracycline-based regimens such as cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) remain the standard first-line treatment choice for systemic ALCL, but in many patients with ALK- ALCL, it is ineffective, and thus it is often followed by consolidative autologous stem cell transplantation.	Cyclophosphamide	37-53	DNA damage inducible transcript 3	Homo sapiens	97-101
26062749-9	2015	Additionally, miR-126-3p was correlated with basal-like breast cancer, and miR-374b-5p modified the therapeutic effects of 5-Fluorouracil and Cyclophosphamide treatments in basal-like breast cancer patients.	Cyclophosphamide	142-158	microRNA 1263	Homo sapiens	14-24
26062749-9	2015	Additionally, miR-126-3p was correlated with basal-like breast cancer, and miR-374b-5p modified the therapeutic effects of 5-Fluorouracil and Cyclophosphamide treatments in basal-like breast cancer patients.	Cyclophosphamide	142-158	microRNA 374b	Homo sapiens	75-83
25907246-0	2015	Antitumor activity of mHSP65-TTL enhanced by administration of low dose cyclophosphamide in pancreatic cancer-bearing mice.	Cyclophosphamide	72-88	heat shock protein 1 (chaperonin)	Mus musculus	22-28
25892657-2	2015	We demonstrate that administration of an ARTN neutralizing antibody, anti-artemin (alpha-ARTN), can block the development of, and reverse already established, bladder hyperalgesia associated with cyclophosphamide-induced cystitis in mice.	Cyclophosphamide	196-212	artemin	Mus musculus	41-45
25892657-2	2015	We demonstrate that administration of an ARTN neutralizing antibody, anti-artemin (alpha-ARTN), can block the development of, and reverse already established, bladder hyperalgesia associated with cyclophosphamide-induced cystitis in mice.	Cyclophosphamide	196-212	artemin	Mus musculus	74-81
25892657-2	2015	We demonstrate that administration of an ARTN neutralizing antibody, anti-artemin (alpha-ARTN), can block the development of, and reverse already established, bladder hyperalgesia associated with cyclophosphamide-induced cystitis in mice.	Cyclophosphamide	196-212	artemin	Mus musculus	89-93
25892657-3	2015	We further demonstrate that alpha-ARTN therapy blocks upregulation of TRPA1, an ion channel contributing to persistent bladder pain during cyclophosphamide-induced cystitis, and decreases phospho-ERK1/2 immunoreactivity in regions of the spinal cord receiving bladder afferent input.	Cyclophosphamide	139-155	artemin	Mus musculus	34-38
25892657-3	2015	We further demonstrate that alpha-ARTN therapy blocks upregulation of TRPA1, an ion channel contributing to persistent bladder pain during cyclophosphamide-induced cystitis, and decreases phospho-ERK1/2 immunoreactivity in regions of the spinal cord receiving bladder afferent input.	Cyclophosphamide	139-155	transient receptor potential cation channel, subfamily A, member 1	Mus musculus	70-75
25892657-4	2015	Thus, alpha-ARTN is a promising novel therapeutic approach for treatment of bladder hyperalgesia that may be associated with interstitial cystitis/painful bladder syndrome, as well as cystitis associated with antitumor or immunosuppressive cyclophosphamide therapy.	Cyclophosphamide	240-256	artemin	Mus musculus	12-16
26557973-0	2015	Squid ink polysaccharide reduces cyclophosphamide-induced testicular damage via Nrf2/ARE activation pathway in mice.	Cyclophosphamide	33-49	nuclear factor, erythroid derived 2, like 2	Mus musculus	80-84
27088062-1	2015	BACKGROUND: We hypothesize that the combination of an mTOR inhibitor, sirolimus, with a well-known cytotoxic agent, cyclophosphamide, provides a well-tolerated and promising alternative treatment for advanced, differentiated thyroid cancers (DTC).	Cyclophosphamide	116-132	mechanistic target of rapamycin kinase	Homo sapiens	54-58
27088062-3	2015	Fifteen patients treated with combination sirolimus and cyclophosphamide were identified as the sirolimus+cyp group.	Cyclophosphamide	56-72	peptidylprolyl isomerase G	Homo sapiens	106-109
25565670-10	2015	GSTM1 expression and high Bu exposure may increase Cy toxicity by reducing intracellular glutathione.	Cyclophosphamide	51-53	glutathione S-transferase mu 1	Homo sapiens	0-5
26041539-5	2015	Cyclophosphamide (CPA) treatment depleted lymphocytes more efficiently than other cytotoxic agents; however, the percentage of CD4(+)CD25(+) Foxp3(+) Tregs was significantly increased in CPA-treated lymphopenic mice.	Cyclophosphamide	187-190	CD4 antigen	Mus musculus	127-130
26041539-8	2015	Using Rag2(-/-) mice or depletion of recipient CD8(+) T cells after CPA treatment abrogated the augmentation of antitumor effects in CPA-treated reconstituted mice.	Cyclophosphamide	133-136	CD8a molecule	Homo sapiens	47-50
26176698-0	2015	Humanized Chronic Graft-versus-Host Disease in NOD-SCID il2rgamma-/- (NSG) Mice with G-CSF-Mobilized Peripheral Blood Mononuclear Cells following Cyclophosphamide and Total Body Irradiation.	Cyclophosphamide	146-162	peripheral blood stem cell response to granulocyte colony stimulating factor 1	Mus musculus	85-90
26176698-4	2015	We evaluated if prolonged inflammation driven by low dose G-CSF-mobilized human PBMCs (G-hPBMCs) would lead to cGvHD following cyclophosphamide (CTX) administration and total body irradiation (TBI) in NSG mice.	Cyclophosphamide	127-143	colony stimulating factor 3	Homo sapiens	58-63
25648098-1	2015	PURPOSE: Rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is the standard chemotherapy in diffuse large B-cell lymphoma (DLBCL) patients.	Cyclophosphamide	24-40	DNA damage inducible transcript 3	Homo sapiens	86-90
25907246-5	2015	The results showed that mHSP65-TTL significantly prolonged the survival of the pancreatic cancer bearing mice and low dose CY enhanced the efficacy of the mHSP65-TTL.	Cyclophosphamide	123-125	heat shock protein 1 (chaperonin)	Mus musculus	155-161
25940712-8	2015	Finally, we found that fludarabine and cyclophosphamide, frequently used before CART administration, downregulated IDO expression in lymphoma cells and improved the antitumor activity of CD19-CART in vivo.	Cyclophosphamide	39-55	CD19 molecule	Homo sapiens	187-191
25675909-1	2015	BACKGROUND: Although the combination of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is considered standard therapy for diffuse large B-cell lymphoma (DLBCL), patterns of use and the impact of R-CHOP on survival in patients aged >80 years are less clear.	Cyclophosphamide	51-67	DNA damage inducible transcript 3	Homo sapiens	113-117
25971528-3	2015	Under the same experimental conditions, larger gold-PPh3 clusters undergo efficient exchange of unsubstituted PPh3 ligands for singly Me- and Cy-substituted PPh2Me and PPh2Cy ligands.	Cyclophosphamide	142-144	caveolin 1	Homo sapiens	52-56
25971528-3	2015	Under the same experimental conditions, larger gold-PPh3 clusters undergo efficient exchange of unsubstituted PPh3 ligands for singly Me- and Cy-substituted PPh2Me and PPh2Cy ligands.	Cyclophosphamide	142-144	caveolin 1	Homo sapiens	110-114
25556071-0	2015	Effect of Cyclophosphamide on Expression of MMP-9 and TGF-beta1 in Renal Tissue of Rats with Diabetes Mellitus.	Cyclophosphamide	10-26	matrix metallopeptidase 9	Rattus norvegicus	44-49
25556071-0	2015	Effect of Cyclophosphamide on Expression of MMP-9 and TGF-beta1 in Renal Tissue of Rats with Diabetes Mellitus.	Cyclophosphamide	10-26	transforming growth factor, beta 1	Rattus norvegicus	54-63
25556071-2	2015	In this study, we investigated the effect of cyclophosphamide (CTX) on expression of matrix metalloproteinases (MMP-9) and transforming growth factor-beta1 (TGF-beta1) in renal tissue of rats with DN.	Cyclophosphamide	45-61	matrix metallopeptidase 9	Rattus norvegicus	112-117
25556071-2	2015	In this study, we investigated the effect of cyclophosphamide (CTX) on expression of matrix metalloproteinases (MMP-9) and transforming growth factor-beta1 (TGF-beta1) in renal tissue of rats with DN.	Cyclophosphamide	45-61	transforming growth factor, beta 1	Rattus norvegicus	123-155
25675909-1	2015	BACKGROUND: Although the combination of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is considered standard therapy for diffuse large B-cell lymphoma (DLBCL), patterns of use and the impact of R-CHOP on survival in patients aged >80 years are less clear.	Cyclophosphamide	51-67	DNA damage inducible transcript 3	Homo sapiens	229-233
25556071-2	2015	In this study, we investigated the effect of cyclophosphamide (CTX) on expression of matrix metalloproteinases (MMP-9) and transforming growth factor-beta1 (TGF-beta1) in renal tissue of rats with DN.	Cyclophosphamide	45-61	transforming growth factor, beta 1	Rattus norvegicus	157-166
25868843-4	2015	Treatment with CY (100-300 mg/kg) increased plasma levels of creatine kinase-MB isoform (CK   MB) and heart-to-body weight ratio to a significantly greater extent in GSTP-null than WT mice.	Cyclophosphamide	15-17	glutathione S-transferase pi 1	Homo sapiens	166-170
25293363-7	2015	Mobilization-related toxicity was also, however, augmented by Cy; 14% of Cy+G-CSF patients were hospitalized because of complications versus none receiving G-CSF (P < 0.0001).	Cyclophosphamide	62-64	colony stimulating factor 3	Homo sapiens	73-81
25293363-7	2015	Mobilization-related toxicity was also, however, augmented by Cy; 14% of Cy+G-CSF patients were hospitalized because of complications versus none receiving G-CSF (P < 0.0001).	Cyclophosphamide	62-64	colony stimulating factor 3	Homo sapiens	76-81
26021670-1	2015	The introduction of glucocorticoids and cyclophosphamide has transformed ANCA associated vasculitis (AAV) from a fatal to a largely treatable condition.	Cyclophosphamide	40-56	adeno-associated virus integration site 1	Homo sapiens	101-104
26316483-2	2015	The aim of this study was to examine the FcgammaRIIIA gene polymorphism distribution of DLBCL patients who had been treated with R-CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisone) chemotherapy.	Cyclophosphamide	137-153	Fc gamma receptor IIIa	Homo sapiens	41-53
26031284-3	2015	RESULTS: In active severe AAV a combination of prednisolone and cyclophosphamide or rituximab leads to a therapeutic response in approximately 90 % of cases.	Cyclophosphamide	64-80	adeno-associated virus integration site 1	Homo sapiens	26-29
25677905-0	2015	Effect of GSTP1 and ABCC4 gene polymorphisms on response and toxicity of cyclophosphamide-epirubicin-5-fluorouracil-based chemotherapy in Bangladeshi breast cancer patients.	Cyclophosphamide	73-89	glutathione S-transferase pi 1	Homo sapiens	10-15
25677905-0	2015	Effect of GSTP1 and ABCC4 gene polymorphisms on response and toxicity of cyclophosphamide-epirubicin-5-fluorouracil-based chemotherapy in Bangladeshi breast cancer patients.	Cyclophosphamide	73-89	ATP binding cassette subfamily C member 4	Homo sapiens	20-25
25677905-1	2015	The most important cytotoxic drug namely, cyclophosphamide used in breast cancer along with epirubicin and 5-fluorouracil, is transported by ABCC transporters and detoxified by glutathione S-transferases (GSTs).	Cyclophosphamide	42-58	ATP binding cassette subfamily C member 1	Homo sapiens	141-145
25677905-1	2015	The most important cytotoxic drug namely, cyclophosphamide used in breast cancer along with epirubicin and 5-fluorouracil, is transported by ABCC transporters and detoxified by glutathione S-transferases (GSTs).	Cyclophosphamide	42-58	glutathione S-transferase pi 1	Homo sapiens	205-209
25797116-3	2015	MATERIALS AND METHODS: The blood deficiency mice model was induced by being hypodermically injected with N-acetyl phenylhydrazine (APH) and being intraperitoneally injected with cyclophosphamide (CTX).	Cyclophosphamide	178-194	V-set and immunoglobulin domain containing 2	Mus musculus	196-199
25868843-5	2015	In addition to modest yet significant echocardiographic changes following acute CY-treatment, GSTP insufficiency was associated with greater phosphorylation of c-Jun and p38 as well as greater accumulation of albumin and protein-acrolein adducts in the heart.	Cyclophosphamide	80-82	glutathione S-transferase pi 1	Homo sapiens	94-98
25868843-6	2015	Mass spectrometric analysis revealed likely prominent modification of albumin, kallikrein-1-related peptidase, myoglobin and transgelin-2 by acrolein in the hearts of CY-treated mice.	Cyclophosphamide	167-169	myoglobin	Mus musculus	111-120
25868843-6	2015	Mass spectrometric analysis revealed likely prominent modification of albumin, kallikrein-1-related peptidase, myoglobin and transgelin-2 by acrolein in the hearts of CY-treated mice.	Cyclophosphamide	167-169	transgelin 2	Mus musculus	125-137
25868843-10	2015	Collectively, these results suggest that CY cardiotoxicity is regulated, in part, by GSTP, which prevents CY toxicity by detoxifying acrolein.	Cyclophosphamide	41-43	glutathione S-transferase pi 1	Homo sapiens	85-89
25860621-4	2015	Experiments using pan- or isoform-selective CYP inhibitors showed that CYP2B6 and CYP3A4 are responsible for the bioactivation of cyclophosphamide.	Cyclophosphamide	130-146	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	71-77
25860621-4	2015	Experiments using pan- or isoform-selective CYP inhibitors showed that CYP2B6 and CYP3A4 are responsible for the bioactivation of cyclophosphamide.	Cyclophosphamide	130-146	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	82-88
25868843-10	2015	Collectively, these results suggest that CY cardiotoxicity is regulated, in part, by GSTP, which prevents CY toxicity by detoxifying acrolein.	Cyclophosphamide	106-108	glutathione S-transferase pi 1	Homo sapiens	85-89
26056479-7	2015	The patient underwent cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) regime of chemotherapy and achieved a complete remission after four cycles.	Cyclophosphamide	22-38	DNA damage inducible transcript 3	Homo sapiens	82-86
25868843-11	2015	Thus, humans with low cardiac GSTP levels or polymorphic forms of GSTP with low acrolein-metabolizing capacity may be more sensitive to CY toxicity.	Cyclophosphamide	136-138	glutathione S-transferase pi 1	Homo sapiens	30-34
25868843-11	2015	Thus, humans with low cardiac GSTP levels or polymorphic forms of GSTP with low acrolein-metabolizing capacity may be more sensitive to CY toxicity.	Cyclophosphamide	136-138	glutathione S-transferase pi 1	Homo sapiens	66-70
25974040-0	2015	The HSP90 Inhibitor Ganetespib Alleviates Disease Progression and Augments Intermittent Cyclophosphamide Therapy in the MRL/lpr Mouse Model of Systemic Lupus Erythematosus.	Cyclophosphamide	88-104	heat shock protein, 3	Mus musculus	4-9
25966271-13	2015	AAP, as the adjuvant of HCV/NS3 DNA vaccine, can widely regulate the humoral immunity and cellular immune function of normal and cyclophosphamide-induced immunocompromised mice.	Cyclophosphamide	129-145	serpin family F member 2	Homo sapiens	0-3
25374388-4	2015	Basal concentrations of AEA were greater, and the severity of cyclophosphamide (CYP)-induced cystitis was reduced in bladders from FAAH KO compared to WT mice.	Cyclophosphamide	62-78	fatty acid amide hydrolase	Mus musculus	131-135
25952672-7	2015	Key upstream regulators activated by metronomic cyclophosphamide include members of the interferon, toll-like receptor, inflammatory response, and PPAR signaling pathways, whose activation may contribute to anti-tumor immunity.	Cyclophosphamide	48-64	peroxisome proliferator activated receptor alpha	Homo sapiens	147-151
25677220-9	2015	Our results suggest that CYP2B6 SNPs influence the efficacy of high-dose Cy and significantly reduce the success of autologous HCT for lymphoma patients with the CYP2B6*5 variant.	Cyclophosphamide	73-75	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	25-31
25677220-9	2015	Our results suggest that CYP2B6 SNPs influence the efficacy of high-dose Cy and significantly reduce the success of autologous HCT for lymphoma patients with the CYP2B6*5 variant.	Cyclophosphamide	73-75	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	162-168
25490907-1	2015	The objective of this study was to analyze and compare the effects of rituximab (RTX) and cyclophosphamide (CTX) on the serum levels of anti-C1q antibodies and antineutrophil cytoplasmic autoantibodies (ANCA) in assessing the prognosis of severe and refractory lupus nephritis (LN).	Cyclophosphamide	90-106	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	108-111
25490907-1	2015	The objective of this study was to analyze and compare the effects of rituximab (RTX) and cyclophosphamide (CTX) on the serum levels of anti-C1q antibodies and antineutrophil cytoplasmic autoantibodies (ANCA) in assessing the prognosis of severe and refractory lupus nephritis (LN).	Cyclophosphamide	90-106	complement C1q A chain	Homo sapiens	141-144
25796551-12	2015	MAIN RESULTS AND THE ROLE OF CHANCE: Cyclophosphamide-induced ovarian injury caused a prompt decrease in AMH level (P < 0.01) and a further long-term decline in serum AMH (P = 0.017), indicating damage to the ovarian reserve.	Cyclophosphamide	37-53	anti-Mullerian hormone	Homo sapiens	105-108
25796551-12	2015	MAIN RESULTS AND THE ROLE OF CHANCE: Cyclophosphamide-induced ovarian injury caused a prompt decrease in AMH level (P < 0.01) and a further long-term decline in serum AMH (P = 0.017), indicating damage to the ovarian reserve.	Cyclophosphamide	37-53	anti-Mullerian hormone	Homo sapiens	170-173
25839127-3	2015	CORM-A1 (2 mg/kg/day) was administered for 10 days to mice induced with MLDS and/or depleted of low dose cyclophosphamide (CY)-sensitive FoxP3+ T regulatory (Treg) cells.	Cyclophosphamide	105-121	forkhead box P3	Mus musculus	137-142
25839127-3	2015	CORM-A1 (2 mg/kg/day) was administered for 10 days to mice induced with MLDS and/or depleted of low dose cyclophosphamide (CY)-sensitive FoxP3+ T regulatory (Treg) cells.	Cyclophosphamide	123-125	forkhead box P3	Mus musculus	137-142
25675382-3	2015	We report the successful treatment of a patient with type B insulin resistance with rituximab, cyclophosphamide, and prednisone.	Cyclophosphamide	95-111	insulin	Homo sapiens	60-67
25893601-6	2015	Moreover, CD226 expression was required for optimal antimyeloma efficacy of cyclophosphamide (CTX) and bortezomib (Btz), which are both standardly used to manage MM in patients.	Cyclophosphamide	76-92	CD226 molecule	Homo sapiens	10-15
25950695-0	2015	The CD4 Lymphocyte Count is a Better Predictor of Overall Infection Than the Total Lymphocyte Count in ANCA-Associated Vasculitis Under a Corticosteroid and Cyclophosphamide Regimen: A Retrospective Cohort.	Cyclophosphamide	157-173	CD4 molecule	Homo sapiens	4-7
25655312-6	2015	Concomitant treatment with cyclophosphamide and temozolomide resulted in less CD4(+) decrease (P = 0.041) than cyclophosphamide only.	Cyclophosphamide	27-43	CD4 molecule	Homo sapiens	78-81
26034479-2	2015	TTP manifestations subsided with rituximab treatment in spite of a persistently low ADAMTS13 activity and continued a detectable inhibitor activity until the patient developed an intolerance to rituximab due to an allergic reaction when cyclophosphamide was added; this resulted in a normalization of ADAMTS13 activity and the disappearance of the inhibitor.	Cyclophosphamide	237-253	ADAM metallopeptidase with thrombospondin type 1 motif 13	Homo sapiens	301-309
26034479-7	2015	We found that ADAMTS13 activity normalized and the inhibitor activity became undetectable when cyclophosphamide was added to rituximab.	Cyclophosphamide	95-111	ADAM metallopeptidase with thrombospondin type 1 motif 13	Homo sapiens	14-22
26034479-8	2015	We suggest adding cyclophosphamide to rituximab for the treatment of patients with persistent ADAMTS13 inhibitors in order to prolong the remission period and lower the rate of relapse.	Cyclophosphamide	18-34	ADAM metallopeptidase with thrombospondin type 1 motif 13	Homo sapiens	94-102
25889496-3	2015	METHODS: We aimed to develop a method based on simple clinical parameters for predicting unsuccessful (<2x10(6)/kg) or sub-optimal (<5x10(6)/kg) collections of CD34+ PBSC in newly diagnosed MM patients eligible for AuSCT, treated with novel agents and receiving an homogeneous mobilizing therapy with cyclophosphamide and granulocyte-colony stimulating factor (G-CSF).	Cyclophosphamide	307-323	CD34 molecule	Homo sapiens	166-170
26451304-7	2015	Furthermore, targeting TNFR2 signaling with a TNF-alpha inhibitor could selectively reduce rapid resurgence of effector Treg cells after cyclophosphamide-induced lymphodepletion and markedly inhibit the growth of established tumors.	Cyclophosphamide	137-153	TNF receptor superfamily member 1B	Homo sapiens	23-28
26451304-7	2015	Furthermore, targeting TNFR2 signaling with a TNF-alpha inhibitor could selectively reduce rapid resurgence of effector Treg cells after cyclophosphamide-induced lymphodepletion and markedly inhibit the growth of established tumors.	Cyclophosphamide	137-153	tumor necrosis factor	Homo sapiens	46-55
26451304-8	2015	Herein, we propose a novel mechanism in which TNF-alpha could promote tumor-associated effector Treg cell expansion and suggest a new cancer immunotherapy strategy using TNF-alpha inhibitors to reduce effector Treg cells expansion after cyclophosphamide-induced lymphodepletion.	Cyclophosphamide	237-253	tumor necrosis factor	Homo sapiens	46-55
26451304-8	2015	Herein, we propose a novel mechanism in which TNF-alpha could promote tumor-associated effector Treg cell expansion and suggest a new cancer immunotherapy strategy using TNF-alpha inhibitors to reduce effector Treg cells expansion after cyclophosphamide-induced lymphodepletion.	Cyclophosphamide	237-253	tumor necrosis factor	Homo sapiens	170-179
25881228-4	2015	METHODS: First, B-cell cancer cell lines were tested successively for resistance towards the chemotherapeutic components of R-CHOP: cyclophosphamide (C), doxorubicin (H), and vincristine (O).	Cyclophosphamide	132-148	DNA damage inducible transcript 3	Homo sapiens	126-130
25430047-1	2015	This study aimed to clarify the association between the TP53 rs1625895 polymorphism and the efficiency of R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisolone) therapy in 106 patients with diffuse large B cell lymphoma (DLBCL).	Cyclophosphamide	125-141	tumor protein p53	Homo sapiens	56-60
25430047-1	2015	This study aimed to clarify the association between the TP53 rs1625895 polymorphism and the efficiency of R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisolone) therapy in 106 patients with diffuse large B cell lymphoma (DLBCL).	Cyclophosphamide	125-141	DNA damage inducible transcript 3	Homo sapiens	108-112
25662405-0	2015	Low-dose cyclophosphamide enhances antigen-specific CD4(+) T cell responses to NY-ESO-1/ISCOMATRIX  vaccine in patients with advanced melanoma.	Cyclophosphamide	9-25	cancer/testis antigen 1A	Homo sapiens	79-87
25662405-5	2015	Therefore, we have enrolled a second cohort of patients with advanced melanoma in the clinical trial LUD2002-013 to investigate whether pre-treatment with cyclophosphamide could improve the immunogenicity of the NY-ESO-1/ISCOMATRIX  vaccine.	Cyclophosphamide	155-171	cancer/testis antigen 1A	Homo sapiens	212-220
25989890-0	2015	Relationship between ABCB1 gene polymorphisms and severe neutropenia in patients with breast cancer treated with doxorubicin/cyclophosphamide chemotherapy.	Cyclophosphamide	125-141	ATP binding cassette subfamily B member 1	Homo sapiens	21-26
25463999-7	2015	RESULTS: Cyclophosphamide induced pain behavior, bladder inflammation and voiding dysfunction associated with increased bladder levels of PEA, up-regulation of CB1 receptor mRNA expression, down-regulation of PPARalpha mRNA and no change in CB2 receptor mRNA expression.	Cyclophosphamide	9-25	cannabinoid receptor 1	Rattus norvegicus	160-163
25463999-7	2015	RESULTS: Cyclophosphamide induced pain behavior, bladder inflammation and voiding dysfunction associated with increased bladder levels of PEA, up-regulation of CB1 receptor mRNA expression, down-regulation of PPARalpha mRNA and no change in CB2 receptor mRNA expression.	Cyclophosphamide	9-25	peroxisome proliferator activated receptor alpha	Rattus norvegicus	209-218
26687958-2	2015	Although it has limited efficacy, cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) therapy is widely used for treatment of de-novo peripheral T-cell lymphoma.	Cyclophosphamide	34-50	DNA damage inducible transcript 3	Homo sapiens	94-98
25454807-0	2015	Temporary elimination of IL-10 enhanced the effectiveness of cyclophosphamide and BMDC-based therapy by decrease of the suppressor activity of MDSCs and activation of antitumour immune response.	Cyclophosphamide	61-77	interleukin 10	Mus musculus	25-30
25677220-0	2015	Cytochrome P450 2B6*5 Increases Relapse after Cyclophosphamide-Containing Conditioning and Autologous Transplantation for Lymphoma.	Cyclophosphamide	46-62	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	0-19
25677220-1	2015	Cyclophosphamide (Cy) is a prodrug that depends on bioactivation by hepatic cytochrome P450 (CYP) enzymes for its cytotoxicity.	Cyclophosphamide	0-16	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	76-91
25677220-1	2015	Cyclophosphamide (Cy) is a prodrug that depends on bioactivation by hepatic cytochrome P450 (CYP) enzymes for its cytotoxicity.	Cyclophosphamide	0-16	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	93-96
25677220-1	2015	Cyclophosphamide (Cy) is a prodrug that depends on bioactivation by hepatic cytochrome P450 (CYP) enzymes for its cytotoxicity.	Cyclophosphamide	0-2	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	76-91
25677220-1	2015	Cyclophosphamide (Cy) is a prodrug that depends on bioactivation by hepatic cytochrome P450 (CYP) enzymes for its cytotoxicity.	Cyclophosphamide	0-2	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	93-96
25830308-10	2015	In cyclophosphamide-induced cystitis, autophagy was detected in detrusor myocytes by increased LC3, p-p70s6k expression, and autophagosomes.	Cyclophosphamide	3-19	ribosomal protein S6 kinase B1	Rattus norvegicus	102-108
25848306-1	2015	OBJECTIVE: The aim of the study reported here was to investigate the protective effect of gonadotropin-releasing hormone analog (GnRHa) against cyclophosphamide (CTX)-induced gonadotoxicity.	Cyclophosphamide	144-160	gonadotropin releasing hormone 1	Rattus norvegicus	129-134
25596528-3	2015	In mice, DNA damage initiated by chemotherapeutic drug cyclophosphamide activated caspase 1 through the formation of the NLRP3 complex resulting in detrusor hyperplasia.	Cyclophosphamide	55-71	caspase 1	Mus musculus	82-91
25596528-3	2015	In mice, DNA damage initiated by chemotherapeutic drug cyclophosphamide activated caspase 1 through the formation of the NLRP3 complex resulting in detrusor hyperplasia.	Cyclophosphamide	55-71	NLR family, pyrin domain containing 3	Mus musculus	121-126
25778658-0	2015	Expression of vascular endothelial growth factor (VEGF-A) in rat mandibular salivary gland during paraneoplastic process and treatment with cyclophosphamide and melatonin.	Cyclophosphamide	140-156	vascular endothelial growth factor A	Rattus norvegicus	14-48
25778658-0	2015	Expression of vascular endothelial growth factor (VEGF-A) in rat mandibular salivary gland during paraneoplastic process and treatment with cyclophosphamide and melatonin.	Cyclophosphamide	140-156	vascular endothelial growth factor A	Rattus norvegicus	50-56
25778658-1	2015	Expression of VEGF-A in Walker 256 carcinosarcoma and mandibular salivary gland of rats during paraneoplastic process and various regimens of chemotherapy with melatonin and cyclophosphamide were studied by immunohistochemical methods.	Cyclophosphamide	174-190	vascular endothelial growth factor A	Rattus norvegicus	14-20
25778658-2	2015	VEGF-A expression increased in the tumor node and salivary gland after monotherapy with melatonin and cyclophosphamide during progression of tumor growth and paraneoplastic syndrome.	Cyclophosphamide	102-118	vascular endothelial growth factor A	Rattus norvegicus	0-6
25778658-3	2015	A decrease in VEGF-A expression in the tumor node and salivary gland was found after monotherapy with melatonin and cyclophosphamide and, especially, after combined treatment, which proves maximum therapeutic efficiency of combined administration of chemical agents with various mechanisms of action.	Cyclophosphamide	116-132	vascular endothelial growth factor A	Rattus norvegicus	14-20
24815955-8	2015	We also performed a correlation analysis between activity and damage index and between the cumulative cyclophosphamide dose and AMH levels.	Cyclophosphamide	102-118	anti-Mullerian hormone	Homo sapiens	128-131
26137402-4	2015	Expression of CTL- and NK-cell-shared effectors peaked on Day 6, and then declined by Day 9 after the second cyclophosphamide injection and correlated inversely with the expression of the regulatory T cell (Treg) marker Foxp3.	Cyclophosphamide	109-125	forkhead box P3	Mus musculus	220-225
26137402-8	2015	Co-depletion of CD8+ T cells and NK cells did not inhibit tumor regression beyond CD8+ T-cell depletion alone, suggesting that the metronomic cyclophosphamide-activated NK cells function via CD8a+ T cells.	Cyclophosphamide	142-158	CD8 antigen, alpha chain	Mus musculus	191-195
25498913-8	2015	We also identified predictive miRNA biomarker signatures in DLBCL, including high expression of miR-155, which is significantly associated with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) treatment failure.	Cyclophosphamide	159-175	microRNA 155	Mus musculus	96-103
25635435-1	2015	BACKGROUND: Rituximab in combination with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) significantly prolonged event-free survival in first-line chemotherapy for patients with diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	42-58	DNA damage inducible transcript 3	Homo sapiens	102-106
25785030-4	2015	Results showed that SCVP and CVP can overcome CY-induced immunosuppression by promoting spleen lymphocyte proliferation, raising serum IFN-gamma and IL-2 levels, enlarging immune organ indexes, and decreasing excessive apoptosis.	Cyclophosphamide	46-48	interferon gamma	Mus musculus	135-144
25454807-5	2015	The high tumour growth inhibition was observed in mice treated with CY+anti-IL-10+BMDC/TAg as well as CY+-anti-IL-10+BMDC/TAg+BMDC/IL-12.	Cyclophosphamide	68-71	interleukin 10	Mus musculus	76-81
25454807-5	2015	The high tumour growth inhibition was observed in mice treated with CY+anti-IL-10+BMDC/TAg as well as CY+-anti-IL-10+BMDC/TAg+BMDC/IL-12.	Cyclophosphamide	102-105	interleukin 10	Mus musculus	111-116
25454807-9	2015	The high cytotoxic activity of spleen-derived NK cells and increased influx of these cells into tumours of mice treated with CY+anti-IL-10+BMDC/TAg indicate that mice from the group developed strong NK-dependent response.	Cyclophosphamide	125-128	interleukin 10	Mus musculus	133-138
25708328-0	2015	Chronodependent effect of interleukin-2 on mouse spleen cells in the model of cyclophosphamide immunosuppression.	Cyclophosphamide	78-94	interleukin 2	Mus musculus	26-39
25708328-1	2015	We studied the chronodependent effect of IL-2 in the experimental model of immunodeficiency, cyclophosphamide-induced immunosuppression in mice.	Cyclophosphamide	93-109	interleukin 2	Mus musculus	41-45
25708328-2	2015	IL-2 in a dose of 100 U/ mouse was administered at 10.00 and 16.00 for 3 days after injection of cyclophosphamide.	Cyclophosphamide	97-113	interleukin 2	Mus musculus	0-4
25596266-10	2015	These data indicate that MLH1 genotype is a predictor of failure to benefit from rituximab-cyclophosphamide-doxorubicin-vincristine-prednisone treatment in advanced follicular lymphoma and confirm that FCGR2A and FCGR3A polymorphisms have no impact when follicular lymphoma is treated with rituximab plus chemotherapy (clinicaltrials.gov identifier: NCT00774826).	Cyclophosphamide	91-107	mutL homolog 1	Homo sapiens	25-29
25298144-9	2015	CPA produced a slight increase in bladder TRPV1 and TRPA1 mRNA expression, which was reversed by all the toxins tested.	Cyclophosphamide	0-3	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	42-47
25298144-9	2015	CPA produced a slight increase in bladder TRPV1 and TRPA1 mRNA expression, which was reversed by all the toxins tested.	Cyclophosphamide	0-3	transient receptor potential cation channel, subfamily A, member 1	Mus musculus	52-57
25727961-1	2015	Cav3.2 T-type Ca(2+) channels targeted by H2S, a gasotransmitter, participate in cyclophosphamide-induced cystitis and bladder pain.	Cyclophosphamide	81-97	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	0-6
25785030-4	2015	Results showed that SCVP and CVP can overcome CY-induced immunosuppression by promoting spleen lymphocyte proliferation, raising serum IFN-gamma and IL-2 levels, enlarging immune organ indexes, and decreasing excessive apoptosis.	Cyclophosphamide	46-48	interleukin 2	Mus musculus	149-153
25448283-0	2015	Activation of the anticancer drugs cyclophosphamide and ifosfamide by cytochrome P450 BM3 mutants.	Cyclophosphamide	35-51	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	70-85
25448283-1	2015	Cyclophosphamide (CPA) and ifosfamide (IFA) are widely used anticancer agents that require metabolic activation by cytochrome P450 (CYP) enzymes.	Cyclophosphamide	0-16	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	115-130
25448283-1	2015	Cyclophosphamide (CPA) and ifosfamide (IFA) are widely used anticancer agents that require metabolic activation by cytochrome P450 (CYP) enzymes.	Cyclophosphamide	0-16	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	132-135
25448283-1	2015	Cyclophosphamide (CPA) and ifosfamide (IFA) are widely used anticancer agents that require metabolic activation by cytochrome P450 (CYP) enzymes.	Cyclophosphamide	18-21	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	115-130
25448283-1	2015	Cyclophosphamide (CPA) and ifosfamide (IFA) are widely used anticancer agents that require metabolic activation by cytochrome P450 (CYP) enzymes.	Cyclophosphamide	18-21	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	132-135
25448283-3	2015	Gene-directed enzyme prodrug therapies (GDEPT) have been suggested to facilitate local CPA and IFA bioactivation by expressing CYP enzymes within the tumor cells, thereby increasing efficacy.	Cyclophosphamide	87-90	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	127-130
25448283-4	2015	We screened bacterial CYP BM3 mutants, previously engineered to metabolize drug-like compounds, for their ability to catalyze 4-hydroxylation of CPA and IFA.	Cyclophosphamide	145-148	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	22-25
25448283-5	2015	Two CYP BM3 mutants showed very rapid initial bioactivation of CPA and IFA, followed by a slower phase of product formation.	Cyclophosphamide	63-66	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	4-7
25448283-7	2015	Using purified CYP BM3 as an extracellular bioactivation tool, cytotoxicity of CPA and IFA metabolism was confirmed in U2OS cells.	Cyclophosphamide	79-82	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	15-18
25448283-9	2015	To our knowledge, the observed rate of CPA and IFA 4-hydroxylation by these CYP BM3 mutants is the fastest reported to date, and might be of potential interest for CPA and IFA GDEPT.	Cyclophosphamide	39-42	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	76-79
25448283-9	2015	To our knowledge, the observed rate of CPA and IFA 4-hydroxylation by these CYP BM3 mutants is the fastest reported to date, and might be of potential interest for CPA and IFA GDEPT.	Cyclophosphamide	164-167	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	76-79
26137775-13	2015	The most widely used and most effective is the combination Cyclophosphamide, Doxorubicin, Vincristine and Prednisone (CHOP).	Cyclophosphamide	59-75	DNA damage inducible transcript 3	Homo sapiens	118-122
25878913-3	2015	The patient received cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) with rituximab and had excellent results.	Cyclophosphamide	21-37	DNA damage inducible transcript 3	Homo sapiens	81-85
26163637-0	2015	Human Chorionic Gonadotropin (hCG) Regression Curve for Predicting Response to EMA/CO (Etoposide, Methotrexate, Actinomycin D, Cyclophosphamide and Vincristine) Regimen in Gestational Trophoblastic Neoplasia.	Cyclophosphamide	127-143	chorionic gonadotropin subunit beta 5	Homo sapiens	30-33
24878927-12	2015	Cyclophosphamide use was reported in only one patient with a low AMH and high FSH level.	Cyclophosphamide	0-16	anti-Mullerian hormone	Homo sapiens	65-68
26257973-3	2015	We report a 65-year-old Hispanic woman with estrogen receptor (ER) and progesterone receptor (PR) positive invasive ductal breast carcinoma who presented with right thigh pain and swelling eight days after her third infusion of docetaxel (a taxane chemotherapeutic) and cyclophosphamide.	Cyclophosphamide	270-286	estrogen receptor 1	Homo sapiens	44-61
26557758-6	2015	In the next experimental groups mice vaccinated with TRAMP-H6 and TRAMP-H11 received cyclophosphamide (CY).	Cyclophosphamide	85-101	translocating chain-associating membrane protein 1	Mus musculus	53-58
25428516-0	2015	Effects of CYP2B6 genetic polymorphisms in patients receiving cyclophosphamide combination chemotherapy for breast cancer.	Cyclophosphamide	62-78	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	11-17
25428516-1	2015	PURPOSE: The purpose of this study was to measure the frequency of three CYP2B6 [CYP2B6*4 (rs2279343), CYP2B6*5 (rs3211371) and CYP2B6*9 (rs3745274)] alleles in patients with breast cancer receiving cyclophosphamide (CP) therapy and test whether these variants are predictors of CP-associated toxicity and efficacy.	Cyclophosphamide	199-215	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	73-79
26557758-6	2015	In the next experimental groups mice vaccinated with TRAMP-H6 and TRAMP-H11 received cyclophosphamide (CY).	Cyclophosphamide	85-101	translocating chain-associating membrane protein 1	Mus musculus	66-71
26557758-6	2015	In the next experimental groups mice vaccinated with TRAMP-H6 and TRAMP-H11 received cyclophosphamide (CY).	Cyclophosphamide	103-105	translocating chain-associating membrane protein 1	Mus musculus	53-58
26557758-15	2015	Cyclophosphamide added to modified TRAMP vaccines demonstrated clinical benefit of treated mice and enhanced anti-tumour immune response.	Cyclophosphamide	0-16	translocating chain-associating membrane protein 1	Mus musculus	35-40
25301295-0	2015	Spectroscopic and DFT investigation of interactions between cyclophosphamide and aspirin with lysozyme as binary and ternary systems.	Cyclophosphamide	60-76	lysozyme	Homo sapiens	94-102
27051922-9	2015	In case of immunodeficiency caused by cyclophosphamide, there was a significant decrease in IL-1beta, IL-4 and IL-6, but the introduction of phenotropil largely restored their levels.	Cyclophosphamide	38-54	interleukin 1 beta	Rattus norvegicus	92-100
27051922-9	2015	In case of immunodeficiency caused by cyclophosphamide, there was a significant decrease in IL-1beta, IL-4 and IL-6, but the introduction of phenotropil largely restored their levels.	Cyclophosphamide	38-54	interleukin 4	Rattus norvegicus	102-106
27051922-9	2015	In case of immunodeficiency caused by cyclophosphamide, there was a significant decrease in IL-1beta, IL-4 and IL-6, but the introduction of phenotropil largely restored their levels.	Cyclophosphamide	38-54	interleukin 6	Rattus norvegicus	111-115
26149512-3	2015	Long-term outcome of AAV dramatically improved with the introduction of cyclophosphamide.	Cyclophosphamide	72-88	adeno-associated virus integration site 1	Homo sapiens	21-24
26774808-9	2015	Assessing functional changes of the ANS caused by prostaglandin synthesis block it should be stated that prostaglandins synthesized by the constitutive COX-1 isoform seem to maintain the parasympathetic activity, which may be associated with the cholinergic anti-inflammatory pathway and resolution of inflammation in course of cyclophosphamide-induced cystitis.	Cyclophosphamide	328-344	cytochrome c oxidase I, mitochondrial	Rattus norvegicus	152-157
26162837-5	2015	In mice with cerulein-induced pancreatitis and cyclophosphamide-induced cystitis, visceral pain and/or referred hyperalgesia are inhibited by CSE inhibitors and by pharmacological blockade or genetic silencing of Cav3.2, and CSE protein is upregulated in the pancreas and bladder.	Cyclophosphamide	47-63	cystathionase (cystathionine gamma-lyase)	Mus musculus	142-145
26162837-5	2015	In mice with cerulein-induced pancreatitis and cyclophosphamide-induced cystitis, visceral pain and/or referred hyperalgesia are inhibited by CSE inhibitors and by pharmacological blockade or genetic silencing of Cav3.2, and CSE protein is upregulated in the pancreas and bladder.	Cyclophosphamide	47-63	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	213-219
26162837-5	2015	In mice with cerulein-induced pancreatitis and cyclophosphamide-induced cystitis, visceral pain and/or referred hyperalgesia are inhibited by CSE inhibitors and by pharmacological blockade or genetic silencing of Cav3.2, and CSE protein is upregulated in the pancreas and bladder.	Cyclophosphamide	47-63	cystathionase (cystathionine gamma-lyase)	Mus musculus	225-228
25468432-3	2015	Molecular analyses support the concept that there is a biological continuum between BL and DLBCL that includes variable activity of MYC, an oncoprotein once thought to be only associated with BL, but now recognized as a major predictor of survival among patients with DLBCL treated with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone).	Cyclophosphamide	306-322	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	132-135
25415283-9	2015	Immunosuppressive pathways, including regulatory T cells and CTLA-4 expression on T cells were overcome by the addition of vaccine and low-dose cyclophosphamide to PD-1 blockade.	Cyclophosphamide	144-160	cytotoxic T-lymphocyte associated protein 4	Homo sapiens	61-67
25415283-9	2015	Immunosuppressive pathways, including regulatory T cells and CTLA-4 expression on T cells were overcome by the addition of vaccine and low-dose cyclophosphamide to PD-1 blockade.	Cyclophosphamide	144-160	programmed cell death 1	Homo sapiens	164-168
25301295-1	2015	Multi-spectroscopic and density functional theory (DFT) calculations was used to study the interaction between cyclophosphamide (CYP) and aspirin (ASA) with lysozyme (LYS).	Cyclophosphamide	111-127	lysozyme	Homo sapiens	157-165
26489498-2	2015	Rituximab, the most widely used anti-CD20 antibody in routine clinical practice, led not only to improvement of progression-free survival, but also to improvement of overall survival in previously untreated patients with good performance status in combination with fludarabine and cyclophosphamide.	Cyclophosphamide	281-297	keratin 20	Homo sapiens	37-41
25587665-3	2015	In the current study, using mice that were intraperitoneally injected with 50 mg/kg cyclophosphamide for 2 days, we reveal that polysaccharides from the ink of Ommastrephes bartrami (OBP) enhanced the mRNA and protein expression levels of Occludin, zonulae occluden (ZO)-1, and E-cadherin.	Cyclophosphamide	84-100	cadherin 1	Mus musculus	278-288
25686648-3	2015	The summary hazard ratios of low ALC/AMC ratio for overall survival were 2.00 (p = 0.000) in the population that received R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone) and 1.12 (p = 0.479) in the population that received CHOP.	Cyclophosphamide	141-157	allantoicase	Homo sapiens	33-36
26798205-0	2015	PK2/PKR1 Signaling Regulates Bladder Function and Sensation in Rats with Cyclophosphamide-Induced Cystitis.	Cyclophosphamide	73-89	prokineticin 2	Rattus norvegicus	0-3
26798205-0	2015	PK2/PKR1 Signaling Regulates Bladder Function and Sensation in Rats with Cyclophosphamide-Induced Cystitis.	Cyclophosphamide	73-89	prokineticin receptor 1	Rattus norvegicus	4-8
26798205-2	2015	This study aimed to explore the potential role of PK2 in modulating bladder activity and sensation in rats with cyclophosphamide- (CYP-) induced cystitis.	Cyclophosphamide	112-128	prokineticin 2	Rattus norvegicus	50-53
26798205-2	2015	This study aimed to explore the potential role of PK2 in modulating bladder activity and sensation in rats with cyclophosphamide- (CYP-) induced cystitis.	Cyclophosphamide	112-128	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	131-134
25997642-12	2015	The potential application of ACE genotyping in predicting cyclophosphamide response deserves further investigation.	Cyclophosphamide	58-74	angiotensin I converting enzyme	Homo sapiens	29-32
26289095-5	2015	CONCLUSION: The TT genotype of 388 C>T FGFR4 may be related to incidence of febrile neutropenia during neoadjuvant TAC (docetaxel, doxorubicin, cyclophosphamide) chemotherapy and is possibly useful as a patient-related risk factor when assessing febrile neutropenia risk.	Cyclophosphamide	147-163	fibroblast growth factor receptor 4	Homo sapiens	42-47
26228581-6	2015	One-hundred and twenty-nine patients (68%) received cyclophosphamide-recombinant human granulocyte colony-stimulating factor for stem cell mobilization.	Cyclophosphamide	52-68	colony stimulating factor 3	Homo sapiens	87-124
25548584-1	2014	PURPOSE: We evaluated the tolerability and cardiac safety of docetaxel, cyclophosphamide, and trastuzumab (TCyH) for the treatment of early-stage human epidermal growth factor receptor 2 (HER2)-positive breast cancer and compared to the standard trastuzumab-based chemotherapy regimens doxorubicin with cyclophosphamide followed by paclitaxel and trastuzumab (AC-TH) and docetaxel, carboplatin, and trastuzumab (TCaH).	Cyclophosphamide	72-88	erb-b2 receptor tyrosine kinase 2	Homo sapiens	152-186
26334344-1	2015	INTRODUCTION: R-CHOP immunochemotherapy (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone) is a standard first-line treatment for diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	52-68	DNA damage inducible transcript 3	Homo sapiens	16-20
25721772-7	2015	A hair-stimulating effect of a PTH/PTHrP receptor antagonist applied topically to the skin has been observed in hairless mice, as well as in mice treated with cyclophosphamide.	Cyclophosphamide	159-175	parathyroid hormone 1 receptor	Mus musculus	31-49
25446862-8	2014	Conclusively, S.montana extract protects the rat testis against cyclophosphamide-induced damage via anti-oxidative and anti-apoptotic mechanisms that seem to be mediated, at least in part, by PPAR-gamma and Akt1 up-regulation.	Cyclophosphamide	64-80	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	192-202
25446862-8	2014	Conclusively, S.montana extract protects the rat testis against cyclophosphamide-induced damage via anti-oxidative and anti-apoptotic mechanisms that seem to be mediated, at least in part, by PPAR-gamma and Akt1 up-regulation.	Cyclophosphamide	64-80	AKT serine/threonine kinase 1	Rattus norvegicus	207-211
25453340-6	2014	Hamsters are immunosuppressed by treatment with cyclophosphamide, then infected intravenously with Ad5, leading to disseminated Ad5 infection, especially in the liver.	Cyclophosphamide	48-64	Alzheimer disease, familial, type 5	Homo sapiens	128-131
24894105-1	2014	Intravenous cyclophosphamide (IV CYC) has been and still used for treatment of severe manifestations of systemic lupus erythematosus (SLE), a disease occurring predominantly in women.	Cyclophosphamide	12-28	cytochrome c, somatic	Homo sapiens	33-36
25251877-0	2014	Human regulatory T cells lack the cyclophosphamide-extruding transporter ABCB1 and are more susceptible to cyclophosphamide-induced apoptosis.	Cyclophosphamide	34-50	ATP binding cassette subfamily B member 1	Homo sapiens	73-78
25251877-2	2014	Susceptibility of CD4(+) regulatory T (Treg) cells to the ABCB1-substrate cyclophosphamide (CPA) has been reported.	Cyclophosphamide	74-90	CD4 molecule	Homo sapiens	18-21
25251877-2	2014	Susceptibility of CD4(+) regulatory T (Treg) cells to the ABCB1-substrate cyclophosphamide (CPA) has been reported.	Cyclophosphamide	74-90	ATP binding cassette subfamily B member 1	Homo sapiens	58-63
25251877-2	2014	Susceptibility of CD4(+) regulatory T (Treg) cells to the ABCB1-substrate cyclophosphamide (CPA) has been reported.	Cyclophosphamide	92-95	CD4 molecule	Homo sapiens	18-21
25251877-2	2014	Susceptibility of CD4(+) regulatory T (Treg) cells to the ABCB1-substrate cyclophosphamide (CPA) has been reported.	Cyclophosphamide	92-95	ATP binding cassette subfamily B member 1	Homo sapiens	58-63
25251877-6	2014	In vitro, the ABCB1-substrate CPA was cytotoxic for Treg cells at a 100-fold lower dose than for nonregulatory counterparts, and, inversely, verapamil, an inhibitor of ABC transporters, increased CPA-toxicity in nonregulatory CD4(+) T cells but not Treg cells.	Cyclophosphamide	30-33	ATP binding cassette subfamily B member 1	Homo sapiens	14-19
25251877-6	2014	In vitro, the ABCB1-substrate CPA was cytotoxic for Treg cells at a 100-fold lower dose than for nonregulatory counterparts, and, inversely, verapamil, an inhibitor of ABC transporters, increased CPA-toxicity in nonregulatory CD4(+) T cells but not Treg cells.	Cyclophosphamide	30-33	CD4 molecule	Homo sapiens	226-229
25308407-3	2014	Using a mouse model of chemotherapy induced intestinal injury by intraperitoneal injection of 50 mg kg(-1) cyclophosphamide, our results showed an enhanced SIgA concentration in intestinal mucosa by OBP administration and the higher production of SIgA relied on the greater expression of IgA, J chain and pIgR.	Cyclophosphamide	107-123	odorant binding protein 2A	Homo sapiens	199-202
25308407-3	2014	Using a mouse model of chemotherapy induced intestinal injury by intraperitoneal injection of 50 mg kg(-1) cyclophosphamide, our results showed an enhanced SIgA concentration in intestinal mucosa by OBP administration and the higher production of SIgA relied on the greater expression of IgA, J chain and pIgR.	Cyclophosphamide	107-123	polymeric immunoglobulin receptor	Mus musculus	305-309
25674205-0	2014	The role of RIP1 and RIP3 in the development of aplastic anemia induced by cyclophosphamide and busulphan in mice.	Cyclophosphamide	75-91	receptor (TNFRSF)-interacting serine-threonine kinase 1	Mus musculus	12-16
25674205-1	2014	This study aimed to investigate the role of RIP1 and RIP3 in the pathogenesis of aplastic anemia (AA) induced by cyclophosphamide and busulphan in mice.	Cyclophosphamide	113-129	receptor (TNFRSF)-interacting serine-threonine kinase 1	Mus musculus	44-48
25674205-16	2014	RIP1 and RIP3-mediated necroptosis may involve in the pathogenesis of AA induced by cyclophosphamide and busulfan in mice.	Cyclophosphamide	84-100	receptor (TNFRSF)-interacting serine-threonine kinase 1	Mus musculus	0-4
25674205-16	2014	RIP1 and RIP3-mediated necroptosis may involve in the pathogenesis of AA induced by cyclophosphamide and busulfan in mice.	Cyclophosphamide	84-100	receptor-interacting serine-threonine kinase 3	Mus musculus	9-13
25973443-1	2015	We hypothesized that cyclophosphamide- (CYP-) induced cystitis results in oxidative stress and contributes to urinary bladder dysfunction.	Cyclophosphamide	21-37	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	40-43
25642443-3	2014	METHODS: The TOP2A gene status was examined by FISH in biopsies from 18 patients who received anthracycline and cyclophosphamide before surgery.	Cyclophosphamide	112-128	DNA topoisomerase II alpha	Homo sapiens	13-18
25489479-5	2014	METHOD: We report details about a patient with treatment-resistant schizophrenia who was given chemotherapy (fludarabine, cyclophosphamide and rituximab) for CLL in the course of concomitant treatment with clozapine and granulocyte-colony stimulating factor (G-CSFs).	Cyclophosphamide	122-138	colony stimulating factor 3	Homo sapiens	220-257
25323007-2	2014	Although patient outcomes have significantly improved to a greater than 40% cure rate by the combinatorial cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) chemotherapy, which is widely used, resistance to the CHOP regimen continues to pose a problem in managing or curing DLBCL.	Cyclophosphamide	107-123	DNA damage inducible transcript 3	Homo sapiens	166-170
25323007-2	2014	Although patient outcomes have significantly improved to a greater than 40% cure rate by the combinatorial cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) chemotherapy, which is widely used, resistance to the CHOP regimen continues to pose a problem in managing or curing DLBCL.	Cyclophosphamide	107-123	DNA damage inducible transcript 3	Homo sapiens	226-230
24996828-9	2014	Receipt of FEC-D or TC (docetaxel 75 mg/m(2) and cyclophosphamide 600 mg/m(2) every 3 weeks for four or six cycles) was associated with odds ratios of 6.5 or 6.77, respectively, for the development of FN.	Cyclophosphamide	49-65	collagen type VIII alpha 2 chain	Homo sapiens	11-22
25344211-2	2014	The aim of this study was to investigate the role of aldehyde dehydrogenase (ALDH) 1A1 in the resistance of diffuse large B cell lymphoma to the chemotherapeutic mixture consisting of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP).	Cyclophosphamide	184-200	aldehyde dehydrogenase 1 family member A1	Homo sapiens	53-86
25332249-11	2014	CONCLUSION: The addition of trastuzumab to paclitaxel after doxorubicin and cyclophosphamide in early-stage HER2-positive breast cancer results in a substantial and durable improvement in survival as a result of a sustained marked reduction in cancer recurrence.	Cyclophosphamide	76-92	erb-b2 receptor tyrosine kinase 2	Homo sapiens	108-112
25425972-6	2014	Low ATM protein level was significantly associated with poor survival including in patients with ER-negative tumors who received adjuvant anthracycline or cyclophosphamide, methotrexate, and 5-fluorouracil-based adjuvant chemotherapy (Ps < .05).	Cyclophosphamide	155-171	ATM serine/threonine kinase	Homo sapiens	4-7
25005330-4	2014	After mobilisation with cyclophosphamide and Granulocyte-Colony-Stimulating Factor stem cells were CD34-selected.	Cyclophosphamide	24-40	CD34 molecule	Homo sapiens	99-103
24773853-8	2014	Serum levels of KL-6 significantly decreased in patients receiving cyclophosphamide treatment in spite of the fact that the spirometry results (FVC and DLCO) did not show a significant change.	Cyclophosphamide	67-83	mucin 1, cell surface associated	Homo sapiens	16-20
24773853-10	2014	Furthermore, following cyclophosphamide treatment serum KL-6 levels may decrease independently of the lung function parameters.	Cyclophosphamide	23-39	mucin 1, cell surface associated	Homo sapiens	56-60
25251877-6	2014	In vitro, the ABCB1-substrate CPA was cytotoxic for Treg cells at a 100-fold lower dose than for nonregulatory counterparts, and, inversely, verapamil, an inhibitor of ABC transporters, increased CPA-toxicity in nonregulatory CD4(+) T cells but not Treg cells.	Cyclophosphamide	196-199	ATP binding cassette subfamily B member 1	Homo sapiens	14-19
24763745-0	2014	Role of c-Jun N-terminal kinase (JNK) activation in micturition reflexes in cyclophosphamide (CYP)-induced cystitis in female rats.	Cyclophosphamide	76-92	mitogen-activated protein kinase 8	Rattus norvegicus	8-31
24763745-0	2014	Role of c-Jun N-terminal kinase (JNK) activation in micturition reflexes in cyclophosphamide (CYP)-induced cystitis in female rats.	Cyclophosphamide	76-92	mitogen-activated protein kinase 8	Rattus norvegicus	33-36
24763745-2	2014	In this study, phosphorylation of JNK was examined in the urinary bladder with cyclophosphamide (CYP)-induced cystitis and the effects of SP600125, a selective inhibitor of phosphorylation of JNK, on urinary bladder function were assessed using conscious, open outlet, cystometry with continuous instillation of intravesical saline.	Cyclophosphamide	79-95	mitogen-activated protein kinase 8	Rattus norvegicus	34-37
25229255-2	2014	Improvements in overall survival have been observed with the introduction of rituximab in combination with cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP), however, prognostic markers are still needed.	Cyclophosphamide	107-123	DNA damage inducible transcript 3	Homo sapiens	169-173
25330205-0	2014	Adjuvant Docetaxel and Cyclophosphamide (DC) with prophylactic granulocyte colony-stimulating factor (G-CSF) on days 8 &12 in breast cancer patients: a retrospective analysis.	Cyclophosphamide	23-39	colony stimulating factor 3	Homo sapiens	63-100
25330205-0	2014	Adjuvant Docetaxel and Cyclophosphamide (DC) with prophylactic granulocyte colony-stimulating factor (G-CSF) on days 8 &12 in breast cancer patients: a retrospective analysis.	Cyclophosphamide	23-39	colony stimulating factor 3	Homo sapiens	102-107
25116755-4	2014	We hypothesized that cyclophosphamide-modulated vaccination with HER2-specific mAb safely induces relevant HER2-specific immunity in neu mice and patients with HER2+ metastatic breast cancer.	Cyclophosphamide	21-37	erb-b2 receptor tyrosine kinase 2	Mus musculus	65-69
25116755-4	2014	We hypothesized that cyclophosphamide-modulated vaccination with HER2-specific mAb safely induces relevant HER2-specific immunity in neu mice and patients with HER2+ metastatic breast cancer.	Cyclophosphamide	21-37	erb-b2 receptor tyrosine kinase 2	Mus musculus	107-111
25116755-4	2014	We hypothesized that cyclophosphamide-modulated vaccination with HER2-specific mAb safely induces relevant HER2-specific immunity in neu mice and patients with HER2+ metastatic breast cancer.	Cyclophosphamide	21-37	erb-b2 receptor tyrosine kinase 2	Homo sapiens	107-111
25116755-5	2014	Adding both cyclophosphamide and the HER2-specific mAb 7.16.4 to vaccination maximized HER2-specific CD8+ T-cell immunity and tumor-free survival in neu transgenic mice.	Cyclophosphamide	12-28	erb-b2 receptor tyrosine kinase 2	Mus musculus	87-91
24469765-0	2014	Inhibition of gene expression of carnitine palmitoyltransferase I and heart fatty acid binding protein in cyclophosphamide and ifosfamide-induced acute cardiotoxic rat models.	Cyclophosphamide	106-122	carnitine palmitoyltransferase 1B	Rattus norvegicus	33-65
25304726-2	2014	The intention of this study was to enhance the antitumor activity of vaccines consisting of bone marrow-derived DCs stimulated with TAg (BMDC/TAg) via single administration of cyclophosphamide and multiple injections of interleukin (IL)-12-transduced DCs (BMDC/IL-12).	Cyclophosphamide	176-192	temporal alpha-galactosidase	Mus musculus	132-135
25895394-1	2014	OBJECTIVE: To study the protective effect of polysaccharides from corn silk (PCS) against cyclophosphamide (CTX) induced host damages in mice bearing H22 tumors.	Cyclophosphamide	90-106	V-set and immunoglobulin domain containing 2	Mus musculus	108-111
25139358-0	2014	Donor CD4+ Foxp3+ regulatory T cells are necessary for posttransplantation cyclophosphamide-mediated protection against GVHD in mice.	Cyclophosphamide	75-91	CD4 antigen	Mus musculus	6-9
25139358-0	2014	Donor CD4+ Foxp3+ regulatory T cells are necessary for posttransplantation cyclophosphamide-mediated protection against GVHD in mice.	Cyclophosphamide	75-91	forkhead box P3	Mus musculus	11-16
25228527-0	2014	Urine uromodulin estimation in partial bladder outlet obstruction and cyclophosphamide-induced haemorrhagic cystitis models in rats.	Cyclophosphamide	70-86	uromodulin	Rattus norvegicus	6-16
25228527-13	2014	The highest UMOD urinary output was observed after the 3rd and 4th doses of cyclophosphamide.	Cyclophosphamide	76-92	uromodulin	Rattus norvegicus	12-16
25228527-17	2014	UMOD assessment in this model may reflect renal and urological toxicity as UMOD excretion rises with the cumulative cyclophosphamide dose.	Cyclophosphamide	116-132	uromodulin	Rattus norvegicus	0-4
25228527-17	2014	UMOD assessment in this model may reflect renal and urological toxicity as UMOD excretion rises with the cumulative cyclophosphamide dose.	Cyclophosphamide	116-132	uromodulin	Rattus norvegicus	75-79
24907514-2	2014	In this study, we examined the therapeutic effect of recombinant human tyrosyl-tRNA synthetase (rhTyrRS) against development of thrombocytopenia in cyclophosphamide (CTX) treated mice.	Cyclophosphamide	148-164	tyrosyl-tRNA synthetase 1	Homo sapiens	71-94
24469765-0	2014	Inhibition of gene expression of carnitine palmitoyltransferase I and heart fatty acid binding protein in cyclophosphamide and ifosfamide-induced acute cardiotoxic rat models.	Cyclophosphamide	106-122	fatty acid binding protein 3	Rattus norvegicus	70-102
25153123-7	2014	A reduction in Ccr2 and dendritic cells was found in injured wildtype cortex after cyclophosphamide treatment resembling effects of Ccr2-deficiency.	Cyclophosphamide	83-99	chemokine (C-C motif) receptor 2	Mus musculus	15-19
25079140-0	2014	Hesperidin protects against cyclophosphamide-induced hepatotoxicity by upregulation of PPARgamma and abrogation of oxidative stress and inflammation.	Cyclophosphamide	28-44	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	87-96
25430593-10	2014	CONCLUSIONS: Cyclophosphamide pulse therapy was associated with a significant increase of the CD4(+) CD25(high) FOXP3(+) Tregs in patients with active LN and NPSLE.	Cyclophosphamide	13-29	CD4 molecule	Homo sapiens	94-97
25430593-10	2014	CONCLUSIONS: Cyclophosphamide pulse therapy was associated with a significant increase of the CD4(+) CD25(high) FOXP3(+) Tregs in patients with active LN and NPSLE.	Cyclophosphamide	13-29	forkhead box P3	Homo sapiens	112-117
24304372-0	2014	Polycomb protein EZH2 expression in diffuse large B-cell lymphoma is associated with better prognosis in patients treated with rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone.	Cyclophosphamide	138-154	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	17-21
25152523-1	2014	The adverse effects of the anti-cancer agent cyclophosphamide (CTX) on follicular growth and ovarian angiogenesis were investigated in mice.	Cyclophosphamide	45-61	V-set and immunoglobulin domain containing 2	Mus musculus	63-66
25178064-6	2014	The results showed that intragastric administration of 150 or 300 mg kg- d-1 of MCP significantly increased the carbolic particle clearance index, serum haemolysin production, spleen index, thymus index and NK cell cytotoxicity to normal control levels in cyclophosphamide (Cy)-induced immunosuppressed mice.	Cyclophosphamide	256-272	complement component (3b/4b) receptor 1-like	Mus musculus	80-83
25178064-6	2014	The results showed that intragastric administration of 150 or 300 mg kg- d-1 of MCP significantly increased the carbolic particle clearance index, serum haemolysin production, spleen index, thymus index and NK cell cytotoxicity to normal control levels in cyclophosphamide (Cy)-induced immunosuppressed mice.	Cyclophosphamide	274-276	complement component (3b/4b) receptor 1-like	Mus musculus	80-83
25337281-5	2014	The patient was treated with 6 courses of CHOP therapy (cyclophosphamide, doxorubicin, vincristine, and prednisolone), which resulted in complete remission (CR).	Cyclophosphamide	56-72	DNA damage inducible transcript 3	Homo sapiens	42-46
24590536-3	2014	Here, we aimed to assess whether SA can be an independent prognostic marker in patients with newly diagnosed DLBCL treated with rituximab, cyclophosphamide, vincristine, doxorubicin, and prednisone (R-CHOP).	Cyclophosphamide	139-155	albumin	Homo sapiens	33-35
25099633-6	2014	Cyclophosphamide-treated mice showed typical storage symptoms including increased urinary frequency and reduced bladder capacity, with concurrent up-regulation of connexin 43 (GJA1), one of the major gap junction proteins in the bladder.	Cyclophosphamide	0-16	gap junction protein, alpha 1	Mus musculus	163-174
25099633-6	2014	Cyclophosphamide-treated mice showed typical storage symptoms including increased urinary frequency and reduced bladder capacity, with concurrent up-regulation of connexin 43 (GJA1), one of the major gap junction proteins in the bladder.	Cyclophosphamide	0-16	gap junction protein, alpha 1	Mus musculus	176-180
28962262-10	2014	In conclusion, immunosuppression therapy with intravenous methylprednisolone and cyclophosphamide may counteract immune mediated inflammation after paraquat poisoning and improve survival of patients with admission eGFR < 50 ml/min/1.73 m2 and WBC count > 11,000/muL.	Cyclophosphamide	81-97	epidermal growth factor receptor	Homo sapiens	215-219
24595405-2	2014	PURPOSE: Primary prophylaxis with granulocyte colony-stimulating factor (G-CSF) is used in many institutions across the UK due to unacceptable febrile neutropenia (FN) rates with FEC-D (fluorouracil, epirubicin, cyclophosphamide-docetaxel).	Cyclophosphamide	212-228	colony stimulating factor 3	Homo sapiens	34-71
24595405-2	2014	PURPOSE: Primary prophylaxis with granulocyte colony-stimulating factor (G-CSF) is used in many institutions across the UK due to unacceptable febrile neutropenia (FN) rates with FEC-D (fluorouracil, epirubicin, cyclophosphamide-docetaxel).	Cyclophosphamide	212-228	colony stimulating factor 3	Homo sapiens	73-78
28962262-10	2014	In conclusion, immunosuppression therapy with intravenous methylprednisolone and cyclophosphamide may counteract immune mediated inflammation after paraquat poisoning and improve survival of patients with admission eGFR < 50 ml/min/1.73 m2 and WBC count > 11,000/muL.	Cyclophosphamide	81-97	tripartite motif containing 37	Homo sapiens	269-272
25054764-7	2014	R-CHOP chemotherapy regimen (rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone) is the most widely accepted treatment.	Cyclophosphamide	40-56	DNA damage inducible transcript 3	Homo sapiens	2-6
25197420-5	2014	The patient was treated with chemotherapeutic regimens-CHOP (cyclophosphamide, doxorubicin, vincristine and prednisolone).	Cyclophosphamide	61-77	DNA damage inducible transcript 3	Homo sapiens	55-59
24768782-1	2014	BACKGROUND: Cyclophosphamide (CP), an alkylating chemotherapeutic drug, is catalyzed by the Phase I cytochrome P450 (CYPs) isozymes - CYP3A4, CYP3A5, CYP2B6, CYP2C8, CYP2C9 and CYP2C19.	Cyclophosphamide	12-28	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	134-140
24780756-6	2014	Here we report that cyclophosphamide treatment drives the expansion of inflammatory monocytic myeloid cells (CD11b(+)Ly6C(hi)CCR2(hi)) that possess immunosuppressive activities.	Cyclophosphamide	20-36	integrin subunit alpha M	Homo sapiens	109-114
24780756-6	2014	Here we report that cyclophosphamide treatment drives the expansion of inflammatory monocytic myeloid cells (CD11b(+)Ly6C(hi)CCR2(hi)) that possess immunosuppressive activities.	Cyclophosphamide	20-36	C-C motif chemokine receptor 2	Homo sapiens	125-129
24780756-7	2014	In mice with advanced lymphoma, adoptive transfer (AT) of tumor-specific CD4(+) T cells following cyclophosphamide treatment (CTX+CD4 AT) provoked a robust initial antitumor immune response, but also resulted in enhanced expansion of monocytic myeloid cells.	Cyclophosphamide	98-114	CD4 antigen	Mus musculus	73-76
24780756-7	2014	In mice with advanced lymphoma, adoptive transfer (AT) of tumor-specific CD4(+) T cells following cyclophosphamide treatment (CTX+CD4 AT) provoked a robust initial antitumor immune response, but also resulted in enhanced expansion of monocytic myeloid cells.	Cyclophosphamide	98-114	CD4 antigen	Mus musculus	130-133
24780756-11	2014	Similarly, targeting inflammatory monocytes by disrupting the CCR2 signaling pathway markedly potentiated the efficacy of cyclophosphamide-based therapy.	Cyclophosphamide	122-138	C-C motif chemokine receptor 2	Homo sapiens	62-66
24768782-1	2014	BACKGROUND: Cyclophosphamide (CP), an alkylating chemotherapeutic drug, is catalyzed by the Phase I cytochrome P450 (CYPs) isozymes - CYP3A4, CYP3A5, CYP2B6, CYP2C8, CYP2C9 and CYP2C19.	Cyclophosphamide	12-28	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	142-148
24768782-1	2014	BACKGROUND: Cyclophosphamide (CP), an alkylating chemotherapeutic drug, is catalyzed by the Phase I cytochrome P450 (CYPs) isozymes - CYP3A4, CYP3A5, CYP2B6, CYP2C8, CYP2C9 and CYP2C19.	Cyclophosphamide	12-28	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	150-156
24768782-1	2014	BACKGROUND: Cyclophosphamide (CP), an alkylating chemotherapeutic drug, is catalyzed by the Phase I cytochrome P450 (CYPs) isozymes - CYP3A4, CYP3A5, CYP2B6, CYP2C8, CYP2C9 and CYP2C19.	Cyclophosphamide	12-28	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	158-164
24768782-1	2014	BACKGROUND: Cyclophosphamide (CP), an alkylating chemotherapeutic drug, is catalyzed by the Phase I cytochrome P450 (CYPs) isozymes - CYP3A4, CYP3A5, CYP2B6, CYP2C8, CYP2C9 and CYP2C19.	Cyclophosphamide	12-28	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	166-172
24768782-1	2014	BACKGROUND: Cyclophosphamide (CP), an alkylating chemotherapeutic drug, is catalyzed by the Phase I cytochrome P450 (CYPs) isozymes - CYP3A4, CYP3A5, CYP2B6, CYP2C8, CYP2C9 and CYP2C19.	Cyclophosphamide	12-28	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	177-184
24612334-1	2014	OBJECTIVES: Chemoimmunotherapy with cyclophosphamide, doxorubicin, vincristine, prednisolone, and rituximab (R-CHOP) is the standard of care for patients with diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	36-52	DNA damage inducible transcript 3	Homo sapiens	111-115
24180329-4	2014	Subanalysis of patients receiving cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) +- rituximab showed higher predictive power for both PFS (HR 2.75, 95% confidence interval [CI] 1.24-6.11, p = 0.01) and OS (HR 3.33, 95% CI 1.15-9.63, p = 0.02).	Cyclophosphamide	34-50	DNA damage inducible transcript 3	Homo sapiens	93-97
24769015-0	2014	Induction of cytochrome P450 3A1 expression by diallyl disulfide: protective effects against cyclophosphamide-induced embryo-fetal developmental toxicity.	Cyclophosphamide	93-109	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	13-32
24981320-3	2014	We report the clinical case of a 7-year-old male patient with CPAN refractory to treatment with high doses of corticoids and cyclophosphamide, who was successfully treated with the TNF-alpha (tumor necrosis factor-alpha) inhibitor, etanercept, in monotherapy.	Cyclophosphamide	125-141	tumor necrosis factor	Homo sapiens	181-190
24981320-3	2014	We report the clinical case of a 7-year-old male patient with CPAN refractory to treatment with high doses of corticoids and cyclophosphamide, who was successfully treated with the TNF-alpha (tumor necrosis factor-alpha) inhibitor, etanercept, in monotherapy.	Cyclophosphamide	125-141	tumor necrosis factor	Homo sapiens	192-219
24719189-1	2014	This study aims to investigate the prognostic significance of the MYC protein expression in diffuse large B cell lymphoma (DLBCL) patients treated with RCHOP (rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone).	Cyclophosphamide	174-190	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	66-69
24965046-3	2014	RESULTS: Intermittent metronomic cyclophosphamide scheduling strongly increased glioma-associated CD11b+ immune cells but not CD11b+Gr1+ myeloid-derived suppressor cells, while bone marrow and spleen reservoirs of the suppressor cells were decreased.	Cyclophosphamide	33-49	integrin subunit alpha M	Homo sapiens	98-103
24440659-12	2014	Compared with day 1 (cyclophosphamide alone), H2AX phosphorylation was increased on day 2 when clofarabine and cyclophosphamide were administered as a couplet (n = 8).	Cyclophosphamide	111-127	H2A.X variant histone	Homo sapiens	46-50
24965046-4	2014	The inhibition of immune cell recruitment and tumor regression by anti-angiogenic receptor tyrosine kinase inhibitors, previously observed in several brain tumor models, was recapitulated in the 9L tumor model with the VEGFR2-specific inhibitory monoclonal antibody DC101 (p < 0.01), implicating VEGFR2 signaling as an essential step in metronomic cyclophosphamide-stimulated immune cell recruitment.	Cyclophosphamide	351-367	kinase insert domain receptor	Homo sapiens	219-225
24635166-5	2014	The frequencies of Th22, IL-22(+) Th17 and Th17 cells and the concentrations of IL-22 and IL-17 were reduced in response to the drugs methylprednisolone, cyclophosphamide and hydroxychloroquine for 4 weeks in the majority of SLE patients.	Cyclophosphamide	154-170	interleukin 22	Homo sapiens	25-30
24635166-5	2014	The frequencies of Th22, IL-22(+) Th17 and Th17 cells and the concentrations of IL-22 and IL-17 were reduced in response to the drugs methylprednisolone, cyclophosphamide and hydroxychloroquine for 4 weeks in the majority of SLE patients.	Cyclophosphamide	154-170	interleukin 22	Homo sapiens	80-85
24635166-5	2014	The frequencies of Th22, IL-22(+) Th17 and Th17 cells and the concentrations of IL-22 and IL-17 were reduced in response to the drugs methylprednisolone, cyclophosphamide and hydroxychloroquine for 4 weeks in the majority of SLE patients.	Cyclophosphamide	154-170	interleukin 17A	Homo sapiens	90-95
25018638-3	2014	Such ALK-positive ALCLs are usually responsive to a multidrug chemotherapy with CHOP (cyclophosphamide, doxorubicin, vincristine, prednisone).	Cyclophosphamide	86-102	ALK receptor tyrosine kinase	Homo sapiens	5-8
24249003-0	2014	Cyclophosphamide treatment induces rejection of established P815 mastocytoma by enhancing CD4 priming and intratumoral infiltration of P1E/H-2K(d) -specific CD8+ T cells.	Cyclophosphamide	0-16	CD4 antigen	Mus musculus	90-93
24249003-0	2014	Cyclophosphamide treatment induces rejection of established P815 mastocytoma by enhancing CD4 priming and intratumoral infiltration of P1E/H-2K(d) -specific CD8+ T cells.	Cyclophosphamide	0-16	histocompatibility 2, K1, K region	Mus musculus	139-146
24249003-3	2014	Treatment of DBA/2 mice bearing P815 mastocytoma with cyclophosphamide induced rejection and long-term protection in a CD4- and CD8-dependent manner.	Cyclophosphamide	54-70	CD4 antigen	Mus musculus	119-122
24249003-6	2014	Importantly, the analysis of CD8+ T cells specific to P1A/H-2L(d) and P1E/H-2K(d) revealed that cyclophosphamide altered the P815-specific CD8 T repertoire by amplifying the response specific to the mutated P1E antigen.	Cyclophosphamide	96-112	zinc finger protein 185	Mus musculus	54-57
24249003-6	2014	Importantly, the analysis of CD8+ T cells specific to P1A/H-2L(d) and P1E/H-2K(d) revealed that cyclophosphamide altered the P815-specific CD8 T repertoire by amplifying the response specific to the mutated P1E antigen.	Cyclophosphamide	96-112	histocompatibility 2, K1, K region	Mus musculus	74-81
24668959-10	2014	In conclusion, either CY or GY supplementation partially mitigated the negative effects of heat stress on performance and HSP70 mRNA expression of lactating cows, and GY supplementation provided additional improvements in energy status and HSP70 gene expression of lactating cows.	Cyclophosphamide	22-24	heat shock 70 kDa protein 1B	Bos taurus	122-127
24989286-9	2014	After 2 cycles of treatment with rituximab, cyclophosphamide, doxorubicin, vincristine and prednisolone(R-CHOP), the images of increasing metabolic activity in subcutaneous soft tissue gap disappeared, but the partial increasing metabolism focus could be observed in soft tissue of left knee hollow.	Cyclophosphamide	44-60	DNA damage inducible transcript 3	Homo sapiens	106-110
24668959-7	2014	Cows supplemented with CY and GY had greater yields of milk, energy-corrected milk and milk fat, and milk fat percent but lower HSP70 mRNA expression in peripheral blood lymphocytes than Control cows (P < 0.05).	Cyclophosphamide	23-25	heat shock 70 kDa protein 1B	Bos taurus	128-133
24932232-0	2014	O6-methylguanine-DNA methyltransferase as a prognostic and predictive marker for basal-like breast cancer treated with cyclophosphamide-based chemotherapy.	Cyclophosphamide	119-135	O-6-methylguanine-DNA methyltransferase	Homo sapiens	0-38
24578329-11	2014	Among cyclophosphamide-treated patients, the likelihood of treatment response was >14% even with highest chronicity index score and eGFR<10 ml/min per 1.73 m(2).	Cyclophosphamide	6-22	epidermal growth factor receptor	Homo sapiens	135-139
24935324-5	2014	The ALT of patients reached the first peak of 144 +- 45.04 U/L, on day 7 after busulfan + cyclophosphamide (BU/CY) pretreatment, and reached the second peak of 220.5 +- 40.58 U/L on day 7 after transplantation.	Cyclophosphamide	90-106	glutamic pyruvic transaminase, soluble	Mus musculus	4-7
24810046-10	2014	Next, we evaluated low-dose docetaxel (DTX; 5, 1, 0.5 mg/kg) or cyclophosphamide (CTX; 10-20 mg/kg) on established s.c. PC3 tumors that conditionally express PEDF anti-tumoral epitope/NT3.	Cyclophosphamide	64-80	chromobox 8	Mus musculus	120-123
24525280-2	2014	They generally define peripheral blood cut-off levels of CD34+ cells at a fixed day after starting chemotherapy, mostly with cyclophosphamide.	Cyclophosphamide	125-141	CD34 molecule	Homo sapiens	57-61
24917007-4	2014	Against this background, we measured the time required to prepare cyclophosphamide(CPA)and estimated the cost incurred.	Cyclophosphamide	66-82	carboxypeptidase A1	Homo sapiens	83-86
24917012-6	2014	The patient began receiving different regimens of chemotherapy: 5-fluorouracil (5-FU), epirubicin (EPI), and cyclophosphamide(CPA), (FEC); PTX; docetaxel (DTX); and gemcitabine (GEM) plus PTX.	Cyclophosphamide	109-125	carboxypeptidase A1	Homo sapiens	126-129
24506571-0	2014	Serum levels of anti-SRP54 antibodies reflect disease activity of necrotizing myopathy in a child treated effectively with combinatorial methylprednisolone pulses and plasma exchanges followed by intravenous cyclophosphamide.	Cyclophosphamide	208-224	signal recognition particle 54	Homo sapiens	21-26
24827566-7	2014	Splenic transcriptomic pathways affected by cyclophosphamide included: iron hemostasis; vascular tissue angiotensin system; hepatic stellate cell activation and fibrosis; complement activation; TGFbeta-induced hypertrophy and fibrosis; monocytes, macrophages, and atherosclerosis; and platelet activation.	Cyclophosphamide	44-60	transforming growth factor, beta 1	Rattus norvegicus	194-201
24506571-1	2014	We describe the effectiveness of combinatorial therapy with plasma exchanges and methylprednisolone pulses followed by intravenous cyclophosphamide in a young girl with anti-signal recognition particle 54 (SRP54) antibody-associated myopathy.	Cyclophosphamide	131-147	signal recognition particle 54	Homo sapiens	174-204
24506571-1	2014	We describe the effectiveness of combinatorial therapy with plasma exchanges and methylprednisolone pulses followed by intravenous cyclophosphamide in a young girl with anti-signal recognition particle 54 (SRP54) antibody-associated myopathy.	Cyclophosphamide	131-147	signal recognition particle 54	Homo sapiens	206-211
24493716-1	2014	PURPOSE: R-CHOP (rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone) is standard care for aggressive B-cell lymphoma.	Cyclophosphamide	32-48	DNA damage inducible transcript 3	Homo sapiens	11-15
24393851-2	2014	PATIENTS AND METHODS: Single-nucleotide polymorphisms (SNPs) of CD24 were genotyped by the Sequenom MassArray iPLEX Gold System in 170 patients with breast cancer, and a total of 120 patients with histologically confirmed T2-4N0-2 M0 breast cancer were recruited to therapy with docetaxel, doxorubicin, and cyclophosphamide (TAC) as neoadjuvant chemotherapy.	Cyclophosphamide	307-323	CD24 molecule	Homo sapiens	64-68
24341930-3	2014	OBJECTIVES: To explore, using a human in vitro model for chemotherapy-induced hair follicle (HF) dystrophy that employs the key cyclophosphamide metabolite (4-hydroperoxy-cyclophosphamide, 4-HC), whether alpha-MSH protects from 4-HC-induced HF dystrophy.	Cyclophosphamide	128-144	proopiomelanocortin	Homo sapiens	204-213
24262494-10	2014	Up-regulated myeloperoxidase, IL-1beta, IL-6 and TNF-alpha expression in cyclophosphamide treated rats was also suppressed in rebamipide treated rats.	Cyclophosphamide	73-89	myeloperoxidase	Rattus norvegicus	13-28
24435807-6	2014	Furthermore, when provoked with cyclophosphamide, or transferred to a secondary lymphopenic host, the latent pool of self-reactive T cells resident in BAFF-deficient NOD mice could elicit beta cell destruction.	Cyclophosphamide	32-48	tumor necrosis factor (ligand) superfamily, member 13b	Mus musculus	151-155
24548980-12	2014	The relationships between transcript expression and patient-level data demonstrated; ABCC2 expression was different by race (1.26 +- 1.82 Caucasian versus 1.37 +- 0.86 non-Caucasian; p = 0.049) and CYP2B6 expression was different by treatment (2.07 +- 2.94 cyclophosphamide versus 0.45 +- 0.5 mycophenolate; p = 0.01).	Cyclophosphamide	257-273	ATP binding cassette subfamily C member 2	Homo sapiens	85-90
24548980-12	2014	The relationships between transcript expression and patient-level data demonstrated; ABCC2 expression was different by race (1.26 +- 1.82 Caucasian versus 1.37 +- 0.86 non-Caucasian; p = 0.049) and CYP2B6 expression was different by treatment (2.07 +- 2.94 cyclophosphamide versus 0.45 +- 0.5 mycophenolate; p = 0.01).	Cyclophosphamide	257-273	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	198-204
24262494-10	2014	Up-regulated myeloperoxidase, IL-1beta, IL-6 and TNF-alpha expression in cyclophosphamide treated rats was also suppressed in rebamipide treated rats.	Cyclophosphamide	73-89	interleukin 1 beta	Rattus norvegicus	30-38
24262494-10	2014	Up-regulated myeloperoxidase, IL-1beta, IL-6 and TNF-alpha expression in cyclophosphamide treated rats was also suppressed in rebamipide treated rats.	Cyclophosphamide	73-89	interleukin 6	Rattus norvegicus	40-44
24262494-10	2014	Up-regulated myeloperoxidase, IL-1beta, IL-6 and TNF-alpha expression in cyclophosphamide treated rats was also suppressed in rebamipide treated rats.	Cyclophosphamide	73-89	tumor necrosis factor	Rattus norvegicus	49-58
24681512-3	2014	Previously, we have demonstrated an important role of recombinant human interleukin-1 receptor antagonist (rhIL-1Ra) in the prevention of cyclophosphamide-induced mucositis in mice.	Cyclophosphamide	138-154	interleukin 1 receptor antagonist	Homo sapiens	72-105
24104394-5	2014	MiR187-overexpressing cells were resistant to chemotherapeutic agents like doxorubicin, cyclophosphamide, cisplatin and gemcitabine, but sensitive to the proteasome inhibitor bortezomib.	Cyclophosphamide	88-104	microRNA 187	Homo sapiens	0-6
24262631-0	2014	Bladder pain relief by HMGB1 neutralization and soluble thrombomodulin in mice with cyclophosphamide-induced cystitis.	Cyclophosphamide	84-100	thrombomodulin	Mus musculus	56-70
24262631-2	2014	Given that no evidence for roles of HMGB1 in visceral pain signaling is available, we asked if HMGB1 participates in bladder pain accompanying cystitis caused by cyclophosphamide in mice, using the anti-HMGB1 neutralizing antibody and recombinant human soluble thrombomodulin (rhsTM) that sequesters HMGB1 and promotes its degradation by thrombin.	Cyclophosphamide	162-178	high mobility group box 1	Mus musculus	95-100
24262631-2	2014	Given that no evidence for roles of HMGB1 in visceral pain signaling is available, we asked if HMGB1 participates in bladder pain accompanying cystitis caused by cyclophosphamide in mice, using the anti-HMGB1 neutralizing antibody and recombinant human soluble thrombomodulin (rhsTM) that sequesters HMGB1 and promotes its degradation by thrombin.	Cyclophosphamide	162-178	high mobility group box 1	Mus musculus	95-100
24262631-2	2014	Given that no evidence for roles of HMGB1 in visceral pain signaling is available, we asked if HMGB1 participates in bladder pain accompanying cystitis caused by cyclophosphamide in mice, using the anti-HMGB1 neutralizing antibody and recombinant human soluble thrombomodulin (rhsTM) that sequesters HMGB1 and promotes its degradation by thrombin.	Cyclophosphamide	162-178	high mobility group box 1	Homo sapiens	95-100
24262631-6	2014	HMGB1, given i.p., facilitated the bladder pain and referred hyperalgesia caused by a subeffective dose of cyclophosphamide, an effect blocked by rhsTM.	Cyclophosphamide	107-123	high mobility group box 1	Mus musculus	0-5
24262631-7	2014	In the cyclophosphamide-treated mice, HMGB1 levels greatly decreased in the bladder tissue, particularly in the urothelial cells, but did not change in the plasma.	Cyclophosphamide	7-23	high mobility group box 1	Mus musculus	38-43
24262631-9	2014	Thus, our data indicate involvement of HMGB1 in the cyclophosphamide-induced bladder pain signaling, but not cystitis itself, and suggest that targeting HMGB1 with rhsTM or blocking RAGE might serve as a novel therapeutic strategy for the management of bladder pain.	Cyclophosphamide	52-68	high mobility group box 1	Mus musculus	39-44
24485462-5	2014	Specifically, the nitrogen mustard cyclophosphamide induces an acute secretory activating phenotype (ASAP), releasing CCL4, IL8, VEGF, and TNFalpha from treated tumor cells.	Cyclophosphamide	35-51	C-C motif chemokine ligand 4	Homo sapiens	118-122
24850459-0	2014	Complete remission achieved in a multiple myeloma patient with elevated serum KL-6 level by a combination regimen with bortezomib, cyclophosphamide, and dexamethasone.	Cyclophosphamide	131-147	mucin 1, cell surface associated	Homo sapiens	78-82
24688606-2	2014	However, the use of cyclophosphamide-based treatment regimens fundamentally altered disease outcomes, transforming AAV into a manageable, chronic illness.	Cyclophosphamide	20-36	adeno-associated virus integration site 1	Homo sapiens	115-118
24688606-3	2014	Despite the tremendous success of cyclophosphamide in the treatment of AAV, there remained a need for alternative therapies, due to high rates of treatment failures and significant toxicities.	Cyclophosphamide	34-50	adeno-associated virus integration site 1	Homo sapiens	71-74
24516666-7	2014	Furthermore, this septic death of pulmonary MVEC was markedly attenuated by cyclophosphamide-mediated depletion of neutrophils (PMN) or use of an anti-CD18 antibody developed for immunohistochemistry but shown to block CD18-dependent signaling.	Cyclophosphamide	76-92	integrin beta 2	Mus musculus	219-223
24395281-9	2014	Combination immunochemotherapy with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP) regimen improved both MALT lymphoma and PLE, whereas rituximab monotherapy was not successful.	Cyclophosphamide	47-63	DNA damage inducible transcript 3	Homo sapiens	111-115
24091681-9	2014	A significantly elevated number of CFU-GM was detected also in the femurs of PSGL-1(-/-) mice, 4 and 5 days after cyclophosphamide treatment and these values paralleled with the elevation of CD34+/CD117+ stem cell counts in the peripheral blood.	Cyclophosphamide	114-130	selectin, platelet (p-selectin) ligand	Mus musculus	77-83
24091681-9	2014	A significantly elevated number of CFU-GM was detected also in the femurs of PSGL-1(-/-) mice, 4 and 5 days after cyclophosphamide treatment and these values paralleled with the elevation of CD34+/CD117+ stem cell counts in the peripheral blood.	Cyclophosphamide	114-130	CD34 antigen	Mus musculus	191-195
23666265-0	2014	The function of P2X3 receptor and NK1 receptor antagonists on cyclophosphamide-induced cystitis in rats.	Cyclophosphamide	62-78	tachykinin receptor 1	Rattus norvegicus	34-46
23666265-1	2014	PURPOSE: The purpose of the study is to explore the function of P2X3 and NK1 receptors antagonists on cyclophosphamide (CYP)-induced cystitis in rats.	Cyclophosphamide	102-118	purinergic receptor P2X 3	Rattus norvegicus	64-68
24498107-3	2014	We examined the association of SOD2 genotype and breast cancer recurrence (BCR) among patients treated with cyclophosphamide-based chemotherapy (Cyclo).	Cyclophosphamide	108-124	superoxide dismutase 2	Homo sapiens	31-35
24663500-3	2014	The expression and activity of CYP1A1, 2B6 and 2E1 were carried out in the cells exposed to CYP inducers viz., 3-methylcholanthrene (3-MC), cyclophosphamide (CPA), ethanol and known neurotoxicant- monocrotophos (MCP), a widely used organophosphorous pesticide.	Cyclophosphamide	140-156	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	31-37
24663500-3	2014	The expression and activity of CYP1A1, 2B6 and 2E1 were carried out in the cells exposed to CYP inducers viz., 3-methylcholanthrene (3-MC), cyclophosphamide (CPA), ethanol and known neurotoxicant- monocrotophos (MCP), a widely used organophosphorous pesticide.	Cyclophosphamide	140-156	peptidylprolyl isomerase G	Homo sapiens	31-34
24663500-3	2014	The expression and activity of CYP1A1, 2B6 and 2E1 were carried out in the cells exposed to CYP inducers viz., 3-methylcholanthrene (3-MC), cyclophosphamide (CPA), ethanol and known neurotoxicant- monocrotophos (MCP), a widely used organophosphorous pesticide.	Cyclophosphamide	158-161	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	31-37
24663500-3	2014	The expression and activity of CYP1A1, 2B6 and 2E1 were carried out in the cells exposed to CYP inducers viz., 3-methylcholanthrene (3-MC), cyclophosphamide (CPA), ethanol and known neurotoxicant- monocrotophos (MCP), a widely used organophosphorous pesticide.	Cyclophosphamide	158-161	peptidylprolyl isomerase G	Homo sapiens	31-34
24663500-8	2014	Similarly, the known CYP inducers- 3-MC, CPA and ethanol have also shown significantly high docking scores with all the three studied CYP regulators.	Cyclophosphamide	41-44	peptidylprolyl isomerase G	Homo sapiens	21-24
24663500-8	2014	Similarly, the known CYP inducers- 3-MC, CPA and ethanol have also shown significantly high docking scores with all the three studied CYP regulators.	Cyclophosphamide	41-44	peptidylprolyl isomerase G	Homo sapiens	134-137
24677340-0	2014	Development of selective inhibitors for human aldehyde dehydrogenase 3A1 (ALDH3A1) for the enhancement of cyclophosphamide cytotoxicity.	Cyclophosphamide	106-122	aldehyde dehydrogenase 3 family member A1	Homo sapiens	46-72
24677340-0	2014	Development of selective inhibitors for human aldehyde dehydrogenase 3A1 (ALDH3A1) for the enhancement of cyclophosphamide cytotoxicity.	Cyclophosphamide	106-122	aldehyde dehydrogenase 3 family member A1	Homo sapiens	74-81
24677340-1	2014	Aldehyde dehydrogenase 3A1 (ALDH3A1) plays an important role in many cellular oxidative processes, including cancer chemoresistance, by metabolizing activated forms of oxazaphosphorine drugs such as cyclophosphamide (CP) and its analogues, such as mafosfamide (MF), ifosfamide (IFM), and 4-hydroperoxycyclophosphamide (4-HPCP).	Cyclophosphamide	199-215	aldehyde dehydrogenase 3 family member A1	Homo sapiens	0-26
24677340-1	2014	Aldehyde dehydrogenase 3A1 (ALDH3A1) plays an important role in many cellular oxidative processes, including cancer chemoresistance, by metabolizing activated forms of oxazaphosphorine drugs such as cyclophosphamide (CP) and its analogues, such as mafosfamide (MF), ifosfamide (IFM), and 4-hydroperoxycyclophosphamide (4-HPCP).	Cyclophosphamide	199-215	aldehyde dehydrogenase 3 family member A1	Homo sapiens	28-35
24637521-5	2014	In rats made neutropenic with cyclophosphamide, G-CSF/IgG1-Fc accelerated recovery of blood neutrophils to normal levels (from Day 9 to Day 5) when administered as 5 daily injections or as a single injection on Day 1.	Cyclophosphamide	30-46	colony stimulating factor 3	Rattus norvegicus	48-53
24637521-5	2014	In rats made neutropenic with cyclophosphamide, G-CSF/IgG1-Fc accelerated recovery of blood neutrophils to normal levels (from Day 9 to Day 5) when administered as 5 daily injections or as a single injection on Day 1.	Cyclophosphamide	30-46	immunoglobulin heavy constant gamma 1 (G1m marker)	Mus musculus	54-58
24724408-3	2014	The current standard of care for DLBCL is CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine, and prednisone) combined with rituximab, anti-CD20 antibody, allowing many patients to achieve disease cure.	Cyclophosphamide	61-77	DNA damage inducible transcript 3	Homo sapiens	42-46
24357324-3	2014	However, after cyclophosphamide was replaced with intravenous tocilizumab, the aortitis was improved, and the prednisolone dose was successfully tapered to 4 mg/day without elevation in C-reactive protein and myeloperoxidase ANCA (MPO-ANCA) levels.	Cyclophosphamide	15-31	myeloperoxidase	Homo sapiens	231-234
23728939-4	2014	Herein we show that PC-3 human prostate cancer xenografts were sensitive to both metronomic cyclophosphamide and metronomic docetaxel, but resistant to metronomic topotecan.	Cyclophosphamide	92-108	chromobox 8	Homo sapiens	20-24
23728939-5	2014	Conventional docetaxel was only moderately active in parental PC-3 and in metronomic cyclophosphamide resistant PC-3 tumors.	Cyclophosphamide	85-101	chromobox 8	Homo sapiens	112-116
23728939-6	2014	However, in metronomic cyclophosphamide resistant PC-3 tumors combining conventional docetaxel or bolus cyclophosphamide therapy with continued metronomic cyclophosphamide was superior to each treatment alone.	Cyclophosphamide	23-39	chromobox 8	Homo sapiens	50-54
23728939-6	2014	However, in metronomic cyclophosphamide resistant PC-3 tumors combining conventional docetaxel or bolus cyclophosphamide therapy with continued metronomic cyclophosphamide was superior to each treatment alone.	Cyclophosphamide	104-120	chromobox 8	Homo sapiens	50-54
23728939-6	2014	However, in metronomic cyclophosphamide resistant PC-3 tumors combining conventional docetaxel or bolus cyclophosphamide therapy with continued metronomic cyclophosphamide was superior to each treatment alone.	Cyclophosphamide	104-120	chromobox 8	Homo sapiens	50-54
23728939-7	2014	Furthermore, bevacizumab had single-agent activity against metronomic cyclophosphamide resistant PC-3 tumors.	Cyclophosphamide	70-86	chromobox 8	Homo sapiens	97-101
24485462-5	2014	Specifically, the nitrogen mustard cyclophosphamide induces an acute secretory activating phenotype (ASAP), releasing CCL4, IL8, VEGF, and TNFalpha from treated tumor cells.	Cyclophosphamide	35-51	C-X-C motif chemokine ligand 8	Homo sapiens	124-127
24485462-5	2014	Specifically, the nitrogen mustard cyclophosphamide induces an acute secretory activating phenotype (ASAP), releasing CCL4, IL8, VEGF, and TNFalpha from treated tumor cells.	Cyclophosphamide	35-51	vascular endothelial growth factor A	Homo sapiens	129-133
24485462-5	2014	Specifically, the nitrogen mustard cyclophosphamide induces an acute secretory activating phenotype (ASAP), releasing CCL4, IL8, VEGF, and TNFalpha from treated tumor cells.	Cyclophosphamide	35-51	tumor necrosis factor	Homo sapiens	139-147
24269385-1	2014	CASE REPORT: A patient diagnosed with necrotizing scleritis, c-ANCA+ an orbital pseudotumour, and possible multiple sclerosis in 2003 was treated with oral cyclophosphamide and steroids with partial response.	Cyclophosphamide	156-172	proteinase 3	Homo sapiens	61-67
24608395-11	2014	CONCLUSION: Corticosteroids and cyclophosphamide are effective in the treatment of MPO-ANCA associated glomerulonephritis in MCTD.	Cyclophosphamide	32-48	myeloperoxidase	Homo sapiens	83-86
24387105-3	2014	Upon activation, cyclophosphamide forms an intermediate, aldophosphamide, which can be detoxified to carboxyphosphamide by aldehyde dehydrogenases (ALDH), especially ALDH1A1 and ALDH3A1.	Cyclophosphamide	17-33	aldehyde dehydrogenase 1 family member A1	Homo sapiens	148-152
24387105-3	2014	Upon activation, cyclophosphamide forms an intermediate, aldophosphamide, which can be detoxified to carboxyphosphamide by aldehyde dehydrogenases (ALDH), especially ALDH1A1 and ALDH3A1.	Cyclophosphamide	17-33	aldehyde dehydrogenase 1 family member A1	Homo sapiens	166-173
24387105-3	2014	Upon activation, cyclophosphamide forms an intermediate, aldophosphamide, which can be detoxified to carboxyphosphamide by aldehyde dehydrogenases (ALDH), especially ALDH1A1 and ALDH3A1.	Cyclophosphamide	17-33	aldehyde dehydrogenase 3 family member A1	Homo sapiens	178-185
24387105-4	2014	Consequently, selective inhibition of ALDH3A1 could increase chemosensitivity toward cyclophosphamide in ALDH3A1 expressing tumors.	Cyclophosphamide	85-101	aldehyde dehydrogenase 3 family member A1	Homo sapiens	38-45
24387105-4	2014	Consequently, selective inhibition of ALDH3A1 could increase chemosensitivity toward cyclophosphamide in ALDH3A1 expressing tumors.	Cyclophosphamide	85-101	aldehyde dehydrogenase 3 family member A1	Homo sapiens	105-112
24466173-6	2014	RESULTS: Cyclophosphamide treatment down-regulated expression of several genes mapped to immune/autoimmune activation and graft rejection including CD3, CD28, CTLA4, MHC II, PRF1, GZMB and IL-2R, and up-regulated immune-related receptor genes, e.g. IL1R2, IL18R1, and FLT3.	Cyclophosphamide	9-25	CD28 molecule	Homo sapiens	153-157
24466173-6	2014	RESULTS: Cyclophosphamide treatment down-regulated expression of several genes mapped to immune/autoimmune activation and graft rejection including CD3, CD28, CTLA4, MHC II, PRF1, GZMB and IL-2R, and up-regulated immune-related receptor genes, e.g. IL1R2, IL18R1, and FLT3.	Cyclophosphamide	9-25	cytotoxic T-lymphocyte associated protein 4	Homo sapiens	159-164
24466173-6	2014	RESULTS: Cyclophosphamide treatment down-regulated expression of several genes mapped to immune/autoimmune activation and graft rejection including CD3, CD28, CTLA4, MHC II, PRF1, GZMB and IL-2R, and up-regulated immune-related receptor genes, e.g. IL1R2, IL18R1, and FLT3.	Cyclophosphamide	9-25	perforin 1	Homo sapiens	174-178
24466173-6	2014	RESULTS: Cyclophosphamide treatment down-regulated expression of several genes mapped to immune/autoimmune activation and graft rejection including CD3, CD28, CTLA4, MHC II, PRF1, GZMB and IL-2R, and up-regulated immune-related receptor genes, e.g. IL1R2, IL18R1, and FLT3.	Cyclophosphamide	9-25	granzyme B	Homo sapiens	180-184
24466173-6	2014	RESULTS: Cyclophosphamide treatment down-regulated expression of several genes mapped to immune/autoimmune activation and graft rejection including CD3, CD28, CTLA4, MHC II, PRF1, GZMB and IL-2R, and up-regulated immune-related receptor genes, e.g. IL1R2, IL18R1, and FLT3.	Cyclophosphamide	9-25	interleukin 2 receptor subunit alpha	Homo sapiens	189-194
24466173-6	2014	RESULTS: Cyclophosphamide treatment down-regulated expression of several genes mapped to immune/autoimmune activation and graft rejection including CD3, CD28, CTLA4, MHC II, PRF1, GZMB and IL-2R, and up-regulated immune-related receptor genes, e.g. IL1R2, IL18R1, and FLT3.	Cyclophosphamide	9-25	interleukin 1 receptor type 2	Homo sapiens	249-254
24466173-6	2014	RESULTS: Cyclophosphamide treatment down-regulated expression of several genes mapped to immune/autoimmune activation and graft rejection including CD3, CD28, CTLA4, MHC II, PRF1, GZMB and IL-2R, and up-regulated immune-related receptor genes, e.g. IL1R2, IL18R1, and FLT3.	Cyclophosphamide	9-25	interleukin 18 receptor 1	Homo sapiens	256-262
24466173-6	2014	RESULTS: Cyclophosphamide treatment down-regulated expression of several genes mapped to immune/autoimmune activation and graft rejection including CD3, CD28, CTLA4, MHC II, PRF1, GZMB and IL-2R, and up-regulated immune-related receptor genes, e.g. IL1R2, IL18R1, and FLT3.	Cyclophosphamide	9-25	fms related receptor tyrosine kinase 3	Homo sapiens	268-272
24466173-7	2014	Moreover, a high and significant expression of ANGPTL1 and c-JUN genes was observed independent of cyclophosphamide treatment.	Cyclophosphamide	99-115	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	59-64
24416401-0	2014	Effective chemoimmunotherapy with anti-TGFbeta antibody and cyclophosphamide in a mouse model of breast cancer.	Cyclophosphamide	60-76	transforming growth factor, beta 1	Mus musculus	39-46
24416401-11	2014	Taken together, our data show that anti-TGFbeta antibody and cyclophosphamide represents an effective chemoimmunotherapeutic combination.	Cyclophosphamide	61-77	transforming growth factor, beta 1	Mus musculus	40-47
29805869-3	2013	The aim of this study was to investigate the effect of new nano-encapsulated forms of recombinant human erythropoietin for oral use on the erythropoiesis in the cyclophosphamide immunosuppression model.	Cyclophosphamide	161-177	erythropoietin	Homo sapiens	104-118
29805869-17	2013	Conclusion: The erythropoietic activity of nano-encapsulated forms of erythropoietin was observed in the 0.05% and 0.005% pectin samples in the cyclophosphamide immunosuppression model setting.	Cyclophosphamide	144-160	erythropoietin	Mus musculus	70-84
25087953-0	2014	Schedule-dependent cytotoxicity of Etoposide and cyclophosphamide in P-glycoprotein-expressing human leukemic K-562 cells.	Cyclophosphamide	49-65	ATP binding cassette subfamily B member 1	Homo sapiens	69-83
25087953-3	2014	Our previous studies showed that K-562 cells pretreated with non-cytotoxic concentrations of 4-hydroperoxycyclophosphamide (4-HPC), which is a preactivated analog of cyclophosphamide (CY), enhanced the cytotoxicity of etoposide (VP-16).	Cyclophosphamide	106-122	host cell factor C1	Homo sapiens	229-234
25087953-6	2014	In the present study, we demonstrated schedule-dependent cytotoxicity of VP-16 and CY in P-gp-overexpressed K-562/P-gp cells.	Cyclophosphamide	83-85	ATP binding cassette subfamily B member 1	Homo sapiens	89-93
25087953-6	2014	In the present study, we demonstrated schedule-dependent cytotoxicity of VP-16 and CY in P-gp-overexpressed K-562/P-gp cells.	Cyclophosphamide	83-85	ATP binding cassette subfamily B member 1	Homo sapiens	114-118
24982868-1	2014	Nitric oxide (NO) has pivotal roles in cyclophosphamide- (CYP-) induced cystitis during which mucosal nitric oxide synthase (NOS) and muscarinic M5 receptor expressions are upregulated.	Cyclophosphamide	39-55	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	58-61
24117268-0	2014	Role of CXCR2 and TRPV1 in functional, inflammatory and behavioural changes in the rat model of cyclophosphamide-induced haemorrhagic cystitis.	Cyclophosphamide	96-112	C-X-C motif chemokine receptor 2	Rattus norvegicus	8-13
24117268-0	2014	Role of CXCR2 and TRPV1 in functional, inflammatory and behavioural changes in the rat model of cyclophosphamide-induced haemorrhagic cystitis.	Cyclophosphamide	96-112	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	18-23
24117268-7	2014	The CXCR2 antagonist, SB225002, the TRPV1 channel antagonist, SB366791 or their combination reduced the mechanical hypersensitivity of paw and abdominal area and nociceptive behaviour after cyclophosphamide.	Cyclophosphamide	190-206	C-X-C motif chemokine receptor 2	Rattus norvegicus	4-9
24117268-7	2014	The CXCR2 antagonist, SB225002, the TRPV1 channel antagonist, SB366791 or their combination reduced the mechanical hypersensitivity of paw and abdominal area and nociceptive behaviour after cyclophosphamide.	Cyclophosphamide	190-206	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	36-41
24117268-9	2014	Up-regulation of CXCR2 and TRPV1 mRNA in the bladder after cyclophosphamide was inhibited by SB225002, SB366791 or their combination.	Cyclophosphamide	59-75	C-X-C motif chemokine receptor 2	Rattus norvegicus	17-22
24117268-9	2014	Up-regulation of CXCR2 and TRPV1 mRNA in the bladder after cyclophosphamide was inhibited by SB225002, SB366791 or their combination.	Cyclophosphamide	59-75	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	27-32
24117268-10	2014	Expression of CXCR2 and TRPV1 channels was increased in the urothelium after cyclophosphamide.	Cyclophosphamide	77-93	C-X-C motif chemokine receptor 2	Rattus norvegicus	14-19
24117268-10	2014	Expression of CXCR2 and TRPV1 channels was increased in the urothelium after cyclophosphamide.	Cyclophosphamide	77-93	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	24-29
24117268-13	2014	CONCLUSIONS AND IMPLICATIONS: CXCR2 and TRPV1 channels play important roles in cyclophosphamide-induced cystitis in rats and could provide potential therapeutic targets for cystitis.	Cyclophosphamide	79-95	C-X-C motif chemokine receptor 2	Rattus norvegicus	30-35
24117268-13	2014	CONCLUSIONS AND IMPLICATIONS: CXCR2 and TRPV1 channels play important roles in cyclophosphamide-induced cystitis in rats and could provide potential therapeutic targets for cystitis.	Cyclophosphamide	79-95	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	40-45
24955264-11	2014	Long-term therapy was initiated with cyclophosphamide and prednisone with normalization of FVIII activity.	Cyclophosphamide	37-53	coagulation factor VIII	Homo sapiens	91-96
24791879-0	2014	Baseline proteinuria, urinary osmotic pressure, and renal function as positive predictors of corticosteroids plus cyclophosphamide treatment efficacy in IgA nephropathy.	Cyclophosphamide	114-130	IGAN1	Homo sapiens	153-168
24403451-5	2014	Flow cytometry to examine expression of the CSC markers C-X-C chemokine receptor type-4 (CXCR4; CD184) and ATP-binding cassette sub-family G member-2 (ABCG2; CDw338) revealed markedly higher levels of CXCR4 and ABCG2 in cyclophosphamide-treated xenograft tumor cells compared to untreated tumor cells.	Cyclophosphamide	220-236	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	158-164
24709186-8	2014	The chemotherapy-induced bone marrow suppression was established by intraperitoneally injecting cyclophosphamide (CTX) into the mice which performed as the chemotherapy group.	Cyclophosphamide	96-112	V-set and immunoglobulin domain containing 2	Mus musculus	114-117
24791879-1	2014	BACKGROUND: Very limited data are available on factors predictive of corticosteroids plus cyclophosphamide treatment efficacy on IgA nephropathy (IgAN).	Cyclophosphamide	90-106	IGAN1	Homo sapiens	129-144
24791879-1	2014	BACKGROUND: Very limited data are available on factors predictive of corticosteroids plus cyclophosphamide treatment efficacy on IgA nephropathy (IgAN).	Cyclophosphamide	90-106	IGAN1	Homo sapiens	146-150
24791879-7	2014	CONCLUSION: The response to the combination of corticosteroids and cyclophosphamide might be well associated with baseline proteinuria, urinary osmotic pressure, and renal function in patients with IgAN.	Cyclophosphamide	67-83	IGAN1	Homo sapiens	198-202
24654464-0	2014	Evaluation of the effect of GnRH agonist on menstrual reverse in breast cancer cases treated with cyclophosphamide.	Cyclophosphamide	98-114	gonadotropin releasing hormone 1	Homo sapiens	28-32
24766134-3	2014	We built a highly efficient suicide gene capable of bioactivating the prodrug cyclophosphamide (CPA) by fusing a CYP2B6 triple mutant with NADPH cytochrome P450 reductase (CYP2B6TM-RED).	Cyclophosphamide	78-94	cytochrome p450 oxidoreductase	Mus musculus	139-170
24766134-3	2014	We built a highly efficient suicide gene capable of bioactivating the prodrug cyclophosphamide (CPA) by fusing a CYP2B6 triple mutant with NADPH cytochrome P450 reductase (CYP2B6TM-RED).	Cyclophosphamide	96-99	cytochrome p450 oxidoreductase	Mus musculus	139-170
24403451-5	2014	Flow cytometry to examine expression of the CSC markers C-X-C chemokine receptor type-4 (CXCR4; CD184) and ATP-binding cassette sub-family G member-2 (ABCG2; CDw338) revealed markedly higher levels of CXCR4 and ABCG2 in cyclophosphamide-treated xenograft tumor cells compared to untreated tumor cells.	Cyclophosphamide	220-236	C-X-C motif chemokine receptor 4	Homo sapiens	56-87
24403451-5	2014	Flow cytometry to examine expression of the CSC markers C-X-C chemokine receptor type-4 (CXCR4; CD184) and ATP-binding cassette sub-family G member-2 (ABCG2; CDw338) revealed markedly higher levels of CXCR4 and ABCG2 in cyclophosphamide-treated xenograft tumor cells compared to untreated tumor cells.	Cyclophosphamide	220-236	C-X-C motif chemokine receptor 4	Homo sapiens	89-94
24654464-3	2014	The aim of this study was to evaluate the effect of gonadotropin releasing hormone (GnRH) agonist on menstrual reverse in breast cancer cases treated with cyclophosphamide regimen.	Cyclophosphamide	155-171	gonadotropin releasing hormone 1	Homo sapiens	52-82
24654464-3	2014	The aim of this study was to evaluate the effect of gonadotropin releasing hormone (GnRH) agonist on menstrual reverse in breast cancer cases treated with cyclophosphamide regimen.	Cyclophosphamide	155-171	gonadotropin releasing hormone 1	Homo sapiens	84-88
25555880-1	2014	OBJECTIVE: Cyclophosphamide (CTX) can attack tumour cells, but can also damage the other cells and microstructures of an organism at different levels, such as haematopoietic cells, liver cells, peripheral lymphocyte DNA, and genetic materials.	Cyclophosphamide	11-27	V-set and immunoglobulin domain containing 2	Mus musculus	29-32
24949077-3	2014	The present paper emphasizes antitumor effect of FZFA combined with cyclophosphamide (CTX) on C57BL/6 mice subcutaneously injected with Lewis lung cancer cells, Comparing it with that of CTX.	Cyclophosphamide	68-84	V-set and immunoglobulin domain containing 2	Mus musculus	86-89
24143112-1	2013	Fludarabine-based regimens and CHOP (doxorubicin, cyclophosphamide, vincristine, prednisone)-like regimens with or without rituximab are the most common treatment modalities for indolent lymphoma.	Cyclophosphamide	50-66	DNA damage inducible transcript 3	Homo sapiens	31-35
24316550-2	2014	CD25 antibodies and cyclophosphamide are well-studied immunomodulators through inhibition of regulatory T cells (Treg) and a blockade the immune-checkpoint molecule, cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) was recently targeted for immunomodulation.	Cyclophosphamide	20-36	cytotoxic T-lymphocyte-associated protein 4	Mus musculus	166-209
24316550-2	2014	CD25 antibodies and cyclophosphamide are well-studied immunomodulators through inhibition of regulatory T cells (Treg) and a blockade the immune-checkpoint molecule, cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) was recently targeted for immunomodulation.	Cyclophosphamide	20-36	cytotoxic T-lymphocyte-associated protein 4	Mus musculus	211-217
24800167-2	2014	Our recent work suggests that anti-commensal effector pTH17 and memory TH1 CD4+ T-cell responses are indispensable for optimal anticancer effects as mediated by cyclophosphamide.	Cyclophosphamide	161-177	negative elongation factor complex member C/D	Homo sapiens	55-58
23494828-0	2014	Protective effects of total flavonoids from Epimedium on the male mouse reproductive system against cyclophosphamide-induced oxidative injury by up-regulating the expressions of SOD3 and GPX1.	Cyclophosphamide	100-116	superoxide dismutase 3, extracellular	Mus musculus	178-182
23494828-0	2014	Protective effects of total flavonoids from Epimedium on the male mouse reproductive system against cyclophosphamide-induced oxidative injury by up-regulating the expressions of SOD3 and GPX1.	Cyclophosphamide	100-116	glutathione peroxidase 1	Mus musculus	187-191
24803924-0	2014	Peroxisome Proliferator Activator Receptor (PPAR)- gamma Ligand, but Not PPAR- alpha , Ameliorates Cyclophosphamide-Induced Oxidative Stress and Inflammation in Rat Liver.	Cyclophosphamide	99-115	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	0-56
24881927-8	2014	Further evaluation of c-SLE patients treated with cyclophosphamide revealed a higher median of FSH levels compared to c-SLE patients not treated with cyclophosphamide and controls (8.8 vs. 5.7 vs. 5.6 IU/L, p = 0.032) and lower median AMH (0.4 vs. 1.5 vs. 1.5 ng/mL, p = 0.004) and AFC (4.0 vs. 6.5 vs. 16 IU/L, p = 0.001) levels.	Cyclophosphamide	50-66	anti-Mullerian hormone	Homo sapiens	235-238
24262132-0	2014	Post-transplant cyclophosphamide and bortezomib inhibit dendritic cell maturation and function and alter their IkappaB and NFkappaB.	Cyclophosphamide	16-32	nuclear factor kappa B subunit 1	Homo sapiens	123-131
24358271-3	2013	Compared to the traditional methodology, our cell-sheet approach resulted in longer-term and 3-5-fold higher expression of FVIII (up to 11% of normal) in recipient hemophilia A mice that lacked a FVIII humoral immune response due to transient immunosuppression with cyclophosphamide.	Cyclophosphamide	266-282	coagulation factor VIII	Mus musculus	123-128
24184018-2	2013	Here we report that phosphoinositide 3-kinase (PI3K)-dependent Akt activation and N-methyl-d-aspartic acid receptor (NMDAR) in lumbosacral spinal cord independently regulate the activation of cAMP response element-binding protein (CREB) in vivo in a rat visceral pain model of cystitis induced by intraperitoneal injection of cyclophosphamide (CYP).	Cyclophosphamide	326-342	phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit gamma	Rattus norvegicus	20-45
24184018-2	2013	Here we report that phosphoinositide 3-kinase (PI3K)-dependent Akt activation and N-methyl-d-aspartic acid receptor (NMDAR) in lumbosacral spinal cord independently regulate the activation of cAMP response element-binding protein (CREB) in vivo in a rat visceral pain model of cystitis induced by intraperitoneal injection of cyclophosphamide (CYP).	Cyclophosphamide	326-342	AKT serine/threonine kinase 1	Rattus norvegicus	63-66
24184018-2	2013	Here we report that phosphoinositide 3-kinase (PI3K)-dependent Akt activation and N-methyl-d-aspartic acid receptor (NMDAR) in lumbosacral spinal cord independently regulate the activation of cAMP response element-binding protein (CREB) in vivo in a rat visceral pain model of cystitis induced by intraperitoneal injection of cyclophosphamide (CYP).	Cyclophosphamide	326-342	cAMP responsive element binding protein 1	Rattus norvegicus	192-229
24184018-2	2013	Here we report that phosphoinositide 3-kinase (PI3K)-dependent Akt activation and N-methyl-d-aspartic acid receptor (NMDAR) in lumbosacral spinal cord independently regulate the activation of cAMP response element-binding protein (CREB) in vivo in a rat visceral pain model of cystitis induced by intraperitoneal injection of cyclophosphamide (CYP).	Cyclophosphamide	326-342	cAMP responsive element binding protein 1	Rattus norvegicus	231-235
23196752-12	2013	Cyclophosphamide increased the level of serum biomarkers: total protein, lactate dehydrogenase, and tumor necrosis factor-alpha (TNF-alpha).	Cyclophosphamide	0-16	tumor necrosis factor	Rattus norvegicus	100-127
23196752-12	2013	Cyclophosphamide increased the level of serum biomarkers: total protein, lactate dehydrogenase, and tumor necrosis factor-alpha (TNF-alpha).	Cyclophosphamide	0-16	tumor necrosis factor	Rattus norvegicus	129-138
24348180-12	2013	Lung myeloperoxidase activity, which was increased by cyclophosphamide, was decreased significantly by EECp (400 mg/kg).	Cyclophosphamide	54-70	myeloperoxidase	Rattus norvegicus	5-20
24219888-7	2013	RESULTS: Our results demonstrate that transient inhibition of eIF4E protects against cyclophosphamide-induced alopecia at the organismal level.	Cyclophosphamide	85-101	eukaryotic translation initiation factor 4E	Homo sapiens	62-67
23942768-12	2013	These results suggest that patients receiving intensive immunosuppressive therapy such as high-dose glucocorticoids and cyclophosphamide are at higher risk for developing CMV-UGT.	Cyclophosphamide	120-136	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	175-178
24080320-4	2013	ELISA experiments showed that COS treatment enhanced production of the cytokines IL-2, IL-12, and IFN-gamma but decreased production of IL-10 in sera of Cy-treated mice.	Cyclophosphamide	153-155	interleukin 10	Mus musculus	136-141
23775435-1	2013	BACKGROUND: High levels of cyclin E (CCNE) are accompanied by shorter survival in cyclophosphamide, hydroxydaunorubicin, oncovin and prednisone (CHOP)-treated diffuse large B-cell lymphomas (DLBCL), independent of the international prognostic index (IPI).	Cyclophosphamide	82-98	cyclin E1	Homo sapiens	27-35
23775435-1	2013	BACKGROUND: High levels of cyclin E (CCNE) are accompanied by shorter survival in cyclophosphamide, hydroxydaunorubicin, oncovin and prednisone (CHOP)-treated diffuse large B-cell lymphomas (DLBCL), independent of the international prognostic index (IPI).	Cyclophosphamide	82-98	cyclin E1	Homo sapiens	37-41
25073258-5	2013	Our patient showed a high dermal Ki-67 level and concomitant C-MYC/8q24 translocation, which may account for the aggressive clinical course and refractoriness to CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisone) chemotherapy.	Cyclophosphamide	168-184	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	61-66
24090996-0	2013	Distinct sensitivity of CD8+ CD4- and CD8+ CD4+ leukemic cell subpopulations to cyclophosphamide and rapamycin in Notch1-induced T-ALL mouse model.	Cyclophosphamide	80-96	CD4 antigen	Mus musculus	43-46
24090996-0	2013	Distinct sensitivity of CD8+ CD4- and CD8+ CD4+ leukemic cell subpopulations to cyclophosphamide and rapamycin in Notch1-induced T-ALL mouse model.	Cyclophosphamide	80-96	notch 1	Mus musculus	114-120
24090996-4	2013	We found that Notch1 induced T-ALL cells could be decreased by chemotherapeutic drug cyclophosphamide (CTX).	Cyclophosphamide	85-101	notch 1	Mus musculus	14-20
23911305-0	2013	Delivery and processing of exogenous double-stranded DNA in mouse CD34+ hematopoietic progenitor cells and their cell cycle changes upon combined treatment with cyclophosphamide and double-stranded DNA.	Cyclophosphamide	161-177	CD34 antigen	Mus musculus	66-70
23911305-9	2013	Cell cycle analysis of CD34+ cells treated with cyclophosphamide only or in combination with dsDNA, suggests that these cells have distinct biologic responses to these treatments.	Cyclophosphamide	48-64	CD34 antigen	Mus musculus	23-27
23911305-12	2013	We observe that cyclophosphamide-only or a combined cyclophosphamide+dsDNA treatment of cells lead to two distinct waves of apoptosis in CD34+ progenitors.	Cyclophosphamide	16-32	CD34 antigen	Mus musculus	137-141
23911305-12	2013	We observe that cyclophosphamide-only or a combined cyclophosphamide+dsDNA treatment of cells lead to two distinct waves of apoptosis in CD34+ progenitors.	Cyclophosphamide	52-68	CD34 antigen	Mus musculus	137-141
23911305-13	2013	We also show that cyclophosphamide and cyclophosphamide+dsDNA injections promote division of CD34+ cells at distinct time periods.	Cyclophosphamide	18-34	CD34 antigen	Mus musculus	93-97
23911305-13	2013	We also show that cyclophosphamide and cyclophosphamide+dsDNA injections promote division of CD34+ cells at distinct time periods.	Cyclophosphamide	39-55	CD34 antigen	Mus musculus	93-97
23868108-0	2014	Long-term remission of atypical HUS with anti-factor H antibodies after cyclophosphamide pulses.	Cyclophosphamide	72-88	complement factor H	Homo sapiens	46-54
23868108-2	2014	METHODS: We report the follow-up of four children with anti-CFH Ab (8,000 to >32,000 arbitrary units)-associated aHUS after plasma exchanges (PEs), prednisone, and cyclophosphamide pulse therapy with the evolution of anti-CFH Ab titers and kidney function.	Cyclophosphamide	167-183	complement factor H	Homo sapiens	60-63
23868108-7	2014	CONCLUSIONS: We demonstrate the long-term efficiency and safety of cyclophosphamide pulses combined with PEs and prednisone in anti-CFH Ab-associated aHUS leading to a prolonged decrease in anti-CFH Ab titers and prevention of relapses without the need for maintenance therapy.	Cyclophosphamide	67-83	complement factor H	Homo sapiens	132-135
23868108-7	2014	CONCLUSIONS: We demonstrate the long-term efficiency and safety of cyclophosphamide pulses combined with PEs and prednisone in anti-CFH Ab-associated aHUS leading to a prolonged decrease in anti-CFH Ab titers and prevention of relapses without the need for maintenance therapy.	Cyclophosphamide	67-83	complement factor H	Homo sapiens	195-198
24106983-8	2014	A robust mitogen-induced IFN-gamma response was seen in samples from 14 patients (88%) despite therapy with high-dose corticosteroids, cyclophosphamide, fludarabine, gemtuzumab ozogamicin, and alemtuzumab.	Cyclophosphamide	135-151	interferon gamma	Homo sapiens	25-34
24376696-0	2013	Human CD4+CD25+ regulatory T cells are sensitive to low dose cyclophosphamide: implications for the immune response.	Cyclophosphamide	61-77	CD4 molecule	Homo sapiens	6-9
24128861-0	2013	CYP2B6*6 is an independent determinant of inferior response to fludarabine plus cyclophosphamide in chronic lymphocytic leukemia.	Cyclophosphamide	80-96	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	0-6
24128861-2	2013	CYP2B6 is a polymorphic cytochrome P450 isoform that converts cyclophosphamide to its active form.	Cyclophosphamide	62-78	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	0-6
24357708-0	2013	Cyclophosphamide for CLL: to be or not CYP2B activated?	Cyclophosphamide	0-16	cytochrome P450 family 2 subfamily B member 7, pseudogene	Homo sapiens	39-44
24075480-9	2013	Lastly, the classic anticancer prodrug cyclophosphamide (CTX) was chosen as a model drug for the study of drug metabolism and the prediction of drug effects.	Cyclophosphamide	39-55	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	57-60
24067072-2	2013	Pre-pubertal female C57BL/6J mice (n = 78) were assigned to receive placebo (controls), 200 mg/kg (group A), or 120 mg/kg (group B) of cyclophosphamide (CTX) on postnatal day 18.	Cyclophosphamide	135-151	V-set and immunoglobulin domain containing 2	Mus musculus	153-156
24036158-6	2013	Cyclophosphamide stimulated OAT1, but did not affect OAT3.	Cyclophosphamide	0-16	solute carrier family 22 member 6	Homo sapiens	28-32
24036158-7	2013	With regard to the apical efflux transporters, mycophenolic acid, cyclophosphamide, hydrocortisone, and tacrolimus inhibited MRP2 and MRP4, whereas mitoxantrone and dexamethasone stimulated [(3)H]-MTX transport by both transporters.	Cyclophosphamide	66-82	ATP binding cassette subfamily C member 2	Homo sapiens	125-129
24036158-7	2013	With regard to the apical efflux transporters, mycophenolic acid, cyclophosphamide, hydrocortisone, and tacrolimus inhibited MRP2 and MRP4, whereas mitoxantrone and dexamethasone stimulated [(3)H]-MTX transport by both transporters.	Cyclophosphamide	66-82	ATP binding cassette subfamily C member 4	Homo sapiens	134-138
24036158-7	2013	With regard to the apical efflux transporters, mycophenolic acid, cyclophosphamide, hydrocortisone, and tacrolimus inhibited MRP2 and MRP4, whereas mitoxantrone and dexamethasone stimulated [(3)H]-MTX transport by both transporters.	Cyclophosphamide	66-82	metaxin 1	Homo sapiens	197-200
24324391-1	2013	Possible genoprotective effect of Citrullus colocynthis (L.) (CCT) fruits extract against cyclophosphamide- (CP-)induced DNA damage in mice bone marrow cells was evaluated using micronucleus assay, as an index of induced chromosomal damage.	Cyclophosphamide	90-106	t-complex protein 1	Mus musculus	62-65
24166716-18	2013	Cyclosporin was as effective as cyclophosphamide (RR 1.07, 95% CI 0.48 to 2.35) and chlorambucil (RR 0.82, 95% CI 0.44 to 1.53) at the end of therapy while levamisole (RR 0.47, 95% CI 0.24 to 0.89) was more effective than steroids alone.	Cyclophosphamide	32-48	ribonucleotide reductase catalytic subunit M1	Homo sapiens	50-54
23672298-1	2013	BACKGROUND: Serum soluble tumor necrosis factor receptor 2 (sTNFR2) concentration predicted the clinical outcome of patients with aggressive non-Hodgkin"s lymphoma including diffuse large B-cell lymphoma (DLBCL) treated with CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisolone) in our previous study.	Cyclophosphamide	231-247	TNF receptor superfamily member 1B	Homo sapiens	26-58
23636313-7	2013	Activation of the PI3K/AKT/mTOR pathway was related to poor disease outcome in DLBCL patients treated with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) but not in those treated with rituximab-CHOP.	Cyclophosphamide	107-123	AKT serine/threonine kinase 1	Homo sapiens	23-26
23636313-7	2013	Activation of the PI3K/AKT/mTOR pathway was related to poor disease outcome in DLBCL patients treated with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) but not in those treated with rituximab-CHOP.	Cyclophosphamide	107-123	mechanistic target of rapamycin kinase	Homo sapiens	27-31
23636313-7	2013	Activation of the PI3K/AKT/mTOR pathway was related to poor disease outcome in DLBCL patients treated with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) but not in those treated with rituximab-CHOP.	Cyclophosphamide	107-123	DNA damage inducible transcript 3	Homo sapiens	167-171
24639699-10	2013	CONCLUSION: These results demonstrated that, analogue of GnRH i.e., decapeptyl protect morphologic, morphometric, and stereologic alterations of the testes tissue, as well as gonadotropic and gonadal hormonal changes preceding cyclophosphamide treatment in male mice.	Cyclophosphamide	227-243	gonadotropin releasing hormone 1	Mus musculus	57-61
23764550-5	2013	Both corticosteroids and ACTH (corticotropin) significantly lowered CCL21 to control levels, as they did in combination with IVIg, rituximab, cyclophosphamide or other treatments, without additional reduction attributable to the other agents.	Cyclophosphamide	142-158	proopiomelanocortin	Homo sapiens	25-29
24007746-0	2013	Adjuvant docetaxel and cyclophosphamide plus trastuzumab in patients with HER2-amplified early stage breast cancer: a single-group, open-label, phase 2 study.	Cyclophosphamide	23-39	erb-b2 receptor tyrosine kinase 2	Homo sapiens	74-78
24007746-15	2013	INTERPRETATION: A short, four-cycle regimen of docetaxel and cyclophosphamide combined with trastuzumab could be an option for adjuvant treatment of women with lower risk HER2-amplified early breast cancer, irrespective of TOP2A status.	Cyclophosphamide	61-77	erb-b2 receptor tyrosine kinase 2	Homo sapiens	171-175
24007746-15	2013	INTERPRETATION: A short, four-cycle regimen of docetaxel and cyclophosphamide combined with trastuzumab could be an option for adjuvant treatment of women with lower risk HER2-amplified early breast cancer, irrespective of TOP2A status.	Cyclophosphamide	61-77	DNA topoisomerase II alpha	Homo sapiens	223-228
23650219-2	2013	Our objective was to describe the outcomes and toxicities for a topotecan and cyclophosphamide (TOPO/CTX) regimen for first relapse or progression of high-risk neuroblastoma.	Cyclophosphamide	78-94	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	101-104
23444104-0	2013	Cyclophosphamide enhances antitumor efficacy of oncolytic adenovirus expressing uracil phosphoribosyltransferase (UPRT) in immunocompetent Syrian hamsters.	Cyclophosphamide	0-16	uracil phosphoribosyltransferase homolog	Mesocricetus auratus	80-112
23444104-0	2013	Cyclophosphamide enhances antitumor efficacy of oncolytic adenovirus expressing uracil phosphoribosyltransferase (UPRT) in immunocompetent Syrian hamsters.	Cyclophosphamide	0-16	uracil phosphoribosyltransferase homolog	Mesocricetus auratus	114-118
24047774-2	2013	A phase I study of sequential S-1 and cyclophosphamide(CPA)therapy was conducted to determine the dose-limiting toxicities(DLTs)and recommended doses(RDs)in patients with metastatic or recurrent breast cancer(MBC).	Cyclophosphamide	38-54	carboxypeptidase A1	Homo sapiens	55-58
23663075-9	2013	Cyclophosphamide treatment led to a significantly lower percentage of apoptotic CD4(+) , CD8(+) and CD4(+) CD25(+) T cells in SPCs from NOD.GzmB(-/-) mice than those from wt-NOD mice.	Cyclophosphamide	0-16	CD4 antigen	Mus musculus	80-83
23663075-9	2013	Cyclophosphamide treatment led to a significantly lower percentage of apoptotic CD4(+) , CD8(+) and CD4(+) CD25(+) T cells in SPCs from NOD.GzmB(-/-) mice than those from wt-NOD mice.	Cyclophosphamide	0-16	CD4 antigen	Mus musculus	100-103
23663075-9	2013	Cyclophosphamide treatment led to a significantly lower percentage of apoptotic CD4(+) , CD8(+) and CD4(+) CD25(+) T cells in SPCs from NOD.GzmB(-/-) mice than those from wt-NOD mice.	Cyclophosphamide	0-16	interleukin 2 receptor, alpha chain	Mus musculus	107-111
23663075-9	2013	Cyclophosphamide treatment led to a significantly lower percentage of apoptotic CD4(+) , CD8(+) and CD4(+) CD25(+) T cells in SPCs from NOD.GzmB(-/-) mice than those from wt-NOD mice.	Cyclophosphamide	0-16	granzyme B	Mus musculus	140-144
23683582-4	2013	CCL2-induced hyperalgesia was abolished by prior systemic leukocyte depletion by cyclophosphamide and was reconstituted by local adoptive transfer of donor macrophages but not of neutrophils.	Cyclophosphamide	81-97	C-C motif chemokine ligand 2	Homo sapiens	0-4
23833039-10	2013	The mean AMH level was low (1.21 +- 1.01 ng/mL) and was significantly lower in patients exposed to cyclophosphamide (P = .03) and in patients older than 30 years (P = .02).	Cyclophosphamide	99-115	anti-Mullerian hormone	Homo sapiens	9-12
23833039-13	2013	CONCLUSION: We confirmed that AMH levels are low in SLE patients and decrease significantly with age and cyclophosphamide exposure.	Cyclophosphamide	105-121	anti-Mullerian hormone	Homo sapiens	30-33
22972016-0	2013	Dynamics of serum angiopoietin-2 levels correlate with efficacy of intravenous pulse cyclophosphamide therapy for interstitial lung disease associated with systemic sclerosis.	Cyclophosphamide	85-101	angiopoietin 2	Homo sapiens	18-32
23810843-3	2013	AIM OF THE STUDY: The purpose of this study is to evaluate the immunostimulatory effects of the hot water extract from the leaves of Artemisia princeps Pampanini (WAPP) in recombinant interferon-gamma (rIFN-gamma)-primed RAW 264.7 macrophages and in cyclophosphamide (20mg/kg, i.p.	Cyclophosphamide	250-266	interferon gamma	Rattus norvegicus	202-212
24244905-3	2013	In particular, we found that cyclophosphamide stimulates anticancer immune responses upon the perception by the immune system of inflammatory danger signals associated with the death of leukocytes, via p53 and type I interferon-related mechanisms.	Cyclophosphamide	29-45	tumor protein p53	Homo sapiens	202-205
23962393-0	2013	Systemic sclerosis sera affect fibrillin-1 deposition by dermal blood microvascular endothelial cells: therapeutic implications of cyclophosphamide.	Cyclophosphamide	131-147	fibrillin 1	Homo sapiens	31-42
23860526-0	2013	VEGF-A polymorphisms predict progression-free survival among advanced castration-resistant prostate cancer patients treated with metronomic cyclophosphamide.	Cyclophosphamide	140-156	vascular endothelial growth factor A	Homo sapiens	0-6
23860526-2	2013	The aim of this study was to evaluate the association between VEGF-A sequence variants and prostate-specific antigen (PSA) progression, progression-free survival (PFS) and overall survival (OS), in advanced castration-resistant prostate cancer patients treated with metronomic cyclophosphamide (CTX), celecoxib and dexamethasone.	Cyclophosphamide	277-293	vascular endothelial growth factor A	Homo sapiens	62-68
23941509-5	2013	More importantly, in combination with temporary depletion of regulatory T cells (Treg) by low-dose cyclophosphamide, vaccination with scFvNLDC-145-HER2/neu induced the regression of established D2F2/E2 breast tumor and significantly retarded the development of spontaneous mammary carcinomas in transgenic BALB-neuT mice.	Cyclophosphamide	99-115	erb-b2 receptor tyrosine kinase 2	Mus musculus	134-155
23791611-2	2013	We aimed to investigate the alterations of mucosal barrier and colonization resistance in mouse treated with cyclophosphamide (CTX) to further understand the translocation mechanism.	Cyclophosphamide	109-125	V-set and immunoglobulin domain containing 2	Mus musculus	127-130
23588565-5	2013	RESULTS: A population PK analysis showed that the ABCC2 1249 genotype and aspartate aminotransferase levels significantly affected non-induced clearance (CL UI) and induced clearance (CL I) of CY, respectively.	Cyclophosphamide	193-195	ATP binding cassette subfamily C member 2	Homo sapiens	50-55
23759676-6	2013	Accordingly, cyclophosphamide induced the expansion/activation of CD14(+)CD16(+) monocytes, of HLA-DR(+), IL-8RA(+), and MARCO(+) monocytes/dendritic cells, and of CD69(+), OX40(+), and IL-8RA(+) lymphocytes.	Cyclophosphamide	13-29	CD14 molecule	Homo sapiens	66-70
23759676-6	2013	Accordingly, cyclophosphamide induced the expansion/activation of CD14(+)CD16(+) monocytes, of HLA-DR(+), IL-8RA(+), and MARCO(+) monocytes/dendritic cells, and of CD69(+), OX40(+), and IL-8RA(+) lymphocytes.	Cyclophosphamide	13-29	Fc gamma receptor IIIa	Homo sapiens	73-77
23759676-6	2013	Accordingly, cyclophosphamide induced the expansion/activation of CD14(+)CD16(+) monocytes, of HLA-DR(+), IL-8RA(+), and MARCO(+) monocytes/dendritic cells, and of CD69(+), OX40(+), and IL-8RA(+) lymphocytes.	Cyclophosphamide	13-29	C-X-C motif chemokine receptor 1	Homo sapiens	106-112
23759676-6	2013	Accordingly, cyclophosphamide induced the expansion/activation of CD14(+)CD16(+) monocytes, of HLA-DR(+), IL-8RA(+), and MARCO(+) monocytes/dendritic cells, and of CD69(+), OX40(+), and IL-8RA(+) lymphocytes.	Cyclophosphamide	13-29	macrophage receptor with collagenous structure	Homo sapiens	121-126
23759676-6	2013	Accordingly, cyclophosphamide induced the expansion/activation of CD14(+)CD16(+) monocytes, of HLA-DR(+), IL-8RA(+), and MARCO(+) monocytes/dendritic cells, and of CD69(+), OX40(+), and IL-8RA(+) lymphocytes.	Cyclophosphamide	13-29	CD69 molecule	Homo sapiens	164-168
23759676-6	2013	Accordingly, cyclophosphamide induced the expansion/activation of CD14(+)CD16(+) monocytes, of HLA-DR(+), IL-8RA(+), and MARCO(+) monocytes/dendritic cells, and of CD69(+), OX40(+), and IL-8RA(+) lymphocytes.	Cyclophosphamide	13-29	C-X-C motif chemokine receptor 1	Homo sapiens	186-192
23759676-7	2013	CONCLUSIONS: Altogether, these data identify the cyclophosphamide-induced immunomodulatory factors in humans and indicate that preconditioning chemotherapy may stimulate immunity as a consequence of danger perception associated with blood cell death, through p53 and IFN-I-related mechanisms.	Cyclophosphamide	49-65	tumor protein p53	Homo sapiens	259-262
23703311-13	2013	Cyclophosphamide is also used for refractory neurosarcoidosis patients, but, because of the drug"s significant toxicity, it is usually reserved for severe cases that have failed oral therapies when tumor necrosis factor alpha antagonists cannot be obtained.	Cyclophosphamide	0-16	tumor necrosis factor	Homo sapiens	198-225
23806407-0	2013	Alterations in deoxyribonucleic acid (DNA) methylation patterns of Calca, Timp3, Mmp2, and Igf2r are associated with chronic cystitis in a cyclophosphamide-induced mouse model.	Cyclophosphamide	139-155	calcitonin/calcitonin-related polypeptide, alpha	Mus musculus	67-72
24074787-8	2013	We reported that TP53 mutated non inflammatory locally advanced breast carcinomas had a high rate of complete pathological response to dose-dense doxorubicin-cyclophosphamide chemotherapy, while TP53 wild-type (WT) tumors never achieved complete response.	Cyclophosphamide	158-174	tumor protein p53	Homo sapiens	17-21
23846384-2	2013	The BM infiltration and the condition of the MF improved following CHOP therapy (cyclophosphamide hydrate, doxorubicin hydrochloride, vincristine sulfate, and prednisolone).	Cyclophosphamide	81-105	DNA damage inducible transcript 3	Homo sapiens	67-71
22512726-5	2013	The effects of paclitaxel, cyclophosphamide, and gemcitabine, are antineoplastic agents, were examined on the in vitro enzyme activity of glutathione S-transferase and were determined to be inhibitors for the enzyme.	Cyclophosphamide	27-43	glutathione S-transferase kappa 1	Homo sapiens	138-163
23137070-3	2013	Patients treated with rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) had significantly superior survival rates.	Cyclophosphamide	33-49	DNA damage inducible transcript 3	Homo sapiens	94-98
23922735-8	2013	RESULTS: Repeated cyclophosphamide injections induce a specific increase in the expression of TRPC1 and TRPC4 in bladder-innervating sensory neurons and the sprouting of sensory fibers in the bladder mucosa.	Cyclophosphamide	18-34	transient receptor potential cation channel, subfamily C, member 1	Mus musculus	94-99
23922735-8	2013	RESULTS: Repeated cyclophosphamide injections induce a specific increase in the expression of TRPC1 and TRPC4 in bladder-innervating sensory neurons and the sprouting of sensory fibers in the bladder mucosa.	Cyclophosphamide	18-34	transient receptor potential cation channel, subfamily C, member 4	Mus musculus	104-109
23922735-9	2013	Interestingly, cyclophosphamide-treated Trpc1/c4(-/-) mice no longer exhibited increased bladder innervations, and, concomitantly, the development of bladder overactivity was diminished in these mice.	Cyclophosphamide	15-31	transient receptor potential cation channel, subfamily C, member 1	Mus musculus	40-45
23894460-2	2013	Because the epidermal growth factor receptor (EGFR) signals anagen hair follicles to enter catagen, we hypothesized that EGFR signaling may be involved in cyclophosphamide-induced alopecia.	Cyclophosphamide	155-171	epidermal growth factor receptor	Mus musculus	12-44
23894460-2	2013	Because the epidermal growth factor receptor (EGFR) signals anagen hair follicles to enter catagen, we hypothesized that EGFR signaling may be involved in cyclophosphamide-induced alopecia.	Cyclophosphamide	155-171	epidermal growth factor receptor	Mus musculus	46-50
23894460-2	2013	Because the epidermal growth factor receptor (EGFR) signals anagen hair follicles to enter catagen, we hypothesized that EGFR signaling may be involved in cyclophosphamide-induced alopecia.	Cyclophosphamide	155-171	epidermal growth factor receptor	Mus musculus	121-125
23894460-4	2013	Cyclophosphamide treatment of control mice resulted in alopecia while Egfr mutant skin was resistant to cyclophosphamide-induced alopecia.	Cyclophosphamide	104-120	epidermal growth factor receptor	Mus musculus	70-74
23894460-6	2013	Egfr mutant follicles responded with less proliferation, apoptosis, and fewer p53-positive cells after cyclophosphamide.	Cyclophosphamide	103-119	epidermal growth factor receptor	Mus musculus	0-4
23894460-7	2013	Treatment of control mice with the EGFR inhibitors erlotinib or gefitinib similarly suppressed alopecia and catagen progression by cyclophosphamide.	Cyclophosphamide	131-147	epidermal growth factor receptor	Mus musculus	35-39
23838374-4	2013	METHODS: Female mice were injected intraperitoneally with 50 mg/kg cyclophosphamide (CTX).	Cyclophosphamide	67-83	V-set and immunoglobulin domain containing 2	Mus musculus	85-88
23737517-10	2013	Profound hypothyroidism likely contributed to the patient"s poor response to cyclophosphamide treatment through its influence on CYP isoenzymes responsible for the activation to 4-hydroxycyclophosphamide and possibly through reduced transport function.	Cyclophosphamide	77-93	peptidylprolyl isomerase G	Homo sapiens	129-132
23686226-0	2013	A bystander cell-based GM-CSF secreting vaccine synergized with a low dose of cyclophosphamide presents therapeutic immune responses against murine hepatocellular carcinoma.	Cyclophosphamide	78-94	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	23-29
23608739-9	2013	Cyclophosphamide, methotrexate, and corticosteroid treatment decreased the number of DN and CD27(high) B cells.	Cyclophosphamide	0-16	CD27 molecule	Homo sapiens	92-96
23473836-0	2013	High-dose cyclophosphamide used to treat aplastic anemia in a patient with respiratory and food allergies has a prolonged effect on serum IgE levels.	Cyclophosphamide	10-26	immunoglobulin heavy constant epsilon	Homo sapiens	138-141
23636721-0	2013	Cyclophosphamide-induced cystitis reduces ASIC channel but enhances TRPV1 receptor function in rat bladder sensory neurons.	Cyclophosphamide	0-16	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	68-73
24649228-2	2013	The reported 5-year overall survival for patients with localized nasal NKTCL treated with cyclophosphamide, hydroxydaunorubicin, oncovin and prednisone (CHOP) is <50%.	Cyclophosphamide	90-106	DNA damage inducible transcript 3	Homo sapiens	153-157
23806407-0	2013	Alterations in deoxyribonucleic acid (DNA) methylation patterns of Calca, Timp3, Mmp2, and Igf2r are associated with chronic cystitis in a cyclophosphamide-induced mouse model.	Cyclophosphamide	139-155	tissue inhibitor of metalloproteinase 3	Mus musculus	74-79
23806407-0	2013	Alterations in deoxyribonucleic acid (DNA) methylation patterns of Calca, Timp3, Mmp2, and Igf2r are associated with chronic cystitis in a cyclophosphamide-induced mouse model.	Cyclophosphamide	139-155	matrix metallopeptidase 2	Mus musculus	81-85
23806407-0	2013	Alterations in deoxyribonucleic acid (DNA) methylation patterns of Calca, Timp3, Mmp2, and Igf2r are associated with chronic cystitis in a cyclophosphamide-induced mouse model.	Cyclophosphamide	139-155	insulin-like growth factor 2 receptor	Mus musculus	91-96
23826324-0	2013	The GSTP1 105Val allele increases breast cancer risk and aggressiveness but enhances response to cyclophosphamide chemotherapy in North China.	Cyclophosphamide	97-113	glutathione S-transferase pi 1	Homo sapiens	4-9
23826324-5	2013	However, the patients with the GSTP1 105Val genotype had a better disease free survival after cyclophosphamide (CTX)-based chemotherapy than those with Ile/Ile (HR = 0.77, 95% CI: 0.45-0.91; P < 0.001).	Cyclophosphamide	94-110	glutathione S-transferase pi 1	Homo sapiens	31-36
23773525-7	2013	That has become the aim of our study, to assess the expression of PGP, BCRP, MRP1 and MRP3 in canine mammary cancer cell lines and to investigate their role in cancer resistance to vinblastine, cisplatin and cyclophosphamide with using RNAi approach.	Cyclophosphamide	208-224	PGP	Canis lupus familiaris	66-69
23396606-0	2013	Genetic variability in the multidrug resistance associated protein-1 (ABCC1/MRP1) predicts hematological toxicity in breast cancer patients receiving (neo-)adjuvant chemotherapy with 5-fluorouracil, epirubicin and cyclophosphamide (FEC).	Cyclophosphamide	214-230	ATP binding cassette subfamily C member 1	Homo sapiens	27-68
23396606-0	2013	Genetic variability in the multidrug resistance associated protein-1 (ABCC1/MRP1) predicts hematological toxicity in breast cancer patients receiving (neo-)adjuvant chemotherapy with 5-fluorouracil, epirubicin and cyclophosphamide (FEC).	Cyclophosphamide	214-230	ATP binding cassette subfamily C member 1	Homo sapiens	70-75
23396606-0	2013	Genetic variability in the multidrug resistance associated protein-1 (ABCC1/MRP1) predicts hematological toxicity in breast cancer patients receiving (neo-)adjuvant chemotherapy with 5-fluorouracil, epirubicin and cyclophosphamide (FEC).	Cyclophosphamide	214-230	ATP binding cassette subfamily C member 1	Homo sapiens	76-80
23656432-4	2013	rLZ-8 treatment also increased the percentage of CD4(+) T cells and the levels of secreted IL-3 and IL-4, which contributed to the cyclophosphamide-induced immune dysfunction and immune system imbalance.	Cyclophosphamide	131-147	interleukin 3	Mus musculus	91-95
23656432-4	2013	rLZ-8 treatment also increased the percentage of CD4(+) T cells and the levels of secreted IL-3 and IL-4, which contributed to the cyclophosphamide-induced immune dysfunction and immune system imbalance.	Cyclophosphamide	131-147	interleukin 4	Mus musculus	100-104
23143555-12	2013	TGF-beta1 (21 +- 14) mug/L level decreased significantly after 3-month treatment, and TNF-alpha level (9.4 +- 1.7) mug/L was decreased after 6 months of cyclophosphamide treatment that may be associated with its inhabitation on production of TNF-alpha, TGF-beta1 and MMP-9.	Cyclophosphamide	153-169	tumor necrosis factor	Homo sapiens	86-95
23659474-8	2013	Correspondingly, significantly higher secretion of perforin, granzyme B, IL-2, and IFN-gamma in tumor tissues with decreased tumor growth was seen in the cyclophosphamide injection group than in the control group.	Cyclophosphamide	154-170	granzyme B	Mus musculus	61-71
23659474-8	2013	Correspondingly, significantly higher secretion of perforin, granzyme B, IL-2, and IFN-gamma in tumor tissues with decreased tumor growth was seen in the cyclophosphamide injection group than in the control group.	Cyclophosphamide	154-170	interleukin 2	Mus musculus	73-77
23659474-8	2013	Correspondingly, significantly higher secretion of perforin, granzyme B, IL-2, and IFN-gamma in tumor tissues with decreased tumor growth was seen in the cyclophosphamide injection group than in the control group.	Cyclophosphamide	154-170	interferon gamma	Mus musculus	83-92
23615461-1	2013	BACKGROUND: Dose intensification with a combination of cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) every 2 weeks improves outcomes in patients older than 60 years with diffuse large B-cell lymphoma compared with CHOP every 3 weeks.	Cyclophosphamide	55-71	DNA damage inducible transcript 3	Homo sapiens	117-121
23615461-1	2013	BACKGROUND: Dose intensification with a combination of cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) every 2 weeks improves outcomes in patients older than 60 years with diffuse large B-cell lymphoma compared with CHOP every 3 weeks.	Cyclophosphamide	55-71	DNA damage inducible transcript 3	Homo sapiens	236-240
23143555-7	2013	TNF-alpha level (0.23 +- 0.19) was significantly decreased 3 months after cyclophosphamide treatment (t = 2.533, p < 0.05), and TGF-beta1 (0.31 +- 0.18) level markedly decreased after 6 months of treatment (t = 2.617, p < 0.05).	Cyclophosphamide	74-90	tumor necrosis factor	Homo sapiens	0-9
23143555-12	2013	TGF-beta1 (21 +- 14) mug/L level decreased significantly after 3-month treatment, and TNF-alpha level (9.4 +- 1.7) mug/L was decreased after 6 months of cyclophosphamide treatment that may be associated with its inhabitation on production of TNF-alpha, TGF-beta1 and MMP-9.	Cyclophosphamide	153-169	transforming growth factor beta 1	Homo sapiens	0-9
23460611-6	2013	FOXO1 mutation was associated with decreased overall survival in patients treated with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (P = .037), independent of cell of origin (COO) and the revised International Prognostic Index (R-IPI).	Cyclophosphamide	98-114	forkhead box O1	Homo sapiens	0-5
23375819-11	2013	eGFR in the MMF group improved more quickly than in the cyclophosphamide group, by 1.51 (95% CI, 0.99-2.02) mL/min/1.73 m(2) each week (P < 0.001).	Cyclophosphamide	56-72	epidermal growth factor receptor	Homo sapiens	0-4
23143555-12	2013	TGF-beta1 (21 +- 14) mug/L level decreased significantly after 3-month treatment, and TNF-alpha level (9.4 +- 1.7) mug/L was decreased after 6 months of cyclophosphamide treatment that may be associated with its inhabitation on production of TNF-alpha, TGF-beta1 and MMP-9.	Cyclophosphamide	153-169	tumor necrosis factor	Homo sapiens	242-251
23143555-12	2013	TGF-beta1 (21 +- 14) mug/L level decreased significantly after 3-month treatment, and TNF-alpha level (9.4 +- 1.7) mug/L was decreased after 6 months of cyclophosphamide treatment that may be associated with its inhabitation on production of TNF-alpha, TGF-beta1 and MMP-9.	Cyclophosphamide	153-169	transforming growth factor beta 1	Homo sapiens	253-262
23143555-12	2013	TGF-beta1 (21 +- 14) mug/L level decreased significantly after 3-month treatment, and TNF-alpha level (9.4 +- 1.7) mug/L was decreased after 6 months of cyclophosphamide treatment that may be associated with its inhabitation on production of TNF-alpha, TGF-beta1 and MMP-9.	Cyclophosphamide	153-169	matrix metallopeptidase 9	Homo sapiens	267-272
23352254-2	2013	METHODS: We report a case of anti-GBM antibody disease with both anti-GBM antibodies and anti-myeloperoxidase (MPO) specific p-ANCA, who developed thrombotic thrombocytopenic purpura (TTP) on high dose prednisone, plasmapheresis, and cyclophosphamide therapy.	Cyclophosphamide	234-250	myeloperoxidase	Homo sapiens	89-109
23352254-2	2013	METHODS: We report a case of anti-GBM antibody disease with both anti-GBM antibodies and anti-myeloperoxidase (MPO) specific p-ANCA, who developed thrombotic thrombocytopenic purpura (TTP) on high dose prednisone, plasmapheresis, and cyclophosphamide therapy.	Cyclophosphamide	234-250	myeloperoxidase	Homo sapiens	111-114
22897584-6	2013	As controls we had the first collections from 12 MM patients mobilized with low-dose CY with G-CSF.	Cyclophosphamide	85-87	colony stimulating factor 3	Homo sapiens	93-98
24082512-6	2013	Similarly, cells were showing substrate specific responses against the specific inducers of CYPs, that is, ethanol (2E1), cyclophosphamide (2B1/2B2), 3-methylcholanthrene (1A1/1A2).	Cyclophosphamide	122-138	UDP glucuronosyltransferase family 2 member B17	Rattus norvegicus	140-147
23228633-0	2013	Thrombospondin-1 and pigment epithelium-derived factor enhance responsiveness of KM12 colon tumor to metronomic cyclophosphamide but have disparate effects on tumor metastasis.	Cyclophosphamide	112-128	thrombospondin 1	Homo sapiens	0-54
23228633-2	2013	Thrombospondin-1 and PEDF decreased KM12 tumor microvessel density, increased macrophage infiltration, and improved responsiveness to metronomic cyclophosphamide (CPA) treatment, but did not activate the anti-tumor innate immunity that metronomic CPA induces in other tumor models.	Cyclophosphamide	163-166	thrombospondin 1	Homo sapiens	0-16
23228633-2	2013	Thrombospondin-1 and PEDF decreased KM12 tumor microvessel density, increased macrophage infiltration, and improved responsiveness to metronomic cyclophosphamide (CPA) treatment, but did not activate the anti-tumor innate immunity that metronomic CPA induces in other tumor models.	Cyclophosphamide	163-166	serpin family F member 1	Homo sapiens	21-25
23228633-3	2013	Moreover, thrombospondin-1, but not PEDF, significantly increased KM12 metastasis to the lung, while PEDF augmented the anti-metastatic activity of metronomic CPA.	Cyclophosphamide	159-162	serpin family F member 1	Homo sapiens	101-105
23228633-4	2013	Thus, while thrombospondin-1 and PEDF both increase the KM12 tumor responsiveness to metronomic CPA, they have disparate effects on tumor metastasis.	Cyclophosphamide	96-99	thrombospondin 1	Homo sapiens	12-28
23228633-4	2013	Thus, while thrombospondin-1 and PEDF both increase the KM12 tumor responsiveness to metronomic CPA, they have disparate effects on tumor metastasis.	Cyclophosphamide	96-99	serpin family F member 1	Homo sapiens	33-37
23578722-1	2013	BACKGROUND: Immunochemotherapy with rituximab and cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) has become the standard of care for elderly patients with diffuse large B-cell lymphoma.	Cyclophosphamide	50-66	DNA damage inducible transcript 3	Homo sapiens	112-116
22897584-8	2013	The numbers of CD19+ B lymphocytes and natural killer cells were higher in patients collected after G-CSF plus plerixafor when compared to the patients mobilized with CY plus G-CSF.	Cyclophosphamide	167-169	CD19 molecule	Homo sapiens	15-19
23523557-0	2013	Antagonism of the transient receptor potential ankyrin 1 (TRPA1) attenuates hyperalgesia and urinary bladder overactivity in cyclophosphamide-induced haemorrhagic cystitis.	Cyclophosphamide	125-141	transient receptor potential cation channel, subfamily A, member 1	Rattus norvegicus	18-56
23523557-0	2013	Antagonism of the transient receptor potential ankyrin 1 (TRPA1) attenuates hyperalgesia and urinary bladder overactivity in cyclophosphamide-induced haemorrhagic cystitis.	Cyclophosphamide	125-141	transient receptor potential cation channel, subfamily A, member 1	Rattus norvegicus	58-63
23523557-1	2013	The aim of this study was to investigate the involvement of the transient receptor potential ankyrin 1 (TRPA1) in haemorrhagic cystitis, the main side effect of cyclophosphamide-based chemotherapy.	Cyclophosphamide	161-177	transient receptor potential cation channel, subfamily A, member 1	Rattus norvegicus	64-102
23523557-1	2013	The aim of this study was to investigate the involvement of the transient receptor potential ankyrin 1 (TRPA1) in haemorrhagic cystitis, the main side effect of cyclophosphamide-based chemotherapy.	Cyclophosphamide	161-177	transient receptor potential cation channel, subfamily A, member 1	Rattus norvegicus	104-109
23523557-6	2013	The treatment with the TRPA1 antagonist HC 030031 significantly decreased mechanical hyperalgesia induced by cyclophosphamide without interfere with locomotor activity.	Cyclophosphamide	109-125	transient receptor potential cation channel, subfamily A, member 1	Rattus norvegicus	23-28
23523557-13	2013	Our data demonstrates that nociceptive symptoms and urinary bladder overactivity caused by cyclophosphamide, in part, are dependent upon the activation of TRPA1.	Cyclophosphamide	91-107	transient receptor potential cation channel, subfamily A, member 1	Rattus norvegicus	155-160
23979202-1	2013	BACKGROUND: Metronomic chemotherapy (MCT) with cyclophosphamide (Cy) and celecoxib (Cel) has therapeutic efficacy and low toxicity profile in advanced breast cancer patients (ABCP), but no reliable biomarkers of response have been found yet that allow patient selection for treatment.	Cyclophosphamide	47-63	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	175-179
23547746-3	2013	In this study, we focus on the characterization of in vivo chemoresistant human hepatocellular carcinoma HUH-REISO established from a metronomically cyclophosphamide (CPA) treated HUH7 xenograft model.	Cyclophosphamide	149-165	MIR7-3 host gene	Homo sapiens	180-184
23547746-3	2013	In this study, we focus on the characterization of in vivo chemoresistant human hepatocellular carcinoma HUH-REISO established from a metronomically cyclophosphamide (CPA) treated HUH7 xenograft model.	Cyclophosphamide	167-170	MIR7-3 host gene	Homo sapiens	180-184
23547746-12	2013	Under therapeutic pressure by CPA, tumors of HUH-PAS and HUH-REISO displayed regulations in Notch-1 and Notch-3 expression.	Cyclophosphamide	30-33	notch receptor 1	Homo sapiens	92-99
23547746-12	2013	Under therapeutic pressure by CPA, tumors of HUH-PAS and HUH-REISO displayed regulations in Notch-1 and Notch-3 expression.	Cyclophosphamide	30-33	notch receptor 3	Homo sapiens	104-111
23218766-0	2013	High expression of class III beta-tubulin predicts good response to neoadjuvant taxane and doxorubicin/cyclophosphamide-based chemotherapy in estrogen receptor-negative breast cancer.	Cyclophosphamide	103-119	estrogen receptor 1	Homo sapiens	142-159
23847953-1	2013	OBJECTIVE: To explore the inhibitory effect of combined administration of bear bile powder (BBP) and cyclophosphamide (Cytoxan, CTX) on colorectal cancer liver metastasis by regulating tumor promotion inflammation microenvironment.	Cyclophosphamide	101-117	V-set and immunoglobulin domain containing 2	Mus musculus	128-131
23335369-1	2013	MYC rearrangements occur in 5% to 10% of diffuse large B-cell lymphomas (DLBCL) and confer an increased risk to cyclophosphamide, hydroxydaunorubicin, oncovin, and prednisone (CHOP) and rituximab (R)-CHOP treated patients.	Cyclophosphamide	112-128	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	0-3
23517575-10	2013	cyclophosphamide pulses monthly for 6 doses, followed by mycophenolate mofetil that resulted in normal lung function tests, hemoglobin concentration, and anti-MPO level within four subsequent weeks.	Cyclophosphamide	0-16	myeloperoxidase	Homo sapiens	159-162
23467454-3	2013	Drugs metabolized mainly by CYP2B6 include artemisinin, bupropion, cyclophosphamide, efavirenz, ketamine, and methadone.	Cyclophosphamide	67-83	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	28-34
22929978-9	2013	G-CSF, cyclophosphamide and AMD3100 have distinct effects on B lymphopoiesis and B-cell mobilization with: 1) G-CSF inhibiting medullar B lymphopoiesis without mobilizing B cells in a mechanism distinct from the TNF-alpha-mediated loss of B lymphopoiesis observed during inflammation or viral infections; 2) CYP mobilizing B cells but blocking their maturation; and 3) AMD3100 mobilizing B cells without affecting B lymphopoiesis.	Cyclophosphamide	7-23	colony stimulating factor 3 (granulocyte)	Mus musculus	110-115
23436656-9	2013	We found that miR-663 was significantly elevated in MDA-MB-231/ADM cells, and the down-regulation of miR-663 sensitized MDA-MB-231/ADM cells to both cyclophosphamide and docetaxel.	Cyclophosphamide	149-165	microRNA 663a	Homo sapiens	14-21
23436656-9	2013	We found that miR-663 was significantly elevated in MDA-MB-231/ADM cells, and the down-regulation of miR-663 sensitized MDA-MB-231/ADM cells to both cyclophosphamide and docetaxel.	Cyclophosphamide	149-165	microRNA 663a	Homo sapiens	101-108
23412107-3	2013	METHODS: We developed a phosphoshift (pShift) flow cytometry-based test that measures RAF signal transduction capacity in peripheral blood cells, and evaluated it in a phase II clinical trial of oral sorafenib plus low-dose cyclophosphamide in patients with advanced neuroendocrine tumours (NETs), in order to predict clinical course and/or guide individual dose-titration.	Cyclophosphamide	224-240	zinc fingers and homeoboxes 2	Homo sapiens	86-89
23412107-8	2013	CONCLUSION: The pharmacodynamic assessment of RAF transduction may identify selected patients with advanced NETs most likely to benefit from the combination of sorafenib plus cyclophosphamide.	Cyclophosphamide	175-191	zinc fingers and homeoboxes 2	Homo sapiens	46-49
23979202-0	2013	Association between baseline VEGF/sVEGFR-2 and VEGF/TSP-1 ratios and response to metronomic chemotherapy using cyclophosphamide and celecoxib in patients with advanced breast cancer.	Cyclophosphamide	111-127	vascular endothelial growth factor A	Homo sapiens	29-33
23979202-0	2013	Association between baseline VEGF/sVEGFR-2 and VEGF/TSP-1 ratios and response to metronomic chemotherapy using cyclophosphamide and celecoxib in patients with advanced breast cancer.	Cyclophosphamide	111-127	thrombospondin 1	Homo sapiens	52-57
23979202-1	2013	BACKGROUND: Metronomic chemotherapy (MCT) with cyclophosphamide (Cy) and celecoxib (Cel) has therapeutic efficacy and low toxicity profile in advanced breast cancer patients (ABCP), but no reliable biomarkers of response have been found yet that allow patient selection for treatment.	Cyclophosphamide	65-67	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	175-179
23498802-4	2013	Immunohistochemical staining demonstrated reduced expression of RANTES and CCR5 in allograft muscle and coronary arteries when the recipients were pretreated with donor splenocytes plus cyclophosphamide.	Cyclophosphamide	186-202	C-C motif chemokine ligand 5	Homo sapiens	64-70
22972488-1	2013	PURPOSE: Treatment of non-Hodgkin lymphoma (NHL) with cyclophosphamide, vincristine, doxorubicin and prednisone (CHOP) is known to be associated with a significant risk of febrile neutropenia (FN) of up to 50% [Osby et al.	Cyclophosphamide	54-70	DNA damage inducible transcript 3	Homo sapiens	113-117
23498802-4	2013	Immunohistochemical staining demonstrated reduced expression of RANTES and CCR5 in allograft muscle and coronary arteries when the recipients were pretreated with donor splenocytes plus cyclophosphamide.	Cyclophosphamide	186-202	C-C motif chemokine receptor 5	Homo sapiens	75-79
22721387-7	2013	Finally, mesothelin expression promotes resistance to certain chemotherapy drugs such as TNF-alpha, paclitaxel, and a combination of platinum and cyclophosphamide.	Cyclophosphamide	146-162	mesothelin	Homo sapiens	9-19
23700724-7	2013	CONCLUSION: CMTM2 antagonizes cyclophosphamide-induced reproductive toxicity via regulating the expression of StAR, and hence plays a protective role in the reproductive system.	Cyclophosphamide	30-46	steroidogenic acute regulatory protein	Mus musculus	110-114
23303666-0	2013	Naturally occurring PD-1+ memory phenotype CD8 T cells belong to nonconventional CD8 T cells and are cyclophosphamide-sensitive regulatory T cells.	Cyclophosphamide	101-117	programmed cell death 1	Mus musculus	20-24
23303666-8	2013	PD-1(+) MP CD8 T cells showed the fastest cell cycling among various T cell subsets in naive mice, which was consistent with the highest sensitivity to cyclophosphamide (CP) treatment.	Cyclophosphamide	152-168	programmed cell death 1	Mus musculus	0-4
23507054-8	2013	We recommend especially to monitor neutrophiles, lymphocytes and if needed CD3-, CD4- and CD8-cell counts in patients receiving steroids and cyclophosphamide or other cytotoxic agents.	Cyclophosphamide	141-157	CD4 molecule	Homo sapiens	81-84
23507054-8	2013	We recommend especially to monitor neutrophiles, lymphocytes and if needed CD3-, CD4- and CD8-cell counts in patients receiving steroids and cyclophosphamide or other cytotoxic agents.	Cyclophosphamide	141-157	CD8a molecule	Homo sapiens	90-93
23407364-1	2013	20(S)-protopanaxadiol (PPD) is an extract of Panax quinquefolius L. The aim of this study was to investigate the effect of PPD on the antitumor activity and toxicity of cyclophosphamide (CTX) in tumor-bearing mice.	Cyclophosphamide	169-185	V-set and immunoglobulin domain containing 2	Mus musculus	187-190
22957713-11	2013	Administration of bestatin after pharmacological immunosuppression partially prevented the suppressive action of cyclophosphamide in the in vivo model of the humoral immune response to SRBC.	Cyclophosphamide	113-129	caveolae associated 3	Mus musculus	185-189
23343906-1	2013	BACKGROUND: The efficacy and safety of tacrolimus (TAC) and cyclophosphamide (CTX) were prospectively examined in steroid-dependent or steroid-resistant primary focal segmental glomerulosclerosis (FSGS).	Cyclophosphamide	60-76	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	78-81
23148924-1	2013	OBJECTIVE: To determine the expression of CatSper1 channel in epididymal spermatozoa in a rat model of asthenozoospermia, induced by cyclophosphamide (CP), and further examine the effects of soluble granules of Sheng-Jing-San (SJS), a traditional Chinese medicine recipe, on CatSper1 expression and sperm motility in the CP-induced asthenozoospermic rats.	Cyclophosphamide	133-149	cation channel, sperm associated 1	Rattus norvegicus	42-50
23275230-2	2013	In the present study, we investigated whether miR-21 is involved in regulating the sensitivity of the diffuse large B-cell lymphoma (DLBCL) cell line CRL2631 to the cyclophosphamide, vincristine, Adriamycin, and prednisone (CHOP) chemotherapeutic regimen.	Cyclophosphamide	165-181	microRNA 21	Homo sapiens	46-52
23142275-11	2013	Taken together, our data suggest that the prevailing Th2 immune response in BALB/c mice may be responsible for the resistance to MLD-STZ diabetes and that ST2 gene deletion reveals the role of highly cyclophosphamide sensitive CD4+Foxp3+ regulatory T cells in the pancreatic lymph nodes in diabetes modulation.	Cyclophosphamide	200-216	interleukin 1 receptor-like 1	Mus musculus	155-158
23142275-11	2013	Taken together, our data suggest that the prevailing Th2 immune response in BALB/c mice may be responsible for the resistance to MLD-STZ diabetes and that ST2 gene deletion reveals the role of highly cyclophosphamide sensitive CD4+Foxp3+ regulatory T cells in the pancreatic lymph nodes in diabetes modulation.	Cyclophosphamide	200-216	CD4 antigen	Mus musculus	227-230
22610787-0	2013	Clinical significance of monitoring serum adiponectin levels during intravenous pulse cyclophosphamide therapy in interstitial lung disease associated with systemic sclerosis.	Cyclophosphamide	86-102	adiponectin, C1Q and collagen domain containing	Homo sapiens	42-53
22610787-1	2013	OBJECTIVE: To investigate the clinical significance of monitoring serum adiponectin levels during intravenous pulse cyclophosphamide (IVCY) in systemic sclerosis (SSc) patients with interstitial lung disease (ILD).	Cyclophosphamide	116-132	adiponectin, C1Q and collagen domain containing	Homo sapiens	72-83
23166041-2	2013	The CHOP chemotherapy             regimen, which includes cyclophosphamide, doxorubicin, vincristine and prednisone,             has been used previously to treat other types of lymphomas.	Cyclophosphamide	58-74	DNA damage inducible transcript 3	Homo sapiens	4-8
23359007-3	2013	We report the clinical case of a 7-year-old male patient with CPAN refractory to treatment with high doses of corticoids and cyclophosphamide, who was successfully treated with the TNF-alpha (tumor necrosis factor-alpha) inhibitor, etanercept, in monotherapy.	Cyclophosphamide	125-141	tumor necrosis factor	Homo sapiens	181-190
23359007-3	2013	We report the clinical case of a 7-year-old male patient with CPAN refractory to treatment with high doses of corticoids and cyclophosphamide, who was successfully treated with the TNF-alpha (tumor necrosis factor-alpha) inhibitor, etanercept, in monotherapy.	Cyclophosphamide	125-141	tumor necrosis factor	Homo sapiens	192-219
23320927-0	2013	A phase 1b study of humanized KS-interleukin-2 (huKS-IL2) immunocytokine with cyclophosphamide in patients with EpCAM-positive advanced solid tumors.	Cyclophosphamide	78-94	epithelial cell adhesion molecule	Homo sapiens	112-117
23160467-0	2013	The constitutive androstane receptor is a novel therapeutic target facilitating cyclophosphamide-based treatment of hematopoietic malignancies.	Cyclophosphamide	80-96	nuclear receptor subfamily 1 group I member 3	Homo sapiens	4-36
23160467-1	2013	Cyclophosphamide (CPA) is one of the most widely used chemotherapeutic prodrugs that undergoes hepatic bioactivation mediated predominantly by cytochrome P450 (CYP) 2B6.	Cyclophosphamide	0-16	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	143-168
23160467-1	2013	Cyclophosphamide (CPA) is one of the most widely used chemotherapeutic prodrugs that undergoes hepatic bioactivation mediated predominantly by cytochrome P450 (CYP) 2B6.	Cyclophosphamide	18-21	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	143-168
23344194-0	2013	Investigation on the interaction between cyclophosphamide and lysozyme in the presence of three different kind of cyclodextrins: determination of the binding mechanism by spectroscopic and molecular modeling techniques.	Cyclophosphamide	41-57	lysozyme	Homo sapiens	62-70
23344194-1	2013	The interactions between cyclophosphamide (CYC) and lysozyme (LYZ) in  the presence of different cyclodextrins (CDs) were investigated by UV absorption, fluorescence spectroscopy, circular dichroism (CD), and molecular modeling techniques under imitated physiological conditions.	Cyclophosphamide	25-41	lysozyme	Homo sapiens	52-60
23344194-1	2013	The interactions between cyclophosphamide (CYC) and lysozyme (LYZ) in  the presence of different cyclodextrins (CDs) were investigated by UV absorption, fluorescence spectroscopy, circular dichroism (CD), and molecular modeling techniques under imitated physiological conditions.	Cyclophosphamide	25-41	lysozyme	Homo sapiens	62-65
23344194-8	2013	The effect of CYC and cyclodextrins on the conformation of LYZ was analyzed using synchronous fluorescence spectroscopy.	Cyclophosphamide	14-17	lysozyme	Homo sapiens	59-62
23344194-9	2013	Our results revealed that the fluorescence quenching of LYZ originated from the Trp and Tyr residues, and demonstrated conformational changes of LYZ with the addition of CYC and CDs.	Cyclophosphamide	170-173	lysozyme	Homo sapiens	56-59
23344194-9	2013	Our results revealed that the fluorescence quenching of LYZ originated from the Trp and Tyr residues, and demonstrated conformational changes of LYZ with the addition of CYC and CDs.	Cyclophosphamide	170-173	lysozyme	Homo sapiens	145-148
23344194-10	2013	The molecular distances between the donor (LYZ) and acceptor (CYC and CDs) in binary and ternary systems were estimated according to Forster"s theory and showed static quenching for protein with CYC in the presence of CDs.	Cyclophosphamide	62-65	lysozyme	Homo sapiens	43-46
23053189-1	2013	R-CHOP chemotherapy composed of rituximab, cyclophosphamide, adriamycin, vincristine, and prednisolone which might increase the risk of Pneumocystis pneumonia in patients with non-Hodgkin lymphoma.	Cyclophosphamide	43-59	DNA damage inducible transcript 3	Homo sapiens	2-6
22971714-0	2013	Inhibition of TNF-alpha by cyclophosphamide reduces myocardial injury after ischemia-reperfusion.	Cyclophosphamide	27-43	tumor necrosis factor	Rattus norvegicus	14-23
22971714-1	2013	PURPOSE: The purpose of this study was to determine whether cyclophosphamide (CP) can decrease myocardial and systemic TNF-alpha expression and thus protects myocardial I/R injury.	Cyclophosphamide	60-76	tumor necrosis factor	Rattus norvegicus	119-128
23641277-3	2013	Harmonized steroids and cyclophosphamide or azathioprine are effective for active AAV.	Cyclophosphamide	24-40	adeno-associated virus integration site 1	Homo sapiens	82-85
23044647-1	2013	OBJECTIVE: To study the level of anti-mullerian hormone (AMH) and its relationship to age and previous exposure to cyclophosphamide (CYC) in patients with systemic lupus erythematosus (SLE).	Cyclophosphamide	115-131	anti-Mullerian hormone	Homo sapiens	57-60
23044647-1	2013	OBJECTIVE: To study the level of anti-mullerian hormone (AMH) and its relationship to age and previous exposure to cyclophosphamide (CYC) in patients with systemic lupus erythematosus (SLE).	Cyclophosphamide	133-136	anti-Mullerian hormone	Homo sapiens	57-60
23044647-7	2013	The mean+-SD AMH level was significantly lower in patients previously exposed to CYC therapy than in those who had not been exposed after adjustment for age (1.58+-2.92 versus 1.73+-2.11 ng/ml; P=0.04).	Cyclophosphamide	81-84	anti-Mullerian hormone	Homo sapiens	13-16
24093110-0	2013	Urinary IgG and alpha2-macroglobulin are powerful predictors of outcome and responsiveness to steroids and cyclophosphamide in idiopathic focal segmental glomerulosclerosis with nephrotic syndrome.	Cyclophosphamide	107-123	alpha-2-macroglobulin	Homo sapiens	16-36
24093110-10	2013	CONCLUSIONS: FEIgG and alpha2m/C are powerful predictors of outcome and responsiveness to steroids and cyclophosphamide; their predictive value, if validated in prospective studies, may be useful in clinical practice suggesting first-line alternative treatments in high risk patients.	Cyclophosphamide	103-119	alpha-2-macroglobulin	Homo sapiens	23-30
23114516-0	2013	Early measurement of CD34+ cells in peripheral blood after cyclophosphamide and granulocyte colony-stimulating factor treatment predicts later CD34+ mobilisation failure and is a possible criterion for guiding "on demand" use of plerixafor.	Cyclophosphamide	59-75	CD34 molecule	Homo sapiens	21-25
23114516-10	2013	DISCUSSION: We propose that patients with <6 x 10(6)/L CD34+ cells in peripheral blood on day 12 and <10 x 10(6)/L on day 13 following mobilisation with cyclophosphamide 4 g/m(2) and granulocyte colony-stimulating factor are candidates for "on demand" use of plerixafor, making the administration of this expensive agent more efficient and avoiding its inappropriate use.	Cyclophosphamide	159-175	CD34 molecule	Homo sapiens	58-62
23011589-4	2013	Cyclophosphamide (CTX) is a systemic chemotherapeutic agent, which can eradicate immune cells, including inhibitory Tregs.	Cyclophosphamide	0-16	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	18-21
24480791-8	2013	CONCLUSION: The association of a homozygous deletion of GSTM1 with hypersensitivity to oxaliplatin and cyclophosphamide combination chemotherapy has not been described to date in ovarian cancer.	Cyclophosphamide	103-119	glutathione S-transferase mu 1	Homo sapiens	56-61
23689569-6	2013	In progressive IgAN patients whose clinical and pathological manifestations are more severe, active therapy may be considered including glucocorticoid therapy, cyclophosphamide, azathioprine, mycophenolate mofetil, tacrolimus, and other immunosuppressants.	Cyclophosphamide	160-176	IGAN1	Homo sapiens	15-19
24617050-11	2013	CD5+ lymphocyte"s P-gp1 function was found to be lower in the patients receiving cyclophosphamide in addition to steroids compared to those on steroids only.	Cyclophosphamide	81-97	CD5 molecule	Homo sapiens	0-3
24617050-11	2013	CD5+ lymphocyte"s P-gp1 function was found to be lower in the patients receiving cyclophosphamide in addition to steroids compared to those on steroids only.	Cyclophosphamide	81-97	ATP binding cassette subfamily B member 1	Homo sapiens	18-23
23231045-2	2013	Cyclophosphamide (CTX) can induce oxidative stress in bone marrow resulting in suppression of anti-oxdiantive enzymes and causes myelosuppression.	Cyclophosphamide	0-16	V-set and immunoglobulin domain containing 2	Mus musculus	18-21
23233155-1	2013	The CTD (cyclophosphamide, thalidomide, and dexamethasone) regimen is known to be an effective primary therapy in patients with newly diagnosed multiple myeloma (MM).	Cyclophosphamide	9-25	CTD	Homo sapiens	4-7
24200545-8	2013	The patient received R-CHOP therapy (cyclophosphamide, doxorubicin, vincristine, prednisone, and rituximab) with good response.	Cyclophosphamide	37-53	DNA damage inducible transcript 3	Homo sapiens	23-27
24240788-9	2013	In the CY group, the hazard ratio after adjusting for age, sex, Birmingham vasculitis activity score values, serum albumin levels and C-reactive protein (CRP) levels was 0.657 (95% CI, 0.254-1.699; p=0.386).	Cyclophosphamide	7-9	C-reactive protein	Homo sapiens	134-152
24240788-9	2013	In the CY group, the hazard ratio after adjusting for age, sex, Birmingham vasculitis activity score values, serum albumin levels and C-reactive protein (CRP) levels was 0.657 (95% CI, 0.254-1.699; p=0.386).	Cyclophosphamide	7-9	C-reactive protein	Homo sapiens	154-157
23042256-1	2013	The aim of this study was to investigate the impact of a Chinese herbal decoction on the intracellular calcium (Ca2+) concentration of sperm and the expression of the cation channel 1 of sperm (CatSper1), which is a calcium-channel protein specific to sperm tail, in a murine model of asthenospermia induced with cyclophosphamide.	Cyclophosphamide	313-329	cation channel, sperm associated 1	Mus musculus	194-202
23042256-8	2013	Intraperitoneal injection of cyclophosphamide reduced sperm concentration, percentage of sperm activity and overall sperm motility, intracellular Ca2+ concentration and CatSper1 expression.	Cyclophosphamide	29-45	cation channel, sperm associated 1	Mus musculus	169-177
23262931-1	2013	OBJECTIVE: To estimate the effectiveness of gonadotropin-releasing hormone (GnRH) analogues cotreatment in preventing chemotherapy-induced amenorrhea in young breast cancer patients undergoing cyclophosphamide-based chemotherapy.	Cyclophosphamide	193-209	gonadotropin releasing hormone 1	Homo sapiens	44-74
23262931-1	2013	OBJECTIVE: To estimate the effectiveness of gonadotropin-releasing hormone (GnRH) analogues cotreatment in preventing chemotherapy-induced amenorrhea in young breast cancer patients undergoing cyclophosphamide-based chemotherapy.	Cyclophosphamide	193-209	gonadotropin releasing hormone 1	Homo sapiens	76-80
23160467-2	2013	Given that the CYP2B6 gene is primarily regulated by the constitutive androstane receptor (CAR, NR1I3), we hypothesize that selective activation of CAR can enhance systemic exposure of the pharmacologically active 4-hydroxycyclophosamide (4-OH-CPA), with improved efficacy of CPA-based chemotherapy.	Cyclophosphamide	244-247	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	15-21
23160467-2	2013	Given that the CYP2B6 gene is primarily regulated by the constitutive androstane receptor (CAR, NR1I3), we hypothesize that selective activation of CAR can enhance systemic exposure of the pharmacologically active 4-hydroxycyclophosamide (4-OH-CPA), with improved efficacy of CPA-based chemotherapy.	Cyclophosphamide	244-247	nuclear receptor subfamily 1 group I member 3	Homo sapiens	57-89
23160467-2	2013	Given that the CYP2B6 gene is primarily regulated by the constitutive androstane receptor (CAR, NR1I3), we hypothesize that selective activation of CAR can enhance systemic exposure of the pharmacologically active 4-hydroxycyclophosamide (4-OH-CPA), with improved efficacy of CPA-based chemotherapy.	Cyclophosphamide	244-247	nuclear receptor subfamily 1 group I member 3	Homo sapiens	91-94
23160467-2	2013	Given that the CYP2B6 gene is primarily regulated by the constitutive androstane receptor (CAR, NR1I3), we hypothesize that selective activation of CAR can enhance systemic exposure of the pharmacologically active 4-hydroxycyclophosamide (4-OH-CPA), with improved efficacy of CPA-based chemotherapy.	Cyclophosphamide	244-247	nuclear receptor subfamily 1 group I member 3	Homo sapiens	96-101
23160467-2	2013	Given that the CYP2B6 gene is primarily regulated by the constitutive androstane receptor (CAR, NR1I3), we hypothesize that selective activation of CAR can enhance systemic exposure of the pharmacologically active 4-hydroxycyclophosamide (4-OH-CPA), with improved efficacy of CPA-based chemotherapy.	Cyclophosphamide	244-247	nuclear receptor subfamily 1 group I member 3	Homo sapiens	148-151
23160467-5	2013	Importantly, coadministration of CPA with a human CAR activator led to significantly enhanced cytotoxicity in leukemia cells by inducing the apoptosis pathways, without concomitant increase in the off-target hepatotoxicity.	Cyclophosphamide	33-36	nuclear receptor subfamily 1 group I member 3	Homo sapiens	50-53
23160467-7	2013	Together, our findings offer proof of concept that CAR as a novel molecular target can facilitate CPA-based chemotherapy by selectively promoting its bioactivation.	Cyclophosphamide	98-101	nuclear receptor subfamily 1 group I member 3	Homo sapiens	51-54
23445734-7	2013	With corticosteroid and cyclophosphamide therapy, his symptoms disappeared in two months along with faded PR3-ANCA.	Cyclophosphamide	24-40	proteinase 3	Homo sapiens	106-109
23629426-5	2013	Intensive regimen of combined immunosuppressive therapy (high-dose corticosteroids, oral cyclosporin and intravenous cyclophosphamide (IVCY, 900-1000 mg/m(2) in every other week)) improved the survival rate of anti-MDA5-positive patients.	Cyclophosphamide	117-133	interferon induced with helicase C domain 1	Homo sapiens	215-219
23569384-0	2013	Dual control of Shuanghuang Shengbai granule on upstream and downstream signal modulators of CyclinD-CDK4/6 signaling pathway of cell cycle in Lewis-bearing mice with cyclophosphamide-induced myelosuppression.	Cyclophosphamide	167-183	cyclin-dependent kinase 4	Mus musculus	101-107
23252950-4	2013	Moreover, glutathione-S-transferase isoenzymes have been associated with cellular outward transport of various alkylating agents, including Cy metabolites, melphalan, Bu and chlorambucil.	Cyclophosphamide	140-142	glutathione S-transferase kappa 1	Homo sapiens	10-35
23555992-13	2013	Additionally, MYC amplification may help in the identification of tumors that are sensitive to doxorubicin plus cyclophosphamide treatment.	Cyclophosphamide	112-128	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	14-17
23996885-4	2013	We describe a patient with follicular lymphoma treated with R-CHOP scheme (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone) who had pulmonary symptoms during chemotherapy which were diagnosed as rituximab-induced interstitial pneumonia.	Cyclophosphamide	86-102	DNA damage inducible transcript 3	Homo sapiens	62-66
23814970-2	2012	Standard chemotherapy is CHOP regimen (cyclophosphamide, doxorubicin, vincristine and prednisone).	Cyclophosphamide	39-55	DNA damage inducible transcript 3	Homo sapiens	25-29
22961095-0	2013	Involvement of interleukin-6-regulated nitric oxide synthase in hemorrhagic cystitis and impaired bladder contractions in young rats induced by acrolein, a urinary metabolite of cyclophosphamide.	Cyclophosphamide	178-194	interleukin 6	Rattus norvegicus	15-28
27335870-6	2013	Cyclophosphamide-induced bladder hyperalgesia correlated with a significant 22% increase in GluR1 AMPA receptor subunit expression in the membrane fraction of the lumbosacral spinal cord, which was attenuated by CTX coadministration.	Cyclophosphamide	0-16	glutamate ionotropic receptor AMPA type subunit 1	Homo sapiens	92-97
27335870-6	2013	Cyclophosphamide-induced bladder hyperalgesia correlated with a significant 22% increase in GluR1 AMPA receptor subunit expression in the membrane fraction of the lumbosacral spinal cord, which was attenuated by CTX coadministration.	Cyclophosphamide	0-16	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	212-215
23091097-3	2012	PATIENTS AND METHODS: We analyzed the ATM gene in 224 patients treated on the Leukemia Research Fund Chronic Lymphocytic Leukemia 4 (LRF-CLL4) trial with chlorambucil or fludarabine with and without cyclophosphamide.	Cyclophosphamide	199-215	ATM serine/threonine kinase	Homo sapiens	38-41
23658994-2	2008	HSPC mobilization is induced clinically or experimentally in animal models by a wide variety of agents, such as cytokines (e.g. G-CSF), chemotherapeutic agents (e.g. cyclophosphamide) and small molecules (e.g. the CXCR4 antagonist AMD3100).	Cyclophosphamide	166-182	proteasome 20S subunit alpha 7	Homo sapiens	0-4
23000307-0	2012	The expression of PAC1 increases in the degenerative thymus and low dose PACAP protects female mice from cyclophosphamide induced thymus atrophy.	Cyclophosphamide	105-121	adenylate cyclase activating polypeptide 1 receptor 1	Mus musculus	18-22
22814394-0	2012	SJSZ glycoprotein (38 kDa) modulates expression of IL-2, IL-12, and IFN-gamma in cyclophosphamide-induced Balb/c.	Cyclophosphamide	81-97	interleukin 2	Mus musculus	51-55
22814394-0	2012	SJSZ glycoprotein (38 kDa) modulates expression of IL-2, IL-12, and IFN-gamma in cyclophosphamide-induced Balb/c.	Cyclophosphamide	81-97	interferon gamma	Mus musculus	68-77
23346482-0	2012	Expression of caveolin-1 in rat urinary bladder with cyclophosphamide-induced cystitis.	Cyclophosphamide	53-69	caveolin 1	Rattus norvegicus	14-24
23346482-1	2012	PURPOSE: The purposes of this study were to investigate the effect of cyclophosphamide (CYP)-induced inflammatory cystitis on caveolin 1 in rat urinary bladder and to determine the role of these molecules in the bladder dysfunction that occurs in inflammatory change in rat urinary bladder.	Cyclophosphamide	70-86	caveolin 1	Rattus norvegicus	126-136
22544540-5	2012	Epidemiological studies have also associated elevated tumor tissue TIMP-1 levels with a poor response to cyclophosphamide/methotrexate/5-fluorouracil and anthracycline-based chemotherapy.	Cyclophosphamide	105-121	TIMP metallopeptidase inhibitor 1	Homo sapiens	67-73
22963679-13	2012	A significant protective effect was observed against cyclophosphamide induced DNA damage and inhibition of hepatic LPO with concomitant increase in reduced glutathione (GSH) glutathione S-transferase (GST), superoxide dismutase (SOD) and catalase (CAT) in mice pretreated with PLE.	Cyclophosphamide	53-69	catalase	Mus musculus	238-246
22963679-13	2012	A significant protective effect was observed against cyclophosphamide induced DNA damage and inhibition of hepatic LPO with concomitant increase in reduced glutathione (GSH) glutathione S-transferase (GST), superoxide dismutase (SOD) and catalase (CAT) in mice pretreated with PLE.	Cyclophosphamide	53-69	catalase	Mus musculus	248-251
23000307-0	2012	The expression of PAC1 increases in the degenerative thymus and low dose PACAP protects female mice from cyclophosphamide induced thymus atrophy.	Cyclophosphamide	105-121	adenylate cyclase activating polypeptide 1	Mus musculus	73-78
23000307-2	2012	In this research, firstly the thymus index and the expression of PAC1 in the normal and degenerative thymus with different gender were assayed; secondly PACAP in different dose was used to treat the female mice with cyclophosphamide (CPS) and the changes in thymus index, the expression of PAC1, histopathology, apoptosis, oxidative status and the caspase 3 activity in thymus were determined and compared.	Cyclophosphamide	216-232	adenylate cyclase activating polypeptide 1	Mus musculus	153-158
23000307-2	2012	In this research, firstly the thymus index and the expression of PAC1 in the normal and degenerative thymus with different gender were assayed; secondly PACAP in different dose was used to treat the female mice with cyclophosphamide (CPS) and the changes in thymus index, the expression of PAC1, histopathology, apoptosis, oxidative status and the caspase 3 activity in thymus were determined and compared.	Cyclophosphamide	234-237	adenylate cyclase activating polypeptide 1	Mus musculus	153-158
23000307-4	2012	And it was found for the first time that the PAC1 expression level in thymus of female mice was significantly higher than that of male mice and the expression of the PAC1 and PACAP increased significantly in the degenerative thymus induced by CPS.	Cyclophosphamide	243-246	adenylate cyclase activating polypeptide 1 receptor 1	Mus musculus	45-49
22955915-1	2012	TP53 mutation is an independent marker of poor prognosis in patients with diffuse large B-cell lymphoma (DLBCL) treated with cyclophosphamide, hydroxydaunorubicin, vincristine, and prednisone (CHOP) therapy.	Cyclophosphamide	125-141	tumor protein p53	Homo sapiens	0-4
23000689-6	2012	Along with the depletion of Tregs by low-dose CY treatment, the expression of interleukin-2 (IL-2) in T effector cells increased, and intracellular cAMP concentrations in immune cells decreased.	Cyclophosphamide	46-48	interleukin 2	Mus musculus	78-91
23000689-6	2012	Along with the depletion of Tregs by low-dose CY treatment, the expression of interleukin-2 (IL-2) in T effector cells increased, and intracellular cAMP concentrations in immune cells decreased.	Cyclophosphamide	46-48	interleukin 2	Mus musculus	93-97
22940261-0	2012	Improvement of ginsenoside Rg1 on hematopoietic function in cyclophosphamide-induced myelosuppression mice.	Cyclophosphamide	60-76	protein phosphatase 1, regulatory subunit 3A	Mus musculus	27-30
22940261-1	2012	This study was aimed to investigate the effects of ginsenoside Rg1 (Rg1) on hematopoietic function of bone marrow in cyclophosphamide-induced bone marrow depression mice.	Cyclophosphamide	117-133	protein phosphatase 1, regulatory subunit 3A	Mus musculus	63-66
22940261-1	2012	This study was aimed to investigate the effects of ginsenoside Rg1 (Rg1) on hematopoietic function of bone marrow in cyclophosphamide-induced bone marrow depression mice.	Cyclophosphamide	117-133	protein phosphatase 1, regulatory subunit 3A	Mus musculus	68-71
22940261-9	2012	Rg1 (7.5 and 15mg/kg) protected against cyclophosphamide-induced bone marrow depression, as evidenced by increased bone marrow cell numbers and improved femoral bone morphology.	Cyclophosphamide	40-56	protein phosphatase 1, regulatory subunit 3A	Mus musculus	0-3
22940261-11	2012	Expression of calcium-sensing receptor mRNA was increased in bone marrow cells on the 10th day after cyclophosphamide, but it was returned to normal level after Rg1 treatment.	Cyclophosphamide	101-117	calcium-sensing receptor	Mus musculus	14-38
22940261-13	2012	These results demonstrated that Rg1 improved hematopoietic function of bone marrow in cyclophosphamide-induced myelosuppression.	Cyclophosphamide	86-102	protein phosphatase 1, regulatory subunit 3A	Mus musculus	32-35
23131146-4	2012	In contrast, while TP53 mutations have shown to predict response to cyclophosphamide high dose therapy, mutations in general have been associated with anthracycline resistance in human breast cancers.	Cyclophosphamide	68-84	tumor protein p53	Homo sapiens	19-23
22752193-1	2012	The combination chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) plus rituximab is the standard treatment for patients with primary gastric diffuse large B cell lymphoma (DLBCL).	Cyclophosphamide	34-50	DNA damage inducible transcript 3	Homo sapiens	96-100
22452546-0	2012	Mechanisms and urodynamic effects of a potent and selective EP4 receptor antagonist, MF191, on cyclophosphamide and prostaglandin E2-induced bladder overactivity in rats.	Cyclophosphamide	95-111	prostaglandin E receptor 4	Rattus norvegicus	60-63
23267908-5	2012	The malignant lymphoma patient was treated by cyclophosphamide+doxorubicin+vincristine+prednisolone(CHOP) with rituximab.	Cyclophosphamide	46-62	DNA damage inducible transcript 3	Homo sapiens	100-104
23267962-13	2012	Cyclophosphamide+doxorubicin+vincristine+prednisolone(CHOP) with rituximab therapy was performed.	Cyclophosphamide	0-16	DNA damage inducible transcript 3	Homo sapiens	54-58
23000307-4	2012	And it was found for the first time that the PAC1 expression level in thymus of female mice was significantly higher than that of male mice and the expression of the PAC1 and PACAP increased significantly in the degenerative thymus induced by CPS.	Cyclophosphamide	243-246	adenylate cyclase activating polypeptide 1 receptor 1	Mus musculus	166-170
23000307-4	2012	And it was found for the first time that the PAC1 expression level in thymus of female mice was significantly higher than that of male mice and the expression of the PAC1 and PACAP increased significantly in the degenerative thymus induced by CPS.	Cyclophosphamide	243-246	adenylate cyclase activating polypeptide 1	Mus musculus	175-180
23000307-5	2012	After PACAP was co-injected with CPS to the female mice, it was shown that only low dose (1 nmol/kg) of PACAP promoted the thymus index, inhibited the cell apoptosis, ameliorated the oxidative status and decreased the caspase activity significantly, while high dose (10 nmol/kg) of PACAP had no significant protective effects against CPS-induced thymus atrophy.	Cyclophosphamide	33-36	adenylate cyclase activating polypeptide 1	Mus musculus	104-109
23000307-5	2012	After PACAP was co-injected with CPS to the female mice, it was shown that only low dose (1 nmol/kg) of PACAP promoted the thymus index, inhibited the cell apoptosis, ameliorated the oxidative status and decreased the caspase activity significantly, while high dose (10 nmol/kg) of PACAP had no significant protective effects against CPS-induced thymus atrophy.	Cyclophosphamide	33-36	adenylate cyclase activating polypeptide 1	Mus musculus	104-109
23000307-5	2012	After PACAP was co-injected with CPS to the female mice, it was shown that only low dose (1 nmol/kg) of PACAP promoted the thymus index, inhibited the cell apoptosis, ameliorated the oxidative status and decreased the caspase activity significantly, while high dose (10 nmol/kg) of PACAP had no significant protective effects against CPS-induced thymus atrophy.	Cyclophosphamide	334-337	adenylate cyclase activating polypeptide 1	Mus musculus	104-109
23000307-5	2012	After PACAP was co-injected with CPS to the female mice, it was shown that only low dose (1 nmol/kg) of PACAP promoted the thymus index, inhibited the cell apoptosis, ameliorated the oxidative status and decreased the caspase activity significantly, while high dose (10 nmol/kg) of PACAP had no significant protective effects against CPS-induced thymus atrophy.	Cyclophosphamide	334-337	adenylate cyclase activating polypeptide 1	Mus musculus	104-109
23000307-6	2012	It was concluded that the expression of PAC1 in the thymus changes in reverse ratio with thymus index and in direct ratio with cell apoptosis and only low dose of PACAP had positive effects against the CPS-induced thymus atrophy.	Cyclophosphamide	202-205	adenylate cyclase activating polypeptide 1	Mus musculus	163-168
23024279-7	2012	Calcium-activated binding of S100A4 to CD16A, promoted by the initial calcium flux, attenuates the phosphorylation of CY, and, acting as a molecular switch, may both serve as a negative feedback on cytokine production pathways during sustained receptor engagement and favor a shift to degranulation, consistent with the importance of granule release following conjugate formation between CD16A(+) effector cells and target cells.	Cyclophosphamide	118-120	S100 calcium binding protein A4	Homo sapiens	29-35
23024279-7	2012	Calcium-activated binding of S100A4 to CD16A, promoted by the initial calcium flux, attenuates the phosphorylation of CY, and, acting as a molecular switch, may both serve as a negative feedback on cytokine production pathways during sustained receptor engagement and favor a shift to degranulation, consistent with the importance of granule release following conjugate formation between CD16A(+) effector cells and target cells.	Cyclophosphamide	118-120	Fc gamma receptor IIIa	Homo sapiens	39-44
22660274-8	2012	We conclude that Cy is an effective and superior preparative regimen with respect to engraftment of lentivirus-transduced cells and functional correction in fanca ( -/- ) mice.	Cyclophosphamide	17-19	Fanconi anemia, complementation group A	Mus musculus	157-162
22307556-0	2012	Improvement in health-related quality of life in MPO-ANCA-associated vasculitis patients treated with cyclophosphamide plus prednisolone: an analysis of 18 months of follow-up data from the JMAAV study.	Cyclophosphamide	102-118	myeloperoxidase	Homo sapiens	49-52
22307556-1	2012	OBJECTIVES: To examine the improvement in health-related quality of life (HRQOL) in association with disease activity in myeloperoxidase (MPO)-antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis patients treated with cyclophosphamide plus prednisolone.	Cyclophosphamide	230-246	myeloperoxidase	Homo sapiens	121-136
22307556-1	2012	OBJECTIVES: To examine the improvement in health-related quality of life (HRQOL) in association with disease activity in myeloperoxidase (MPO)-antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis patients treated with cyclophosphamide plus prednisolone.	Cyclophosphamide	230-246	myeloperoxidase	Homo sapiens	138-141
22646666-13	2012	CONCLUSION AND IMPLICATIONS: Endogenous H(2) S, generated by up-regulated CSE, caused bladder pain and referred hyperalgesia through the activation of Ca(v) 3.2 channels, one of the T-type Ca(2+) channels, in mice with cyclophosphamide-induced cystitis.	Cyclophosphamide	219-235	cystathionase (cystathionine gamma-lyase)	Mus musculus	74-77
22646666-13	2012	CONCLUSION AND IMPLICATIONS: Endogenous H(2) S, generated by up-regulated CSE, caused bladder pain and referred hyperalgesia through the activation of Ca(v) 3.2 channels, one of the T-type Ca(2+) channels, in mice with cyclophosphamide-induced cystitis.	Cyclophosphamide	219-235	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	151-160
22840047-4	2012	The results showed that SFPS stimulated proliferation and the cytokines (IL-2, IL-6 and IFN-gamma) secretion of splenic lymphocytes in cyclophosphamide-induced immunosuppressed mice.	Cyclophosphamide	135-151	interferon gamma	Mus musculus	88-97
22851565-0	2012	Concurrent expression of MYC and BCL2 in diffuse large B-cell lymphoma treated with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone.	Cyclophosphamide	99-115	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	25-28
23170130-6	2012	Lymphocytes, obtained from three patients with severely active SLE, with high levels of P-gp expression were treated with cyclophosphamide, mycophenolic acid or emodin in vitro and Rh123-efflux activity was measured.	Cyclophosphamide	122-138	ATP binding cassette subfamily B member 1	Homo sapiens	88-92
21883784-2	2012	AIMS: We report the largest study to date assessing FCGR3A-V158F polymorphisms in diffuse large B-cell lymphoma (DLBCL) treated with cyclophosphamide/hydroxydaunorubicin/Oncovin (vincristine)/prednisone/rituximab (CHOP-R).	Cyclophosphamide	133-149	Fc gamma receptor IIIa	Homo sapiens	52-58
22851565-0	2012	Concurrent expression of MYC and BCL2 in diffuse large B-cell lymphoma treated with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone.	Cyclophosphamide	99-115	BCL2 apoptosis regulator	Homo sapiens	33-37
22139992-0	2012	Potentiation of a p53-SLP vaccine by cyclophosphamide in ovarian cancer: a single-arm phase II study.	Cyclophosphamide	37-53	tumor protein p53	Homo sapiens	18-21
22139992-1	2012	The purpose of the current phase II single-arm clinical trial was to evaluate whether pretreatment with low-dose cyclophosphamide improves immunogenicity of a p53-synthetic long peptide (SLP) vaccine in patients with recurrent ovarian cancer.	Cyclophosphamide	113-129	tumor protein p53	Homo sapiens	159-162
22139992-10	2012	The outcome of this phase II trial warrants new studies on the use of low-dose cyclophosphamide to potentiate the immunogenicity of the p53-SLP vaccine or other antitumor vaccines.	Cyclophosphamide	79-95	tumor protein p53	Homo sapiens	136-139
22543673-3	2012	PATIENTS AND METHODS: This study aimed to evaluate the associations between ABCB1 polymorphisms G2677T/A, C3435T, and their haplotype with progression-free survival (PFS) and overall survival (OS) in 177 SCLC patients treated with cisplatin-etoposide or cyclophosphamide-epirubicin-vincristine chemotherapy.	Cyclophosphamide	254-270	ATP binding cassette subfamily B member 1	Homo sapiens	76-81
22837483-5	2012	In this study, we demonstrate that B7-DC-Ig can enhance the therapeutic efficacy of vaccine when combined with cyclophosphamide.	Cyclophosphamide	111-127	programmed cell death 1 ligand 2	Mus musculus	35-40
22983648-0	2012	Cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) in the treatment of stage IE/IIE extranodal natural killer/T cell lymphoma, nasal type: 13-year follow-up in 135 patients.	Cyclophosphamide	0-16	DNA damage inducible transcript 3	Homo sapiens	60-64
22767414-0	2012	Early treatment with glucocorticoids or cyclophosphamide retains the slit diaphragm proteins nephrin and podocin in experimental lupus nephritis.	Cyclophosphamide	40-56	nephrosis 1, nephrin	Mus musculus	93-100
22767414-0	2012	Early treatment with glucocorticoids or cyclophosphamide retains the slit diaphragm proteins nephrin and podocin in experimental lupus nephritis.	Cyclophosphamide	40-56	nephrosis 2, podocin	Mus musculus	105-112
22767414-6	2012	Nephrin and podocin protein expression significantly increased in both glucocorticoid and cyclophosphamide groups as early as after three months of therapy.	Cyclophosphamide	90-106	nephrosis 1, nephrin	Mus musculus	0-7
22767414-6	2012	Nephrin and podocin protein expression significantly increased in both glucocorticoid and cyclophosphamide groups as early as after three months of therapy.	Cyclophosphamide	90-106	nephrosis 2, podocin	Mus musculus	12-19
22962380-1	2012	The authors present the first case report of a patient with lymphoma who developed disseminated cryptococcal osteomyelitis and meningitis while being treated with the PEP-C (prednisone, etoposide, procarbazine and cyclophosphamide) chemotherapy regimen.	Cyclophosphamide	214-230	peptidase C	Homo sapiens	167-172
22796409-5	2012	As a result, mice deficient in Dicer manifest enhanced P2X expression in the detrusor on cyclophosphamide treatment, predisposing to the increased risk for OAB development.	Cyclophosphamide	89-105	purinergic receptor P2X, ligand-gated ion channel, 1	Mus musculus	55-58
22721383-1	2012	R (rituximab)-CHOP (cyclophosphamide, adriamycin, vincristin, and prednisone) is given to outpatients with CD20-positive lymphoma as a standard treatment.	Cyclophosphamide	20-36	DNA damage inducible transcript 3	Homo sapiens	14-18
22721383-6	2012	After combining with either adriamycin or cyclophosphamide, the binding capacity of R to the CD20 antigen was equivalent to controls, and no molecular changes in adriamycin and cyclophosphamide were detected after combination with R. Twenty-one cases of DLBCL were treated safely with concurrent administration of R and CHOP.	Cyclophosphamide	42-58	keratin 20	Homo sapiens	93-97
22380717-12	2012	CYP2B6*9 variants vs. wildtype were found to have decreased elimination rate constant (P = 0.0005, 95% CI 0.033, 0.103), increased V(d) (P = 0.0271, 95% CI -57.5, -4.2) and decreased C(max) (P = 0.0176, 95% CI 0.696, 6179) for cyclophosphamide.	Cyclophosphamide	227-243	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	0-6
22380717-13	2012	ABCB1 C3435T variants had a borderline decrease in cyclophosphamide elimination rate constant (P = 0.0858; 95% CI -0.005, 0.102).	Cyclophosphamide	51-67	ATP binding cassette subfamily B member 1	Homo sapiens	0-5
22380717-17	2012	The CYP2B6*9 and ABCB1 C3435T polymorphisms alter the pharmacokinetics of cyclophosphamide and 4-hydroxycyclophosphamide in glomerulonephritis.	Cyclophosphamide	74-90	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	4-10
22380717-17	2012	The CYP2B6*9 and ABCB1 C3435T polymorphisms alter the pharmacokinetics of cyclophosphamide and 4-hydroxycyclophosphamide in glomerulonephritis.	Cyclophosphamide	74-90	ATP binding cassette subfamily B member 1	Homo sapiens	17-22
22804669-7	2012	We also demonstrated that sera from mice with human MM xenografts contained human BCMA, and levels correlated with the change in tumour volume in response to melphalan or cyclophosphamide with bortezomib.	Cyclophosphamide	171-187	TNF receptor superfamily member 17	Homo sapiens	82-86
22213394-0	2012	Prognostic significance of MYC, BCL2, and BCL6 rearrangements in patients with diffuse large B-cell lymphoma treated with cyclophosphamide, doxorubicin, vincristine, and prednisone plus rituximab.	Cyclophosphamide	122-138	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	27-30
22213394-0	2012	Prognostic significance of MYC, BCL2, and BCL6 rearrangements in patients with diffuse large B-cell lymphoma treated with cyclophosphamide, doxorubicin, vincristine, and prednisone plus rituximab.	Cyclophosphamide	122-138	BCL6 transcription repressor	Homo sapiens	42-46
22213394-2	2012	The aim of this study was to investigate the frequency and prognostic impact of BCL2, BCL6, and MYC rearrangements in cyclophosphamide, doxorubicin, vincristine, and prednisone plus rituximab (R-CHOP)-treated DLBCL cases.	Cyclophosphamide	118-134	BCL2 apoptosis regulator	Homo sapiens	80-84
22213394-2	2012	The aim of this study was to investigate the frequency and prognostic impact of BCL2, BCL6, and MYC rearrangements in cyclophosphamide, doxorubicin, vincristine, and prednisone plus rituximab (R-CHOP)-treated DLBCL cases.	Cyclophosphamide	118-134	BCL6 transcription repressor	Homo sapiens	86-90
22213394-2	2012	The aim of this study was to investigate the frequency and prognostic impact of BCL2, BCL6, and MYC rearrangements in cyclophosphamide, doxorubicin, vincristine, and prednisone plus rituximab (R-CHOP)-treated DLBCL cases.	Cyclophosphamide	118-134	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	96-99
22759738-4	2012	SUMMARY: Rituximab administered as induction or maintenance therapy in combination with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) significantly prolonged event-free survival.	Cyclophosphamide	88-104	DNA damage inducible transcript 3	Homo sapiens	148-152
22759219-0	2012	The treatment of retinoblastoma with four-drug regimen including cisplatin, etoposide, vincristine, and cyclophosphamide.	Cyclophosphamide	104-120	RB transcriptional corepressor 1	Homo sapiens	17-31
23094815-4	2012	Greater success was achieved with thalidomide regimen (CTD: cyclophosphamide, thalidomide, dexamethasone, 10 cycles, 3/2009-1/2010) leading to reduction in the size of the hypervascularized lymph nodes (almost by 50%) as well as their radiopharmaceutical (fluorodeoxyglucose) uptake as seen on a combined positron emission tomography and computed tomography (PET/CT) scan imaging.	Cyclophosphamide	60-76	CTD	Homo sapiens	55-58
22608309-1	2012	The study was aimed to investigate modifications of apoptotic gene expression profile by microarray technique in 10 patients with chronic lymphocytic leukemia by treatment with rituximab, cladribine and cyclophosphamide (RCC) according to IGHV mutational status.	Cyclophosphamide	203-219	immunoglobulin heavy variable 3-69-1 (pseudogene)	Homo sapiens	239-243
22789848-4	2012	The incidences of spontaneous diabetes as well as cyclophosphamide-induced diabetes were significantly reduced and delayed in the Stat5b transgenic NOD mice compared to their littermate controls.	Cyclophosphamide	50-66	signal transducer and activator of transcription 5B	Mus musculus	130-136
22865806-4	2012	A brain biopsy confirmed the diagnosis of intravascular B-cell lymphoma and he was treated with CHOP chemotherapy (cyclophosphamide, hydroxydaunorubicin, vincristine and prednisolone).	Cyclophosphamide	115-131	DNA damage inducible transcript 3	Homo sapiens	96-100
23185784-3	2012	The treatment of L-TACB-bearing rats with a single low-dose cyclophosphamide decreased IL-10 production, reverted immunosuppression and induced the immunologic rejection of tumor metastasis without any effect on primary tumor growth.	Cyclophosphamide	60-76	interleukin 10	Rattus norvegicus	87-92
23185784-4	2012	Our current aim was to investigate the effects of cyclophosphamide on the expression of IL-10 and IL-10R on primary and metastatic L-TACB cells.	Cyclophosphamide	50-66	interleukin 10	Rattus norvegicus	88-93
22526409-0	2012	Metronomic oral combination chemotherapy with capecitabine and cyclophosphamide: a phase II study in patients with HER2-negative metastatic breast cancer.	Cyclophosphamide	63-79	erb-b2 receptor tyrosine kinase 2	Homo sapiens	115-119
22487925-9	2012	Moreover, CD4(+)CD25(+) cells from wild-type NOD mice suppressed and delayed the onset of diabetes compared with those from Cxcr3                            (                               -/-                            ) NOD mice in a cyclophosphamide-induced diabetes model system.	Cyclophosphamide	236-252	CD4 antigen	Mus musculus	10-13
22280534-0	2012	Serum soluble CD27 level is associated with outcome in patients with diffuse large B-cell lymphoma treated with rituximab, cyclophosphamide, doxorubicin, vincristine and prednisolone.	Cyclophosphamide	123-139	CD27 molecule	Homo sapiens	14-18
22111969-0	2012	Importance of granulocyte colony-stimulating factor prophylaxis in therapy with rituximab, cyclophosphamide, doxorubicin, vincristine and prednisolone given every 14 days for diffuse large B-cell lymphoma in routine clinical practice.	Cyclophosphamide	91-107	colony stimulating factor 3	Homo sapiens	14-51
21672106-6	2012	We report the first case of post-transplant recurrence of nephrotic syndrome in a 4-yr-old child with CNS due to NPHS-1 mutation in whom CNI, corticosteroid and cyclophosphamide therapy was unsuccessful, but who achieved remission after depletion of B cells with RTX, associated with a decrease in the level of anti-nephrin antibodies.	Cyclophosphamide	161-177	NPHS1 adhesion molecule, nephrin	Homo sapiens	113-119
22613676-10	2012	The stronger inhibiting effects of MMF, LEF, CsA and Cy on CD4(+)CD25(+)Foxp3(+) Tregs than on T effectors may block the host immune tolerance potentiality.	Cyclophosphamide	53-55	CD4 antigen	Mus musculus	59-62
22613676-10	2012	The stronger inhibiting effects of MMF, LEF, CsA and Cy on CD4(+)CD25(+)Foxp3(+) Tregs than on T effectors may block the host immune tolerance potentiality.	Cyclophosphamide	53-55	forkhead box P3	Mus musculus	72-77
22586064-3	2012	Extending these findings in vitro, we found that knockdown of Fra-1 in breast tumor cells was sufficient to confer resistance to doxorubicin and cyclophosphamide, whereas enhanced Fra-1 expression could render these cells chemosensitive.	Cyclophosphamide	145-161	FOS like 1, AP-1 transcription factor subunit	Homo sapiens	62-67
22249209-8	2012	Of the 105 patients who received rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisolone therapy, those who were CD20 negative (FCM) showed significantly inferior overall (hazard ratios (HR): 6.79, 95% CI: 1.32-34.96, p = 0.04) and progression-free survival (HR: 7.3, 95% CI: 1.49-35.8, p = 0.04) compared to patients who were CD20 normal.	Cyclophosphamide	48-64	keratin 20	Homo sapiens	133-137
22753738-2	2012	MAF is a cyclophosphamide analog which spontaneously degrades to 4-hydroxy-cyclophosphamide.	Cyclophosphamide	9-25	MAF bZIP transcription factor	Homo sapiens	0-3
22248715-1	2012	Peripheral blood progenitor cell mobilization with intermediate-dose cyclophosphamide (ID-CY) and granulocyte colony-stimulating factor (G-CSF) has been shown to be more efficacious, albeit more toxic, than low-dose cyclophosphamide (LD-CY) mobilization regimens in patients with multiple myeloma treated with conventional therapies.	Cyclophosphamide	216-232	colony stimulating factor 3	Homo sapiens	137-142
22315133-2	2012	The aim of this study was to investigate whether 14-3-3sigma expression is also associated with resistance to neoadjuvant chemotherapy consisting of paclitaxel followed by 5-FU/epirubicin/cyclophosphamide (P-FEC) in human breast cancer patients.	Cyclophosphamide	188-204	stratifin	Homo sapiens	49-60
22626517-6	2012	Cyclophosphamide-immunosuppressed mice have greatly reduced amounts of CD8(+), CD4(+) and CD3(+) T cells and CD19(+) B cells.	Cyclophosphamide	0-16	CD4 antigen	Mus musculus	79-82
22626517-6	2012	Cyclophosphamide-immunosuppressed mice have greatly reduced amounts of CD8(+), CD4(+) and CD3(+) T cells and CD19(+) B cells.	Cyclophosphamide	0-16	CD3 antigen, epsilon polypeptide	Mus musculus	90-93
21792892-0	2012	The tumor microenvironment expression of p-STAT3 influences the efficacy of cyclophosphamide with WP1066 in murine melanoma models.	Cyclophosphamide	76-92	signal transducer and activator of transcription 3	Mus musculus	43-48
21792892-3	2012	We hypothesized that WP1066, a novel inhibitor of STAT3 signaling, would enhance the antitumor activity of cyclophosphamide (CTX) against melanoma, including disease within the CNS.	Cyclophosphamide	107-123	signal transducer and activator of transcription 3	Mus musculus	50-55
21792892-3	2012	We hypothesized that WP1066, a novel inhibitor of STAT3 signaling, would enhance the antitumor activity of cyclophosphamide (CTX) against melanoma, including disease within the CNS.	Cyclophosphamide	107-123	V-set and immunoglobulin domain containing 2	Mus musculus	125-128
22469755-8	2012	Furthermore, Cav3.1 knockdown blocked cyclophosphamide-induced apoptosis.	Cyclophosphamide	38-54	calcium voltage-gated channel subunit alpha1 G	Homo sapiens	13-19
22754788-2	2012	Administration of cyclophosphamide (CY) prior to intratumoral IL-12 and GM-CSF delivery blocked post-treatment T-suppressor cell rebound via elimination of the pre-existing T-suppressor cell pool, allowed repeated activation of antitumor cytotoxic T-cells and resulted in the cure of advanced spontaneous tumors.	Cyclophosphamide	18-34	colony stimulating factor 2	Homo sapiens	72-78
22742729-3	2012	RESULTS: In a rat cystitis model induced by cyclophosphamide (CYP) for 48 h, the mRNA and protein levels of the excitatory neurotransmitter calcitonin gene-related peptide (CGRP) are increased in the L6 dorsal root ganglia (DRG) in response to bladder inflammation.	Cyclophosphamide	44-60	calcitonin-related polypeptide alpha	Rattus norvegicus	140-171
22742729-3	2012	RESULTS: In a rat cystitis model induced by cyclophosphamide (CYP) for 48 h, the mRNA and protein levels of the excitatory neurotransmitter calcitonin gene-related peptide (CGRP) are increased in the L6 dorsal root ganglia (DRG) in response to bladder inflammation.	Cyclophosphamide	44-60	calcitonin-related polypeptide alpha	Rattus norvegicus	173-177
22310172-7	2012	The results showed that Rg3 significantly inhibited Cy-induced oxidative stress in mice by increasing the indices of the spleen and thymus and total antioxidant capacity, elevating the activities of catalase, superoxidase dismutase and lysozyme as well as decreasing the activity of xanthine oxidase and the levels of malondialdehyde and nitric oxide.	Cyclophosphamide	52-54	xanthine dehydrogenase	Mus musculus	283-299
22245954-1	2012	PURPOSE: The prodrug cyclophosphamide is metabolized by cytochrome P450(CYP)2B6 to the active metabolite, 4-hydroxycyclophosphamide (4-OH), and by CYP3A4/5 to toxic chloracetaldehyde and 2-dechloroethylcyclophosphamide (DCE).	Cyclophosphamide	21-37	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	56-79
22245954-1	2012	PURPOSE: The prodrug cyclophosphamide is metabolized by cytochrome P450(CYP)2B6 to the active metabolite, 4-hydroxycyclophosphamide (4-OH), and by CYP3A4/5 to toxic chloracetaldehyde and 2-dechloroethylcyclophosphamide (DCE).	Cyclophosphamide	21-37	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	147-153
22035416-1	2012	The prognosis of patients with peripheral T-cell lymphoma (PTCL) treated with cyclophosphamide, adriamycin, vincristine and prednisone (CHOP) is poor, but their laboratory prognostic parameters had not previously been evaluated.	Cyclophosphamide	78-94	DNA damage inducible transcript 3	Homo sapiens	136-140
22266913-1	2012	The CXCR4 antagonist AMD3100 is progressively replacing cyclophosphamide (CYP) as adjuvant to granulocyte colony-stimulating factor (G-CSF) to mobilize hematopoietic stem cells (HSC) for autologous transplants in patients who failed prior mobilization with G-CSF alone.	Cyclophosphamide	56-72	C-X-C motif chemokine receptor 4	Homo sapiens	4-9
22807977-2	2012	Thus, we hypothesized that BRCA1 protein expression and activating PIK3CA mutations are potential tumor biomarkers for the chemotherapeutic response to doxorubicin/cyclophosphamide plus docetaxel in locally advanced breast cancer.	Cyclophosphamide	164-180	BRCA1 DNA repair associated	Homo sapiens	27-32
22807977-2	2012	Thus, we hypothesized that BRCA1 protein expression and activating PIK3CA mutations are potential tumor biomarkers for the chemotherapeutic response to doxorubicin/cyclophosphamide plus docetaxel in locally advanced breast cancer.	Cyclophosphamide	164-180	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	67-73
22349930-10	2012	Four weeks of CYC or MMF treatment led to a significant increase in CD3+CD4+ T cells (P < 0.05).	Cyclophosphamide	14-17	CD4 molecule	Homo sapiens	72-75
22430613-8	2012	The sensitivity to other genotoxic agents such as carboplatin, cyclophosphamide and 5-fluorouracil was also increased by silencing the expression of elafin.	Cyclophosphamide	63-79	peptidase inhibitor 3	Homo sapiens	149-155
22589273-5	2012	Shortly after cyclophosphamide treatment, there was an abrupt expansion of myeloid lineage cells in the bone marrow and the peripheral blood, associated with increases in cytokines with myelogenic potential such as C-C chemokine ligand (CCL)2, interleukin (IL)-6, and VEGF-A.	Cyclophosphamide	14-30	chemokine (C-C motif) ligand 2	Mus musculus	237-242
22589273-5	2012	Shortly after cyclophosphamide treatment, there was an abrupt expansion of myeloid lineage cells in the bone marrow and the peripheral blood, associated with increases in cytokines with myelogenic potential such as C-C chemokine ligand (CCL)2, interleukin (IL)-6, and VEGF-A.	Cyclophosphamide	14-30	interleukin 6	Mus musculus	244-262
22589273-5	2012	Shortly after cyclophosphamide treatment, there was an abrupt expansion of myeloid lineage cells in the bone marrow and the peripheral blood, associated with increases in cytokines with myelogenic potential such as C-C chemokine ligand (CCL)2, interleukin (IL)-6, and VEGF-A.	Cyclophosphamide	14-30	vascular endothelial growth factor A	Mus musculus	268-274
22589273-6	2012	More importantly, neutralizing host-derived murine CCL2, but not IL-6, in the premetastatic murine host significantly reduced the prometastatic effects of cyclophosphamide.	Cyclophosphamide	155-171	chemokine (C-C motif) ligand 2	Mus musculus	51-55
22320227-1	2012	The purpose of the present study was to investigate the association of glutathione S-transferase P1 (GSTP1) expression with resistance to neoadjuvant paclitaxel followed by 5-fluorouracil/epirubicin/cyclophosphamide (P-FEC) in human breast cancers.	Cyclophosphamide	199-215	glutathione S-transferase pi 1	Homo sapiens	71-99
22441388-8	2012	In contrast, the administration of cyclophosphamide (200 mg/kg) after immunization significantly reduced anti-TNF-alpha antibody titers and their neutralizing capacity.	Cyclophosphamide	35-51	tumor necrosis factor	Mus musculus	110-119
22539294-5	2012	Our data indicate that adoptive transfer of donor-derived T-cell receptor (TCR) alphabeta(+) CD3(+) CD4(-) CD8(-) NK1.1(-) (double negative, DN) Treg cells prior to C57BL/6 to BALB/c BM transplantation, in combination with cyclophosphamide, induced a stable-mixed chimerism and acceptance of C57BL/6 skin allografts but rejection of third-party C3H (H-2k) skin grafts.	Cyclophosphamide	223-239	CD4 molecule	Homo sapiens	100-103
22539294-5	2012	Our data indicate that adoptive transfer of donor-derived T-cell receptor (TCR) alphabeta(+) CD3(+) CD4(-) CD8(-) NK1.1(-) (double negative, DN) Treg cells prior to C57BL/6 to BALB/c BM transplantation, in combination with cyclophosphamide, induced a stable-mixed chimerism and acceptance of C57BL/6 skin allografts but rejection of third-party C3H (H-2k) skin grafts.	Cyclophosphamide	223-239	CD8a molecule	Homo sapiens	107-110
21821547-0	2012	Recurrence risk score based on the specific activity of CDK1 and CDK2 predicts response to neoadjuvant paclitaxel followed by 5-fluorouracil, epirubicin and cyclophosphamide in breast cancers.	Cyclophosphamide	157-173	cyclin dependent kinase 1	Homo sapiens	56-60
22566972-7	2012	Finally, in mice with cyclophosphamide induced lymphopenia, the administration of P3 mAb accelerated the recovery of both CD4(+) and CD8(+) T cells.	Cyclophosphamide	22-38	CD4 antigen	Mus musculus	122-125
21821547-0	2012	Recurrence risk score based on the specific activity of CDK1 and CDK2 predicts response to neoadjuvant paclitaxel followed by 5-fluorouracil, epirubicin and cyclophosphamide in breast cancers.	Cyclophosphamide	157-173	cyclin dependent kinase 2	Homo sapiens	65-69
21947259-3	2012	The aim of the present work was to study the relationship between tumor growth rate, aggressiveness, and response to cyclophosphamide (Cy) therapy with regard to Gal-1 expression in murine T-cell lymphoma models.	Cyclophosphamide	117-133	lectin, galactose binding, soluble 1	Mus musculus	162-167
21706156-0	2012	MDM2 SNP309 and TP53 R72P associated with severe and febrile neutropenia in breast cancer patients treated with 5-FU/epirubicin/cyclophosphamide.	Cyclophosphamide	128-144	MDM2 proto-oncogene	Homo sapiens	0-4
21706156-0	2012	MDM2 SNP309 and TP53 R72P associated with severe and febrile neutropenia in breast cancer patients treated with 5-FU/epirubicin/cyclophosphamide.	Cyclophosphamide	128-144	tumor protein p53	Homo sapiens	16-20
21947259-3	2012	The aim of the present work was to study the relationship between tumor growth rate, aggressiveness, and response to cyclophosphamide (Cy) therapy with regard to Gal-1 expression in murine T-cell lymphoma models.	Cyclophosphamide	135-137	lectin, galactose binding, soluble 1	Mus musculus	162-167
22012257-1	2012	PURPOSE: The cytotoxic drug cyclophosphamide (CP) is bioactivated into 4-hydroxy-cyclophosphamide (4-OH-CP) through cytochrome P450 enzymes and cleared through aldehyde dehydrogenase and glutathione S-transferase.	Cyclophosphamide	28-44	glutathione S-transferase kappa 1	Homo sapiens	187-212
22690149-5	2012	ELISA measurement suggested that ASTA treatment (10 microM) reduced pro-inflammatory cytokines secretion (IL-1beta, IL-6 and TNF-alpha) induced through H(2)O(2), (100 microM).	Cyclophosphamide	33-37	interleukin 1 beta	Homo sapiens	106-114
22690149-5	2012	ELISA measurement suggested that ASTA treatment (10 microM) reduced pro-inflammatory cytokines secretion (IL-1beta, IL-6 and TNF-alpha) induced through H(2)O(2), (100 microM).	Cyclophosphamide	33-37	interleukin 6	Homo sapiens	116-120
22690149-5	2012	ELISA measurement suggested that ASTA treatment (10 microM) reduced pro-inflammatory cytokines secretion (IL-1beta, IL-6 and TNF-alpha) induced through H(2)O(2), (100 microM).	Cyclophosphamide	33-37	tumor necrosis factor	Homo sapiens	125-134
22345563-3	2012	Using genetically based manipulations of neuronal activity, we show that activation of neurons (or neuroendocrine cells) expressing the neuropeptide allatostatin A (AstA) inhibits or limits several starvation-induced changes in feeding behavior in adult Drosophila, including increased food intake and enhanced behavioral responsiveness to sugar.	Cyclophosphamide	165-169	Allatostatin A	Drosophila melanogaster	149-163
22803439-1	2012	OBJECTIVE: To explore the mechanism of polypeptide extract from scorpion venom (PESV) on promoting anti-tumor effects of cyclophosphamide (CTX).	Cyclophosphamide	121-137	V-set and immunoglobulin domain containing 2	Mus musculus	139-142
22352711-7	2012	It was also observed that the hepatic beta-oxidation enzymes (ACO, CPT1) and PPARalpha expressions tended to increase in the livers of the Lo- and Cy-treated rats compared with those in ZDF-control rats.	Cyclophosphamide	147-149	peroxisome proliferator activated receptor alpha	Rattus norvegicus	77-86
22307137-2	2012	PARP inhibition potentiates effects of cyclophosphamide in preclinical models.	Cyclophosphamide	39-55	collagen type XI alpha 2 chain	Homo sapiens	0-4
22307137-10	2012	CONCLUSIONS: The combination of veliparib with metronomic cyclophosphamide is well tolerated and shows promising activity in a subset of patients with BRCA mutations.	Cyclophosphamide	58-74	BRCA1 DNA repair associated	Homo sapiens	151-155
22483282-1	2012	This study describes molecular interactions between human brain acetylcholinesterase (AChE) and the well known anti-neoplastic drug, methotrexate (MTX) and its comparison to "AChE-cyclophosphamide (CP) interactions" that we reported previously.	Cyclophosphamide	180-196	acetylcholinesterase (Cartwright blood group)	Homo sapiens	175-179
22560674-1	2012	Recently, we showed that post cyclophosphamide (CTX) microenvironment benefits the function of transferred T cells.	Cyclophosphamide	30-46	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	48-51
22159699-0	2012	Which CYP2B6 variants have functional consequences for cyclophosphamide bioactivation?	Cyclophosphamide	55-71	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	6-12
22303814-11	2012	Dogs receiving toceranib and CYC demonstrated a significant increase in serum concentrations of IFN-gamma, which was inversely correlated with Treg numbers after 6 weeks of combination treatment.	Cyclophosphamide	29-32	interferon gamma	Canis lupus familiaris	96-105
22285846-0	2012	Cyclophosphamide inhibits the generation and function of CD8(+) regulatory T cells.	Cyclophosphamide	0-16	CD8a molecule	Homo sapiens	57-60
22285846-3	2012	Cyclophosphamide (CY) has been demonstrated to be effective in counteracting CD4(+)CD25(+) Treg activity.	Cyclophosphamide	0-16	CD4 molecule	Homo sapiens	77-80
22285846-3	2012	Cyclophosphamide (CY) has been demonstrated to be effective in counteracting CD4(+)CD25(+) Treg activity.	Cyclophosphamide	0-16	interleukin 2 receptor subunit alpha	Homo sapiens	83-87
22285846-3	2012	Cyclophosphamide (CY) has been demonstrated to be effective in counteracting CD4(+)CD25(+) Treg activity.	Cyclophosphamide	18-20	CD4 molecule	Homo sapiens	77-80
22285846-3	2012	Cyclophosphamide (CY) has been demonstrated to be effective in counteracting CD4(+)CD25(+) Treg activity.	Cyclophosphamide	18-20	interleukin 2 receptor subunit alpha	Homo sapiens	83-87
22285846-10	2012	These data demonstrate that CD8(+) Treg are inhibited through cytotoxic phenomena by CY, thus supporting the use of this drug at adequate concentrations and schedules of administration as a Treg inhibitor in combinatorial chemo- or immunotherapeutic anticancer protocols.	Cyclophosphamide	85-87	CD8a molecule	Homo sapiens	28-31
22291182-5	2012	Injection of the anti-CD98hc mAb completely prevented the onset of cyclophosphamide-induced diabetes in NOD mice.	Cyclophosphamide	67-83	solute carrier family 3 (activators of dibasic and neutral amino acid transport), member 2	Mus musculus	22-28
22080062-2	2012	ALDH1A1 inactivates cyclophosphamide, which is an integral agent in breast cancer chemotherapy regimens.	Cyclophosphamide	20-36	aldehyde dehydrogenase 1 family member A1	Homo sapiens	0-7
22080062-3	2012	The purposes of this study were to verify these results, to correlate ALDH1A1 expression with clinical outcome in patients treated with cyclophosphamide as part of the chemotherapy (adjuvant or neoadjuvant), and to evaluate ALDH1A1 as a useful marker to predict the clinical outcome of breast cancer subsets.	Cyclophosphamide	136-152	aldehyde dehydrogenase 1 family member A1	Homo sapiens	70-77
22217702-1	2012	This study was designed to examine the interaction of two anti-breast cancer drugs, i.e., fluoxymesterone (FLU) and cyclophosphamide (CYC), with human serum albumin (HSA) using different kinds of spectroscopic, zeta potential and molecular modeling techniques under imitated physiological conditions.	Cyclophosphamide	116-132	albumin	Homo sapiens	151-164
22265744-6	2012	Furthermore, CDy::UPRT-MSCs were significantly more sensitive to 5-fluorouracil (5FU), cisplatin, cyclophosphamide and cytosine arabinoside as determined by increased Caspase 3/7 activation and/or decreased relative proliferation.	Cyclophosphamide	98-114	chromodomain Y-linked 1B	Homo sapiens	13-16
22333190-12	2012	The patient was treated with chemotherapy (CHOP: cyclophosphamide, hydroxydaunorbicin, vincristine, and predonisone), and the lung tumor disappeared.	Cyclophosphamide	49-65	DNA damage inducible transcript 3	Homo sapiens	43-47
20449626-0	2012	Circulating thrombospondin 1 level as a surrogate marker in patients receiving cyclophosphamide-based metronomic chemotherapy.	Cyclophosphamide	79-95	thrombospondin 1	Homo sapiens	12-28
20449626-1	2012	Several previous reports suggest that thrombospondin (TSP-1) may be a mediator of the antiangiogenic effects of low-dose metronomic cyclophosphamide-based chemotherapy (MC).	Cyclophosphamide	132-148	thrombospondin 1	Homo sapiens	54-59
20449626-5	2012	TSP-1 levels decreased in patients receiving metronomic cyclophosphamide (from 16.6 +- 7.2 microg/ml to 12.8 +- 7.4 microg/ml; p = 0.057).	Cyclophosphamide	56-72	thrombospondin 1	Homo sapiens	0-5
22822676-6	2012	They both could antagonize immunosuppressive action caused by Cyclophosphamide, which could promote T lymphocyte proliferation, kill and wound activity, quantity of T lymphocyte subgroup, and production of IL-1beta with different degree.	Cyclophosphamide	62-78	interleukin 1 beta	Mus musculus	206-214
22227404-7	2012	In the case of cyclophosphamide, elevated blood MN-RET frequencies were observed 2 days after treatment began, and the maximal frequency was achieved 1 day later.	Cyclophosphamide	15-31	ret proto-oncogene	Canis lupus familiaris	51-54
21649551-5	2012	Treatment of mice with CPA suppressed the formation of Th1 cytokines (TNF-alpha, IFN-gamma, and IL-2), shifting the overall balance toward Th2 (IL-4 and IL-5).	Cyclophosphamide	23-26	negative elongation factor complex member C/D, Th1l	Mus musculus	55-58
21649551-5	2012	Treatment of mice with CPA suppressed the formation of Th1 cytokines (TNF-alpha, IFN-gamma, and IL-2), shifting the overall balance toward Th2 (IL-4 and IL-5).	Cyclophosphamide	23-26	tumor necrosis factor	Mus musculus	70-79
21649551-5	2012	Treatment of mice with CPA suppressed the formation of Th1 cytokines (TNF-alpha, IFN-gamma, and IL-2), shifting the overall balance toward Th2 (IL-4 and IL-5).	Cyclophosphamide	23-26	interferon gamma	Mus musculus	81-90
21649551-5	2012	Treatment of mice with CPA suppressed the formation of Th1 cytokines (TNF-alpha, IFN-gamma, and IL-2), shifting the overall balance toward Th2 (IL-4 and IL-5).	Cyclophosphamide	23-26	interleukin 2	Mus musculus	96-100
21649551-5	2012	Treatment of mice with CPA suppressed the formation of Th1 cytokines (TNF-alpha, IFN-gamma, and IL-2), shifting the overall balance toward Th2 (IL-4 and IL-5).	Cyclophosphamide	23-26	heart and neural crest derivatives expressed 2	Mus musculus	139-142
21649551-5	2012	Treatment of mice with CPA suppressed the formation of Th1 cytokines (TNF-alpha, IFN-gamma, and IL-2), shifting the overall balance toward Th2 (IL-4 and IL-5).	Cyclophosphamide	23-26	interleukin 4	Mus musculus	144-148
21649551-5	2012	Treatment of mice with CPA suppressed the formation of Th1 cytokines (TNF-alpha, IFN-gamma, and IL-2), shifting the overall balance toward Th2 (IL-4 and IL-5).	Cyclophosphamide	23-26	interleukin 5	Mus musculus	153-157
21649551-6	2012	MMW irradiation of CPA-treated groups up-regulated the production of Th1 cytokines suppressed by CPA.	Cyclophosphamide	19-22	negative elongation factor complex member C/D, Th1l	Mus musculus	69-72
21649551-6	2012	MMW irradiation of CPA-treated groups up-regulated the production of Th1 cytokines suppressed by CPA.	Cyclophosphamide	97-100	negative elongation factor complex member C/D, Th1l	Mus musculus	69-72
21649551-7	2012	Treatment of the CPA+MMW group with selective kappa (kappa) ORA further potentiated this effect of MMWs on Th1 cytokine production, whereas treatment with mu or delta ORA increased the imbalance of cytokine production in the Th2 direction.	Cyclophosphamide	17-20	negative elongation factor complex member C/D, Th1l	Mus musculus	107-110
21649551-7	2012	Treatment of the CPA+MMW group with selective kappa (kappa) ORA further potentiated this effect of MMWs on Th1 cytokine production, whereas treatment with mu or delta ORA increased the imbalance of cytokine production in the Th2 direction.	Cyclophosphamide	17-20	heart and neural crest derivatives expressed 2	Mus musculus	225-228
22226750-0	2012	IFN-gamma producing T cells contribute to the increase of myeloid derived suppressor cells in tumor-bearing mice after cyclophosphamide treatment.	Cyclophosphamide	119-135	interferon gamma	Mus musculus	0-9
22180248-2	2012	The aim of this work was to study the mechanism of neuroprotection conferred by targeting cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) in the acute brain injury following subarachnoid hemorrhage.	Cyclophosphamide	90-106	DNA-damage inducible transcript 3	Rattus norvegicus	150-154
22217702-1	2012	This study was designed to examine the interaction of two anti-breast cancer drugs, i.e., fluoxymesterone (FLU) and cyclophosphamide (CYC), with human serum albumin (HSA) using different kinds of spectroscopic, zeta potential and molecular modeling techniques under imitated physiological conditions.	Cyclophosphamide	134-137	albumin	Homo sapiens	151-164
22319498-3	2012	In addition, AKR1B10 has been recently reported to be significantly up-regulated in some cancer cell lines (medulloblastoma D341 and colon cancer HT29) acquiring resistance toward chemotherapeutic agents (cyclophosphamide and mitomycin c), suggesting the validity of the enzyme as a chemoresistance marker.	Cyclophosphamide	205-221	aldo-keto reductase family 1 member B10	Homo sapiens	13-20
22803083-3	2012	Experiments on RLS(40) tumor cells derived from RLS lymphosarcoma and characterized by more intensive expression of mdr1a/1b genes showed that the therapeutic effects of cyclophosphamide increased under conditions of simultaneous suppression of these genes by specific small interfering RNA (siRNA).	Cyclophosphamide	170-186	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	116-121
22667143-3	2012	The immunocompromised mice model was established by intraperitoneal injection cyclophosphamide to detected the content of IL-2, IL-6 in serum, CD4+, CD8+ in the peripheral blood by ELISA and flow cytometry, respectively.	Cyclophosphamide	78-94	interleukin 2	Mus musculus	122-126
22667143-3	2012	The immunocompromised mice model was established by intraperitoneal injection cyclophosphamide to detected the content of IL-2, IL-6 in serum, CD4+, CD8+ in the peripheral blood by ELISA and flow cytometry, respectively.	Cyclophosphamide	78-94	interleukin 6	Mus musculus	128-132
22667143-3	2012	The immunocompromised mice model was established by intraperitoneal injection cyclophosphamide to detected the content of IL-2, IL-6 in serum, CD4+, CD8+ in the peripheral blood by ELISA and flow cytometry, respectively.	Cyclophosphamide	78-94	CD4 antigen	Mus musculus	143-146
22260632-4	2012	The patient initially received 6 cycles of chemotherapy with CHOP regimen (cyclophosphamide, vincristine, adriamycin, prednisone), but his symptoms did not disappear.	Cyclophosphamide	75-91	DNA damage inducible transcript 3	Homo sapiens	61-65
22260632-9	2012	CHOP-R chemotherapy (cyclophosphamide, doxorubicin, vincristine, prednisone and rituximab) was then administered, resulting in partial response of the disease with pancytopenia and suppression of cellular immunity.	Cyclophosphamide	21-37	DNA damage inducible transcript 3	Homo sapiens	0-4
21351093-11	2012	Patients carrying the high activity Ala/Ala genotype in SOD2 (rs4880) had significantly poorer PFS than Val allele carriers in the group treated by cyclophosphamide but not hormonal regimens (p = 0.004).	Cyclophosphamide	148-164	superoxide dismutase 2	Homo sapiens	56-60
21351096-5	2012	The number of recipient CD4+ CD25+ Foxp3+ Tregs significantly decreased 3 days after an intraperitoneal injection of cyclophosphamide in C3H/HeN mice that had been injected with spleen cells and BMC of donor AKR/J mice, compared with the number of CD4+ CD25+ Foxp3- T cells.	Cyclophosphamide	117-133	CD4 antigen	Mus musculus	24-27
21351096-5	2012	The number of recipient CD4+ CD25+ Foxp3+ Tregs significantly decreased 3 days after an intraperitoneal injection of cyclophosphamide in C3H/HeN mice that had been injected with spleen cells and BMC of donor AKR/J mice, compared with the number of CD4+ CD25+ Foxp3- T cells.	Cyclophosphamide	117-133	interleukin 2 receptor, alpha chain	Mus musculus	29-33
21351096-5	2012	The number of recipient CD4+ CD25+ Foxp3+ Tregs significantly decreased 3 days after an intraperitoneal injection of cyclophosphamide in C3H/HeN mice that had been injected with spleen cells and BMC of donor AKR/J mice, compared with the number of CD4+ CD25+ Foxp3- T cells.	Cyclophosphamide	117-133	forkhead box P3	Mus musculus	35-40
21351096-5	2012	The number of recipient CD4+ CD25+ Foxp3+ Tregs significantly decreased 3 days after an intraperitoneal injection of cyclophosphamide in C3H/HeN mice that had been injected with spleen cells and BMC of donor AKR/J mice, compared with the number of CD4+ CD25+ Foxp3- T cells.	Cyclophosphamide	117-133	CD4 antigen	Mus musculus	248-251
21351096-5	2012	The number of recipient CD4+ CD25+ Foxp3+ Tregs significantly decreased 3 days after an intraperitoneal injection of cyclophosphamide in C3H/HeN mice that had been injected with spleen cells and BMC of donor AKR/J mice, compared with the number of CD4+ CD25+ Foxp3- T cells.	Cyclophosphamide	117-133	interleukin 2 receptor, alpha chain	Mus musculus	253-257
21351096-5	2012	The number of recipient CD4+ CD25+ Foxp3+ Tregs significantly decreased 3 days after an intraperitoneal injection of cyclophosphamide in C3H/HeN mice that had been injected with spleen cells and BMC of donor AKR/J mice, compared with the number of CD4+ CD25+ Foxp3- T cells.	Cyclophosphamide	117-133	forkhead box P3	Mus musculus	259-264
21351096-7	2012	These results indicated that cyclophosphamide-induced reduction of recipient Tregs is associated with retardation of tumor progression via the expansion of host-reactive donor T cells and IFN-gamma production after DLI in our nonmyeloablative SCT system.	Cyclophosphamide	29-45	interferon gamma	Homo sapiens	188-197
22946026-7	2012	A decreased cyclophosphamide dose in combination with two doses of vasostatin (V2 + CTX scheme) inhibits tumor growth similarly to a larger dose of cyclophosphamide alone.	Cyclophosphamide	12-28	V-set and immunoglobulin domain containing 2	Mus musculus	84-87
21460380-3	2012	The combination chemotherapy with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) with addition of etoposide (CHOEP) has in other patient groups been shown to be effective.	Cyclophosphamide	34-50	DNA damage inducible transcript 3	Homo sapiens	93-97
22997596-2	2012	We present the results of a long-term followup of two patients who were diagnosed with PRL and treated with cyclophosphamide, adriamycin, vincristine, prednisolone and rituximab (CHOP + R) regimen.	Cyclophosphamide	108-124	DNA damage inducible transcript 3	Homo sapiens	179-183
21675966-0	2012	The role of P2X7 purinergic receptors in inflammatory and nociceptive changes accompanying cyclophosphamide-induced haemorrhagic cystitis in mice.	Cyclophosphamide	91-107	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	12-16
21675966-3	2012	Here we have evaluated the role of P2X7 receptors in a model of HC induced by cyclophosphamide.	Cyclophosphamide	78-94	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	35-39
21675966-4	2012	EXPERIMENTAL APPROACH: Effects of pharmacological antagonism or genetic deletion of P2X7 receptor on cyclophosphamide-induced HC in mice was assessed by nociceptive and inflammatory measures.	Cyclophosphamide	101-117	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	84-97
21675966-10	2012	Finally, P2X7 receptors were markedly up-regulated in the bladders of mice with cyclophosphamide-induced HC.	Cyclophosphamide	80-96	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	9-13
21675966-11	2012	CONCLUSIONS AND IMPLICATIONS: P2X7 receptors were significantly involved in a model of HC induced by cyclophosphamide.	Cyclophosphamide	101-117	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	30-34
22536046-2	2012	A 68-year-old male patient with anti-proteinase-3 ANCA-positive Wegener"s granulomatosis who was receiving immunosuppressive therapy with methylprednisolone, cyclophosphamide, and azathioprine developed CMV retinitis.	Cyclophosphamide	158-174	proteinase 3	Homo sapiens	37-49
21976622-1	2012	Results from retrospective studies on the relationship between cytochrome P450 (P450) 2B6 (CYP2B6) genotype and cyclophosphamide (CY) efficacy and toxicity in adult cancer patients have been conflicting.	Cyclophosphamide	112-128	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	74-89
21976622-1	2012	Results from retrospective studies on the relationship between cytochrome P450 (P450) 2B6 (CYP2B6) genotype and cyclophosphamide (CY) efficacy and toxicity in adult cancer patients have been conflicting.	Cyclophosphamide	112-128	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	91-97
21976622-1	2012	Results from retrospective studies on the relationship between cytochrome P450 (P450) 2B6 (CYP2B6) genotype and cyclophosphamide (CY) efficacy and toxicity in adult cancer patients have been conflicting.	Cyclophosphamide	91-93	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	74-89
23028242-3	2012	MATERIALS AND METHODS: The CD44+/CD105+ subpopulation were isolated from HuAFCs, cultured in vitro, and injected into a cyclophosphamide-induced mouse model of POF.	Cyclophosphamide	120-136	POF1B actin binding protein	Homo sapiens	160-163
22864129-5	2012	Combination chemotherapy composed of cyclophosphamide, vincristine, doxorubicin and prednisolone (CHOP) was effective for polyneuropathy as well as for lymphoma.	Cyclophosphamide	37-53	DNA damage inducible transcript 3	Homo sapiens	98-102
23249637-1	2012	The aim of this study was to evaluate preoperative           tumour expression of NAD(P)H:quinone           oxidoreductase 1 (NQO1) along with other biological           markers as potential predictors of pathological complete           response (pCR) to neoadjuvant docetaxel, doxorubicin,           and cyclophosphamide-containing (TAC)           chemotherapy in patients with primary breast cancer.	Cyclophosphamide	305-321	NAD(P)H quinone dehydrogenase 1	Homo sapiens	82-124
21741706-1	2012	CYP2B6, CYP2C19, ABCC4, and SOD2 have been implicated in adverse drug reactions and survival after cyclophosphamide (CPA) treatment.	Cyclophosphamide	99-115	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	0-6
21741706-1	2012	CYP2B6, CYP2C19, ABCC4, and SOD2 have been implicated in adverse drug reactions and survival after cyclophosphamide (CPA) treatment.	Cyclophosphamide	99-115	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	8-15
21741706-1	2012	CYP2B6, CYP2C19, ABCC4, and SOD2 have been implicated in adverse drug reactions and survival after cyclophosphamide (CPA) treatment.	Cyclophosphamide	99-115	ATP binding cassette subfamily C member 4	Homo sapiens	17-22
21741706-1	2012	CYP2B6, CYP2C19, ABCC4, and SOD2 have been implicated in adverse drug reactions and survival after cyclophosphamide (CPA) treatment.	Cyclophosphamide	99-115	superoxide dismutase 2	Homo sapiens	28-32
21741706-1	2012	CYP2B6, CYP2C19, ABCC4, and SOD2 have been implicated in adverse drug reactions and survival after cyclophosphamide (CPA) treatment.	Cyclophosphamide	117-120	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	0-6
21741706-1	2012	CYP2B6, CYP2C19, ABCC4, and SOD2 have been implicated in adverse drug reactions and survival after cyclophosphamide (CPA) treatment.	Cyclophosphamide	117-120	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	8-15
21741706-1	2012	CYP2B6, CYP2C19, ABCC4, and SOD2 have been implicated in adverse drug reactions and survival after cyclophosphamide (CPA) treatment.	Cyclophosphamide	117-120	ATP binding cassette subfamily C member 4	Homo sapiens	17-22
21741706-1	2012	CYP2B6, CYP2C19, ABCC4, and SOD2 have been implicated in adverse drug reactions and survival after cyclophosphamide (CPA) treatment.	Cyclophosphamide	117-120	superoxide dismutase 2	Homo sapiens	28-32
21741706-5	2012	SOD2 rs4880 V16A polymorphism was associated with significantly less CPA-related overall toxicity and significantly lower relapse rates by Kaplan-Meier analysis although the SOD2 finding regarding relapse was not significant when evaluated by the cumulative incidence function.	Cyclophosphamide	69-72	superoxide dismutase 2	Homo sapiens	0-4
21864040-1	2012	In the rituximab era, several large studies have suggested that full-dose rituximab plus cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) might be the best treatment for patients with diffuse large B-cell lymphoma (DLBCL) aged 60 years and older.	Cyclophosphamide	89-105	DNA damage inducible transcript 3	Homo sapiens	150-154
22720230-2	2012	Disruption of tumor microenvironment homeostasis by low-dose cyclophosphamide prior to interleukin-12 gene therapy led to CD8+ T cell-driven established tumor rejection.	Cyclophosphamide	61-77	CD8a molecule	Homo sapiens	122-125
22321016-4	2012	Recently it was shown that alkylating drugs (ADs), such as melphalan and cyclophosphamide (Cy) in the dose 100-fold lower than cytostatic one are capable to disturb signal transduction by IL-2R.	Cyclophosphamide	73-89	interleukin 2 receptor, alpha chain	Mus musculus	188-193
22321016-4	2012	Recently it was shown that alkylating drugs (ADs), such as melphalan and cyclophosphamide (Cy) in the dose 100-fold lower than cytostatic one are capable to disturb signal transduction by IL-2R.	Cyclophosphamide	91-93	interleukin 2 receptor, alpha chain	Mus musculus	188-193
22384158-3	2012	Our experiments demonstrated that a peptide created as combination of fragments of tenascin X and fibrillin 1 (comb1) applied into cranial dermal wounds created in mice treated with cyclophosphamide to impair wound healing, can improve the rate of wound closure.	Cyclophosphamide	182-198	tenascin XB	Mus musculus	83-93
22384158-3	2012	Our experiments demonstrated that a peptide created as combination of fragments of tenascin X and fibrillin 1 (comb1) applied into cranial dermal wounds created in mice treated with cyclophosphamide to impair wound healing, can improve the rate of wound closure.	Cyclophosphamide	182-198	fibrillin 1	Mus musculus	98-109
22359647-10	2012	Analysis of Treg subsets revealed a Cy-sensitive CD4(+)Foxp3(+)CD25(low) tumor-seeking migratory phenotype, characteristic of effector/memory Tregs, and capable of high avidity T cell suppression.	Cyclophosphamide	36-38	CD4 antigen	Mus musculus	49-52
22359647-10	2012	Analysis of Treg subsets revealed a Cy-sensitive CD4(+)Foxp3(+)CD25(low) tumor-seeking migratory phenotype, characteristic of effector/memory Tregs, and capable of high avidity T cell suppression.	Cyclophosphamide	36-38	interleukin 2 receptor, alpha chain	Mus musculus	63-67
22851904-2	2012	The combination of topotecan and cyclophosphamide (TC) has activity in pediatric patients with recurrent sarcoma, especially Ewing"s sarcoma (EWS).	Cyclophosphamide	33-49	EWS RNA binding protein 1	Homo sapiens	142-145
23323070-8	2012	The association of this antibody to the cyclophosphamide, hydroxydaunorubicin, oncovin and prednisolone (CHOP) regimen has increased overall survival of diffuse large B-Cell lymphoma and follicular lymphoma patients by 20%.	Cyclophosphamide	40-56	DNA damage inducible transcript 3	Homo sapiens	105-109
22310616-9	2012	In conclusion, our investigation suggested that potent immunosuppression with splenectomy and cyclophosphamide for ABOi LDRT may not be a risk factor for malignancy.	Cyclophosphamide	94-110	ABO, alpha 1-3-N-acetylgalactosaminyltransferase and alpha 1-3-galactosyltransferase	Homo sapiens	115-124
21933893-1	2011	PURPOSE: We have previously shown the prognostic significance of BCL2 expression in the activated B-cell-like diffuse large B-cell lymphoma (ABC-DLBCL) patients treated with cyclophosphamide-Adriamycin-vincristine-prednisone (CHOP) or CHOP-like therapy.	Cyclophosphamide	174-190	BCL2 apoptosis regulator	Homo sapiens	65-69
21421542-8	2011	CONCLUSION: The combination of PLD-cyclophosphamide-concurrent trastuzumab is a feasible, safe, and effective first-line regimen for HER2-overexpressing MBC.	Cyclophosphamide	35-51	erb-b2 receptor tyrosine kinase 2	Homo sapiens	133-137
21750397-0	2011	Prevention of chemotherapy-induced osteoporosis by cyclophosphamide with a long-acting form of parathyroid hormone.	Cyclophosphamide	51-67	parathyroid hormone	Mus musculus	95-114
22229321-0	2011	Human platelet acetylcholinesterase inhibition by cyclophosphamide: a combined experimental and computational approach.	Cyclophosphamide	50-66	acetylcholinesterase (Cartwright blood group)	Homo sapiens	15-35
22229321-2	2011	In the present study, a comparative multiple 4 dimensional (4D)-approach was applied to analyze human platelet AChE-inhibition by cyclophosphamide (CP).	Cyclophosphamide	130-146	acetylcholinesterase (Cartwright blood group)	Homo sapiens	111-115
21931035-1	2011	PURPOSE: Rituximab with cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is one of the most effective front-line therapies to treat indolent B-cell lymphoma.	Cyclophosphamide	24-40	DNA damage inducible transcript 3	Homo sapiens	86-90
23038003-5	2012	Time- and dose-related increases in Pig-a mutant frequency were found in all the chemical-treated groups, except for the groups treated with cyclophosphamide, which was a potent inducer of micronuclei.	Cyclophosphamide	141-157	phosphatidylinositol glycan anchor biosynthesis class A	Sus scrofa	36-41
21946896-0	2011	Two minor NQO1 and NQO2 alleles predict poor response of breast cancer patients to adjuvant doxorubicin and cyclophosphamide therapy.	Cyclophosphamide	108-124	NAD(P)H quinone dehydrogenase 1	Homo sapiens	10-14
21946896-0	2011	Two minor NQO1 and NQO2 alleles predict poor response of breast cancer patients to adjuvant doxorubicin and cyclophosphamide therapy.	Cyclophosphamide	108-124	N-ribosyldihydronicotinamide:quinone reductase 2	Homo sapiens	19-23
21946896-3	2011	We aimed to determine whether functional NQO2 variants are associated with altered response to adjuvant doxorubicin and cyclophosphamide therapy, with or without tamoxifen, in the treatment of breast cancer.	Cyclophosphamide	120-136	N-ribosyldihydronicotinamide:quinone reductase 2	Homo sapiens	41-45
22241155-5	2011	We show a case of a 39-year-old woman with recurrent CNS involvement of IVLBCL receiving autologous peripheral blood stem cell transplantation (auto-PBSCT) preconditioned with high-dose thiotepa, busulfan, cyclophosphamide (TBC regimen).	Cyclophosphamide	206-222	TBC1 domain family member 1	Homo sapiens	224-227
21546064-10	2011	Anti-TNF inhibitors should be considered in patients who do not respond to treatment with corticosteroids and cyclophosphamide.	Cyclophosphamide	110-126	tumor necrosis factor	Homo sapiens	5-8
21868068-8	2011	The difference in the long-term POF remained significant even after adjusting the groups for comparable age and cumulative cyclophosphamide doses.	Cyclophosphamide	123-139	POF1B actin binding protein	Homo sapiens	32-35
23556105-7	2011	A prospective, multicenter, international phase II trial evaluating sequential treatment with rituximab and CHOP-based chemotherapy (cyclophosphamide, doxorubicin, vincristine, prednisone) is ongoing and preliminary results have been promising.	Cyclophosphamide	133-149	DNA damage inducible transcript 3	Homo sapiens	108-112
22172885-3	2011	Standard therapy for recurrent posttransplantation FSGS includes the use of intensive plasmapheresis (PP) in conjunction with cyclophosphamide or high-dose cyclosporine.	Cyclophosphamide	126-142	actinin alpha 4	Homo sapiens	51-55
22129044-8	2011	DISCUSSION: This phase I-II study is designed to determine whether metronomic cyclophosphamide can be used to counter the mTOR inhibitor everolimus induced Treg expansion in patients with metastatic renal cell carcinoma and increase the antitumor efficacy of everolimus.	Cyclophosphamide	78-94	mechanistic target of rapamycin kinase	Homo sapiens	122-126
22007908-8	2011	Taken together, our results showed that cyclophosphamide perturbed temporarily global cytosine methylation in Jurkat-T cells via regulation of the lysine methylation level in DNMT1.	Cyclophosphamide	40-56	DNA methyltransferase 1	Homo sapiens	175-180
21908423-5	2011	The CCR4 antagonist was more efficient than cyclophosphamide to elicit anti-self CD8(+) T cells.	Cyclophosphamide	44-60	CD8a molecule	Homo sapiens	81-84
21837479-2	2011	We evaluated immunohistochemical AR expression on a tissue microarray of 673 core biopsies from primary breast cancer patients treated with neoadjuvant docetaxel/doxorubicin/cyclophosphamide (TAC) chemotherapy in the prospective GeparTrio phase-III trial.	Cyclophosphamide	174-190	androgen receptor	Homo sapiens	33-35
21999734-0	2011	Interaction of human brain acetylcholinesterase with cyclophosphamide: a molecular modeling and docking study.	Cyclophosphamide	53-69	acetylcholinesterase (Cartwright blood group)	Homo sapiens	27-47
21999734-1	2011	This study describes the interaction between human acetylcholinesterase (AChE), a key regulator of central and peripheral cholinergic function, and the widely used nitrogen mustard alkylating agent, cyclophosphamide (CP).	Cyclophosphamide	199-215	acetylcholinesterase (Cartwright blood group)	Homo sapiens	51-71
21999734-1	2011	This study describes the interaction between human acetylcholinesterase (AChE), a key regulator of central and peripheral cholinergic function, and the widely used nitrogen mustard alkylating agent, cyclophosphamide (CP).	Cyclophosphamide	199-215	acetylcholinesterase (Cartwright blood group)	Homo sapiens	73-77
21821736-0	2011	Q172H replacement overcomes effects on the metabolism of cyclophosphamide and efavirenz caused by CYP2B6 variant with Arg262.	Cyclophosphamide	57-73	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	98-104
21821736-1	2011	There are a number of reports indicating that CYP2B6*6 (c.516G>T and c.785A>G) is responsible for decreased clearance of efavirenz (EFV), although increased disposition of cyclophosphamide (CPA) in individuals with this polymorphism was observed.	Cyclophosphamide	178-194	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	46-52
21821736-1	2011	There are a number of reports indicating that CYP2B6*6 (c.516G>T and c.785A>G) is responsible for decreased clearance of efavirenz (EFV), although increased disposition of cyclophosphamide (CPA) in individuals with this polymorphism was observed.	Cyclophosphamide	196-199	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	46-52
21723424-4	2011	Furthermore, SEP elevated CD4(+) T lymphocyte counts as well as the CD4/CD8 ratio dose-dependently, and it increased interleukin-2 (IL-2), IgA, IgM, and IgG levels in the sera of Cy-treated mice.	Cyclophosphamide	179-181	epoxide hydrolase 2, cytoplasmic	Mus musculus	13-16
21723424-6	2011	Finally, SEP significantly induced Akt phosphorylation in splenocytes from Cy-treated mice, suggesting that chemoprotection by SEP was mediated through the PI3K/Akt signaling pathway.	Cyclophosphamide	75-77	epoxide hydrolase 2, cytoplasmic	Mus musculus	9-12
21723424-6	2011	Finally, SEP significantly induced Akt phosphorylation in splenocytes from Cy-treated mice, suggesting that chemoprotection by SEP was mediated through the PI3K/Akt signaling pathway.	Cyclophosphamide	75-77	thymoma viral proto-oncogene 1	Mus musculus	35-38
21723424-6	2011	Finally, SEP significantly induced Akt phosphorylation in splenocytes from Cy-treated mice, suggesting that chemoprotection by SEP was mediated through the PI3K/Akt signaling pathway.	Cyclophosphamide	75-77	epoxide hydrolase 2, cytoplasmic	Mus musculus	127-130
21723424-6	2011	Finally, SEP significantly induced Akt phosphorylation in splenocytes from Cy-treated mice, suggesting that chemoprotection by SEP was mediated through the PI3K/Akt signaling pathway.	Cyclophosphamide	75-77	thymoma viral proto-oncogene 1	Mus musculus	161-164
21723424-7	2011	These findings indicate that SEP plays an important role in the protection against myelosuppression and immunosuppression in Cy-treated mice and could be a potential immunomodulatory agent.	Cyclophosphamide	125-127	epoxide hydrolase 2, cytoplasmic	Mus musculus	29-32
21702643-0	2011	Granulocyte-macrophage colony stimulating factor-induced immune priming of cyclophosphamide, doxorubicin, vincristine, and prednisone with rituximab chemoimmunotherapy in previously untreated patients with diffuse large B-cell lymphoma and mantle cell lymphoma.	Cyclophosphamide	75-91	colony stimulating factor 2	Homo sapiens	0-48
21788064-7	2011	The amount of IFN-gamma and LT-alpha were markedly reduced by the time of inhibitor disappearance in the patients responding to GC therapy but remained high in the non-responder until cyclophosphamide was added.	Cyclophosphamide	184-200	interferon gamma	Homo sapiens	14-23
21788064-7	2011	The amount of IFN-gamma and LT-alpha were markedly reduced by the time of inhibitor disappearance in the patients responding to GC therapy but remained high in the non-responder until cyclophosphamide was added.	Cyclophosphamide	184-200	lymphotoxin alpha	Homo sapiens	28-36
22586509-2	2011	The cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) treatment regimen has been the standard of care for more than 20 years.	Cyclophosphamide	4-20	DNA damage inducible transcript 3	Homo sapiens	64-68
22586511-1	2011	Chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) has long been a standard treatment for lymphoma.	Cyclophosphamide	18-34	DNA damage inducible transcript 3	Homo sapiens	78-82
22586511-2	2011	Improvements to the efficacy of this regimen can be made by increasing the doses of doxorubicin and cyclophosphamide, as in the chemotherapeutic regimen of doxorubicin, cyclophosphamide, vindesine, bleomycin, and prednisone (ACVBP), and by reducing the standard dosing interval, as seen with the CHOP-14 regimen.	Cyclophosphamide	100-116	DNA damage inducible transcript 3	Homo sapiens	296-300
21908736-4	2011	Administration of CY mediated a significant delay in the post-IL-12/GM-CSF T suppressor cell rebound, resulting in a 7-fold increase in the CD8(+) CTL/T suppressor cell ratio, a 3-fold enhancement of CTL cytotoxicity, and an extension of the effector window from 3 to 7 d. In long-term therapy studies, chronic chemoimmunotherapy promoted a dramatic enhancement of tumor regression, resulting in complete cure in 44% of the mice receiving CY plus IL-12/GM-CSF.	Cyclophosphamide	18-20	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	68-74
21908736-4	2011	Administration of CY mediated a significant delay in the post-IL-12/GM-CSF T suppressor cell rebound, resulting in a 7-fold increase in the CD8(+) CTL/T suppressor cell ratio, a 3-fold enhancement of CTL cytotoxicity, and an extension of the effector window from 3 to 7 d. In long-term therapy studies, chronic chemoimmunotherapy promoted a dramatic enhancement of tumor regression, resulting in complete cure in 44% of the mice receiving CY plus IL-12/GM-CSF.	Cyclophosphamide	18-20	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	453-459
21617923-0	2011	Prolonged progression-free survival in patients with chronic lymphocytic leukemia receiving granulocyte colony-stimulating factor during treatment with fludarabine, cyclophosphamide, and rituximab.	Cyclophosphamide	165-181	colony stimulating factor 3	Homo sapiens	92-129
22563154-3	2011	We report a patient with primary ovarian diffuse large B-cell lymphoma (DLBCL) and associated auto-immune hemolytic anemia (AIHA) who achieved complete remission after treatment with Rituximab-cyclophosphamide-doxorubicin-vincristine and prednisolone (R-CHOP) chemotherapy.	Cyclophosphamide	193-209	DNA damage inducible transcript 3	Homo sapiens	254-258
22331716-8	2011	Paclitaxel, doxorubicin, tamoxifen, cyclophosphamide and docetaxel application downregulated SK-1 expression while paclitaxel, tamoxifen, cyclophosphamide and docetaxel but not doxorubicin downregulated GCS comparing to untreated control cells.	Cyclophosphamide	36-52	sphingosine kinase 1	Homo sapiens	93-97
22331716-8	2011	Paclitaxel, doxorubicin, tamoxifen, cyclophosphamide and docetaxel application downregulated SK-1 expression while paclitaxel, tamoxifen, cyclophosphamide and docetaxel but not doxorubicin downregulated GCS comparing to untreated control cells.	Cyclophosphamide	36-52	UDP-glucose ceramide glucosyltransferase	Homo sapiens	203-206
21769435-11	2011	These preliminary data indicate that therapy-induced HER4 gene up-regulation may be associated with response to NAC with epirubicine, cyclophosphamide and docetaxel.	Cyclophosphamide	134-150	erb-b2 receptor tyrosine kinase 4	Homo sapiens	53-57
21257672-1	2011	BACKGROUND: Rituximab plus combination chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is widely recommended for the treatment of aggressive B-cell lymphomas.	Cyclophosphamide	57-73	DNA damage inducible transcript 3	Homo sapiens	119-123
21561436-7	2011	The cardiac precursor cells were sensitive to CPA in non-cytotoxic concentrations for the expression of the cardiac-specific mRNA markers Nkx2.5 (NK2 transcription factor related, locus 5), GATA-4 (GATA binding protein 4 transcription factor) and TNNT2 (troponin T type 2).	Cyclophosphamide	46-49	NK2 homeobox 5	Homo sapiens	138-144
21561436-7	2011	The cardiac precursor cells were sensitive to CPA in non-cytotoxic concentrations for the expression of the cardiac-specific mRNA markers Nkx2.5 (NK2 transcription factor related, locus 5), GATA-4 (GATA binding protein 4 transcription factor) and TNNT2 (troponin T type 2).	Cyclophosphamide	46-49	NK2 homeobox 5	Homo sapiens	146-187
21561436-7	2011	The cardiac precursor cells were sensitive to CPA in non-cytotoxic concentrations for the expression of the cardiac-specific mRNA markers Nkx2.5 (NK2 transcription factor related, locus 5), GATA-4 (GATA binding protein 4 transcription factor) and TNNT2 (troponin T type 2).	Cyclophosphamide	46-49	GATA binding protein 4	Homo sapiens	190-196
21561436-7	2011	The cardiac precursor cells were sensitive to CPA in non-cytotoxic concentrations for the expression of the cardiac-specific mRNA markers Nkx2.5 (NK2 transcription factor related, locus 5), GATA-4 (GATA binding protein 4 transcription factor) and TNNT2 (troponin T type 2).	Cyclophosphamide	46-49	GATA binding protein 4	Homo sapiens	198-220
21561436-7	2011	The cardiac precursor cells were sensitive to CPA in non-cytotoxic concentrations for the expression of the cardiac-specific mRNA markers Nkx2.5 (NK2 transcription factor related, locus 5), GATA-4 (GATA binding protein 4 transcription factor) and TNNT2 (troponin T type 2).	Cyclophosphamide	46-49	troponin T2, cardiac type	Homo sapiens	247-252
21561436-7	2011	The cardiac precursor cells were sensitive to CPA in non-cytotoxic concentrations for the expression of the cardiac-specific mRNA markers Nkx2.5 (NK2 transcription factor related, locus 5), GATA-4 (GATA binding protein 4 transcription factor) and TNNT2 (troponin T type 2).	Cyclophosphamide	46-49	troponin T2, cardiac type	Homo sapiens	254-271
21575062-1	2011	BACKGROUND: We have previously reported that serum interleukin-18 (IL-18) concentration predicted the clinical outcome of patients with aggressive non-Hodgkin"s lymphoma treated with cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP).	Cyclophosphamide	183-199	interleukin 18	Homo sapiens	51-65
21575062-1	2011	BACKGROUND: We have previously reported that serum interleukin-18 (IL-18) concentration predicted the clinical outcome of patients with aggressive non-Hodgkin"s lymphoma treated with cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP).	Cyclophosphamide	183-199	interleukin 18	Homo sapiens	67-72
21918347-0	2011	[A case of effective combination therapy with docetaxel, cyclophosphamide and trastuzumab as primary systemic therapy for locally advanced HER2-positive breast cancer].	Cyclophosphamide	57-73	erb-b2 receptor tyrosine kinase 2	Homo sapiens	139-143
21918347-1	2011	We experienced a case of locally advanced breast cancer achieving a significant improvement by using a combination of docetaxel(DOC), cyclophosphamide(CPA)and trastuzumab as a primary systemic therapy.The patient was a 54-year-old woman suffering from a right breast mass, who was referred to our hospital and diagnosed with HER2-positive breast cancer with subclavicular lymph nodes metastases.The combination therapy of DOC(75 mg/m / 2), CPA(600 mg/m2)and trastuzumab(loading dose 8 mg/kg, then 6 mg/kg)for 6 courses at q3 week intervals, was started as the primary systemic therapy.	Cyclophosphamide	134-150	carboxypeptidase A1	Homo sapiens	151-154
21788566-1	2011	PURPOSE: To evaluate efficacy and safety of epirubicin and cyclophosphamide followed by paclitaxel and trastuzumab as neoadjuvant treatment in patients with human epidermal growth factor receptor 2 (HER2)-overexpressing breast cancer.	Cyclophosphamide	59-75	erb-b2 receptor tyrosine kinase 2	Homo sapiens	163-197
21788566-1	2011	PURPOSE: To evaluate efficacy and safety of epirubicin and cyclophosphamide followed by paclitaxel and trastuzumab as neoadjuvant treatment in patients with human epidermal growth factor receptor 2 (HER2)-overexpressing breast cancer.	Cyclophosphamide	59-75	erb-b2 receptor tyrosine kinase 2	Homo sapiens	199-203
21705143-3	2011	Here we studied the activation of ERK1/2 in the lumbosacral spinal cord after innocuous and noxious distention of the inflamed (cyclophosphamide-treated) and noninflamed urinary bladder in mice.	Cyclophosphamide	128-144	mitogen-activated protein kinase 3	Mus musculus	34-40
20358205-5	2011	Logistic regression was applied to assess CYP2C19 polymorphism as an effect modifier of cyclophosphamide.	Cyclophosphamide	88-104	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	42-49
20358205-8	2011	Patients with CYP2C19*1/*1 genotype and higher cumulative dose of cyclophosphamide (>23.75 g) had the highest odds of ovarian toxicity, i.e. 11.0 (95% CI: 1.2-99.1) times higher than patients with the CYP2C19*1/*2 or *2/*2 genotypes who received less cyclophosphamide (<23.75 g).	Cyclophosphamide	66-82	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	14-21
20358205-8	2011	Patients with CYP2C19*1/*1 genotype and higher cumulative dose of cyclophosphamide (>23.75 g) had the highest odds of ovarian toxicity, i.e. 11.0 (95% CI: 1.2-99.1) times higher than patients with the CYP2C19*1/*2 or *2/*2 genotypes who received less cyclophosphamide (<23.75 g).	Cyclophosphamide	66-82	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	204-211
20358205-8	2011	Patients with CYP2C19*1/*1 genotype and higher cumulative dose of cyclophosphamide (>23.75 g) had the highest odds of ovarian toxicity, i.e. 11.0 (95% CI: 1.2-99.1) times higher than patients with the CYP2C19*1/*2 or *2/*2 genotypes who received less cyclophosphamide (<23.75 g).	Cyclophosphamide	254-270	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	14-21
21132301-7	2011	Furthermore, serum hBD2 was raised in patients with meningeal granulomas (n = 4) or in those undergoing treatment with cyclophosphamide (n = 4).	Cyclophosphamide	119-135	defensin beta 4A	Homo sapiens	19-23
22092799-6	2011	Neutropenic rats treated with anti-neutrophil mAb or cyclophosphamide exhibited significant attenuation in re-epithelialization, epidermal cell proliferation, neo-vascularization, and TNF-alpha synthesis compared with control; administration of TNF-alpha reversed these attenuations.	Cyclophosphamide	53-69	tumor necrosis factor	Rattus norvegicus	184-193
22092799-6	2011	Neutropenic rats treated with anti-neutrophil mAb or cyclophosphamide exhibited significant attenuation in re-epithelialization, epidermal cell proliferation, neo-vascularization, and TNF-alpha synthesis compared with control; administration of TNF-alpha reversed these attenuations.	Cyclophosphamide	53-69	tumor necrosis factor	Rattus norvegicus	245-254
21514041-0	2011	Gene expression signature of TP53 but not its mutation status predicts response to sequential paclitaxel and 5-FU/epirubicin/cyclophosphamide in human breast cancer.	Cyclophosphamide	125-141	tumor protein p53	Homo sapiens	29-33
21693655-3	2011	PATIENTS AND METHODS: Epithelial p53 expression was evaluated using two immunohistochemical antibodies (DO7 and 1801) in formalin-fixed, paraffin-embedded tissue from patients with node-positive breast cancer who were randomized to four cycles of cyclophosphamide and one of three doses of doxorubicin (60, 75, or 90 mg/m(2); AC) and to receive four subsequent cycles of paclitaxel (T) or not.	Cyclophosphamide	247-263	tumor protein p53	Homo sapiens	33-36
21487929-1	2011	PURPOSE: To investigate the roles of the constitutive androstane receptor (CAR) in cyclophosphamide (CPA)- and ifosfamide (IFO)-mediated induction of hepatic drug-metabolizing enzymes (DME).	Cyclophosphamide	83-99	nuclear receptor subfamily 1 group I member 3	Homo sapiens	41-73
21741827-1	2011	BACKGROUND: The aim of this study was to investigate whether c-myc amplification in human breast cancer is associated with response to neoadjuvant chemotherapy comprising paclitaxel followed by 5-FU/epirubicin/cyclophosphamide (P-FEC).	Cyclophosphamide	210-226	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	61-66
21487929-1	2011	PURPOSE: To investigate the roles of the constitutive androstane receptor (CAR) in cyclophosphamide (CPA)- and ifosfamide (IFO)-mediated induction of hepatic drug-metabolizing enzymes (DME).	Cyclophosphamide	83-99	nuclear receptor subfamily 1 group I member 3	Homo sapiens	75-78
21487929-1	2011	PURPOSE: To investigate the roles of the constitutive androstane receptor (CAR) in cyclophosphamide (CPA)- and ifosfamide (IFO)-mediated induction of hepatic drug-metabolizing enzymes (DME).	Cyclophosphamide	101-104	nuclear receptor subfamily 1 group I member 3	Homo sapiens	41-73
21487929-1	2011	PURPOSE: To investigate the roles of the constitutive androstane receptor (CAR) in cyclophosphamide (CPA)- and ifosfamide (IFO)-mediated induction of hepatic drug-metabolizing enzymes (DME).	Cyclophosphamide	101-104	nuclear receptor subfamily 1 group I member 3	Homo sapiens	75-78
21487929-3	2011	Activation of CAR, pregnane X receptor (PXR), and aryl hydrocarbon receptor by CPA and IFO was assessed in cell-based reporter assays in HepG2 cells and/or nuclear translocation assays in HPHs.	Cyclophosphamide	79-82	nuclear receptor subfamily 1 group I member 3	Homo sapiens	14-17
21487929-3	2011	Activation of CAR, pregnane X receptor (PXR), and aryl hydrocarbon receptor by CPA and IFO was assessed in cell-based reporter assays in HepG2 cells and/or nuclear translocation assays in HPHs.	Cyclophosphamide	79-82	nuclear receptor subfamily 1 group I member 2	Homo sapiens	19-38
21487929-3	2011	Activation of CAR, pregnane X receptor (PXR), and aryl hydrocarbon receptor by CPA and IFO was assessed in cell-based reporter assays in HepG2 cells and/or nuclear translocation assays in HPHs.	Cyclophosphamide	79-82	nuclear receptor subfamily 1 group I member 2	Homo sapiens	40-43
21487929-3	2011	Activation of CAR, pregnane X receptor (PXR), and aryl hydrocarbon receptor by CPA and IFO was assessed in cell-based reporter assays in HepG2 cells and/or nuclear translocation assays in HPHs.	Cyclophosphamide	79-82	aryl hydrocarbon receptor	Homo sapiens	50-75
21487929-4	2011	RESULTS: CYP2B6 reporter activity was significantly enhanced by CPA and IFO in HepG2 cells co-transfected with CYP2B6 reporter plasmid and a chemical-responsive human CAR variant (CAR1 + A) construct.	Cyclophosphamide	64-67	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	9-15
21487929-4	2011	RESULTS: CYP2B6 reporter activity was significantly enhanced by CPA and IFO in HepG2 cells co-transfected with CYP2B6 reporter plasmid and a chemical-responsive human CAR variant (CAR1 + A) construct.	Cyclophosphamide	64-67	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	111-117
21487929-4	2011	RESULTS: CYP2B6 reporter activity was significantly enhanced by CPA and IFO in HepG2 cells co-transfected with CYP2B6 reporter plasmid and a chemical-responsive human CAR variant (CAR1 + A) construct.	Cyclophosphamide	64-67	nuclear receptor subfamily 1 group I member 3	Homo sapiens	167-170
21487929-4	2011	RESULTS: CYP2B6 reporter activity was significantly enhanced by CPA and IFO in HepG2 cells co-transfected with CYP2B6 reporter plasmid and a chemical-responsive human CAR variant (CAR1 + A) construct.	Cyclophosphamide	64-67	nuclear receptor subfamily 1 group I member 3	Homo sapiens	180-184
21487929-5	2011	Real-time RT-PCR and Western blotting analysis in HPHs showed that both CPA and IFO induced the expressions of CYP2B6 and CYP3A4.	Cyclophosphamide	72-75	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	111-117
21487929-5	2011	Real-time RT-PCR and Western blotting analysis in HPHs showed that both CPA and IFO induced the expressions of CYP2B6 and CYP3A4.	Cyclophosphamide	72-75	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	122-128
21487929-6	2011	Notably, treatment of HPHs with CPA but not IFO resulted in significant nuclear accumulation of CAR, which represents the initial step of CAR activation.	Cyclophosphamide	32-35	nuclear receptor subfamily 1 group I member 3	Homo sapiens	96-99
21487929-6	2011	Notably, treatment of HPHs with CPA but not IFO resulted in significant nuclear accumulation of CAR, which represents the initial step of CAR activation.	Cyclophosphamide	32-35	nuclear receptor subfamily 1 group I member 3	Homo sapiens	138-141
21487929-7	2011	Further studies in HPHs demonstrated that selective inhibition of PXR by sulforaphane preferentially repressed IFO- over CPA-mediated induction of CYP2B6.	Cyclophosphamide	121-124	nuclear receptor subfamily 1 group I member 2	Homo sapiens	66-69
21487929-7	2011	Further studies in HPHs demonstrated that selective inhibition of PXR by sulforaphane preferentially repressed IFO- over CPA-mediated induction of CYP2B6.	Cyclophosphamide	121-124	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	147-153
21487929-8	2011	CONCLUSION: These results provide novel insights into the differential roles of CAR in the regulation of CPA- and IFO-induced DME expression and potential drug-drug interactions.	Cyclophosphamide	105-108	nuclear receptor subfamily 1 group I member 3	Homo sapiens	80-83
21234567-5	2011	Within this study, the exposure of MSCs to the chemotherapeutic agents cyclophosphamide or melphalan had strong negative effects on MSC expansion and CD44 expression.	Cyclophosphamide	71-87	CD44 molecule (Indian blood group)	Homo sapiens	150-154
22093786-1	2011	OBJECTIVE: To compare the efficacy and toxicity of neoadjuvant chemotherapy of docetaxel with paclitaxel plus pirarubicin hydrochloride (THP) and cyclophosphamide (CTX) in locally advanced breast cancer (LABC).	Cyclophosphamide	146-162	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	164-167
21722394-8	2011	Cyclophosphamide-induced diabetes at 10 weeks post-B cell reconstitution reorganized the predominant TCR repertoires by removing potential regulatory clonotypes (BV1, BV8 and BV11) and increasing the frequency of others (BV4, BV5S2, BV9, BV16-20).	Cyclophosphamide	0-16	T cell receptor alpha variable 6-3	Mus musculus	101-104
21722394-8	2011	Cyclophosphamide-induced diabetes at 10 weeks post-B cell reconstitution reorganized the predominant TCR repertoires by removing potential regulatory clonotypes (BV1, BV8 and BV11) and increasing the frequency of others (BV4, BV5S2, BV9, BV16-20).	Cyclophosphamide	0-16	endogenous ecotropic MuLV 2	Mus musculus	162-165
21722394-8	2011	Cyclophosphamide-induced diabetes at 10 weeks post-B cell reconstitution reorganized the predominant TCR repertoires by removing potential regulatory clonotypes (BV1, BV8 and BV11) and increasing the frequency of others (BV4, BV5S2, BV9, BV16-20).	Cyclophosphamide	0-16	prokineticin 2	Mus musculus	167-170
21279551-8	2011	The high-dose of zymosan markedly showed a depressant effect on S(180) tumor, enhanced by the action of Cy that increased mRNA expression levels of TNF-alpha and IL-2.	Cyclophosphamide	104-106	tumor necrosis factor	Mus musculus	148-157
21279551-8	2011	The high-dose of zymosan markedly showed a depressant effect on S(180) tumor, enhanced by the action of Cy that increased mRNA expression levels of TNF-alpha and IL-2.	Cyclophosphamide	104-106	interleukin 2	Mus musculus	162-166
21519830-7	2011	Furthermore, cyclophosphamide (CY) added to SAg plus tumor-antigens (OVA(257-264), tumor lysate, or TRP-2) pulsed DC immunization markedly enhanced tumor-specific T-cell expansion and had a significant therapeutic effect against various tumors (EG7, 2LL, and B16).	Cyclophosphamide	13-29	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	69-72
22570925-5	2011	By combining the purified fraction with Cyclophosphamide the release of HMGB1 from tumor cells was strongly decreased.	Cyclophosphamide	40-56	high mobility group box 1	Mus musculus	72-77
21519830-7	2011	Furthermore, cyclophosphamide (CY) added to SAg plus tumor-antigens (OVA(257-264), tumor lysate, or TRP-2) pulsed DC immunization markedly enhanced tumor-specific T-cell expansion and had a significant therapeutic effect against various tumors (EG7, 2LL, and B16).	Cyclophosphamide	13-29	tRNA proline 2	Mus musculus	100-105
21519830-7	2011	Furthermore, cyclophosphamide (CY) added to SAg plus tumor-antigens (OVA(257-264), tumor lysate, or TRP-2) pulsed DC immunization markedly enhanced tumor-specific T-cell expansion and had a significant therapeutic effect against various tumors (EG7, 2LL, and B16).	Cyclophosphamide	31-33	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	69-72
21519830-7	2011	Furthermore, cyclophosphamide (CY) added to SAg plus tumor-antigens (OVA(257-264), tumor lysate, or TRP-2) pulsed DC immunization markedly enhanced tumor-specific T-cell expansion and had a significant therapeutic effect against various tumors (EG7, 2LL, and B16).	Cyclophosphamide	31-33	tRNA proline 2	Mus musculus	100-105
21842694-6	2011	Because CD20 immunostaining was positive, the patient received 6 cycles of rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) without any signs of major toxicity.	Cyclophosphamide	90-106	keratin 20	Homo sapiens	8-12
21611872-2	2011	Since 1959, alkylating agents, such as the lead compound cyclophosphamide (CTX), have always been conceived, at high dosages, as potent cytotoxic and lymphoablative drugs, indispensable for dose intensity and immunosuppressive regimen in the oncological and internal medicine armamentarium.	Cyclophosphamide	57-73	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	75-78
24331101-2	2011	In this study, we investigated the effects of Lo and Cy on peroxisome proliferator activated receptors (PPAR) using a luciferase reporter assay.	Cyclophosphamide	53-55	peroxisome proliferator activated receptor alpha	Mus musculus	59-102
24331101-2	2011	In this study, we investigated the effects of Lo and Cy on peroxisome proliferator activated receptors (PPAR) using a luciferase reporter assay.	Cyclophosphamide	53-55	peroxisome proliferator activated receptor alpha	Mus musculus	104-108
21396778-5	2011	Cyclophosphamide treatment caused bladder pain-like nociceptive behavior and referred hyperalgesia accompanying cystitis symptoms, including increased bladder weight and vascular permeability and upregulation of cyclooxygenase-2 in the bladder tissue.	Cyclophosphamide	0-16	prostaglandin-endoperoxide synthase 2	Mus musculus	212-228
21641409-3	2011	We sought to determine whether inhibition of PDGF-B signaling can increase delivery and efficacy of cyclophosphamide in Lewis lung carcinomas or RIP-Tag2 tumors.	Cyclophosphamide	100-116	platelet derived growth factor, B polypeptide	Mus musculus	45-51
20814790-0	2011	Interleukin-1 receptor antagonist attenuates cyclophosphamide-induced mucositis in a murine model.	Cyclophosphamide	45-61	interleukin 1 receptor antagonist	Homo sapiens	0-33
20814790-2	2011	The aim of this study is to evaluate the protective effects of recombinant human interleukin-1 receptor antagonist (rhIL-1Ra) on chemotherapy-induced mucositis (CIM) in a murine model of cyclophosphamide chemotherapy.	Cyclophosphamide	187-203	interleukin 1 receptor antagonist	Homo sapiens	81-114
21747882-1	2011	BACKGROUND: The addition of rituximab to cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy (R-CHOP) has significantly improved clinical outcomes for patients with diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	41-57	DNA damage inducible transcript 3	Homo sapiens	101-105
21747882-1	2011	BACKGROUND: The addition of rituximab to cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy (R-CHOP) has significantly improved clinical outcomes for patients with diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	41-57	DNA damage inducible transcript 3	Homo sapiens	123-127
22041773-7	2011	TNF-alpha level (0.23 +- 0.19) was significantly decreased 3 months after cyclophosphamide treatment (t = 2.533, P < 0.05), and TGF-beta(1) (0.31 +- 0.18) level markedly decreased after 6 months of treatment (t = 2.617, P < 0.05).	Cyclophosphamide	74-90	tumor necrosis factor	Homo sapiens	0-9
22041773-12	2011	TGF-beta(1) (21 +- 14) microg/L level decreased significantly after 3-month treatment, and TNF-alpha level (9.4 +- 1.7) microg/L was decreased after 6 months of cyclophosphamide treatment (t = 2.215, P < 0.05).	Cyclophosphamide	161-177	tumor necrosis factor	Homo sapiens	91-100
22041773-13	2011	MMP-9 level (13 +- 5) microg/L decreased after 12 months of cyclophosphamide treatment (t = 2.576, P < 0.05).	Cyclophosphamide	60-76	matrix metallopeptidase 9	Homo sapiens	0-5
22041773-14	2011	CONCLUSION: The mechanisms of cyclophosphamide treatment may be associated with its inhibition on production of TNF-alpha, TGF-beta(1)and MMP-9.	Cyclophosphamide	30-46	tumor necrosis factor	Homo sapiens	112-121
22041773-14	2011	CONCLUSION: The mechanisms of cyclophosphamide treatment may be associated with its inhibition on production of TNF-alpha, TGF-beta(1)and MMP-9.	Cyclophosphamide	30-46	transforming growth factor beta 1	Homo sapiens	123-134
22041773-14	2011	CONCLUSION: The mechanisms of cyclophosphamide treatment may be associated with its inhibition on production of TNF-alpha, TGF-beta(1)and MMP-9.	Cyclophosphamide	30-46	matrix metallopeptidase 9	Homo sapiens	138-143
21512138-5	2011	In adult urothelial cells, Sox9 was quiescent but was rapidly induced by a variety of injuries, including exposure to the carcinogen cyclophosphamide, culture with hydrogen peroxide, and osmotic stress.	Cyclophosphamide	133-149	SRY-box transcription factor 9	Homo sapiens	27-31
21998601-3	2011	This study was undertaken to test the hypothesis that cyclophosphamide may produce water retention via the proximal nephron, where aquaporin-1 (AQP1) and aquaporin-7 (AQP7) water channels participate in water absorption.	Cyclophosphamide	54-70	aquaporin 1	Rattus norvegicus	131-142
21998601-3	2011	This study was undertaken to test the hypothesis that cyclophosphamide may produce water retention via the proximal nephron, where aquaporin-1 (AQP1) and aquaporin-7 (AQP7) water channels participate in water absorption.	Cyclophosphamide	54-70	aquaporin 1	Rattus norvegicus	144-148
21998601-5	2011	In the short-term 3-day rat study, AQP1 protein expression was significantly increased in the whole kidney homogenates by cyclophosphamide administration at 48 (614 +- 194%, P < 0.005), and 96 (460 +- 46%, P < 0.05) mg/kg BW compared with vehicle-treated controls.	Cyclophosphamide	122-138	aquaporin 1	Rattus norvegicus	35-39
21998601-9	2011	From these preliminary data, we conclude that the proximal nephron may be involved in cyclophosphamide-induced water retention via AQP1 and AQP7 water channels.	Cyclophosphamide	86-102	aquaporin 1	Rattus norvegicus	131-135
21998601-9	2011	From these preliminary data, we conclude that the proximal nephron may be involved in cyclophosphamide-induced water retention via AQP1 and AQP7 water channels.	Cyclophosphamide	86-102	aquaporin 7	Rattus norvegicus	140-144
21130889-4	2011	Relative to single-agent regimens, combination regimens with pentostatin and cyclophosphamide (PC) and with fludarabine and cyclophosphamide (FC) worked synergistically to deplete host CD4(+) and CD8(+) T cells.	Cyclophosphamide	77-93	CD4 antigen	Mus musculus	185-188
21497079-4	2011	By using MWCNT, the limit of detection was enhanced from 59 to 12 muM in case of Cyclophosphamide and from to 187 to 82 muM in case of Naproxen.	Cyclophosphamide	81-97	latexin	Homo sapiens	66-69
21130889-4	2011	Relative to single-agent regimens, combination regimens with pentostatin and cyclophosphamide (PC) and with fludarabine and cyclophosphamide (FC) worked synergistically to deplete host CD4(+) and CD8(+) T cells.	Cyclophosphamide	124-140	CD4 antigen	Mus musculus	185-188
20957680-8	2011	Cyclophosphamide resulted in a significant increase in serum creatine kinase, lactate dehydrogenase, cholesterol, triglycerides, creatinine, urea, and tumor necrosis factor-alpha.	Cyclophosphamide	0-16	tumor necrosis factor	Rattus norvegicus	151-178
21543025-4	2011	Cyclophosphamide is metabolized and activated by the cytochrome P450 (CYP) system and in particular CYP enzymes 2B6 and 2C19.	Cyclophosphamide	0-16	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	53-68
21543025-4	2011	Cyclophosphamide is metabolized and activated by the cytochrome P450 (CYP) system and in particular CYP enzymes 2B6 and 2C19.	Cyclophosphamide	0-16	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	70-73
21543025-4	2011	Cyclophosphamide is metabolized and activated by the cytochrome P450 (CYP) system and in particular CYP enzymes 2B6 and 2C19.	Cyclophosphamide	0-16	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	100-103
21543025-6	2011	This investigation was done to determine the impact of CYP2B6*5 and CYP2C19*2 on the renal response in cyclophosphamide-treated lupus nephritis (LN) patients.	Cyclophosphamide	103-119	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	55-61
21543025-6	2011	This investigation was done to determine the impact of CYP2B6*5 and CYP2C19*2 on the renal response in cyclophosphamide-treated lupus nephritis (LN) patients.	Cyclophosphamide	103-119	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	68-75
21337384-0	2011	Cyclophosphamide-induced apoptosis in A431 cells is inhibited by fucosyltransferase IV.	Cyclophosphamide	0-16	fucosyltransferase 4	Homo sapiens	65-86
21337384-3	2011	Here, we investigated the effect of FUT4 overexpression on cyclophosphamide (CPA)-induced apoptosis in A431 cells.	Cyclophosphamide	59-75	fucosyltransferase 4	Homo sapiens	36-40
21337384-3	2011	Here, we investigated the effect of FUT4 overexpression on cyclophosphamide (CPA)-induced apoptosis in A431 cells.	Cyclophosphamide	77-80	fucosyltransferase 4	Homo sapiens	36-40
21498532-1	2011	UNLABELLED: R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone)-like chemotherapy is the standard therapy in aggressive B-cell lymphoma.	Cyclophosphamide	31-47	DNA damage inducible transcript 3	Homo sapiens	14-18
21337384-6	2011	The results showed that FUT4 overexpression up-regulated phosphorylation of ERK1/2 and Akt which was inhibited by CPA in dose-dependent manner.	Cyclophosphamide	114-117	fucosyltransferase 4	Homo sapiens	24-28
21337384-6	2011	The results showed that FUT4 overexpression up-regulated phosphorylation of ERK1/2 and Akt which was inhibited by CPA in dose-dependent manner.	Cyclophosphamide	114-117	mitogen-activated protein kinase 3	Homo sapiens	76-82
21337384-6	2011	The results showed that FUT4 overexpression up-regulated phosphorylation of ERK1/2 and Akt which was inhibited by CPA in dose-dependent manner.	Cyclophosphamide	114-117	AKT serine/threonine kinase 1	Homo sapiens	87-90
21337384-8	2011	We concluded that FUT4 inhibited cell apoptosis induced by CPA through decreasing the expression of apoptotic proteins Bax, Caspase 3, and PARP and increasing the expression of anti-apoptotic protein Bcl-2 via the ERK/MAPK and PI3K/Akt signaling pathways in A431 cells.	Cyclophosphamide	59-62	fucosyltransferase 4	Homo sapiens	18-22
21337384-8	2011	We concluded that FUT4 inhibited cell apoptosis induced by CPA through decreasing the expression of apoptotic proteins Bax, Caspase 3, and PARP and increasing the expression of anti-apoptotic protein Bcl-2 via the ERK/MAPK and PI3K/Akt signaling pathways in A431 cells.	Cyclophosphamide	59-62	BCL2 associated X, apoptosis regulator	Homo sapiens	119-122
21337384-8	2011	We concluded that FUT4 inhibited cell apoptosis induced by CPA through decreasing the expression of apoptotic proteins Bax, Caspase 3, and PARP and increasing the expression of anti-apoptotic protein Bcl-2 via the ERK/MAPK and PI3K/Akt signaling pathways in A431 cells.	Cyclophosphamide	59-62	caspase 3	Homo sapiens	124-133
21337384-8	2011	We concluded that FUT4 inhibited cell apoptosis induced by CPA through decreasing the expression of apoptotic proteins Bax, Caspase 3, and PARP and increasing the expression of anti-apoptotic protein Bcl-2 via the ERK/MAPK and PI3K/Akt signaling pathways in A431 cells.	Cyclophosphamide	59-62	collagen type XI alpha 2 chain	Homo sapiens	139-143
21323512-1	2011	Development of resistance to the CHOP chemotherapeutic regimen (cyclophosphamide, doxorubicin, vincristine, prednisone) remains a major cause of treatment failure and mortality in approximately 40% of patients with diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	64-80	DNA damage inducible transcript 3	Homo sapiens	33-37
21381781-1	2011	The aim of this study was to investigate the enhancement of Ganoderma atrum polysaccharide (PSG-1) on cyclophosphamide (CTX)-induced antitumor effect in sarcoma 180 (S-180)-bearing mice.	Cyclophosphamide	102-118	V-set and immunoglobulin domain containing 2	Mus musculus	120-123
21482186-3	2011	We aimed to investigate the efficacy and safety of a decreased dose of CHOP (doxorubicin, cyclophosphamide, vincristine, and prednisone) chemotherapy with a conventional dose of rituximab in elderly patients with diffuse large B-cell lymphoma.	Cyclophosphamide	90-106	DNA damage inducible transcript 3	Homo sapiens	71-75
21442647-0	2011	The importance of correct assignment of CYP2B6 genetic variants with respect to cyclophosphamide metabolizer status.	Cyclophosphamide	80-96	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	40-46
21363914-4	2011	Here, we use a new mathematical model to compare the effects of conventional cyclophosphamide therapy with those induced when macrophages are used to deliver hypoxia-inducible cytochrome P450 to locally activate cyclophosphamide.	Cyclophosphamide	77-93	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	176-191
21363914-4	2011	Here, we use a new mathematical model to compare the effects of conventional cyclophosphamide therapy with those induced when macrophages are used to deliver hypoxia-inducible cytochrome P450 to locally activate cyclophosphamide.	Cyclophosphamide	212-228	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	176-191
20938662-3	2011	In this study, we performed immunohistochemical analysis for IDO expression using mouse anti-human IDO monoclonal antibody in 119 tissue samples of diffuse large B-cell lymphoma (DLBCL) obtained before treatment with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP).	Cyclophosphamide	228-244	indoleamine 2,3-dioxygenase 1	Homo sapiens	61-64
21216274-5	2011	RESULTS: Mad2(+/-) HPCs were protected from cytotoxic effects in vivo of a cell-cycle-specific agent, Ara-C, events consistent with Mad2(+/-) HPCs being in a slow or noncycling state, but not from recovery of functional HPC after treatment with non-cycle-specific cyclophosphamide or sublethal irradiation.	Cyclophosphamide	264-280	MAD2 mitotic arrest deficient-like 1	Mus musculus	9-13
21508361-0	2011	Beta-(1-3),(1-6)-D-glucan enhances the effect of low-dose cyclophosphamide treatment on A20 lymphoma in mice.	Cyclophosphamide	58-74	hemoglobin, beta adult major chain	Mus musculus	0-9
21508361-0	2011	Beta-(1-3),(1-6)-D-glucan enhances the effect of low-dose cyclophosphamide treatment on A20 lymphoma in mice.	Cyclophosphamide	58-74	tumor necrosis factor, alpha-induced protein 3	Mus musculus	88-91
21508361-6	2011	CONCLUSION: Beta-(1-3),(1-6)-D-glucan could be useful in the treatment of lymphoma after low-dose chemotherapy with CY.	Cyclophosphamide	116-118	hemoglobin, beta adult major chain	Mus musculus	12-21
21539449-0	2011	Knockdown of osteopontin chemosensitizes MDA-MB-231 cells to cyclophosphamide by enhancing apoptosis through activating p38 MAPK pathway.	Cyclophosphamide	61-77	secreted phosphoprotein 1	Homo sapiens	13-24
21423807-10	2011	IL-8 production by carcinoma cells can be modulated by low doses of cyclophosphamide at the transcription level.	Cyclophosphamide	68-84	C-X-C motif chemokine ligand 8	Homo sapiens	0-4
21438831-2	2011	We previously described the benefit of the THP-COP regimen comprising cyclophosphamide, THP, vincristine, and prednisolone for elderly patients with diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	70-86	uromodulin	Homo sapiens	43-46
21438831-2	2011	We previously described the benefit of the THP-COP regimen comprising cyclophosphamide, THP, vincristine, and prednisolone for elderly patients with diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	70-86	caspase recruitment domain family member 16	Homo sapiens	47-50
21320281-11	2011	In vivo, treatment of mice with cyclophosphamide and acrolein resulted in elevations of plasma TAT complex levels, whereas APC levels remained low.	Cyclophosphamide	32-48	APC, WNT signaling pathway regulator	Mus musculus	123-126
21106858-0	2011	Cyclophosphamide induces NR2B phosphorylation-dependent facilitation on spinal reflex potentiation.	Cyclophosphamide	0-16	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	25-29
21312191-6	2011	A short course of cyclophosphamide caused a sharp drop in IFN-alpha-elicited short-lived plasma cells, but the levels recovered within days following termination of treatment.	Cyclophosphamide	18-34	interferon alpha	Mus musculus	58-67
21519545-6	2011	Remarkably, the levels of CK5 and CK14 expression were enhanced in mTECs, and CK8 expression was upregulated in cTECs during mouse thymus regeneration after cyclophosphamide-induced acute thymic involution.	Cyclophosphamide	157-173	keratin 8	Mus musculus	78-81
21487460-0	2011	Transient effectiveness of an oral 5-Fluorouracil derivative, s-1, for epirubicin, cyclophosphamide and Paclitaxel refractory skin metastases from possible occult breast cancer in a male.	Cyclophosphamide	83-99	proteasome 26S subunit, non-ATPase 1	Homo sapiens	62-65
22099932-7	2011	AIM: The aim of the study was to evaluate the clinical risk stratification models including the age adjusted International prognostic index (aaIPI), patients profile and dose intensity (DI) of Cyclophosphamide and Doxorubicin as effective tools for predicting the outcome and prognosis of our DLBCL patients treated with first line CHOP regimen.	Cyclophosphamide	193-209	DNA damage inducible transcript 3	Homo sapiens	332-336
21078813-7	2011	Injection of EPO (30 IU/kg) and PrB (0.5 ml) led to a significant increase in the MN frequency in the PBMN assay in response to cyclophosphamide and zidovudine.	Cyclophosphamide	128-144	erythropoietin	Rattus norvegicus	13-16
20354901-4	2011	The patient was treated with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) with rituximab, and a dramatic improvement of renal function was noticed after two weeks of treatment.	Cyclophosphamide	29-45	DNA damage inducible transcript 3	Homo sapiens	89-93
21189395-6	2011	RESULTS: Test set cases containing HER2 amplification treated with doxorubicin and cyclophosphamide (AC) plus trastuzumab, demonstrated longer progression-free survival compared to those treated with AC alone (P = .0002).	Cyclophosphamide	83-99	erb-b2 receptor tyrosine kinase 2	Homo sapiens	35-39
21487460-2	2011	We describe the case of a 76-year-old male showing transient effectiveness with an oral 5-fluorouracil derivative, S-1 (tegafur, 5-chloro-2,4-dihydroxypyridine and potassium oxonate), for epirubicin, cyclophosphamide and paclitaxel refractory skin metastases from possible occult breast cancer.	Cyclophosphamide	200-216	proteasome 26S subunit, non-ATPase 1	Homo sapiens	115-118
20882053-9	2011	Moreover, cyclophosphamide reduced the infiltration of inflammatory cells, including total leukocytes, lymphocytes, CD4+ and CD8+T cells.	Cyclophosphamide	10-26	CD4 antigen	Mus musculus	116-119
21373362-0	2011	Increased expression of interleukin-6 family members and receptors in urinary bladder with cyclophosphamide-induced bladder inflammation in female rats.	Cyclophosphamide	91-107	interleukin 6	Rattus norvegicus	24-37
21148486-1	2011	Low doses of the alkylating agent cyclophosphamide (CTX) mediate antiangiogenic and immunostimulatory effects, leading to potent tumoricidal activity in association with various immunotherapeutic strategies.	Cyclophosphamide	34-50	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	52-55
21165551-2	2011	Here, we have utilised the tumour-infiltrating properties of macrophages as vehicles to deliver a gene encoding a prodrug-activating enzyme such as human cytochrome P450 2B6 (CYP2B6) inside tumours followed by killing the tumour cells with the prodrug cyclophosphamide (CPA).	Cyclophosphamide	252-268	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	154-173
21233415-5	2011	Four weeks after BM transplantation, we treated mice with steroid/cyclophosphamide (S/CYC) or BTZ.	Cyclophosphamide	66-82	peptidylprolyl isomerase A, pseudogene 1	Mus musculus	86-89
21207214-8	2011	The patient was treated according to the CTD protocol (cyclophosphamide, thalidomide, and dexamethasone) which was effective against the myeloma as well as the systemic sclerosis and patient achieved complete remission.	Cyclophosphamide	55-71	CTD	Homo sapiens	41-44
21425582-0	2011	[Study on dynamic effect of acupuncture on marrow cell cycle regulatory protein cyclin D1 expression and cell cycle in mice with cyclophosphamide induced myelosuppression].	Cyclophosphamide	129-145	cyclin D1	Mus musculus	80-89
21255398-11	2011	Knockdown of RAD21 in the MDA-MB-231 breast cancer cell line significantly enhanced sensitivity to cyclophosphamide, 5-fluorouracil and etoposide.	Cyclophosphamide	99-115	RAD21 cohesin complex component	Homo sapiens	13-18
21865687-3	2011	Evidence that pulse steroid plus intravenous or oral cyclophosphamide can retard the rate of progression of advanced IgAN was provided by several groups worldwide.	Cyclophosphamide	53-69	IGAN1	Homo sapiens	117-121
21875286-3	2011	In this study, we therefore examined the anticlastogenic and anticarcinogenic effect of TBG against clastogens, cyclophosphamide (CYP) and DMBA, in mice using the in vivo erythrocyte micronucleus assay and azoxymethane (AOM)-induced colon carcinogenesis in rats, respectively.	Cyclophosphamide	112-128	serine (or cysteine) peptidase inhibitor, clade A (alpha-1 antiproteinase, antitrypsin), member 7	Mus musculus	88-91
20798686-6	2011	Furthermore, all patients who received cyclophosphamide (CP), epirubicin plus taxotere/CP, epirubicin plus 5-fluorouracil chemotherapy showed miR-448 suppression, an increased SATB1, Twist1 expression and acquisition of mesenchymal phenotypes.	Cyclophosphamide	39-55	microRNA 448	Homo sapiens	142-149
20857100-7	2011	Analysis of peripheral blood samples from patients prior and during fludarabine/cyclophosphamide therapy revealed rapid and sustained reduction of tumour cells but also of CD4(+) and CD8(+) T cells.	Cyclophosphamide	80-96	CD4 molecule	Homo sapiens	172-175
20857100-7	2011	Analysis of peripheral blood samples from patients prior and during fludarabine/cyclophosphamide therapy revealed rapid and sustained reduction of tumour cells but also of CD4(+) and CD8(+) T cells.	Cyclophosphamide	80-96	CD8a molecule	Homo sapiens	183-186
20798686-6	2011	Furthermore, all patients who received cyclophosphamide (CP), epirubicin plus taxotere/CP, epirubicin plus 5-fluorouracil chemotherapy showed miR-448 suppression, an increased SATB1, Twist1 expression and acquisition of mesenchymal phenotypes.	Cyclophosphamide	39-55	SATB homeobox 1	Homo sapiens	176-181
20798686-6	2011	Furthermore, all patients who received cyclophosphamide (CP), epirubicin plus taxotere/CP, epirubicin plus 5-fluorouracil chemotherapy showed miR-448 suppression, an increased SATB1, Twist1 expression and acquisition of mesenchymal phenotypes.	Cyclophosphamide	39-55	twist family bHLH transcription factor 1	Homo sapiens	183-189
21893984-0	2011	Aminoguanidine, a selective nitric oxide synthase inhibitor, attenuates cyclophosphamide-induced renal damage by inhibiting protein nitration and poly(ADP-Ribose) polymerase activation.	Cyclophosphamide	72-88	poly (ADP-ribose) polymerase 1	Rattus norvegicus	146-173
21362365-2	2011	The metabolism of epirubicin (EPI) and cyclophosphamide (CTX) is mainly mediated by cytochrome P450s (CYPs) and glutathione S-transferases (GSTs).	Cyclophosphamide	39-55	glutathione S-transferase pi 1	Homo sapiens	140-144
22232912-3	2011	Under these conditions, changes of the catalase activity exhibited some specific features: in the animals under LPS action, the catalase activity increased in the spleen, while being decreased in the thymus; under the influence of CPHA, the activity of this enzyme decreased in both organs.	Cyclophosphamide	231-235	catalase	Rattus norvegicus	39-47
22232912-3	2011	Under these conditions, changes of the catalase activity exhibited some specific features: in the animals under LPS action, the catalase activity increased in the spleen, while being decreased in the thymus; under the influence of CPHA, the activity of this enzyme decreased in both organs.	Cyclophosphamide	231-235	catalase	Rattus norvegicus	128-136
22144989-0	2011	TRAIL and DcR1 expressions are differentially regulated in the pancreatic islets of STZ- versus CY-applied NOD mice.	Cyclophosphamide	96-98	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	0-5
22144989-6	2011	TRAIL ligand expression followed a completely different pattern in STZ- versus CY-accelerated disease, displaying a prominent increase in the former, while appearing at reduced levels in the latter.	Cyclophosphamide	79-81	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	0-5
20693809-3	2011	Anti-TNF antibody therapy (infliximab) may help control AAV by providing more targeted immunosuppression and allow reductions in the use of corticosteroids and cyclophosphamide, thereby reducing the burden of immunosuppression with its associated morbidity and mortality.	Cyclophosphamide	160-176	tumor necrosis factor	Homo sapiens	5-8
21731212-2	2011	Glutathione S-transferases (GSTs) are involved in the metabolism of several anticancer drugs, including alkylating agents, anthracyclines, and cyclophosphamides.	Cyclophosphamide	143-160	glutathione S-transferase mu 1	Homo sapiens	28-32
22454706-5	2011	He received chemotherapy with CHOP regimen (cyclophosphamide, adriamycin, vincristine and prednisolone) resulting in reduction in lesion size leaving a phthysical eyeball and a ptotic lid.	Cyclophosphamide	44-60	DNA damage inducible transcript 3	Homo sapiens	30-34
21738257-0	2011	Hepatotoxicity following cyclophosphamide treatment in a patient with MPO-ANCA vasculitis.	Cyclophosphamide	25-41	myeloperoxidase	Homo sapiens	70-73
22358096-5	2011	It was found that bestatin administered at doses of 1 and 0.1 mg/kg five times on alternating days increased the synthesis and release of IL-1beta by resident peritoneal murine macrophages stimulated in vitro with LPS in cyclophosphamide-treated mice.	Cyclophosphamide	221-237	interleukin 1 beta	Mus musculus	138-146
21894752-21	2011	Cyclophosphamide dose 4 g/m2 provides collection of CD34+ cells number sufficient for two autotransplantations in moderate thrombocytopenia and in less number of substitute transfusions in the absence of serious toxic complications.	Cyclophosphamide	0-16	CD34 molecule	Homo sapiens	52-56
21165551-2	2011	Here, we have utilised the tumour-infiltrating properties of macrophages as vehicles to deliver a gene encoding a prodrug-activating enzyme such as human cytochrome P450 2B6 (CYP2B6) inside tumours followed by killing the tumour cells with the prodrug cyclophosphamide (CPA).	Cyclophosphamide	252-268	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	175-181
21165551-2	2011	Here, we have utilised the tumour-infiltrating properties of macrophages as vehicles to deliver a gene encoding a prodrug-activating enzyme such as human cytochrome P450 2B6 (CYP2B6) inside tumours followed by killing the tumour cells with the prodrug cyclophosphamide (CPA).	Cyclophosphamide	270-273	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	154-173
21165551-2	2011	Here, we have utilised the tumour-infiltrating properties of macrophages as vehicles to deliver a gene encoding a prodrug-activating enzyme such as human cytochrome P450 2B6 (CYP2B6) inside tumours followed by killing the tumour cells with the prodrug cyclophosphamide (CPA).	Cyclophosphamide	270-273	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	175-181
21894752-1	2011	AIM: To determine an optimal cyclophosphamide dose in the mobilization scheme providing adequate collection of CD34+ cells in patients with multiple myeloma (MM), to optimize the time of initiation of granulocytic colony-stimulating factor (G-CSF) administration, to study effects of induction therapy schemes on results of mobilization and collection of CD34+ cells.	Cyclophosphamide	29-45	CD34 molecule	Homo sapiens	111-115
21894752-1	2011	AIM: To determine an optimal cyclophosphamide dose in the mobilization scheme providing adequate collection of CD34+ cells in patients with multiple myeloma (MM), to optimize the time of initiation of granulocytic colony-stimulating factor (G-CSF) administration, to study effects of induction therapy schemes on results of mobilization and collection of CD34+ cells.	Cyclophosphamide	29-45	CD34 molecule	Homo sapiens	355-359
21894752-19	2011	CONCLUSION: Administration of high cyclophosphamide doses in combination with G-CSF is an effective and safe method of BHSC mobilization providing collection of adequate number of CD34+ cells for double autotransplantation in 96.8% patients.	Cyclophosphamide	35-51	CD34 molecule	Homo sapiens	180-184
21339937-5	2010	On the basis of these findings, the US Food and Drug Administration (FDA) recently approved rituximab in combination with fludarabine and cyclophosphamide for the treatment of patients with relapsed/refractory or previously untreated CD20-postive CLL.	Cyclophosphamide	138-154	keratin 20	Homo sapiens	234-238
21068404-6	2010	Analysis of the tumor microenvironment disclosed that long-term Treg depletion by 0.5 mg cyclophosphamide treatment induced Gr-1(+)CD11b(+) myeloid-derived suppressor cells (MDSCs).	Cyclophosphamide	89-105	integrin subunit alpha M	Homo sapiens	131-136
21159176-0	2010	VEGFR2 heterogeneity and response to anti-angiogenic low dose metronomic cyclophosphamide treatment.	Cyclophosphamide	73-89	kinase insert domain receptor	Homo sapiens	0-6
21159176-9	2010	We observed a significant decrease in microvascular density (MVD) in response to low dose metronomic cyclophosphamide chemotherapy in both malignant melanoma (with higher proportion VEGFR2 positive blood vessels; 93%) and colorectal carcinoma (with lower proportion VEGFR2 positive blood vessels; 60%) xenografts.	Cyclophosphamide	101-117	kinase insert domain receptor	Homo sapiens	182-188
21159176-9	2010	We observed a significant decrease in microvascular density (MVD) in response to low dose metronomic cyclophosphamide chemotherapy in both malignant melanoma (with higher proportion VEGFR2 positive blood vessels; 93%) and colorectal carcinoma (with lower proportion VEGFR2 positive blood vessels; 60%) xenografts.	Cyclophosphamide	101-117	kinase insert domain receptor	Homo sapiens	266-272
21068378-5	2010	We find that suppression of Rev1, an essential TLS scaffold protein and dCMP transferase, inhibits both cisplatin- and cyclophosphamide-induced mutagenesis.	Cyclophosphamide	119-135	REV1, DNA directed polymerase	Mus musculus	28-32
21108329-0	2010	Allelic variations in CYP2B6 and CYP2C19 and survival of patients receiving cyclophosphamide prior to myeloablative hematopoietic stem cell transplantation.	Cyclophosphamide	76-92	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	22-28
21108329-0	2010	Allelic variations in CYP2B6 and CYP2C19 and survival of patients receiving cyclophosphamide prior to myeloablative hematopoietic stem cell transplantation.	Cyclophosphamide	76-92	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	33-40
21175440-0	2010	The combined impact of CYP2C19 and CYP2B6 pharmacogenetics on cyclophosphamide bioactivation.	Cyclophosphamide	62-78	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	23-30
21175440-0	2010	The combined impact of CYP2C19 and CYP2B6 pharmacogenetics on cyclophosphamide bioactivation.	Cyclophosphamide	62-78	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	35-41
21175440-7	2010	This dual genotype relationship was also observed in a preliminary clinical study, with patients who had >=1 LoF allele at either CYP2C19 or CYP2B6 also displaying significantly (P= 0.0316) lower bioactivation of cyclophosphamide.	Cyclophosphamide	216-232	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	133-140
21175440-7	2010	This dual genotype relationship was also observed in a preliminary clinical study, with patients who had >=1 LoF allele at either CYP2C19 or CYP2B6 also displaying significantly (P= 0.0316) lower bioactivation of cyclophosphamide.	Cyclophosphamide	216-232	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	144-150
21175440-9	2010	CONCLUSIONS: The presence of >=1 LoF allele(s) at either CYP2B6 or CYP2C19 appeared to result in decreased bioactivation of cyclophosphamide both in vitro and in patients.	Cyclophosphamide	127-143	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	60-66
21175440-9	2010	CONCLUSIONS: The presence of >=1 LoF allele(s) at either CYP2B6 or CYP2C19 appeared to result in decreased bioactivation of cyclophosphamide both in vitro and in patients.	Cyclophosphamide	127-143	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	70-77
21103787-1	2010	In breast cancer patients submitted to neoadjuvant chemotherapy (4 cycles of doxorubicin and cyclophosphamide, AC), expression of groups of three genes (gene trio signatures) could distinguish responsive from non-responsive tumors, as demonstrated by cDNA microarray profiling in a previous study by our group.	Cyclophosphamide	93-109	trio Rho guanine nucleotide exchange factor	Homo sapiens	158-162
21103787-10	2010	Therefore, the combined expression of MTSS1, RPL37 and SMYD2, as evaluated by real-time RT-PCR, is a potential candidate to predict response to neoadjuvant doxorubicin and cyclophosphamide in breast cancer patients.	Cyclophosphamide	172-188	MTSS I-BAR domain containing 1	Homo sapiens	38-43
21103787-10	2010	Therefore, the combined expression of MTSS1, RPL37 and SMYD2, as evaluated by real-time RT-PCR, is a potential candidate to predict response to neoadjuvant doxorubicin and cyclophosphamide in breast cancer patients.	Cyclophosphamide	172-188	ribosomal protein L37	Homo sapiens	45-50
21103787-10	2010	Therefore, the combined expression of MTSS1, RPL37 and SMYD2, as evaluated by real-time RT-PCR, is a potential candidate to predict response to neoadjuvant doxorubicin and cyclophosphamide in breast cancer patients.	Cyclophosphamide	172-188	SET and MYND domain containing 2	Homo sapiens	55-60
20964639-6	2010	On the other hand, using cyclophosphamide and gemcitabine, we demonstrated that regulatory/suppressor CD4(+) CD25(+) forkhead boxP3(+) and GR-1(+) CD11b(+) cells do not play a major role in the establishment or the maintenance of endotoxin tolerance, a central mechanism for inducing an immunosuppression state.	Cyclophosphamide	25-41	CD4 molecule	Homo sapiens	102-105
20964639-6	2010	On the other hand, using cyclophosphamide and gemcitabine, we demonstrated that regulatory/suppressor CD4(+) CD25(+) forkhead boxP3(+) and GR-1(+) CD11b(+) cells do not play a major role in the establishment or the maintenance of endotoxin tolerance, a central mechanism for inducing an immunosuppression state.	Cyclophosphamide	25-41	integrin subunit alpha M	Homo sapiens	147-152
20624446-1	2010	The polysaccharide (PAP) from Potentilla anserina was evaluated for modulating effects by using mouse peritoneal macrophage and the immunosuppressed-model cyclophosphamide-induced.	Cyclophosphamide	155-171	phospholipid phosphatase 1	Mus musculus	20-23
21160270-0	2010	[A case of HER2 overexpressing advanced breast cancer with CTF therapy [cyclophosphamide, pirarubicin (THPADM), fluorouracil] showed long-term effectiveness after paclitaxel shock].	Cyclophosphamide	72-88	erb-b2 receptor tyrosine kinase 2	Homo sapiens	11-15
21160270-0	2010	[A case of HER2 overexpressing advanced breast cancer with CTF therapy [cyclophosphamide, pirarubicin (THPADM), fluorouracil] showed long-term effectiveness after paclitaxel shock].	Cyclophosphamide	72-88	nuclear factor I C	Homo sapiens	59-62
20937032-1	2010	The interaction between cyclophosphamide monohydrate with human serum albumin (HSA) and human serum transferrin (hTf) was studied with UV absorption, fluorescence and circular dichroism (CD) spectroscopies as well as molecular modeling.	Cyclophosphamide	24-52	albumin	Homo sapiens	64-77
21068378-6	2010	Additionally, by performing repeated cycles of tumor engraftment and treatment, we show that Rev1 plays a critical role in the development of acquired cyclophosphamide resistance.	Cyclophosphamide	151-167	REV1, DNA directed polymerase	Mus musculus	93-97
20956320-0	2010	Inhibition of the cation channel TRPV4 improves bladder function in mice and rats with cyclophosphamide-induced cystitis.	Cyclophosphamide	87-103	transient receptor potential cation channel, subfamily V, member 4	Mus musculus	33-38
21054711-0	2010	Therapeutic hotline: Primary cutaneous CD4 + small/medium-sized pleomorphic T cell lymphoma coexisting with myelodysplastic syndrome transforming into chronic myelomonocytic leukemia successfully treated with cyclophosphamide.	Cyclophosphamide	209-225	CD4 molecule	Homo sapiens	39-42
21050466-10	2010	Pre-treatment of recipient mice with cyclophosphamide dramatically increased the number of interferon-gamma producing cells.	Cyclophosphamide	37-53	interferon gamma	Mus musculus	91-107
21050466-13	2010	Cyclophosphamide pre-treatment augments the anti-tumor effect by increasing the proliferation of interferon-gamma producing cells in the adoptive host.	Cyclophosphamide	0-16	interferon gamma	Mus musculus	97-113
21030533-3	2010	DLBCL is associated with an aggressive natural history, but it can be cured with combination chemotherapy regimens like cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP), which has been the mainstay of therapy for several decades.	Cyclophosphamide	120-136	DNA damage inducible transcript 3	Homo sapiens	180-184
21076492-2	2010	The objective of this study was to investigate its protective activity against cyclophosphamide (CTX)-induced toxicity in mouse models.	Cyclophosphamide	79-95	V-set and immunoglobulin domain containing 2	Mus musculus	97-100
20689431-6	2010	The chemokine receptor 4 (CXCR4) inhibitor, AMD-3100, is recommended for patients who have received lenalidomide and failed to mobilize stem cells after G-SCF and cyclophosphamide.	Cyclophosphamide	163-179	C-X-C motif chemokine receptor 4	Homo sapiens	26-31
21054711-4	2010	We report a case of primary cutaneous CD4 + small/medium-sized pleomorphic T cell lymphoma accompanied with myelodysplastic syndrome successfully treated with cyclophosphamide.	Cyclophosphamide	159-175	CD4 molecule	Homo sapiens	38-41
21050687-8	2010	The classic CHOP protocol (combination of doxorubicin-cyclophosphamide-vincristine-prednisone) does not have satisfactory results and survival remains poor, especially in patients with underlying RCD.	Cyclophosphamide	54-70	DNA damage inducible transcript 3	Homo sapiens	12-16
20631380-9	2010	When treated in vivo with cyclophosphamide, tumors coexpressing Mcl-1 and Myc transgenes were significantly more resistant than conventional Emu-Myc lymphomas.	Cyclophosphamide	26-42	myeloid cell leukemia sequence 1	Mus musculus	64-69
20631380-9	2010	When treated in vivo with cyclophosphamide, tumors coexpressing Mcl-1 and Myc transgenes were significantly more resistant than conventional Emu-Myc lymphomas.	Cyclophosphamide	26-42	myelocytomatosis oncogene	Mus musculus	74-77
21103206-3	2010	We describe a 51-year-old man with jejunal B-cell lymphoma who developed recurrent episodes of ischemic colitis following chemotherapy with cyclophosphamide, vincristine, doxorubicine and prednisolone plus rituximab (R-CHOP).	Cyclophosphamide	140-156	DNA damage inducible transcript 3	Homo sapiens	219-223
21179332-0	2010	Expression of nitric oxide synthase and aquaporin-3 in cyclophosphamide treated rat bladder.	Cyclophosphamide	55-71	aquaporin 3 (Gill blood group)	Rattus norvegicus	40-51
21179332-2	2010	The aim of this study is to evaluate the expression of inducible NOS (iNOS), aquaporin-3 (AQP-3) in cyclophosphamide (CYP) induced rat bladder.	Cyclophosphamide	100-116	nitric oxide synthase 2	Rattus norvegicus	55-68
21179332-2	2010	The aim of this study is to evaluate the expression of inducible NOS (iNOS), aquaporin-3 (AQP-3) in cyclophosphamide (CYP) induced rat bladder.	Cyclophosphamide	100-116	nitric oxide synthase 2	Rattus norvegicus	70-74
21179332-2	2010	The aim of this study is to evaluate the expression of inducible NOS (iNOS), aquaporin-3 (AQP-3) in cyclophosphamide (CYP) induced rat bladder.	Cyclophosphamide	100-116	aquaporin 3 (Gill blood group)	Rattus norvegicus	77-88
21179332-2	2010	The aim of this study is to evaluate the expression of inducible NOS (iNOS), aquaporin-3 (AQP-3) in cyclophosphamide (CYP) induced rat bladder.	Cyclophosphamide	100-116	aquaporin 3 (Gill blood group)	Rattus norvegicus	90-95
20627385-0	2010	The efficacy and safety of the low-thalidomide dose CTD (cyclophosphamide, thalidomide, dexamethasone) regimen in patients with multiple myeloma--a report by the Polish Myeloma Study Group.	Cyclophosphamide	57-73	CTD	Homo sapiens	52-55
21180996-1	2010	OBJECTIVE: To evaluate the immunohistochemical expression of cox-2 before primary chemotherapy with 5-fluorouracil, epirubicin and cyclophosphamide (FEC) and its association with initial tumor size, lymph node status, hormone receptors, expression of HER2 and the clinical and pathological response in patients with breast cancer.	Cyclophosphamide	131-147	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	61-66
20877570-3	2010	METHODS AND FINDINGS: Here it was found that specific inhibition of cathepsin L affords strong protection from cyclophosphamide (CY)-induced insulitis and diabetes of NOD mice at the advanced stage of CD8(+) T cell infiltration via inhibiting granzyme activity.	Cyclophosphamide	111-127	cathepsin L	Mus musculus	68-79
20877570-3	2010	METHODS AND FINDINGS: Here it was found that specific inhibition of cathepsin L affords strong protection from cyclophosphamide (CY)-induced insulitis and diabetes of NOD mice at the advanced stage of CD8(+) T cell infiltration via inhibiting granzyme activity.	Cyclophosphamide	129-131	cathepsin L	Mus musculus	68-79
20877570-5	2010	Moreover, the gene targeting for cathepsin L with application of in vivo siRNA administration successfully prevented CY-induced diabetes of NOD mice.	Cyclophosphamide	117-119	cathepsin L	Mus musculus	33-44
20836875-0	2010	Adenoviral delivery of pan-caspase inhibitor p35 enhances bystander killing by P450 gene-directed enzyme prodrug therapy using cyclophosphamide+.	Cyclophosphamide	127-143	interleukin 12A	Homo sapiens	45-48
20836875-0	2010	Adenoviral delivery of pan-caspase inhibitor p35 enhances bystander killing by P450 gene-directed enzyme prodrug therapy using cyclophosphamide+.	Cyclophosphamide	127-143	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	79-83
20836875-1	2010	BACKGROUND: Cytochrome P450-based suicide gene therapy for cancer using prodrugs such as cyclophosphamide (CPA) increases anti-tumor activity, both directly and via a bystander killing mechanism.	Cyclophosphamide	89-105	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	23-27
20836875-1	2010	BACKGROUND: Cytochrome P450-based suicide gene therapy for cancer using prodrugs such as cyclophosphamide (CPA) increases anti-tumor activity, both directly and via a bystander killing mechanism.	Cyclophosphamide	107-110	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	23-27
20836875-3	2010	Previous studies have shown that the pan-caspase inhibitor p35 significantly increases CPA-induced bystander killing by tumor cells that stably express P450 enzyme CYP2B6 (Schwartz et al, (2002) Cancer Res.	Cyclophosphamide	87-90	interleukin 12A	Homo sapiens	59-62
20836875-3	2010	Previous studies have shown that the pan-caspase inhibitor p35 significantly increases CPA-induced bystander killing by tumor cells that stably express P450 enzyme CYP2B6 (Schwartz et al, (2002) Cancer Res.	Cyclophosphamide	87-90	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	164-170
20041327-7	2010	RESULTS: Our study showed that vincristine, tamoxifen, vinblastine, docetaxel, cyclophosphamide, flutamide, ifosfamide and paclitaxel activate PXR-mediated Pgp induction, and were additionally shown to affect the intracellular accumulation of the Pgp probe rhodamine 123.	Cyclophosphamide	79-95	nuclear receptor subfamily 1 group I member 2	Homo sapiens	143-146
20041327-7	2010	RESULTS: Our study showed that vincristine, tamoxifen, vinblastine, docetaxel, cyclophosphamide, flutamide, ifosfamide and paclitaxel activate PXR-mediated Pgp induction, and were additionally shown to affect the intracellular accumulation of the Pgp probe rhodamine 123.	Cyclophosphamide	79-95	ATP binding cassette subfamily B member 1	Homo sapiens	156-159
20041327-7	2010	RESULTS: Our study showed that vincristine, tamoxifen, vinblastine, docetaxel, cyclophosphamide, flutamide, ifosfamide and paclitaxel activate PXR-mediated Pgp induction, and were additionally shown to affect the intracellular accumulation of the Pgp probe rhodamine 123.	Cyclophosphamide	79-95	ATP binding cassette subfamily B member 1	Homo sapiens	247-250
20664354-5	2010	Cyclophosphamide (CTX) plus Fludarabine depleted lymphocytes more profoundly, with a maximal effect using high doses of CTX.	Cyclophosphamide	0-16	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	18-21
20664354-5	2010	Cyclophosphamide (CTX) plus Fludarabine depleted lymphocytes more profoundly, with a maximal effect using high doses of CTX.	Cyclophosphamide	0-16	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	120-123
20607281-5	2010	Replacement of proline residues by alanines (188-ASTA) decreased Cavbeta(2) affinity about 20-fold.	Cyclophosphamide	49-53	calcium channel, voltage-dependent, beta 2 subunit	Mus musculus	65-75
20687516-10	2010	The results demonstrate up to 4-fold increases in cell death in PARG null-TS cells after treatment with epirubicin or sub-IC(50) doses of cisplatin and cyclophosphamide.	Cyclophosphamide	152-168	poly(ADP-ribose) glycohydrolase	Homo sapiens	64-68
20435884-3	2010	Losses of TP53 and CDKN2A, observed in 8% and 35% of patients, respectively, were significantly associated with a shorter survival after rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) treatment, independently of the International Prognostic Index and of the cell of origin.	Cyclophosphamide	148-164	tumor protein p53	Homo sapiens	10-14
20435884-3	2010	Losses of TP53 and CDKN2A, observed in 8% and 35% of patients, respectively, were significantly associated with a shorter survival after rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) treatment, independently of the International Prognostic Index and of the cell of origin.	Cyclophosphamide	148-164	cyclin dependent kinase inhibitor 2A	Homo sapiens	19-25
20660823-1	2010	PURPOSE: The adverse prognosis of CD20 expression in adults with de novo precursor B-lineage acute lymphoblastic leukemia (ALL) prompted incorporation of monoclonal antibody therapy with rituximab into the intensive chemotherapy regimen hyper-CVAD (fractionated cyclophosphamide, vincristine, doxorubicin, dexamethasone).	Cyclophosphamide	262-278	keratin 20	Homo sapiens	34-38
21188112-0	2010	Positive response to neoadjuvant cyclophosphamide and doxorubicin in topoisomerase II nonamplified/HER2/neu negative/polysomy 17 absent breast cancer patients.	Cyclophosphamide	33-49	erb-b2 receptor tyrosine kinase 2	Homo sapiens	99-103
21188112-0	2010	Positive response to neoadjuvant cyclophosphamide and doxorubicin in topoisomerase II nonamplified/HER2/neu negative/polysomy 17 absent breast cancer patients.	Cyclophosphamide	33-49	erb-b2 receptor tyrosine kinase 2	Homo sapiens	104-107
21042682-6	2010	Immunosuppressive treatment with a combination of oral prednisone (1 mg/kg daily) and cyclophosphamide (1,5 mg/kg daily) was administered to reduce the FVIII inhibitor.	Cyclophosphamide	86-102	coagulation factor VIII	Homo sapiens	152-157
21218650-8	2010	CONCLUSION: Intraperitoneal injection of cyclophosphamide decreases the sperm count, percentages of grades a + b and a + b + c sperm, and the expression of CatSper1 in mice, while large-dose Yijingfang can increase the above parameters, and hence contributes to the treatment of oligoasthenospermia.	Cyclophosphamide	41-57	cation channel, sperm associated 1	Mus musculus	156-164
20655369-7	2010	While cyclophosphamide showed an elevation of activated P53 in the presence of S9, 7,12-dimethylbenz[a]anthracene and aflatoxin B(1) responded without the MAS.	Cyclophosphamide	6-22	tumor protein p53	Homo sapiens	56-59
20638924-4	2010	CONCLUSION: We introduced new data related to the contribution of p53 codon 72 to toxicity due to 5-fluorouracil and cyclophosphamide-based neoadjuvant chemotherapy in patients with breast cancer.	Cyclophosphamide	117-133	tumor protein p53	Homo sapiens	66-69
20652634-0	2010	Multiple approaches to analyse the data for rat brain acetylcholinesterase inhibition by cyclophosphamide.	Cyclophosphamide	89-105	acetylcholinesterase	Rattus norvegicus	54-74
20405259-2	2010	MRP4 could have an influence on the resistance and transport of the two oxazaphosphorines, cyclophosphamide (CP) and ifosfamide (IF).	Cyclophosphamide	91-107	ATP binding cassette subfamily C member 4	Homo sapiens	0-4
20842604-8	2010	TREATMENT AND COURSE: After 6 cycles of rituximab, cyclophosphamide, doxorubicin, vincristin and prednisolone (R-CHOP), an early relapse developed which was treated with rituximab, ifosphamid, methotrexate and etoposide.	Cyclophosphamide	51-67	DNA damage inducible transcript 3	Homo sapiens	113-117
20830228-1	2010	BACKGROUND/AIMS: Rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone chemotherapy (R-CHOP) has improved survival in patients with diffuse large B-cell lymphoma (DLBCL) and weakened the prognostic power of the international prognostic index (IPI).	Cyclophosphamide	32-48	DNA damage inducible transcript 3	Homo sapiens	107-111
19434371-1	2010	PURPOSE: This was a phase I study evaluating the dose limiting toxicity (DLT) and the maximum tolerated dose (MTD) of weekly docetaxel, doxorubicin and daily oral cyclophosphamide with G-CSF support (ConTAC regimen).	Cyclophosphamide	163-179	colony stimulating factor 3	Homo sapiens	185-190
20417682-0	2010	Human serum butyrylcholinesterase interactions with cisplatin and cyclophosphamide.	Cyclophosphamide	66-82	butyrylcholinesterase	Homo sapiens	12-33
20417682-2	2010	The inhibitory effect of cisplatin (CDDP) and cyclophosphamide (CY) on BChE is characterized.	Cyclophosphamide	46-62	butyrylcholinesterase	Homo sapiens	71-75
20417682-2	2010	The inhibitory effect of cisplatin (CDDP) and cyclophosphamide (CY) on BChE is characterized.	Cyclophosphamide	64-66	butyrylcholinesterase	Homo sapiens	71-75
20417682-9	2010	These results suggest that used in combination therapy, CY and CDDP cause considerable BChE inhibition and may aggravate conditions observed during chemotherapy.	Cyclophosphamide	56-58	butyrylcholinesterase	Homo sapiens	87-91
20484479-11	2010	CONCLUSIONS: In seven patients with type B insulin resistance, standardized treatment with rituximab, cyclophosphamide, and pulse steroids results in remission of the disease.	Cyclophosphamide	102-118	insulin	Homo sapiens	43-50
21246940-3	2010	This study aimed to determine whether the ratio of hepatocyte growth factor (HGF) to transforming growth factor beta 1 (TGF beta1) in lupus nephritis could be a prognostic factor for response to therapy with cyclophosphamide and steroids at six months.	Cyclophosphamide	208-224	hepatocyte growth factor	Homo sapiens	51-75
21246940-3	2010	This study aimed to determine whether the ratio of hepatocyte growth factor (HGF) to transforming growth factor beta 1 (TGF beta1) in lupus nephritis could be a prognostic factor for response to therapy with cyclophosphamide and steroids at six months.	Cyclophosphamide	208-224	hepatocyte growth factor	Homo sapiens	77-80
21246940-3	2010	This study aimed to determine whether the ratio of hepatocyte growth factor (HGF) to transforming growth factor beta 1 (TGF beta1) in lupus nephritis could be a prognostic factor for response to therapy with cyclophosphamide and steroids at six months.	Cyclophosphamide	208-224	transforming growth factor beta 1	Homo sapiens	85-118
21246940-3	2010	This study aimed to determine whether the ratio of hepatocyte growth factor (HGF) to transforming growth factor beta 1 (TGF beta1) in lupus nephritis could be a prognostic factor for response to therapy with cyclophosphamide and steroids at six months.	Cyclophosphamide	208-224	transforming growth factor beta 1	Homo sapiens	120-129
20338811-0	2010	CD4+FOXP3+ regulatory T cell depletion by low-dose cyclophosphamide prevents recurrence in patients with large condylomata acuminata after laser therapy.	Cyclophosphamide	51-67	CD4 molecule	Homo sapiens	0-3
21351585-9	2010	Furthermore, CMTM4 down-expressed remarkably in the gossypol and cyclophosphamide treated rats, the expression of the CMTM4 was up-expressed after testosterone administration.	Cyclophosphamide	65-81	CKLF-like MARVEL transmembrane domain containing 4	Rattus norvegicus	13-18
20498406-2	2010	The aim of this study was to determine the frequency of MYC translocations in DLBCL and their prognostic impact in the era of cyclophosphamide, doxorubicin, vincristine, and prednisone plus rituximab (CHOP-R) therapy.	Cyclophosphamide	126-142	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	56-59
20338811-0	2010	CD4+FOXP3+ regulatory T cell depletion by low-dose cyclophosphamide prevents recurrence in patients with large condylomata acuminata after laser therapy.	Cyclophosphamide	51-67	forkhead box P3	Homo sapiens	4-9
20371502-6	2010	After adjusting for methylprednisolone pulse and/or cyclophosphamide pulse therapy, KIR2DL5 carriers were at significantly greater risk of infectious events overall (adjusted OR = 2.45; 95% CI 1.24, 4.81; P = 0.0095).	Cyclophosphamide	52-68	killer cell immunoglobulin like receptor, two Ig domains and long cytoplasmic tail 5A	Homo sapiens	84-91
20140691-7	2010	It is noticeable that serum IL-18 levels in the patients treated with glucocorticoids and cyclophosphamide was lower than those treated with glucocorticoids only or glucocorticoids and other immune inhibitors such as chloroquine/hydroxychloroquine and azathioprine.	Cyclophosphamide	90-106	interleukin 18	Homo sapiens	28-33
19460060-11	2010	In treatment of ILD, rheumatologists used intravenous (IV) cyclophosphamide more often (CYC) (59% vs 28%, P= 0.003) and more respiratory physicians used oral CYC (44% vs 28%, P= 0.012).	Cyclophosphamide	59-75	cytochrome c, somatic	Homo sapiens	88-91
20299497-9	2010	Quasi-pathological complete response to the docetaxel and cyclophosphamide regimen was associated with low estrogen receptor and progesterone receptor expression and high MIB-1 and topoisomerase IIalpha expression, in univariate analyses, but only with low estrogen receptor expression in multivariate analysis.	Cyclophosphamide	58-74	progesterone receptor	Homo sapiens	129-150
20299497-9	2010	Quasi-pathological complete response to the docetaxel and cyclophosphamide regimen was associated with low estrogen receptor and progesterone receptor expression and high MIB-1 and topoisomerase IIalpha expression, in univariate analyses, but only with low estrogen receptor expression in multivariate analysis.	Cyclophosphamide	58-74	MIB E3 ubiquitin protein ligase 1	Homo sapiens	171-202
20501834-4	2010	In this model, GM-CSF reversed cyclophosphamide-induced leukopenia but also promoted breast cancer and prostate cancer growth in the bone but not in soft tissue sites.	Cyclophosphamide	31-47	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	15-21
21179613-8	2010	Cyclophosphamide and natalizumab could be offered as second-line treatment in patients with a poor response to IFNB or GA.	Cyclophosphamide	0-16	interferon beta 1	Homo sapiens	111-115
20479407-1	2010	PURPOSE: We tested the hypothesis that Akt-Ser473 phosphorylation (pAkt) predicts benefit from the sequential addition of paclitaxel to adjuvant doxorubicin plus cyclophosphamide (AC) chemotherapy in patients with node-positive breast cancer participating in the National Surgical Adjuvant Breast and Bowel Project (NSABP) B-28 trial.	Cyclophosphamide	162-178	AKT serine/threonine kinase 1	Homo sapiens	39-42
20501849-0	2010	Selective depletion of CD4+CD25+Foxp3+ regulatory T cells by low-dose cyclophosphamide is explained by reduced intracellular ATP levels.	Cyclophosphamide	70-86	forkhead box P3	Homo sapiens	32-37
20501849-6	2010	The transfection of miR-142-3p or the blockade of CD39 could increase intracellular ATP levels of Treg cells, consequently decreasing the sensitivity of Treg cells to low-dose CY.	Cyclophosphamide	176-178	ectonucleoside triphosphate diphosphohydrolase 1	Homo sapiens	50-54
20501849-7	2010	On the other hand, the transfection of miR-142-3p inhibitor or the addition of soluble CD39 to the cultured CD4(+)CD25(-) T cells resulted in the decrease of intracellular ATP levels and increase of sensitivity of conventional T cells to low-dose CY.	Cyclophosphamide	247-249	ectonucleoside triphosphate diphosphohydrolase 1	Homo sapiens	87-91
20501849-7	2010	On the other hand, the transfection of miR-142-3p inhibitor or the addition of soluble CD39 to the cultured CD4(+)CD25(-) T cells resulted in the decrease of intracellular ATP levels and increase of sensitivity of conventional T cells to low-dose CY.	Cyclophosphamide	247-249	CD4 molecule	Homo sapiens	108-111
20501849-7	2010	On the other hand, the transfection of miR-142-3p inhibitor or the addition of soluble CD39 to the cultured CD4(+)CD25(-) T cells resulted in the decrease of intracellular ATP levels and increase of sensitivity of conventional T cells to low-dose CY.	Cyclophosphamide	247-249	interleukin 2 receptor subunit alpha	Homo sapiens	114-118
20235190-2	2010	The authors report safety, activity, and angiogenic profiling results with the rituximab and thalidomide plus prednisone, etoposide, procarbazine, and cyclophosphamide (RT-PEPC) regimen in patients with recurrent mantle cell lymphoma (MCL).	Cyclophosphamide	151-167	peptidase C	Homo sapiens	172-176
20610938-1	2010	We report the case of a patient with non-Hodgkin"s lymphoma who, during chemotherapy according to the r-CHOP schedule (rituximab-cyclophosphamide-doxorubicin-vincristine and prednisone), showed a hepatic flare with jaundice.	Cyclophosphamide	129-145	DNA damage inducible transcript 3	Homo sapiens	104-108
20563255-5	2010	Cells bearing the CD44(+) CD24(-) phenotype were reduced by 90% (2.5% to 0.24%) in CPA-treated tumors, whereas cells with aldehyde dehydrogenase activity were reduced by 64% (4.7% to 1.7%).	Cyclophosphamide	83-86	CD44 molecule (Indian blood group)	Homo sapiens	18-22
20563255-5	2010	Cells bearing the CD44(+) CD24(-) phenotype were reduced by 90% (2.5% to 0.24%) in CPA-treated tumors, whereas cells with aldehyde dehydrogenase activity were reduced by 64% (4.7% to 1.7%).	Cyclophosphamide	83-86	CD24 molecule	Homo sapiens	26-30
20482803-0	2010	Assessment of fertility protection and ovarian reserve with GnRH antagonist in rats undergoing chemotherapy with cyclophosphamide.	Cyclophosphamide	113-129	gonadotropin releasing hormone 1	Rattus norvegicus	60-64
20202729-0	2010	Pulse cyclophosphamide therapy and clinical remission in atypical hemolytic uremic syndrome with anti-complement factor H autoantibodies.	Cyclophosphamide	6-22	complement factor H	Homo sapiens	113-121
20202729-1	2010	We report 3 children with atypical hemolytic uremic syndrome associated with anti-complement factor H (CFH) autoantibodies who presented with sustained remission with low antibody titers and normal kidney function after plasma exchanges (PEs) and cyclophosphamide pulses.	Cyclophosphamide	247-263	complement factor H	Homo sapiens	77-101
20202729-1	2010	We report 3 children with atypical hemolytic uremic syndrome associated with anti-complement factor H (CFH) autoantibodies who presented with sustained remission with low antibody titers and normal kidney function after plasma exchanges (PEs) and cyclophosphamide pulses.	Cyclophosphamide	247-263	complement factor H	Homo sapiens	103-106
20207185-0	2010	Vascular endothelial growth factor in the early stage of skin incision wounds in cyclophosphamide-induced leukocytopenic rats.	Cyclophosphamide	81-97	vascular endothelial growth factor A	Rattus norvegicus	0-34
20007128-1	2010	BACKGROUND: Cyclophosphamide is an alkylating agent and was traditionally known to potentiate the renal action of vasopressin.	Cyclophosphamide	12-28	arginine vasopressin	Homo sapiens	114-125
20568461-1	2010	OBJECTIVE: To compare the methods for developing immune-suppressed mice models induced by cyclophosphamide (CTX) with different dosages and ways.	Cyclophosphamide	90-106	V-set and immunoglobulin domain containing 2	Mus musculus	108-111
21150336-0	2010	Probucol attenuates cyclophosphamide-induced oxidative apoptosis, p53 and Bax signal expression in rat cardiac tissues.	Cyclophosphamide	20-36	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	66-69
21150336-0	2010	Probucol attenuates cyclophosphamide-induced oxidative apoptosis, p53 and Bax signal expression in rat cardiac tissues.	Cyclophosphamide	20-36	BCL2 associated X, apoptosis regulator	Rattus norvegicus	74-77
20096776-1	2010	The chemotherapeutic agents used to treat non-Hodgkin lymphoma, cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP), have adverse effects on male reproductive function and progeny outcome.	Cyclophosphamide	64-80	DNA-damage inducible transcript 3	Rattus norvegicus	124-128
20219715-1	2010	A human prostate cancer (PC3) xenograft model was established which reflects acquired in vivo resistance towards metronomic cyclophosphamide (CPA) treatment.	Cyclophosphamide	124-140	chromobox 8	Homo sapiens	25-28
20219715-1	2010	A human prostate cancer (PC3) xenograft model was established which reflects acquired in vivo resistance towards metronomic cyclophosphamide (CPA) treatment.	Cyclophosphamide	142-145	chromobox 8	Homo sapiens	25-28
20219715-5	2010	Thioredoxin containing protein 5 was up-regulated in resistant xenografts only upon in vivo CPA therapy.	Cyclophosphamide	92-95	thioredoxin	Homo sapiens	0-11
20219715-7	2010	Annexin A3 (ANXA3) presents a very interesting candidate which was found to be up-regulated both in vitro and in xenografts, with protein levels further increased by metronomic CPA treatment in vivo.	Cyclophosphamide	177-180	annexin A3	Homo sapiens	0-10
20219715-7	2010	Annexin A3 (ANXA3) presents a very interesting candidate which was found to be up-regulated both in vitro and in xenografts, with protein levels further increased by metronomic CPA treatment in vivo.	Cyclophosphamide	177-180	annexin A3	Homo sapiens	12-17
19850640-2	2010	cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) is recognized as the standard chemotherapy regimen and the addition of rituximab to B-cell subtypes has been shown to significantly improve treatment outcomes.	Cyclophosphamide	0-16	DNA damage inducible transcript 3	Homo sapiens	59-63
19861575-1	2010	BACKGROUND: The addition of rituximab to CHOP (R-CHOP; CHOP, cyclophosphamide, doxorubicin, vincristine, and prednisone) chemotherapy improves outcome in patients with diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	61-77	DNA damage inducible transcript 3	Homo sapiens	41-45
20433640-0	2010	Effect of melatonin on the expression of Nrf2 and NF-kappaB during cyclophosphamide-induced urinary bladder injury in rat.	Cyclophosphamide	67-83	NFE2 like bZIP transcription factor 2	Rattus norvegicus	41-45
20501849-0	2010	Selective depletion of CD4+CD25+Foxp3+ regulatory T cells by low-dose cyclophosphamide is explained by reduced intracellular ATP levels.	Cyclophosphamide	70-86	CD4 molecule	Homo sapiens	23-26
20501849-0	2010	Selective depletion of CD4+CD25+Foxp3+ regulatory T cells by low-dose cyclophosphamide is explained by reduced intracellular ATP levels.	Cyclophosphamide	70-86	interleukin 2 receptor subunit alpha	Homo sapiens	27-31
19377876-9	2010	Additionally, splenic myeloid cells Gr1(+)/CD11b(+) associated with a suppressor phenotype were significantly reduced in F3II tumor-bearing mice immunized with 1E10 mAb alone or in combination with low-dose Cyclophosphamide.	Cyclophosphamide	207-223	integrin alpha M	Mus musculus	43-48
20371444-2	2010	PATIENTS AND METHODS: We retrospectively analyzed 46 patients all treated with standard chemotherapy ([CHOP] cyclophosphamide/doxorubicin/vincristine/prednisone-like); of these, 16 received rituximab.	Cyclophosphamide	109-125	DNA damage inducible transcript 3	Homo sapiens	103-107
19659514-3	2010	We describe a case of a patient with alpha-1-antitrypsin deficiency who underwent single lung transplantation in 2005 and was maintained on tacrolimus, cytoxan and prednisone.	Cyclophosphamide	152-159	serpin family A member 1	Homo sapiens	37-56
19711345-3	2010	In this study, immunohistochemical expression of MIB1 was studied in a well-characterised series of early (Stages I and II) node-negative breast carcinoma cases (n = 100) with long-term follow-up that have received adjuvant chemotherapy (cyclophosphamide/methotrexate/5-fluorouracil regimen).	Cyclophosphamide	238-254	MIB E3 ubiquitin protein ligase 1	Homo sapiens	49-53
20198460-1	2010	The addition of rituximab to cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) improved the outcome of patients with diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	29-45	DNA damage inducible transcript 3	Homo sapiens	88-92
20032115-0	2010	Expression and function of CXCL12/CXCR4 in rat urinary bladder with cyclophosphamide-induced cystitis.	Cyclophosphamide	68-84	C-X-C motif chemokine ligand 12	Rattus norvegicus	27-33
20032115-0	2010	Expression and function of CXCL12/CXCR4 in rat urinary bladder with cyclophosphamide-induced cystitis.	Cyclophosphamide	68-84	C-X-C motif chemokine receptor 4	Rattus norvegicus	34-39
19653275-5	2010	NSPC were then coinjected into mouse brain with GBM cells, employing NSPC expressing cyclophosphamide (CPA)-activating enzyme cytochrome p450 2B6 (CYP2B6), which catalyzes CPA prodrug transformation into membrane diffusible DNA-alkylating metabolites.	Cyclophosphamide	85-101	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	147-153
20214520-1	2010	For more than 25 years, the combination of cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) was considered the "gold standard" for the treatment of aggressive lymphomas, 90% of which are diffuse large B-cell lymphomas (DLBCLs).	Cyclophosphamide	43-59	DNA damage inducible transcript 3	Homo sapiens	102-106
19464751-0	2010	High-dose cyclophosphamide-mediated anti-tumor effects by the superior expansion of CD44(high) cells after their selective depletion.	Cyclophosphamide	10-26	CD44 antigen	Mus musculus	84-88
19464751-1	2010	As alkylating agents, cyclophosphamides (CTX) are used to treat various cancers and, ironically, to boost immune responses.	Cyclophosphamide	22-39	V-set and immunoglobulin domain containing 2	Mus musculus	41-44
19653275-5	2010	NSPC were then coinjected into mouse brain with GBM cells, employing NSPC expressing cyclophosphamide (CPA)-activating enzyme cytochrome p450 2B6 (CYP2B6), which catalyzes CPA prodrug transformation into membrane diffusible DNA-alkylating metabolites.	Cyclophosphamide	103-106	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	147-153
19653275-5	2010	NSPC were then coinjected into mouse brain with GBM cells, employing NSPC expressing cyclophosphamide (CPA)-activating enzyme cytochrome p450 2B6 (CYP2B6), which catalyzes CPA prodrug transformation into membrane diffusible DNA-alkylating metabolites.	Cyclophosphamide	172-175	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	147-153
19653275-6	2010	Upon CPA administration, NSPC containing CYP2B6 elicited substantial impairment of tumor growth.	Cyclophosphamide	5-8	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	41-47
19637093-0	2010	Cyclophosphamide reduces dectin-1 expression in the lungs of naive and Aspergillus fumigatus-infected mice.	Cyclophosphamide	0-16	C-type lectin domain family 7, member a	Mus musculus	25-33
20195409-0	2010	Severe pulmonary adverse effects in lymphoma patients treated with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) regimen plus rituximab.	Cyclophosphamide	67-83	DNA damage inducible transcript 3	Homo sapiens	127-131
20195409-1	2010	BACKGROUND/AIMS: The aim of our study was to determine the incidence and clinical features of severe pulmonary complications in patients receiving cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) or rituximab plus CHOP (R-CHOP) as the initial treatment for lymphoma.	Cyclophosphamide	147-163	DNA damage inducible transcript 3	Homo sapiens	207-211
20195409-1	2010	BACKGROUND/AIMS: The aim of our study was to determine the incidence and clinical features of severe pulmonary complications in patients receiving cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) or rituximab plus CHOP (R-CHOP) as the initial treatment for lymphoma.	Cyclophosphamide	147-163	DNA damage inducible transcript 3	Homo sapiens	237-243
19637093-4	2010	Therefore, we tested whether cyclophosphamide treatment could cause alterations in dectin-1 expression in the lung, which could contribute to invasive pulmonary Aspergillus infections in patients.	Cyclophosphamide	29-45	C-type lectin domain family 7, member a	Mus musculus	83-91
19637093-8	2010	Infected mice treated with cyclophosphamide showed decreased levels of dectin-1 and a higher fungal burden in the lung than the infected mice without cyclophosphamide treatment.	Cyclophosphamide	27-43	C-type lectin domain family 7, member a	Mus musculus	71-79
19637093-9	2010	These results suggest that dectin-1 is involved in host defense against A. fumigatus infection and that suppression of dectin-1 expression caused by cyclophosphamide may contribute to susceptibility to infections caused by this fungus in the immunocompromised host.	Cyclophosphamide	149-165	C-type lectin domain family 7, member a	Mus musculus	119-127
20048181-4	2010	PATIENTS AND METHODS We studied the immunohistochemical protein expression of HIF-1alpha on tissue microarrays from 153 patients with DLBCL treated in sequential cohorts with cyclophosphamide, doxorubicin, oncovin, and prednisone (CHOP) or rituximab-CHOP (R-CHOP) from 1999 to 2002.	Cyclophosphamide	175-191	hypoxia inducible factor 1 subunit alpha	Homo sapiens	78-88
20060418-9	2010	The combination decreased the damage of CPA, such as damaged nuclear DNA, early apoptotic morphological changes, Bax and P53 expressions on embryo brains and in vivo.	Cyclophosphamide	40-43	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	121-124
20083664-0	2010	Cyclophosphamide induces dynamic alterations in the host microenvironments resulting in a Flt3 ligand-dependent expansion of dendritic cells.	Cyclophosphamide	0-16	fms related receptor tyrosine kinase 3	Homo sapiens	90-94
20083664-3	2010	In a recent study, we observed a significant increase in the circulating levels of dendritic cells (DCs; CD11c(+)CD11b(+)) during the recovery from cyclophosphamide (CTX)-induced lymphodepletion.	Cyclophosphamide	148-164	integrin subunit alpha X	Homo sapiens	105-110
20083664-3	2010	In a recent study, we observed a significant increase in the circulating levels of dendritic cells (DCs; CD11c(+)CD11b(+)) during the recovery from cyclophosphamide (CTX)-induced lymphodepletion.	Cyclophosphamide	148-164	integrin subunit alpha M	Homo sapiens	113-118
20083664-3	2010	In a recent study, we observed a significant increase in the circulating levels of dendritic cells (DCs; CD11c(+)CD11b(+)) during the recovery from cyclophosphamide (CTX)-induced lymphodepletion.	Cyclophosphamide	148-164	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	166-169
20040700-9	2010	Cyclophosphamide and vincristine are metabolized via the CYP3A4 isoenzyme.	Cyclophosphamide	0-16	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	57-63
20145127-8	2010	Reducing IGF-I/IGF-I signaling protected primary glia, but not glioma cells, against cyclophosphamide and protected mouse embryonic fibroblasts against doxorubicin.	Cyclophosphamide	85-101	insulin-like growth factor 1	Mus musculus	9-14
20145127-8	2010	Reducing IGF-I/IGF-I signaling protected primary glia, but not glioma cells, against cyclophosphamide and protected mouse embryonic fibroblasts against doxorubicin.	Cyclophosphamide	85-101	insulin-like growth factor 1	Mus musculus	15-20
20133257-8	2010	CONCLUSION: Sequential administration of preoperative doxorubicin and cyclophosphamide followed by a taxane and trastuzumab combination is safe in women with primary operable HER2+ breast cancer and is associated with a high pCR rate.	Cyclophosphamide	70-86	erb-b2 receptor tyrosine kinase 2	Homo sapiens	175-179
20332474-7	2010	This report suggests that combination therapy with epirubicin and cyclophosphamide followed by trastuzumab and paclitaxel was useful for HER2-positive IBC.	Cyclophosphamide	66-82	erb-b2 receptor tyrosine kinase 2	Homo sapiens	137-141
19895616-0	2010	Circulating CD52 and CD20 levels at end of treatment predict for progression and survival in patients with chronic lymphocytic leukaemia treated with fludarabine, cyclophosphamide and rituximab (FCR).	Cyclophosphamide	163-179	CD52 molecule	Homo sapiens	12-16
19526361-0	2010	Sequential administration of dose-dense epirubicin/cyclophosphamide followed by docetaxel/capecitabine for patients with HER2-negative and locally advanced or node-positive breast cancer.	Cyclophosphamide	51-67	erb-b2 receptor tyrosine kinase 2	Homo sapiens	121-125
20208453-5	2010	As results of CPA treatment, dramatical decreases of the CD3+, CD4+, CD8+ and TNF-alpha+ cells were detected in thymus and spleen with decreases of thymus and spleen weights.	Cyclophosphamide	14-17	tumor necrosis factor	Mus musculus	78-87
19946662-7	2010	Administration of one dose of IL2-cas decreased the incidence of diabetes in NOD mice, showing a superior beneficial effect when administered at young age, and effectively blocked induction of hyperglycaemia by cyclophosphamide, reducing the severity of islet inflammation.	Cyclophosphamide	211-227	interleukin 2	Mus musculus	30-33
20047504-4	2010	The study by Wada and colleagues employed an autochthonous prostate cancer mouse model to demonstrate that low-dose cyclophosphamide given prior to a cell-based GM-CSF-secreting vaccine (T-GVAX) abrogated immune tolerance, augmented prostatic CD8(+) T-cell infiltration, mediated depletion of regulatory T cells (Tregs), and increased expression of dendritic cell maturation markers.	Cyclophosphamide	116-132	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	161-167
20139774-0	2010	Low-dose cyclophosphamide treatment impairs regulatory T cells and unmasks AFP-specific CD4+ T-cell responses in patients with advanced HCC.	Cyclophosphamide	9-25	alpha fetoprotein	Homo sapiens	75-78
20139774-0	2010	Low-dose cyclophosphamide treatment impairs regulatory T cells and unmasks AFP-specific CD4+ T-cell responses in patients with advanced HCC.	Cyclophosphamide	9-25	CD4 molecule	Homo sapiens	88-91
20022034-2	2010	Studies show that PACAP has a role in detrusor smooth muscle contraction to facilitate adenosine triphosphate release from urothelium and PACAP antagonism decreases cyclophosphamide induced bladder hyperreflexia.	Cyclophosphamide	165-181	adenylate cyclase activating polypeptide 1	Mus musculus	138-143
20039429-6	2010	Levels of complement C3, C4, and CH50 and titers of anti-double-stranded DNA antibodies were normalized after treatment with either mycophenolate mofetil or intravenous cyclophosphamide.	Cyclophosphamide	169-185	complement C3	Homo sapiens	10-23
19963133-2	2010	This study was performed to evaluate the effect of polymorphisms and haplotypes of the XRCC1 gene on the risk of diffuse large B-cell lymphoma (DLBCL) and treatment outcomes after rituximab plus cyclophosphamide/doxorubicin/vincristine/prednisone (R-CHOP) chemotherapy in a Korean population.	Cyclophosphamide	195-211	X-ray repair cross complementing 1	Homo sapiens	87-92
20206921-0	2010	Consecutive low doses of cyclophosphamide preferentially target Tregs and potentiate T cell responses induced by DNA PLG microparticle immunization.	Cyclophosphamide	25-41	plasminogen	Homo sapiens	117-120
20206921-3	2010	We investigated cyclophosphamide dosing in combination with ZYC300, a PLG-encapsulated plasmid DNA vaccine which encodes the cytochrome P450 family member, CYP1B1, a known human tumor-associated antigen.	Cyclophosphamide	16-32	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	156-162
20124494-0	2010	Initial insights regarding the role of p53 in maintaining sperm DNA integrity following treatment of mice with ethylnitrosourea or cyclophosphamide.	Cyclophosphamide	131-147	transformation related protein 53, pseudogene	Mus musculus	39-42
19590872-2	2010	We observed that Cy administration resulted in expansion of tumor antigen-specific T cells and transient depletion of CD4(+)Foxp3(+) regulatory T cells (Tregs).	Cyclophosphamide	17-19	CD4 molecule	Homo sapiens	118-121
19962321-2	2010	The cytokine interleukin-21 (IL-21) is known to enhance immune function, and in this study we have investigated its ability to boost the efficacy of chemoimmunotherapy-cyclophosphamide and adoptive cell transfer (ACT)-in the B16-OVA/OT-I murine model of malignant melanoma.	Cyclophosphamide	168-184	interleukin 21	Mus musculus	13-27
19962321-2	2010	The cytokine interleukin-21 (IL-21) is known to enhance immune function, and in this study we have investigated its ability to boost the efficacy of chemoimmunotherapy-cyclophosphamide and adoptive cell transfer (ACT)-in the B16-OVA/OT-I murine model of malignant melanoma.	Cyclophosphamide	168-184	interleukin 21	Mus musculus	29-34
19857547-3	2010	With the growing number of associated molecules found to form functional complexes with CD44, we analyzed a larger cohort of cyclophosphamide, doxorubicin, vincristine, prednisone, and equivalently treated DLBCL patients to define the prognostic role of such CD44-associated molecules.	Cyclophosphamide	125-141	CD44 molecule (Indian blood group)	Homo sapiens	88-92
19857547-10	2010	CONCLUSION: Evaluation of CD44v-RHAMM coexpression may improve the accuracy of DLBCL prognosis and identify a subgroup of patients who will benefit from therapeutic alternatives to cyclophosphamide, doxorubicin, vincristine, and prednisone.	Cyclophosphamide	181-197	hyaluronan mediated motility receptor	Homo sapiens	32-37
20133977-3	2010	injected recombinant human granulocyte colony-stimulating factor (G-CSF/filgrastim) was tested in cyclophosphamide (CY)-conditioned mice.	Cyclophosphamide	98-114	colony stimulating factor 3	Homo sapiens	27-64
20133977-3	2010	injected recombinant human granulocyte colony-stimulating factor (G-CSF/filgrastim) was tested in cyclophosphamide (CY)-conditioned mice.	Cyclophosphamide	116-118	colony stimulating factor 3	Homo sapiens	27-64
20663416-4	2010	Cyclophosphamide has selective effects on the immune response, including the suppression of Th1/Th17 responses and the enhancement of cells secreting anti-inflammatory cytokines such as interleukin (IL) IL-4, IL-10 and TGF-b.	Cyclophosphamide	0-16	negative elongation factor complex member C/D	Homo sapiens	92-95
20663416-4	2010	Cyclophosphamide has selective effects on the immune response, including the suppression of Th1/Th17 responses and the enhancement of cells secreting anti-inflammatory cytokines such as interleukin (IL) IL-4, IL-10 and TGF-b.	Cyclophosphamide	0-16	interleukin 10	Homo sapiens	209-214
20663416-4	2010	Cyclophosphamide has selective effects on the immune response, including the suppression of Th1/Th17 responses and the enhancement of cells secreting anti-inflammatory cytokines such as interleukin (IL) IL-4, IL-10 and TGF-b.	Cyclophosphamide	0-16	transforming growth factor beta 1	Homo sapiens	219-224
20663416-7	2010	Cyclophosphamide is used in relapsing or actively progressive MS as second-line therapy in patients unresponsive to interferon beta or glatiramer acetate who are not candidates for natalizumab.	Cyclophosphamide	0-16	interferon beta 1	Homo sapiens	116-131
19911397-0	2010	R-roscovitine (Seliciclib) affects CLL cells more strongly than combinations of fludarabine or cladribine with cyclophosphamide: Inhibition of CDK7 sensitizes leukemic cells to caspase-dependent apoptosis.	Cyclophosphamide	111-127	cyclin dependent kinase 7	Homo sapiens	143-147
20117996-1	2010	OBJECTIVE: To study the effects of gonadotroph-releasing hormone (GnRH) agonist (GnRH-a) and GnRH antagonist (GnRH-ant) on cyclophosphamide (CTX)-induced follicle apoptosis in female rats.	Cyclophosphamide	123-139	gonadotropin releasing hormone 1	Rattus norvegicus	35-64
20228131-0	2010	Cyclophosphamide dose intensification may circumvent anthracycline resistance of p53 mutant breast cancers.	Cyclophosphamide	0-16	tumor protein p53	Homo sapiens	81-84
20228131-7	2010	A sharp statistical interaction was detected between p53 status and cyclophosphamide dose intensity.	Cyclophosphamide	68-84	tumor protein p53	Homo sapiens	53-56
20939436-10	2010	The increase of tumor-induced IL-10 levels was reverted by the treatment with Cy.	Cyclophosphamide	78-80	interleukin 10	Rattus norvegicus	30-35
20228131-10	2010	Thus, our data strongly suggest that cyclophosphamide dose intensification in ER(-) p53-mutated breast cancer patients could significantly improve their response.	Cyclophosphamide	37-53	estrogen receptor 1	Homo sapiens	78-80
20228131-10	2010	Thus, our data strongly suggest that cyclophosphamide dose intensification in ER(-) p53-mutated breast cancer patients could significantly improve their response.	Cyclophosphamide	37-53	tumor protein p53	Homo sapiens	84-87
19861704-1	2010	The aim of the current study was to examine the effects of gonadotropin-releasing hormone agonist (GnRH-a) and antagonist (GnRH-ant) on the expression of GnRH receptor-I (GnRHR-I) in pituitary and ovaries in cyclophosphamide (CTX) chemotherapeutic rats and to investigate the possible mechanism of interventions of GnRH-a and GnRH-ant in CTX-induced ovarian damage.	Cyclophosphamide	208-224	gonadotropin releasing hormone 1	Rattus norvegicus	59-89
19861704-1	2010	The aim of the current study was to examine the effects of gonadotropin-releasing hormone agonist (GnRH-a) and antagonist (GnRH-ant) on the expression of GnRH receptor-I (GnRHR-I) in pituitary and ovaries in cyclophosphamide (CTX) chemotherapeutic rats and to investigate the possible mechanism of interventions of GnRH-a and GnRH-ant in CTX-induced ovarian damage.	Cyclophosphamide	208-224	gonadotropin releasing hormone 1	Rattus norvegicus	99-105
19861704-1	2010	The aim of the current study was to examine the effects of gonadotropin-releasing hormone agonist (GnRH-a) and antagonist (GnRH-ant) on the expression of GnRH receptor-I (GnRHR-I) in pituitary and ovaries in cyclophosphamide (CTX) chemotherapeutic rats and to investigate the possible mechanism of interventions of GnRH-a and GnRH-ant in CTX-induced ovarian damage.	Cyclophosphamide	208-224	gonadotropin releasing hormone 1	Rattus norvegicus	99-103
19861704-1	2010	The aim of the current study was to examine the effects of gonadotropin-releasing hormone agonist (GnRH-a) and antagonist (GnRH-ant) on the expression of GnRH receptor-I (GnRHR-I) in pituitary and ovaries in cyclophosphamide (CTX) chemotherapeutic rats and to investigate the possible mechanism of interventions of GnRH-a and GnRH-ant in CTX-induced ovarian damage.	Cyclophosphamide	208-224	gonadotropin releasing hormone 1	Rattus norvegicus	123-127
19861704-1	2010	The aim of the current study was to examine the effects of gonadotropin-releasing hormone agonist (GnRH-a) and antagonist (GnRH-ant) on the expression of GnRH receptor-I (GnRHR-I) in pituitary and ovaries in cyclophosphamide (CTX) chemotherapeutic rats and to investigate the possible mechanism of interventions of GnRH-a and GnRH-ant in CTX-induced ovarian damage.	Cyclophosphamide	208-224	gonadotropin releasing hormone receptor	Rattus norvegicus	171-176
19861704-1	2010	The aim of the current study was to examine the effects of gonadotropin-releasing hormone agonist (GnRH-a) and antagonist (GnRH-ant) on the expression of GnRH receptor-I (GnRHR-I) in pituitary and ovaries in cyclophosphamide (CTX) chemotherapeutic rats and to investigate the possible mechanism of interventions of GnRH-a and GnRH-ant in CTX-induced ovarian damage.	Cyclophosphamide	208-224	gonadotropin releasing hormone 1	Rattus norvegicus	123-129
19861704-1	2010	The aim of the current study was to examine the effects of gonadotropin-releasing hormone agonist (GnRH-a) and antagonist (GnRH-ant) on the expression of GnRH receptor-I (GnRHR-I) in pituitary and ovaries in cyclophosphamide (CTX) chemotherapeutic rats and to investigate the possible mechanism of interventions of GnRH-a and GnRH-ant in CTX-induced ovarian damage.	Cyclophosphamide	208-224	gonadotropin releasing hormone 1	Rattus norvegicus	123-127
19745604-3	2009	In this study, the expression of 4-1BB and 4-1BBL was examined during regeneration of the murine thymus following acute cyclophosphamide- induced involution.	Cyclophosphamide	120-136	tumor necrosis factor receptor superfamily, member 9	Mus musculus	33-49
21794679-1	2010	Male with diagnosis of Wegener"s granulomatosis associated to anti-proteinase 3 antibodies that improved initially to the treatment with high dose glucocorticoids and ciclophosphamide, but in a relapse he did not have good response to glucocorticoid treatment, ciclophosphamide, methotrexate nor azathioprine.	Cyclophosphamide	167-183	proteinase 3	Homo sapiens	67-79
21794679-1	2010	Male with diagnosis of Wegener"s granulomatosis associated to anti-proteinase 3 antibodies that improved initially to the treatment with high dose glucocorticoids and ciclophosphamide, but in a relapse he did not have good response to glucocorticoid treatment, ciclophosphamide, methotrexate nor azathioprine.	Cyclophosphamide	261-277	proteinase 3	Homo sapiens	67-79
21048851-5	2010	Studies conducted in our laboratory revealed that the primitive Sca-1(+) BM-HSCs (bone marrow hematopoietic stem cell) are significantly affected in experimental Aplastic animals pretreated with chemotherapeutic drugs (Busulfan and Cyclophosphamide) and there is increased Caspase-3 activity with consecutive high Annexin-V positivity leading to premature apoptosis in the bone marrow hematopoietic stem cell population in Aplastic condition.	Cyclophosphamide	232-248	caspase 3	Mus musculus	64-69
20302754-12	2010	Ten patients received adjuvant chemotherapy with the regimen of CHOP (cyclophosphamide + epirubicin + vincristine + prednisone) after the operation.	Cyclophosphamide	70-86	DNA damage inducible transcript 3	Homo sapiens	64-68
19340428-0	2009	IGHV gene mutational status and LPL/ADAM29 gene expression as clinical outcome predictors in CLL patients in remission following treatment with oral fludarabine plus cyclophosphamide.	Cyclophosphamide	166-182	immunoglobulin heavy variable 3-69-1 (pseudogene)	Homo sapiens	0-4
19805669-8	2009	HER2-specific delayed-type hypersensitivity developed in most patients who received vaccine alone or with 200 mg/m(2) CY.	Cyclophosphamide	118-120	erb-b2 receptor tyrosine kinase 2	Homo sapiens	0-4
19805669-9	2009	HER2-specific antibody responses were enhanced by 200 mg/m(2) CY and 35 mg/m(2) DOX, but higher CY doses suppressed immunity.	Cyclophosphamide	62-64	erb-b2 receptor tyrosine kinase 2	Homo sapiens	0-4
19805669-9	2009	HER2-specific antibody responses were enhanced by 200 mg/m(2) CY and 35 mg/m(2) DOX, but higher CY doses suppressed immunity.	Cyclophosphamide	96-98	erb-b2 receptor tyrosine kinase 2	Homo sapiens	0-4
19805669-11	2009	CONCLUSION: First, immunotherapy with an allogeneic, HER2-positive, GM-CSF-secreting breast tumor vaccine alone or with CY and DOX is safe and induces HER2-specific immunity in patients with metastatic breast cancer.	Cyclophosphamide	120-122	erb-b2 receptor tyrosine kinase 2	Homo sapiens	151-155
19340428-0	2009	IGHV gene mutational status and LPL/ADAM29 gene expression as clinical outcome predictors in CLL patients in remission following treatment with oral fludarabine plus cyclophosphamide.	Cyclophosphamide	166-182	lipoprotein lipase	Homo sapiens	32-35
19340428-10	2009	Our results support the use of LPL and ADAM29 gene expression associated to IGHV mutational status for predicting the clinical outcome of patients treated by oral fludarabine + cyclophosphamide and could be considered for treatment strategies.	Cyclophosphamide	177-193	lipoprotein lipase	Homo sapiens	31-34
19340428-10	2009	Our results support the use of LPL and ADAM29 gene expression associated to IGHV mutational status for predicting the clinical outcome of patients treated by oral fludarabine + cyclophosphamide and could be considered for treatment strategies.	Cyclophosphamide	177-193	ADAM metallopeptidase domain 29	Homo sapiens	39-45
19340428-10	2009	Our results support the use of LPL and ADAM29 gene expression associated to IGHV mutational status for predicting the clinical outcome of patients treated by oral fludarabine + cyclophosphamide and could be considered for treatment strategies.	Cyclophosphamide	177-193	immunoglobulin heavy variable 3-69-1 (pseudogene)	Homo sapiens	76-80
19841877-8	2009	In addition, DAC treatment in vivo was effective in improving the clinical course of diabetes in cyclophosphamide (CY)-potentiated non-obese diabetic mice (CY-NOD).	Cyclophosphamide	97-113	dachshund family transcription factor 1	Mus musculus	13-16
19780759-11	2009	Also, we predicted that G-CSF administration 48 h after cyclophosphamide would be superior to its administration after 2 or 24 h, for both derivatives.	Cyclophosphamide	56-72	colony stimulating factor 3	Rattus norvegicus	24-29
19747716-7	2009	We found that the sensitivity to other genotoxic agents such as cyclophosphamide, doxorubicine and etoposide was also increased by down-regulation of MUC16.	Cyclophosphamide	64-80	mucin 16, cell surface associated	Homo sapiens	150-155
19841877-8	2009	In addition, DAC treatment in vivo was effective in improving the clinical course of diabetes in cyclophosphamide (CY)-potentiated non-obese diabetic mice (CY-NOD).	Cyclophosphamide	115-117	dachshund family transcription factor 1	Mus musculus	13-16
20016232-2	2009	Conventional chemotherapy (CHOP: cyclophosphamide, doxorubicin, vincristine, prednisone) seems unsatisfactory, so modifications of CHOP are used to improve the efficacy.	Cyclophosphamide	33-49	DNA damage inducible transcript 3	Homo sapiens	27-31
19860620-1	2009	The prognostic significance of O6-methylguanine DNA methyltransferase (MGMT) inactivation was evaluated in patients with diffuse large B-cell lymphoma (DLBCL) who received cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) in addition to rituximab.	Cyclophosphamide	172-188	O-6-methylguanine-DNA methyltransferase	Homo sapiens	31-69
19860620-1	2009	The prognostic significance of O6-methylguanine DNA methyltransferase (MGMT) inactivation was evaluated in patients with diffuse large B-cell lymphoma (DLBCL) who received cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) in addition to rituximab.	Cyclophosphamide	172-188	O-6-methylguanine-DNA methyltransferase	Homo sapiens	71-75
20016232-2	2009	Conventional chemotherapy (CHOP: cyclophosphamide, doxorubicin, vincristine, prednisone) seems unsatisfactory, so modifications of CHOP are used to improve the efficacy.	Cyclophosphamide	33-49	DNA damage inducible transcript 3	Homo sapiens	131-135
19861288-1	2009	Treatment with cyclophosphamide, doxorubicin, vincristine and prednisolone (CHOP) has been considered as the standard therapy for diffuse large B-cell lymphoma (DLBCL) for more than 20 years.	Cyclophosphamide	15-31	DNA damage inducible transcript 3	Homo sapiens	76-80
19666069-0	2009	Involvement of orexin-A on micturition reflex in normal and cyclophosphamide-induced cystitis bladder in rat.	Cyclophosphamide	60-76	hypocretin neuropeptide precursor	Rattus norvegicus	15-23
19638304-2	2009	ERK1/2 activation with cyclophosphamide (CYP)-induced cystitis has been demonstrated in urinary bladder and inhibitors of ERK1/2 phosphorylation reduce CYP-induced bladder hyperreflexia.	Cyclophosphamide	23-39	mitogen activated protein kinase 3	Rattus norvegicus	0-6
19638304-2	2009	ERK1/2 activation with cyclophosphamide (CYP)-induced cystitis has been demonstrated in urinary bladder and inhibitors of ERK1/2 phosphorylation reduce CYP-induced bladder hyperreflexia.	Cyclophosphamide	23-39	mitogen activated protein kinase 3	Rattus norvegicus	122-128
19839010-7	2009	Low-dose cyclophosphamide treatment could restore the T-cell responses lost after high-dose gp96 adjuvant injection by suppression of Treg activation.	Cyclophosphamide	9-25	heat shock protein 90 beta family member 1	Homo sapiens	92-96
19731257-3	2009	The dependence of p53-mediated chemosensitivity on pRb status was first investigated in a prospective study on the prognostic relevance of p53 in breast cancer patients treated with adjuvant chemotherapy (5-fluorouracil, methotrexate and cyclophosphamide).	Cyclophosphamide	238-254	tumor protein p53	Homo sapiens	18-21
19731257-3	2009	The dependence of p53-mediated chemosensitivity on pRb status was first investigated in a prospective study on the prognostic relevance of p53 in breast cancer patients treated with adjuvant chemotherapy (5-fluorouracil, methotrexate and cyclophosphamide).	Cyclophosphamide	238-254	RB transcriptional corepressor 1	Homo sapiens	51-54
19696094-3	2009	Herein, we tested the hypothesis that glutathione S-transferase P (GSTP), the GST isoform that displays high catalytic efficiency with acrolein, protects against CY-induced urotoxicity by detoxifying acrolein.	Cyclophosphamide	162-164	glutathione S-transferase pi 1	Homo sapiens	67-71
19696094-4	2009	Treatment of wild-type (WT) and mGstP1/P2 null (GSTP-null) mice with CY caused hemorrhagic cystitis, edema, albumin extravasation, and sloughing of bladder epithelium; however, CY-induced bladder ulcerations of the lamina propria were more numerous and more severe in GSTP-null mice.	Cyclophosphamide	69-71	glutathione S-transferase, pi 1	Mus musculus	32-41
19696094-4	2009	Treatment of wild-type (WT) and mGstP1/P2 null (GSTP-null) mice with CY caused hemorrhagic cystitis, edema, albumin extravasation, and sloughing of bladder epithelium; however, CY-induced bladder ulcerations of the lamina propria were more numerous and more severe in GSTP-null mice.	Cyclophosphamide	69-71	glutathione S-transferase pi 1	Homo sapiens	48-52
19696094-4	2009	Treatment of wild-type (WT) and mGstP1/P2 null (GSTP-null) mice with CY caused hemorrhagic cystitis, edema, albumin extravasation, and sloughing of bladder epithelium; however, CY-induced bladder ulcerations of the lamina propria were more numerous and more severe in GSTP-null mice.	Cyclophosphamide	69-71	glutathione S-transferase pi 1	Homo sapiens	268-272
19696094-5	2009	CY treatment also led to greater accumulation of myeloperoxidase-positive cells and specific protein-acrolein adducts in the bladder of GSTP-null than WT mice.	Cyclophosphamide	0-2	glutathione S-transferase pi 1	Homo sapiens	136-140
19696094-6	2009	There was no difference in hepatic microsomal production of acrolein from CY or urinary hydroxypropyl mercapturic acid output between WT and GSTP-null mice, but CY induced greater c-Jun NH(2)-terminal kinase (JNK) and c-Jun, but not extracellular signal-regulated kinase or p38, activation in GSTP-null than in WT mice.	Cyclophosphamide	161-163	mitogen-activated protein kinase 8	Mus musculus	180-207
19696094-6	2009	There was no difference in hepatic microsomal production of acrolein from CY or urinary hydroxypropyl mercapturic acid output between WT and GSTP-null mice, but CY induced greater c-Jun NH(2)-terminal kinase (JNK) and c-Jun, but not extracellular signal-regulated kinase or p38, activation in GSTP-null than in WT mice.	Cyclophosphamide	161-163	mitogen-activated protein kinase 8	Mus musculus	209-212
19696094-6	2009	There was no difference in hepatic microsomal production of acrolein from CY or urinary hydroxypropyl mercapturic acid output between WT and GSTP-null mice, but CY induced greater c-Jun NH(2)-terminal kinase (JNK) and c-Jun, but not extracellular signal-regulated kinase or p38, activation in GSTP-null than in WT mice.	Cyclophosphamide	161-163	jun proto-oncogene	Mus musculus	180-185
19696094-6	2009	There was no difference in hepatic microsomal production of acrolein from CY or urinary hydroxypropyl mercapturic acid output between WT and GSTP-null mice, but CY induced greater c-Jun NH(2)-terminal kinase (JNK) and c-Jun, but not extracellular signal-regulated kinase or p38, activation in GSTP-null than in WT mice.	Cyclophosphamide	161-163	mitogen-activated protein kinase 14	Mus musculus	274-277
19696094-6	2009	There was no difference in hepatic microsomal production of acrolein from CY or urinary hydroxypropyl mercapturic acid output between WT and GSTP-null mice, but CY induced greater c-Jun NH(2)-terminal kinase (JNK) and c-Jun, but not extracellular signal-regulated kinase or p38, activation in GSTP-null than in WT mice.	Cyclophosphamide	161-163	glutathione S-transferase pi 1	Homo sapiens	293-297
19696094-8	2009	Taken together, these data support the view that GSTP prevents CY-induced bladder toxicity, in part by detoxifying acrolein.	Cyclophosphamide	63-65	glutathione S-transferase pi 1	Homo sapiens	49-53
19356801-4	2009	We show that low dose cyclophosphamide (CY) sensitive CD4(+)CD25(+)FoxP3(+) Treg cell-dependent mechanisms can be demonstrated in C57Bl/6 mice susceptible to MLD-STZ diabetes induction.	Cyclophosphamide	22-38	CD4 antigen	Mus musculus	54-57
19356801-4	2009	We show that low dose cyclophosphamide (CY) sensitive CD4(+)CD25(+)FoxP3(+) Treg cell-dependent mechanisms can be demonstrated in C57Bl/6 mice susceptible to MLD-STZ diabetes induction.	Cyclophosphamide	22-38	forkhead box P3	Mus musculus	67-72
19356801-4	2009	We show that low dose cyclophosphamide (CY) sensitive CD4(+)CD25(+)FoxP3(+) Treg cell-dependent mechanisms can be demonstrated in C57Bl/6 mice susceptible to MLD-STZ diabetes induction.	Cyclophosphamide	40-42	CD4 antigen	Mus musculus	54-57
19356801-4	2009	We show that low dose cyclophosphamide (CY) sensitive CD4(+)CD25(+)FoxP3(+) Treg cell-dependent mechanisms can be demonstrated in C57Bl/6 mice susceptible to MLD-STZ diabetes induction.	Cyclophosphamide	40-42	forkhead box P3	Mus musculus	67-72
19356801-5	2009	CY pretreatment decreased Foxp3(+) cell count, glycemia, glycosuria and insulitis.	Cyclophosphamide	0-2	forkhead box P3	Mus musculus	26-31
19691848-0	2009	Gender-based reciprocal expression of transforming growth factor-beta1 and the inducible nitric oxide synthase in a rat model of cyclophosphamide-induced cystitis.	Cyclophosphamide	129-145	transforming growth factor, beta 1	Rattus norvegicus	38-70
19497016-12	2009	Cyclophosphamide treatment and diabetic condition per se led to increase in the p53 + and TUNEL + cells in the liver and kidney of rats.	Cyclophosphamide	0-16	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	80-83
19497016-13	2009	Under diabetic condition, further increase in the p53 + and TUNEL + cells was observed in response to cyclophosphamide.	Cyclophosphamide	102-118	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	50-53
19696793-0	2009	Association study of genetic polymorphism in ABCC4 with cyclophosphamide-induced adverse drug reactions in breast cancer patients.	Cyclophosphamide	56-72	ATP binding cassette subfamily C member 4	Homo sapiens	45-50
19696793-5	2009	The association study revealed that one SNP, rs9561778 in ABCC4, showed a significant association with CPA-induced ADRs (Cochran-Armitage trend"s P-value=0.00031; odds ratio (OR)=2.06).	Cyclophosphamide	103-106	ATP binding cassette subfamily C member 4	Homo sapiens	58-63
19696793-8	2009	The SNPs in ABCC4 might be applicable in predicting the risk of ADRs in patients receiving CPA combination chemotherapy.	Cyclophosphamide	91-94	ATP binding cassette subfamily C member 4	Homo sapiens	12-17
19873920-6	2009	RESULTS: Acupuncture and moxibustion markedly up-regulated the expression of bone marrow cell DNA pol beta and XPD, and promoted the base excision repair and nucleotide excision repair, which leads to the relieving Cyclophosphamide-induced myelosuppression and increasing the number of white blood cells.	Cyclophosphamide	215-231	excision repair cross-complementing rodent repair deficiency, complementation group 2	Mus musculus	111-114
19746156-0	2009	Cyclophosphamide chemotherapy sensitizes tumor cells to TRAIL-dependent CD8 T cell-mediated immune attack resulting in suppression of tumor growth.	Cyclophosphamide	0-16	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	56-61
19781388-11	2009	Cyclophosphamide inhibited the clearance of pathogens and the expression of dectin-1 with or without A. fumigatus infection in the lungs as well.	Cyclophosphamide	0-16	C-type lectin domain family 7, member a	Mus musculus	76-84
19781388-14	2009	Inhibition of dectin-1 expression may be one of the mechanisms of cyclophosphamide in the development of IPA.	Cyclophosphamide	66-82	C-type lectin domain family 7, member a	Mus musculus	14-22
19694643-0	2009	Tumor necrosis factor-alpha-associated mechanisms affecting the embryonic response to cyclophosphamide.	Cyclophosphamide	86-102	tumor necrosis factor	Homo sapiens	0-27
19694643-1	2009	PROBLEM: We have previously shown that TNF-alpha(-/-) embryos are more sensitive to the exposure to cyclophosphamide (CP) compared with TNF-alpha(+/+) embryos; however, the underlying mechanisms are not fully understood.	Cyclophosphamide	100-116	tumor necrosis factor	Homo sapiens	39-48
19224214-20	2009	Furthermore, it is active against the CPA-resistant, ALDH3A1 overexpressing, OS xenograft suggesting that it might have the potential of overcoming this resistance mechanism against oxazaphosphorines and may be an active agent in resistant/relapsed sarcomas in patients.	Cyclophosphamide	38-41	aldehyde dehydrogenase 3 family member A1	Homo sapiens	53-60
19706817-3	2009	EXPERIMENTAL DESIGN: We studied 84 cases of cyclophosphamide-doxorubicin-vincristine-prednisone (CHOP)-treated DLBCL (47 GCB, 37 ABC) with GCET1, CD10, BCL6, MUM1, FOXP1, BCL2, MTA3, and cyclin D2 immunostains, and compared different combinations of the immunostaining results with the GEP classification.	Cyclophosphamide	44-60	serpin family A member 9	Homo sapiens	139-144
19776000-1	2009	BACKGROUND: The results of CHOP-21 (cyclophosphamide, doxorubicin, vincristine and prednisone given every 21 days) for the treatment of aggressive B-cell lymphoma have recently been improved by the addition of rituximab and by increasing the dose density.	Cyclophosphamide	36-52	DNA damage inducible transcript 3	Homo sapiens	27-31
19754361-11	2009	CPA induced increases in VEGF RNA, which reached a maximum on day 1, and in PLGF RNA which was sustained throughout the treatment, while anti-angiogenic host thrombospondin-1 increased dramatically through day 7 post-CPA treatment.	Cyclophosphamide	0-3	vascular endothelial growth factor A	Mus musculus	25-29
19754361-11	2009	CPA induced increases in VEGF RNA, which reached a maximum on day 1, and in PLGF RNA which was sustained throughout the treatment, while anti-angiogenic host thrombospondin-1 increased dramatically through day 7 post-CPA treatment.	Cyclophosphamide	0-3	placental growth factor	Mus musculus	76-80
19754361-11	2009	CPA induced increases in VEGF RNA, which reached a maximum on day 1, and in PLGF RNA which was sustained throughout the treatment, while anti-angiogenic host thrombospondin-1 increased dramatically through day 7 post-CPA treatment.	Cyclophosphamide	217-220	thrombospondin 1	Mus musculus	158-174
19636007-3	2009	PATIENTS AND METHODS: We retrospectively analyzed 38 patients with ALK-positive DLBCL treated with cyclophosphamide, doxorubicin, vincristine, prednisone (CHOP) or CHOP-like regimens from different institutions to better define the presenting features, clinical course, and response to treatment.	Cyclophosphamide	99-115	ALK receptor tyrosine kinase	Homo sapiens	67-70
19703244-3	2009	However, when the mice were pretreated with cyclophosphamide, bacteremia-induced mortality was significantly greater in the IL-1-deficient mice than in the WT mice (P < 0.01).	Cyclophosphamide	44-60	interleukin 1 complex	Mus musculus	124-128
19620488-2	2009	We determined the status of the HER2 and TOP2A genes in a large cohort of breast cancer patients treated with adjuvant doxorubicin (A) and cyclophosphamide (C).	Cyclophosphamide	139-155	erb-b2 receptor tyrosine kinase 2	Homo sapiens	32-36
19620488-2	2009	We determined the status of the HER2 and TOP2A genes in a large cohort of breast cancer patients treated with adjuvant doxorubicin (A) and cyclophosphamide (C).	Cyclophosphamide	139-155	DNA topoisomerase II alpha	Homo sapiens	41-46
20190490-4	2010	Intravenous boluses of cyclophosphamide (IVCY) with oral prednisolone and cyclosporin A induced remission of SLE, and a subsequent disappearance of anti-insulin receptor autoantibodies, followed by a recovery of glucose intolerance.	Cyclophosphamide	23-39	insulin receptor	Homo sapiens	153-169
19752340-8	2009	CONCLUSION: These results, observed in two independent study populations, indicate that high-activity MPO genotypes are associated with better survival among women receiving cyclophosphamide-containing therapy, particularly when followed by tamoxifen therapy.	Cyclophosphamide	174-190	myeloperoxidase	Homo sapiens	102-105
19825954-0	2009	Comparative impact of trastuzumab and cyclophosphamide on HER-2-positive human breast cancer xenografts.	Cyclophosphamide	38-54	erb-b2 receptor tyrosine kinase 2	Homo sapiens	58-63
19825954-8	2009	CONCLUSIONS: Trastuzumab combined with metronomic cyclophosphamide may be an effective long-term maintenance strategy for the treatment of Her-2-positive metastatic breast cancer.	Cyclophosphamide	50-66	erb-b2 receptor tyrosine kinase 2	Homo sapiens	139-144
19851987-1	2009	BACKGROUND: Cyclophosphamide induces fetal defects through metabolic activation by cytochrome P-450 monooxygenases (CYP).	Cyclophosphamide	12-28	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	83-114
19851987-1	2009	BACKGROUND: Cyclophosphamide induces fetal defects through metabolic activation by cytochrome P-450 monooxygenases (CYP).	Cyclophosphamide	12-28	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	116-119
20396763-3	2009	The use of melatonin as monotherapy or in combination with cyclophosphamide was followed by a significant decrease in Bcl-2 expression in carcinosarcoma cells.	Cyclophosphamide	59-75	BCL2, apoptosis regulator	Rattus norvegicus	118-123
19581388-11	2009	Furthermore, overexpression of miR-27b or mmu-miR-298 in PANC1 cells led to a lower sensitivity to cyclophosphamide.	Cyclophosphamide	99-115	microRNA 27b	Homo sapiens	31-38
19581388-11	2009	Furthermore, overexpression of miR-27b or mmu-miR-298 in PANC1 cells led to a lower sensitivity to cyclophosphamide.	Cyclophosphamide	99-115	microRNA 298	Mus musculus	42-53
19815119-7	2009	Longevity of ovalbumin-specific plasma cells was determined by cyclophosphamide treatment, which depletes proliferating plasmablasts but leaves plasma cells untouched.	Cyclophosphamide	63-79	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	13-22
19882369-3	2009	Cy is most effective in young patients, with very active MS (frequent relapses, rapid accumulation of disability, and gad+ lesions on brain MRI).	Cyclophosphamide	0-2	glutamate decarboxylase 1	Homo sapiens	118-121
19882369-7	2009	As second-line therapy, Cy can be used in non-responders to IFN-beta or glatiramer acetate.	Cyclophosphamide	24-26	interferon beta 1	Homo sapiens	60-68
19935295-0	2009	Effect of sustained-release PDGF and TGF-beta on cyclophosphamide-induced impaired wound healing.	Cyclophosphamide	49-65	transforming growth factor, beta 1	Rattus norvegicus	37-45
19935295-10	2009	CONCLUSIONS: Sustained-release delivery of TGF-beta and PDGF in combination, but not separately, by a subcutaneously implanted drug delivery system significantly improves cyclophosphamide-induced impaired wound healing in rats.	Cyclophosphamide	171-187	transforming growth factor, beta 1	Rattus norvegicus	43-51
19633198-6	2009	Furthermore, anti-CD79b-vcMMAE was significantly more effective than a standard-of-care regimen, R-CHOP (ie, rituximab with a single intravenous injection of 30 mg/kg cyclophosphamide, 2.475 mg/kg doxorubicin, 0.375 mg/kg vincristine, and oral dosing of 0.15 mg/kg prednisone once a day for 5 days), in 3 xenograft models of NHL.	Cyclophosphamide	167-183	CD79b molecule	Homo sapiens	18-23
21319009-12	2009	MINI-ABSTRACT: Combination therapy by trastuzumab with 5"-DFUR and cyclophosphamide can be safely administered on an outpatient basis and is useful to treat patients with HER2-overexpressing metastatic breast cancer.	Cyclophosphamide	67-83	erb-b2 receptor tyrosine kinase 2	Homo sapiens	171-175
20396740-1	2009	Preparation containing ultralow doses of antibodies to stem cell factor considerably activates bone marrow myelopoiesis suppressed by cyclophosphamide.	Cyclophosphamide	134-150	KIT ligand	Homo sapiens	55-71
19464156-9	2009	Recent studies revealed an increased locoregional control and a slight toxicity when radiotherapy was given concurrently with cyclophosphamide, mitoxantrone and fluorouracil (CNF).	Cyclophosphamide	126-142	NPHS1 adhesion molecule, nephrin	Homo sapiens	175-178
19702527-4	2009	CYP2B6 can metabolise approximately 8% of clinically used drugs (n > 60), including cyclophosphamide, ifosfamide, tamoxifen, ketamine, artemisinin, nevirapine, efavirenz, bupropion, sibutramine, and propofol.	Cyclophosphamide	87-103	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	0-6
19691848-0	2009	Gender-based reciprocal expression of transforming growth factor-beta1 and the inducible nitric oxide synthase in a rat model of cyclophosphamide-induced cystitis.	Cyclophosphamide	129-145	nitric oxide synthase 2	Rattus norvegicus	79-110
19691848-2	2009	Previous studies have implicated a role for NO, presumably derived from iNOS, in cyclophosphamide (CYP)-induced cystitis in the bladder.	Cyclophosphamide	81-97	nitric oxide synthase 2	Rattus norvegicus	72-76
19428837-4	2009	Resulting combination, limitedly operational in Btk deficient xid mice, suggests that preferential B-cell lymphocyte space promoted by cyclophosphamide facilitates remaining EGF-specific AFC undergo homeostatic proliferation driven by boosting, amplifying the response.	Cyclophosphamide	135-151	Bruton agammaglobulinemia tyrosine kinase	Mus musculus	48-51
19470942-1	2009	PURPOSE We have demonstrated that patients with HER2-amplified tumors derive more benefit from higher doses of doxorubicin-containing chemotherapy (cyclophosphamide, doxorubicin, and fluorouracil [CAF]).	Cyclophosphamide	148-164	erb-b2 receptor tyrosine kinase 2	Homo sapiens	48-52
18514386-3	2009	OBJECTIVE: To investigate the effect of intravesical botulinum toxin A (BoNT-A) on COX-2 and EP4 expression in cyclophosphamide (CYP)-induced cystitis in rats.	Cyclophosphamide	111-127	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	83-88
19918307-0	2009	A case of crescentic IgA nephropathy treated with prednisolone and cyclophosphamide.	Cyclophosphamide	67-83	CD79a molecule	Homo sapiens	21-24
19761687-2	2009	SMMC-7721 cells were inoculated into mice treated with 0, 2, 5 or 10 mg/kg cyclophosphamide (CTX).	Cyclophosphamide	75-91	V-set and immunoglobulin domain containing 2	Mus musculus	93-96
19513730-3	2009	The introduction of cytokine blockers in RA using tumor necrosis factor (TNF)-alpha and interleukin (IL)-1 inhibitors presented the first original therapy modalities in rheumatology, after proliferation-inhibiting drugs, such as methotrexate and cyclophosphamide, had been accepted in oncology.	Cyclophosphamide	246-262	tumor necrosis factor	Homo sapiens	50-83
19414558-3	2009	We report that the combined use of the alkylating agent cyclophosphamide (CTX) and an agonist antibody targeting the co-stimulatory receptor OX40 (OX86) provides potent antitumor immunity capable of regressing established, poorly immunogenic B16 melanoma tumors.	Cyclophosphamide	56-72	TNF receptor superfamily member 4	Homo sapiens	141-145
19052741-4	2009	We found that the efficacy of cyclophosphamide to eradicate established tumors, which has been linked to regulatory T cell depletion, was negated by adoptive transfer of CD25+ regulatory T cells.	Cyclophosphamide	30-46	interleukin 2 receptor, alpha chain	Mus musculus	170-174
19622584-2	2009	standard dose of cyclophosphamide (CTX) immediately followed by an oral metronomic CTX regimen with celecoxib (CXB) and dexamethasone (DEX) in advanced hormone-refractory prostate cancer patients.	Cyclophosphamide	17-33	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	35-38
19557622-0	2009	Influence of MBL-2 mutations in the infection risk of patients with follicular lymphoma treated with rituximab, fludarabine, and cyclophosphamide.	Cyclophosphamide	129-145	mannose binding lectin 2	Homo sapiens	13-18
19015854-0	2009	Protein nitration, PARP activation and NAD+ depletion may play a critical role in the pathogenesis of cyclophosphamide-induced hemorrhagic cystitis in the rat.	Cyclophosphamide	102-118	poly (ADP-ribose) polymerase 1	Rattus norvegicus	19-23
19223077-5	2009	Some PPCPs with amide bonds, such as cyclophosphamide and DEET, were highly resistant to photodegradation by UV/Lamp1.	Cyclophosphamide	37-53	lysosomal associated membrane protein 1	Homo sapiens	112-117
18751888-1	2009	PURPOSE: Granulocyte-colony stimulating factor (G-CSF) was used in CALGB 9741 to support dose-dense sequential chemotherapy with doxorubicin and cyclophosphamide (AC) followed by paclitaxel (P) (Citron et al.	Cyclophosphamide	145-161	colony stimulating factor 3	Homo sapiens	48-53
19240057-11	2009	CONCLUSIONS: Our results indicate that AS101 can significantly protect against Cy-induced testicular damage and sperm DNA damage, probably by acting through Akt/GSK-3beta phosphorylation.	Cyclophosphamide	79-81	thymoma viral proto-oncogene 1	Mus musculus	157-160
19240057-11	2009	CONCLUSIONS: Our results indicate that AS101 can significantly protect against Cy-induced testicular damage and sperm DNA damage, probably by acting through Akt/GSK-3beta phosphorylation.	Cyclophosphamide	79-81	glycogen synthase kinase 3 beta	Mus musculus	161-170
19627214-0	2009	Treatment with Astragali radix and Angelicae radix enhances erythropoietin gene expression in the cyclophosphamide-induced anemic rat.	Cyclophosphamide	98-114	erythropoietin	Rattus norvegicus	60-74
19627214-2	2009	This study examined the effect of a combination treatment (AAC) using Astragali radix (AMW) and Angelicae radix (AGW) in cyclophosphamide (CYP)-induced anemic rats on erythropoietin (EPO) expression and hematological parameters.	Cyclophosphamide	121-137	glycine-N-acyltransferase	Rattus norvegicus	59-62
19501186-6	2009	Among these transformants, benzo(a)pyrene-induced or cyclophosphamide-produced micronucleus (MN) frequency was markedly increased in transformants expressing CYP1A2 or CYP2C9, respectively.	Cyclophosphamide	53-69	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	158-164
19501186-6	2009	Among these transformants, benzo(a)pyrene-induced or cyclophosphamide-produced micronucleus (MN) frequency was markedly increased in transformants expressing CYP1A2 or CYP2C9, respectively.	Cyclophosphamide	53-69	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	168-174
18976765-0	2009	Lactoferrin is associated with a decrease in oocyte depletion in mice receiving cyclophosphamide.	Cyclophosphamide	80-96	lactotransferrin	Mus musculus	0-11
18976765-1	2009	OBJECTIVE: To investigate new important molecules involved in the regulation of chemotherapy-induced ovarian damage and, based on those results, to examine the effect of lactoferrin on cyclophosphamide (CPM)-induced ovarian failure.	Cyclophosphamide	185-201	lactotransferrin	Mus musculus	170-181
18976765-1	2009	OBJECTIVE: To investigate new important molecules involved in the regulation of chemotherapy-induced ovarian damage and, based on those results, to examine the effect of lactoferrin on cyclophosphamide (CPM)-induced ovarian failure.	Cyclophosphamide	203-206	lactotransferrin	Mus musculus	170-181
19303104-2	2009	Evidence suggests that tumor necrosis factor-alpha (R&D Systems), interleukin-1beta and cyclooxygenase-2 are directly involved in the pathogenesis of cyclophosphamide induced cystitis and these molecules depend on transcription factor NF-kappaB for maximal secretion.	Cyclophosphamide	154-170	tumor necrosis factor	Rattus norvegicus	23-50
19303104-2	2009	Evidence suggests that tumor necrosis factor-alpha (R&D Systems), interleukin-1beta and cyclooxygenase-2 are directly involved in the pathogenesis of cyclophosphamide induced cystitis and these molecules depend on transcription factor NF-kappaB for maximal secretion.	Cyclophosphamide	154-170	interleukin 1 beta	Rattus norvegicus	70-87
19303104-2	2009	Evidence suggests that tumor necrosis factor-alpha (R&D Systems), interleukin-1beta and cyclooxygenase-2 are directly involved in the pathogenesis of cyclophosphamide induced cystitis and these molecules depend on transcription factor NF-kappaB for maximal secretion.	Cyclophosphamide	154-170	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	92-108
19318495-6	2009	Treatment of mice with low-dose cyclophosphamide or anti-CD25 antibody to deplete regulatory T cells unmasked latent T-cell antitumor activity; the number of activated CD8(+) T cells in tumors increased and B16/3L86 tumors were completely rejected in a CD8(+) and CD4(+) T-cell-dependent fashion.	Cyclophosphamide	32-48	CD4 antigen	Mus musculus	264-267
19428837-4	2009	Resulting combination, limitedly operational in Btk deficient xid mice, suggests that preferential B-cell lymphocyte space promoted by cyclophosphamide facilitates remaining EGF-specific AFC undergo homeostatic proliferation driven by boosting, amplifying the response.	Cyclophosphamide	135-151	Bruton agammaglobulinemia tyrosine kinase	Mus musculus	62-65
19089911-3	2009	We found significantly increased numbers of CD34(+)/Flk-1(+) endothelial progenitor cells in the peripheral blood of mice 1 week after the administration of 100 mg/kg cyclophosphamide vs. a saline injection (0.39 +/- 0.09% vs. 0.20 +/- 0.10%, respectively; p < 0.05).	Cyclophosphamide	167-183	CD34 antigen	Mus musculus	44-48
19417562-7	2009	Compared to adenovirus and cyclophosphamide alone, adenovirus-mediated anti-4-1BB scFv in combination with low dose CTX treatment could obviously augment the antitumor activity, in which some established TC-1 tumors were eradicated and the survival of mice was significantly extended.	Cyclophosphamide	27-43	tumor necrosis factor receptor superfamily, member 9	Mus musculus	76-81
19115204-7	2009	Furthermore, analysis of 203 clinically well characterized primary breast cancers displayed a significant correlation of reduced EFEMP1 protein expression with poor disease-free (p = 0.037) and overall survival (p = 0.032), particularly in those node-positive patients who received adjuvant anthracycline-based chemotherapy, but not in those treated by either cyclophosphamide-methotrexate-5-fluorouracil (CMF) or Tamoxifen.	Cyclophosphamide	360-376	EGF containing fibulin extracellular matrix protein 1	Homo sapiens	129-135
18989352-4	2009	We showed that the combination of vaccination with high-dose cyclophosphamide was able to skew the response toward the target antigen and enhanced both the quantity and quality of antigen-specific CD8+ and CD4+ T-cell responses in tumor-bearing mice, which resulted in the inhibition of tumor growth.	Cyclophosphamide	61-77	CD4 antigen	Mus musculus	206-209
19089911-3	2009	We found significantly increased numbers of CD34(+)/Flk-1(+) endothelial progenitor cells in the peripheral blood of mice 1 week after the administration of 100 mg/kg cyclophosphamide vs. a saline injection (0.39 +/- 0.09% vs. 0.20 +/- 0.10%, respectively; p < 0.05).	Cyclophosphamide	167-183	kinase insert domain protein receptor	Mus musculus	52-57
19372630-8	2009	Additional analyses indicated the significant up-regulation (P = 0.001) of tumor suppressor p53 and p53-regulated pro-apoptotic Bax and Fas in MCF-7 cells following CPA treatment in combination with RES, which may contribute to the enhancement of the antitumor effect of CPA.	Cyclophosphamide	165-168	tumor protein p53	Homo sapiens	92-95
19372630-8	2009	Additional analyses indicated the significant up-regulation (P = 0.001) of tumor suppressor p53 and p53-regulated pro-apoptotic Bax and Fas in MCF-7 cells following CPA treatment in combination with RES, which may contribute to the enhancement of the antitumor effect of CPA.	Cyclophosphamide	165-168	tumor protein p53	Homo sapiens	100-103
19372630-8	2009	Additional analyses indicated the significant up-regulation (P = 0.001) of tumor suppressor p53 and p53-regulated pro-apoptotic Bax and Fas in MCF-7 cells following CPA treatment in combination with RES, which may contribute to the enhancement of the antitumor effect of CPA.	Cyclophosphamide	165-168	BCL2 associated X, apoptosis regulator	Homo sapiens	128-131
19372630-8	2009	Additional analyses indicated the significant up-regulation (P = 0.001) of tumor suppressor p53 and p53-regulated pro-apoptotic Bax and Fas in MCF-7 cells following CPA treatment in combination with RES, which may contribute to the enhancement of the antitumor effect of CPA.	Cyclophosphamide	271-274	tumor protein p53	Homo sapiens	92-95
19327529-0	2009	Cyclophosphamide protects against myocardial ischemia/reperfusion injury in rats: one of the therapeutic targets is high sensitivity C-reactive protein.	Cyclophosphamide	0-16	C-reactive protein	Rattus norvegicus	133-151
19327529-1	2009	OBJECTIVE: Cyclophosphamide has a role of decreasing high-sensitivity C-reactive protein in the treatment of autoimmune disorders.	Cyclophosphamide	11-27	C-reactive protein	Rattus norvegicus	70-88
19327529-13	2009	CONCLUSION: Cyclophosphamide protects myocardial ischemia/reperfusion injury in the rat with a decrease in plasma concentration of high-sensitivity C-reactive protein.	Cyclophosphamide	12-28	C-reactive protein	Rattus norvegicus	148-166
19372630-8	2009	Additional analyses indicated the significant up-regulation (P = 0.001) of tumor suppressor p53 and p53-regulated pro-apoptotic Bax and Fas in MCF-7 cells following CPA treatment in combination with RES, which may contribute to the enhancement of the antitumor effect of CPA.	Cyclophosphamide	271-274	tumor protein p53	Homo sapiens	100-103
19372630-8	2009	Additional analyses indicated the significant up-regulation (P = 0.001) of tumor suppressor p53 and p53-regulated pro-apoptotic Bax and Fas in MCF-7 cells following CPA treatment in combination with RES, which may contribute to the enhancement of the antitumor effect of CPA.	Cyclophosphamide	271-274	BCL2 associated X, apoptosis regulator	Homo sapiens	128-131
19372630-9	2009	Furthermore, downregulation of anti-apoptotic Bcl-2 (P = 0.001) was observed in MCF-7 cells treated with CPA with or without RES when compared to untreated MCF-7.	Cyclophosphamide	105-108	BCL2 apoptosis regulator	Homo sapiens	46-51
19162187-0	2009	delta-Aminolevulinate dehydratase activity and oxidative stress during melphalan and cyclophosphamide-BCNU-etoposide (CBV) conditioning regimens in autologous bone marrow transplantation patients.	Cyclophosphamide	85-101	aminolevulinate dehydratase	Homo sapiens	0-33
19318401-10	2009	High-dose of corticosteroids, chloroquine and cyclophosphamide therapy had resulted in remission of hypoglycaemia associated with resolution of circulating antibodies to insulin and insulin receptor, and improvement in clinical and laboratory features of SLE.	Cyclophosphamide	46-62	insulin	Homo sapiens	170-177
19318401-10	2009	High-dose of corticosteroids, chloroquine and cyclophosphamide therapy had resulted in remission of hypoglycaemia associated with resolution of circulating antibodies to insulin and insulin receptor, and improvement in clinical and laboratory features of SLE.	Cyclophosphamide	46-62	insulin receptor	Homo sapiens	182-198
19095022-6	2009	The metronomic CPA dosing clearly promoted accumulation and subsequent deep diffusion of SL in the solid tumor as a result of rather a transient increase in the density of CD31(+)-microvessels, which shows high permeability to SL.	Cyclophosphamide	15-18	platelet/endothelial cell adhesion molecule 1	Mus musculus	172-176
19429390-3	2009	Here we identify components of the signaling network triggered by in vitro exposure of CD-1 murine limbs to 4-hydroperoxycyclophosphamide (4-OOHCPA), a preactivated analog of cyclophosphamide.	Cyclophosphamide	121-137	CD1 antigen complex	Mus musculus	87-91
19233728-7	2009	CONCLUSION: Our data suggested that adequate yields of CD34+ cells may be achieved in multiple myeloma or pre-treated Non-Hodgkin"s lymphoma mobilized with low-dose Cy plus G-CSF regardless of the daily monitoring of peripheral blood CD34+ cells.	Cyclophosphamide	165-167	CD34 molecule	Homo sapiens	55-59
19445875-11	2009	Furthermore, an improved immunologic response was observed in all cases after cyclophosphamide treatment, with decreased anti-DSG1 and anti-DSG3 antibody titers and well as decreased circulating anti-EIS antibody titers.	Cyclophosphamide	78-94	desmoglein 1	Homo sapiens	126-130
19240166-6	2009	Ectopic expression of FGFR4 in cancer cells led to reduced apoptosis sensitivity on treatment with doxorubicin or cyclophosphamide, whereas knockdown of endogenous FGFR4 expression in breast cancer cell lines had the opposite effect.	Cyclophosphamide	114-130	fibroblast growth factor receptor 4	Homo sapiens	22-27
19445875-11	2009	Furthermore, an improved immunologic response was observed in all cases after cyclophosphamide treatment, with decreased anti-DSG1 and anti-DSG3 antibody titers and well as decreased circulating anti-EIS antibody titers.	Cyclophosphamide	78-94	desmoglein 3	Homo sapiens	140-144
19201856-0	2009	Recovery from cyclophosphamide-induced lymphopenia results in expansion of immature dendritic cells which can mediate enhanced prime-boost vaccination antitumor responses in vivo when stimulated with the TLR3 agonist poly(I:C).	Cyclophosphamide	14-30	toll like receptor 3	Homo sapiens	204-208
19619437-1	2009	BACKGROUND AND OBJECTIVE: Cyclophosphamide (CTX) is a commonly used clinical antitumor drug with severe side effects.	Cyclophosphamide	26-42	V-set and immunoglobulin domain containing 2	Mus musculus	44-47
18643850-6	2009	Cyclophosphamide almost completely suppressed the production of anti-Dsg3 IgG, development of body weight loss and the appearance of the PV phenotype in contrast with the control group without the drug.	Cyclophosphamide	0-16	desmoglein 3	Mus musculus	69-73
19005482-7	2009	Among other clinical and genetic factors, polymorphisms of CYP2B6 genes that interfere with cyclophosphamide metabolism were associated with OM (recipient CYP2B6(*)4; P=0.0067), HC (recipient CYP2B6(*)2; P=0.03) and VOD (donor CYP2B6(*)6; P=0.03).	Cyclophosphamide	92-108	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	59-65
19005482-7	2009	Among other clinical and genetic factors, polymorphisms of CYP2B6 genes that interfere with cyclophosphamide metabolism were associated with OM (recipient CYP2B6(*)4; P=0.0067), HC (recipient CYP2B6(*)2; P=0.03) and VOD (donor CYP2B6(*)6; P=0.03).	Cyclophosphamide	92-108	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	155-161
19005482-7	2009	Among other clinical and genetic factors, polymorphisms of CYP2B6 genes that interfere with cyclophosphamide metabolism were associated with OM (recipient CYP2B6(*)4; P=0.0067), HC (recipient CYP2B6(*)2; P=0.03) and VOD (donor CYP2B6(*)6; P=0.03).	Cyclophosphamide	92-108	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	155-161
19005482-7	2009	Among other clinical and genetic factors, polymorphisms of CYP2B6 genes that interfere with cyclophosphamide metabolism were associated with OM (recipient CYP2B6(*)4; P=0.0067), HC (recipient CYP2B6(*)2; P=0.03) and VOD (donor CYP2B6(*)6; P=0.03).	Cyclophosphamide	92-108	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	155-161
18971422-6	2009	Hematopoietic cells from Aldh1a1-deficient mice exhibited increased sensitivity to cyclophosphamide in a non-cell-autonomous manner, consistent with its role in cyclophosphamide metabolism in the liver.	Cyclophosphamide	83-99	aldehyde dehydrogenase family 1, subfamily A1	Mus musculus	25-32
18971422-6	2009	Hematopoietic cells from Aldh1a1-deficient mice exhibited increased sensitivity to cyclophosphamide in a non-cell-autonomous manner, consistent with its role in cyclophosphamide metabolism in the liver.	Cyclophosphamide	161-177	aldehyde dehydrogenase family 1, subfamily A1	Mus musculus	25-32
19201856-3	2009	We show herein that induction of lymphodepletion by a single 4 mg cyclophosphamide (CTX) treatment induces a marked expansion of immature dendritic cells (DCs) in the peripheral blood on days 8-16 post-CTX (termed restoration phase).	Cyclophosphamide	66-82	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	84-87
19201856-3	2009	We show herein that induction of lymphodepletion by a single 4 mg cyclophosphamide (CTX) treatment induces a marked expansion of immature dendritic cells (DCs) in the peripheral blood on days 8-16 post-CTX (termed restoration phase).	Cyclophosphamide	66-82	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	202-205
19168513-0	2009	Cyclophosphamide-evoked heart failure involves pronounced co-suppression of cytoplasmic thioredoxin reductase activity and non-protein free thiol level.	Cyclophosphamide	0-16	thioredoxin 1	Mus musculus	88-99
19168513-1	2009	AIMS: Heart failure is a life-threatening complication of high-dose cyclophosphamide (CTX) chemotherapy, and the present study aimed at identifying the mechanism involved in mice.	Cyclophosphamide	68-84	V-set and immunoglobulin domain containing 2	Mus musculus	86-89
18997060-0	2009	Anti-Ccl2 Spiegelmer permits 75% dose reduction of cyclophosphamide to control diffuse proliferative lupus nephritis and pneumonitis in MRL-Fas(lpr) mice.	Cyclophosphamide	51-67	chemokine (C-C motif) ligand 2	Mus musculus	5-9
19008456-0	2009	Mcl-1 expression predicts progression-free survival in chronic lymphocytic leukemia patients treated with pentostatin, cyclophosphamide, and rituximab.	Cyclophosphamide	119-135	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	0-5
19177203-10	2009	Cyclophosphamide also increased CD31 reactivity, a marker of vascular endothelium, and macrophage (CD68-positive) infiltration into glioma cell-inoculated rat brains.	Cyclophosphamide	0-16	platelet and endothelial cell adhesion molecule 1	Rattus norvegicus	32-36
19177203-10	2009	Cyclophosphamide also increased CD31 reactivity, a marker of vascular endothelium, and macrophage (CD68-positive) infiltration into glioma cell-inoculated rat brains.	Cyclophosphamide	0-16	Cd68 molecule	Rattus norvegicus	99-103
19351038-1	2009	The influence of the untitumor drugs, cyclophosphamide (CPA) and nitrosomethylurea (NMM) on the activity of lysosomal cysteine proteases cathepsin B and L in the tumor tissue was studied.	Cyclophosphamide	38-54	cathepsin B	Homo sapiens	137-148
19351038-1	2009	The influence of the untitumor drugs, cyclophosphamide (CPA) and nitrosomethylurea (NMM) on the activity of lysosomal cysteine proteases cathepsin B and L in the tumor tissue was studied.	Cyclophosphamide	56-59	cathepsin B	Homo sapiens	137-148
19351038-2	2009	Regression or reduction in the rate of growth of LS and RLS (drug sensitive and resistant sarcomas, respectively) during injection of CPA or NMM was accompanied by the increase in the activity of cysteine proteases cathepsin B and L in the tumor tissue.	Cyclophosphamide	134-137	cathepsin B	Homo sapiens	215-226
18620786-2	2009	In phase 3 clinical trials, giving rituximab with cyclophosphamide, vincristine, doxorubicin, and prednisone (CHOP) every 3 weeks (R-CHOP-21) has been associated with improved survival, without increased toxicity, in all patient groups studied.	Cyclophosphamide	50-66	DNA damage inducible transcript 3	Homo sapiens	110-114
18620786-2	2009	In phase 3 clinical trials, giving rituximab with cyclophosphamide, vincristine, doxorubicin, and prednisone (CHOP) every 3 weeks (R-CHOP-21) has been associated with improved survival, without increased toxicity, in all patient groups studied.	Cyclophosphamide	50-66	DNA damage inducible transcript 3	Homo sapiens	133-137
19309506-6	2009	RESULTS: TLE3 staining was associated with improved 5-year disease-free interval (DFI) in the overall cohort (n = 441, P < 0.004), in patients treated with cyclophosphamide (C), methotrexate, and 5-fluorouracil (n = 72, P < 0.02), and in those treated with regimens containing doxorubicin (A) and a T (n = 65, P < 0.04).	Cyclophosphamide	159-175	TLE family member 3, transcriptional corepressor	Homo sapiens	9-13
19899124-1	2009	The yield of CD34+ cells collected by apheresis for autologous peripheral blood stem cell (PBSC) transplantation was greatly increased when the appropriate timing was determined to begin using G-CSF after COAEP (Cytoxan, Vinblastine, Arabinosylcytosin, Etoposide and Prednisone) mobilization.	Cyclophosphamide	212-219	CD34 molecule	Homo sapiens	13-17
18214709-1	2009	INTRODUCTION: Lupus nephritis (LN) is a severe manifestation of systemic lupus erythematosus (SLE) that is usually treated with an extended course of intravenous (IV) cyclophosphamide (CYC).	Cyclophosphamide	167-183	cytochrome c, somatic	Homo sapiens	185-188
19293492-7	2009	Treatment with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) plus etoposide established complete remission.	Cyclophosphamide	15-31	DNA damage inducible transcript 3	Homo sapiens	75-79
19103281-8	2009	The results suggest that repeated intake of GTE may aggravate cyclophosphamide-induced body weight loss and malformations of fetuses by modulating CYP2B and CYP3A.	Cyclophosphamide	62-78	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	157-162
19204436-5	2009	There was significant improvement in response to the first 4 cycles of CHOP chemotherapy (consisting of cyclophosphamide, doxorubicin, vincristine and prednisolone) instituted, but then there were features of relapse.	Cyclophosphamide	104-120	DNA damage inducible transcript 3	Homo sapiens	71-75
19103281-0	2009	Green tea extract increases cyclophosphamide-induced teratogenesis by modulating the expression of cytochrome P-450 mRNA.	Cyclophosphamide	28-44	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	99-115
19103281-7	2009	Moreover, repeated treatment with GTE greatly increased mRNA expression and activity of hepatic cytochrome P-450 (CYP) 2B, which metabolizes cyclophosphamide into teratogenic acrolein and cytotoxic phosphoramide mustard, while reducing CYP3A expression (a detoxifying enzyme).	Cyclophosphamide	141-157	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	96-112
19103281-7	2009	Moreover, repeated treatment with GTE greatly increased mRNA expression and activity of hepatic cytochrome P-450 (CYP) 2B, which metabolizes cyclophosphamide into teratogenic acrolein and cytotoxic phosphoramide mustard, while reducing CYP3A expression (a detoxifying enzyme).	Cyclophosphamide	141-157	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	236-241
18971681-3	2008	The GnRH-a cotreatment may also prevent premature ovarian failure in patients with nonmalignant, autoimmune diseases, such as systemic lupus erythematosus, exposed to cyclophosphamide pulsatile therapy.	Cyclophosphamide	167-183	gonadotropin releasing hormone 1	Homo sapiens	4-8
18726131-0	2008	Neural progenitor cell-mediated delivery of interferon beta improves neuroblastoma response to cyclophosphamide.	Cyclophosphamide	95-111	interferon beta 1	Homo sapiens	44-59
18483878-0	2008	Exaggerated expression of inflammatory mediators in vasoactive intestinal polypeptide knockout (VIP-/-) mice with cyclophosphamide (CYP)-induced cystitis.	Cyclophosphamide	114-130	vasoactive intestinal polypeptide	Mus musculus	52-85
18483878-0	2008	Exaggerated expression of inflammatory mediators in vasoactive intestinal polypeptide knockout (VIP-/-) mice with cyclophosphamide (CYP)-induced cystitis.	Cyclophosphamide	114-130	vasoactive intestinal polypeptide	Mus musculus	96-99
18483878-2	2008	VIP(-/-) mice exhibit altered bladder function and neurochemical properties in micturition pathways after cyclophosphamide (CYP)-induced cystitis.	Cyclophosphamide	106-122	vasoactive intestinal polypeptide	Mus musculus	0-3
19033116-0	2008	[Effect of GnRH analogs on the expression of Bcl-2 gene family in the ovary of rats with cyclophosphamide-induced ovarian damage].	Cyclophosphamide	89-105	BCL2, apoptosis regulator	Rattus norvegicus	45-50
19227835-0	2008	Antimutagenic efficacy of some natural compounds on cyclophosphamide-induced p53 alterations.	Cyclophosphamide	52-68	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	77-80
18854824-1	2008	CYP2C19 is a drug-metabolising enzyme involved in the metabolism of a number of chemotherapeutic agents including cyclophosphamide.	Cyclophosphamide	114-130	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
18854824-11	2008	There is increasing interest in using pharmacogenetics to "individualise medicine", however, the results of this study indicate that in a cancer population genotyping for CYP2C19 would significantly underestimate the number of phenotypic PM of drugs, such as cyclophosphamide, which may be metabolised by this enzyme.	Cyclophosphamide	259-275	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	171-178
18797299-2	2008	Here, we studied, using real-time polymerase chain reaction, whether cyclophosphamide injection-evoked cystitis is associated with altered TRPV1/TRPV1b expression in the L5-L6 dorsal root ganglia, which innervate the urinary bladder.	Cyclophosphamide	69-85	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	139-144
19340966-2	2009	Cyclophosphan (CP) administered to mice four times with 24 hours intervals decreased levels of T-, B-, T-regulatory (T-reg CD4/CD25/Foxp3) lymphocytes, increased quantity of cells expressing early activation marker CD25 (assessment after 4 hours).	Cyclophosphamide	0-13	CD4 antigen	Mus musculus	123-126
19340966-2	2009	Cyclophosphan (CP) administered to mice four times with 24 hours intervals decreased levels of T-, B-, T-regulatory (T-reg CD4/CD25/Foxp3) lymphocytes, increased quantity of cells expressing early activation marker CD25 (assessment after 4 hours).	Cyclophosphamide	0-13	interleukin 2 receptor, alpha chain	Mus musculus	127-131
19340966-2	2009	Cyclophosphan (CP) administered to mice four times with 24 hours intervals decreased levels of T-, B-, T-regulatory (T-reg CD4/CD25/Foxp3) lymphocytes, increased quantity of cells expressing early activation marker CD25 (assessment after 4 hours).	Cyclophosphamide	0-13	forkhead box P3	Mus musculus	132-137
19340966-2	2009	Cyclophosphan (CP) administered to mice four times with 24 hours intervals decreased levels of T-, B-, T-regulatory (T-reg CD4/CD25/Foxp3) lymphocytes, increased quantity of cells expressing early activation marker CD25 (assessment after 4 hours).	Cyclophosphamide	0-13	interleukin 2 receptor, alpha chain	Mus musculus	215-219
19020250-7	2008	RESULTS: Cyclophosphamide, but not paclitaxel, significantly inhibited tumor growth and caused a significant increase in HIF-1alpha protein levels, which peaked at a 10-fold increase from baseline on day 10 after administration.	Cyclophosphamide	9-25	hypoxia inducible factor 1, alpha subunit	Mus musculus	121-131
18842820-0	2008	Role of p75NTR in female rat urinary bladder with cyclophosphamide-induced cystitis.	Cyclophosphamide	50-66	nerve growth factor receptor	Rattus norvegicus	8-14
18842820-1	2008	Previous studies demonstrated changes in urinary bladder neurotrophin content and upregulation of neurotrophin receptors, TrkA and the p75 neurotrophin receptor (p75(NTR)), in micturition reflex pathways after cyclophosphamide (CYP)-induced cystitis.	Cyclophosphamide	210-226	nerve growth factor receptor	Rattus norvegicus	162-170
19032367-0	2008	ABCG2 Q141K polymorphism is associated with chemotherapy-induced diarrhea in patients with diffuse large B-cell lymphoma who received frontline rituximab plus cyclophosphamide/doxorubicin/vincristine/prednisone chemotherapy.	Cyclophosphamide	159-175	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-5
18266977-7	2008	Acrolein treatment modulated expression of thrombospondin-1 (TSP-1), an endogenous inhibitor of angiogenesis known to be linked to antiangiogenic effects of metronomic CPA therapy.	Cyclophosphamide	168-171	thrombospondin 1	Mus musculus	43-59
18266977-7	2008	Acrolein treatment modulated expression of thrombospondin-1 (TSP-1), an endogenous inhibitor of angiogenesis known to be linked to antiangiogenic effects of metronomic CPA therapy.	Cyclophosphamide	168-171	thrombospondin 1	Mus musculus	61-66
18771470-1	2008	OBJECTIVE: To compare the effects, relapse ratio and outcomes between mycophenolate mofetil (MMF) and pulse intravenous cyclophosphamide (CTX) for the induction therapy in patients with crescentic lupus nephritis.	Cyclophosphamide	120-136	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	138-141
19189667-3	2008	The work presented here shows that the mTOR inhibitor everolimus, in combination with cyclophosphamide, exhibits synergistic antitumor activity in gastric cancer xenografts.	Cyclophosphamide	86-102	mechanistic target of rapamycin kinase	Homo sapiens	39-43
19205423-2	2008	The treatment of K562 cells with cyclophosphane and the t-butylamine thiazophosphol derivative was accompanied by the induction of erythroid differentiation, activation of caspase 3 and caspase 9, followed by subsequent induction of apoptosis.	Cyclophosphamide	33-47	caspase 3	Homo sapiens	172-181
19205423-2	2008	The treatment of K562 cells with cyclophosphane and the t-butylamine thiazophosphol derivative was accompanied by the induction of erythroid differentiation, activation of caspase 3 and caspase 9, followed by subsequent induction of apoptosis.	Cyclophosphamide	33-47	caspase 9	Homo sapiens	186-195
18922107-9	2008	Both temozolomide + irinotecan and cyclophosphamide + topotecan combinations are very active in ES and are likely to be tested with anti-IGF-1R antibodies against ES.	Cyclophosphamide	35-51	insulin like growth factor 1 receptor	Homo sapiens	137-143
18299998-0	2008	Expression of phosphorylated cAMP response element binding protein (p-CREB) in bladder afferent pathways in VIP-/- mice with cyclophosphamide (CYP)-induced cystitis.	Cyclophosphamide	125-141	cAMP responsive element binding protein 1	Mus musculus	70-74
18299998-0	2008	Expression of phosphorylated cAMP response element binding protein (p-CREB) in bladder afferent pathways in VIP-/- mice with cyclophosphamide (CYP)-induced cystitis.	Cyclophosphamide	143-146	cAMP responsive element binding protein 1	Mus musculus	70-74
18561033-7	2008	With the induction of bladder inflammation by acute administration of cyclophosphamide, an exaggerated or prolonged bladder hyperreflexia and hindpaw and pelvic sensitivity were demonstrated in VIP(-/-) mice.	Cyclophosphamide	70-86	vasoactive intestinal polypeptide	Mus musculus	194-197
18563302-0	2008	PACAP-mediated ATP release from rat urothelium and regulation of PACAP/VIP and receptor mRNA in micturition pathways after cyclophosphamide (CYP)-induced cystitis.	Cyclophosphamide	123-139	adenylate cyclase activating polypeptide 1	Rattus norvegicus	0-5
18563302-0	2008	PACAP-mediated ATP release from rat urothelium and regulation of PACAP/VIP and receptor mRNA in micturition pathways after cyclophosphamide (CYP)-induced cystitis.	Cyclophosphamide	123-139	adenylate cyclase activating polypeptide 1	Rattus norvegicus	65-70
18563302-0	2008	PACAP-mediated ATP release from rat urothelium and regulation of PACAP/VIP and receptor mRNA in micturition pathways after cyclophosphamide (CYP)-induced cystitis.	Cyclophosphamide	123-139	vasoactive intestinal peptide	Rattus norvegicus	71-87
18953436-6	2008	Cyclophosphamide (CPM) induced a complete remission in p53 wild type TH-MYCN tumors, mirroring the sensitivity of childhood neuroblastoma to this agent.	Cyclophosphamide	0-16	transformation related protein 53, pseudogene	Mus musculus	55-58
18953436-6	2008	Cyclophosphamide (CPM) induced a complete remission in p53 wild type TH-MYCN tumors, mirroring the sensitivity of childhood neuroblastoma to this agent.	Cyclophosphamide	0-16	v-myc avian myelocytomatosis viral related oncogene, neuroblastoma derived	Mus musculus	72-76
18953436-6	2008	Cyclophosphamide (CPM) induced a complete remission in p53 wild type TH-MYCN tumors, mirroring the sensitivity of childhood neuroblastoma to this agent.	Cyclophosphamide	18-21	transformation related protein 53, pseudogene	Mus musculus	55-58
18953436-6	2008	Cyclophosphamide (CPM) induced a complete remission in p53 wild type TH-MYCN tumors, mirroring the sensitivity of childhood neuroblastoma to this agent.	Cyclophosphamide	18-21	v-myc avian myelocytomatosis viral related oncogene, neuroblastoma derived	Mus musculus	72-76
18957084-0	2008	CXCL10 blockade protects mice from cyclophosphamide-induced cystitis.	Cyclophosphamide	35-51	chemokine (C-X-C motif) ligand 10	Mus musculus	0-6
18937726-0	2008	A case report of plasma exchange, steroids, mycophenolate mofetil and cyclophosphamide in acquired factor VIII inhibitors.	Cyclophosphamide	70-86	coagulation factor VIII	Homo sapiens	99-110
18854288-4	2008	After treatment with cyclophosphamide and dexamethasone, the peripheral blood plasma cells disappeared and there was a dramatic decrease in the CA125 and CA15.3 tumor markers.	Cyclophosphamide	21-37	mucin 16, cell surface associated	Homo sapiens	144-149
19144262-3	2008	The TCTP transgene prevents Tregs from undergoing apoptosis induced by interleukin-2 withdrawal-, dexamethasone-, cyclophosphamide-, and anti-Fas treatment in vitro.	Cyclophosphamide	114-130	tumor protein, translationally-controlled 1	Homo sapiens	4-8
18937726-12	2008	Hence, we present a case of severe idiopathic FVIII inhibitor-positive hemophilia successfully treated with the combination of plasma exchange, corticosteroids, cyclophosphamide and MMF.	Cyclophosphamide	161-177	coagulation factor VIII	Homo sapiens	46-51
18692125-1	2008	AIM OF THE STUDY: The objectives of this study were to investigate the protective effect of the triterpenoid fractions from the rhizomes of Astilbe chinensis (Saxifragaceae) (ATF) on cyclophosphamide (CTX)-induced toxicity in tumor-bearing mice.	Cyclophosphamide	183-199	glial cell line derived neurotrophic factor	Mus musculus	175-178
18632792-0	2008	Upregulation of vascular endothelial growth factor isoform VEGF-164 and receptors (VEGFR-2, Npn-1, and Npn-2) in rats with cyclophosphamide-induced cystitis.	Cyclophosphamide	123-139	vascular endothelial growth factor A	Rattus norvegicus	59-67
18632792-1	2008	Regulation of the VEGF-VEGF receptor system was examined in the urinary bladder after acute (2-48 h) and chronic (10 days) cyclophosphamide (CYP)-induced cystitis.	Cyclophosphamide	123-139	vascular endothelial growth factor A	Mus musculus	18-22
18632792-1	2008	Regulation of the VEGF-VEGF receptor system was examined in the urinary bladder after acute (2-48 h) and chronic (10 days) cyclophosphamide (CYP)-induced cystitis.	Cyclophosphamide	123-139	vascular endothelial growth factor A	Mus musculus	23-27
18708754-4	2008	We hypothesized that mTORC1 inhibition by everolimus (RAD001) leads to suppression of HIF-1alpha and VEGF resulting in synergistic anti-tumor activity in combination with anti-angiogenically dosed cyclophosphamide.	Cyclophosphamide	197-213	CREB regulated transcription coactivator 1	Mus musculus	21-27
18781911-5	2008	These individual differences may result in variable systemic exposure to drugs metabolized by CYP2B6, including the antineoplastics cyclophosphamide and ifosfamide, the antiretrovirals nevirapine and efavirenz, the anesthetics propofol and ketamine, the synthetic opioid methadone, and the anti-Parkinsonian selegiline.	Cyclophosphamide	132-148	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	94-100
18853118-6	2008	The level of IL-2 and INF-gamma could be decreased by Cy to 38.12+/-6.88 ng/L and 139.23+/-29.87 ng/L, respectively, while RIP in high dose could increase the secretion of IL-2 and INF-gamma to 53.54+/-14.43 ng/L and 189.91+/-32.63 ng/L, respectively.	Cyclophosphamide	54-56	interleukin 2	Mus musculus	13-17
18853118-6	2008	The level of IL-2 and INF-gamma could be decreased by Cy to 38.12+/-6.88 ng/L and 139.23+/-29.87 ng/L, respectively, while RIP in high dose could increase the secretion of IL-2 and INF-gamma to 53.54+/-14.43 ng/L and 189.91+/-32.63 ng/L, respectively.	Cyclophosphamide	54-56	interleukin 2	Mus musculus	172-176
18644830-0	2008	Protection of IFN-gamma signaling-deficient NOD mice from diabetes by cyclophosphamide.	Cyclophosphamide	70-86	interferon gamma	Mus musculus	14-23
18548196-9	2008	During all three cycles there was a significant increase in baseline BNP concentrations and BNP levels measured at day 1 after treatment with CY and MEL (CY: P = 0.0001, MEL I: P = 0.001, MEL II: P = 0.001).	Cyclophosphamide	142-144	natriuretic peptide B	Homo sapiens	92-95
18644830-2	2008	In the current study, we demonstrated that treatment of IFN-gamma signaling-deficient NOD mice with cyclophosphamide (CY) not only fails to induce acute diabetes but also confers permanent protection from diabetes.	Cyclophosphamide	100-116	interferon gamma	Mus musculus	56-65
18548196-10	2008	The highest BNP concentration occurred during CY treatment (0.517 +/- 0.391 microg/L).	Cyclophosphamide	46-48	natriuretic peptide B	Homo sapiens	12-15
18644830-2	2008	In the current study, we demonstrated that treatment of IFN-gamma signaling-deficient NOD mice with cyclophosphamide (CY) not only fails to induce acute diabetes but also confers permanent protection from diabetes.	Cyclophosphamide	118-120	interferon gamma	Mus musculus	56-65
18644830-4	2008	Moreover, CY treatment of IFN-gamma signaling-deficient NOD mice reversed the ongoing pathogenic process and eliminated cellular infiltrates of pancreatic islets.	Cyclophosphamide	10-12	interferon gamma	Mus musculus	26-35
18502831-1	2008	Chemotherapy with alemtuzumab and the combination of cyclophosphamide, adriamycin, oncovin, and prednisone (CHOP) has become experimental trial therapy for aggressive T-cell lymphoma.	Cyclophosphamide	53-69	DNA damage inducible transcript 3	Homo sapiens	108-112
18477655-0	2008	Survival and tumorigenesis in O6-methylguanine DNA methyltransferase-deficient mice following cyclophosphamide exposure.	Cyclophosphamide	94-110	O-6-methylguanine-DNA methyltransferase	Mus musculus	30-68
18665163-1	2008	tAnGo is a large randomised trial assessing the addition of gemcitabine(G) to paclitaxel(T), following epirubicin(E) and cyclophosphamide(C) in women with invasive higher risk early breast cancer.	Cyclophosphamide	121-137	MIA SH3 domain ER export factor 3	Homo sapiens	0-5
18324350-0	2008	Long-term follow-up of patients with IgA nephropathy treated with prednisolone and cyclophosphamide therapy.	Cyclophosphamide	83-99	CD79a molecule	Homo sapiens	37-40
18937075-3	2008	We describe the clinical course of hypopituitarism as a complication of IVL, successfully treated with immunochemotherapy (cyclophosphamide/doxorubicin/vincristine/prednisone-CHOP) plus Rituximab anti-CD20 humanized antibody).	Cyclophosphamide	123-139	DNA damage inducible transcript 3	Homo sapiens	175-179
18541199-5	2008	In conclusion, Cy can be added to G-CSF for stem cell mobilization to successfully overcome the suppressive effect of prior treatment with lenalidomide.	Cyclophosphamide	15-17	colony stimulating factor 3	Homo sapiens	34-39
18463353-7	2008	An analysis of the literature shows that the most effective first-line treatment for the eradication of factor VIII autoantibodies is the combination of steroids and cyclophosphamide.	Cyclophosphamide	166-182	cytochrome c oxidase subunit 8A	Homo sapiens	111-115
18199598-9	2008	Treatment with glucocorticoids and cyclophosphamide reduced CD4(+)CD25(-)Foxp3(+) T cells in 8 of 10 patients with active disease.	Cyclophosphamide	35-51	CD4 molecule	Homo sapiens	60-63
18199598-9	2008	Treatment with glucocorticoids and cyclophosphamide reduced CD4(+)CD25(-)Foxp3(+) T cells in 8 of 10 patients with active disease.	Cyclophosphamide	35-51	interleukin 2 receptor subunit alpha	Homo sapiens	66-70
18199598-9	2008	Treatment with glucocorticoids and cyclophosphamide reduced CD4(+)CD25(-)Foxp3(+) T cells in 8 of 10 patients with active disease.	Cyclophosphamide	35-51	forkhead box P3	Homo sapiens	73-78
18325917-2	2008	We analysed the efficacy of a preoperative combination between 5-fluorouracil, anthracyclines and cyclophosphamide according to both p53 status and molecular classification.	Cyclophosphamide	98-114	tumor protein p53	Homo sapiens	133-136
18477047-0	2008	The combination of cyclophosphamide and human T cells genetically engineered to target CD19 can eradicate established B-cell lymphoma.	Cyclophosphamide	19-35	CD19 molecule	Homo sapiens	87-91
18223682-0	2008	Low-dose metronomic cyclophosphamide treatment mediates ischemia-dependent K-ras mutation in colorectal carcinoma xenografts.	Cyclophosphamide	20-36	KRAS proto-oncogene, GTPase	Homo sapiens	75-80
18537979-6	2008	The addition of the monoclonal anti-CD20 antibody rituximab to standard CHOP (cyclophosphamide, doxorubicin, vincristine, prednisone) chemotherapy improved outcome of adults with DLBCL significantly.	Cyclophosphamide	78-94	keratin 20	Homo sapiens	36-40
18597657-5	2008	Marsh and colleagues analyzed the CYP1B1*3 (Val432Leu) polymorphism in patients with high-risk stage III and IV breast cancer, who received dose-intense paclitaxel in combination with doxorubicin and cyclophosphamide.	Cyclophosphamide	200-216	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	34-40
18760704-1	2008	The concurrent use of rituximab with cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) has established the utility of chemoimmunotherapy for the treatment of aggressive non-Hodgkin"s lymphoma (NHL).	Cyclophosphamide	37-53	DNA damage inducible transcript 3	Homo sapiens	99-103
18560594-9	2008	Aldehyde dehydrogenase 1 gene expression and enzymatic activity are elevated in CoCSC and using an in vitro culture system that maintains CoCSC as demonstrated by serial transplants and lentiviral marking of single cell-derived clones, we further show that ALDH1 enzymatic activity is a major mediator of resistance to cyclophosphamide: a classical chemotherapeutic agent.	Cyclophosphamide	319-335	aldehyde dehydrogenase 1 family member A1	Homo sapiens	257-262
19110568-3	2008	Addition of 1 mg/ml cyclophosphamide to the culture medium suppressed cell proliferation, which was associated with enhanced expression of proapoptotic p53 protein.	Cyclophosphamide	20-36	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	152-155
18538114-13	2008	CONCLUSIONS: These results indicate that MMF could be an alternative therapy for anti-MPO renal vasculitis associated with cyclophosphamide or azathioprine-related toxicity.	Cyclophosphamide	123-139	myeloperoxidase	Homo sapiens	86-89
20029469-2	2008	PATIENTS AND METHODS: In this phase II study we evaluated the clinical efficacy and tolerability of low dose, oral Methotrexate (MTX) and Cyclophosphamide (CTX) in patients with metastatic breast cancer.	Cyclophosphamide	138-154	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	156-159
18583880-1	2008	The objective of the current study was to investigate the treatment outcomes for the use of cyclophosphamide, adriamycin, vincristine, and prednisolone (CHOP) chemotherapy in adult patients with hemophagocytic lymphohistiocytosis (HLH).	Cyclophosphamide	92-108	DNA damage inducible transcript 3	Homo sapiens	153-157
18278567-10	2008	Cyclophosphamide and phosphoramide mustard, DNA cross-linking agents, decreased tau phosphorylation at Ser-396/404 site, but increased phosphorylation at Ser-202.	Cyclophosphamide	0-16	microtubule associated protein tau	Homo sapiens	80-83
18395765-2	2008	Here, a teratogen such as cyclophosphamide (CP) was used to test whether teratogenic insult alters the classical NF-kappaB activation pathway, and how these alterations correlate with the ability of mouse embryos to resist the teratogen-induced process of maldevelopment.	Cyclophosphamide	26-42	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	113-122
18533195-2	2008	In this paper, the optimal controller represents the optimal drug dosage of CAF (Cyclophosphamide, Adriamycin and Fluorouracil) regimen in adjuvant chemotherapy after surgery for these patients.	Cyclophosphamide	81-97	lysine acetyltransferase 2B	Homo sapiens	76-79
17917716-0	2008	Therapeutic effects of the putative P2X3/P2X2/3 antagonist A-317491 on cyclophosphamide-induced cystitis in rats.	Cyclophosphamide	71-87	purinergic receptor P2X 3	Rattus norvegicus	36-40
18496131-1	2008	PURPOSE: The anticancer agent, cyclophosphamide, is metabolized by cytochrome P450 (CYP), glutathione S-transferase (GST) and aldehyde dehydrogenase (ALDH) enzymes.	Cyclophosphamide	31-47	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	67-82
18496131-1	2008	PURPOSE: The anticancer agent, cyclophosphamide, is metabolized by cytochrome P450 (CYP), glutathione S-transferase (GST) and aldehyde dehydrogenase (ALDH) enzymes.	Cyclophosphamide	31-47	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	84-87
18496131-1	2008	PURPOSE: The anticancer agent, cyclophosphamide, is metabolized by cytochrome P450 (CYP), glutathione S-transferase (GST) and aldehyde dehydrogenase (ALDH) enzymes.	Cyclophosphamide	31-47	glutathione S-transferase kappa 1	Homo sapiens	90-115
18496131-1	2008	PURPOSE: The anticancer agent, cyclophosphamide, is metabolized by cytochrome P450 (CYP), glutathione S-transferase (GST) and aldehyde dehydrogenase (ALDH) enzymes.	Cyclophosphamide	31-47	glutathione S-transferase kappa 1	Homo sapiens	117-120
18390970-0	2008	Influence of activation state of ErbB-2 (HER-2) on response to adjuvant cyclophosphamide, doxorubicin, and fluorouracil for stage II, node-positive breast cancer: study 8541 from the Cancer and Leukemia Group B.	Cyclophosphamide	72-88	erb-b2 receptor tyrosine kinase 2	Homo sapiens	33-39
19040069-1	2008	OBJECTIVE: To evaluate the effects of four agents including cyclophosphamide, thalidomide, total glucosides of peony (TGP) and simvastatin on cell-proliferation and endothelin-1 secretion of human endothelial cells (ECs).	Cyclophosphamide	60-76	endothelin 1	Homo sapiens	165-177
19040069-7	2008	(2) Cyclophosphamide (50-2000 micromol/L) and simvastatin (5-10 micromol/L) decreased endothelin-1 secretion but not in dose dependent manner.	Cyclophosphamide	4-20	endothelin 1	Homo sapiens	86-98
19040069-9	2008	Cyclophosphamide and simvastatin can decrease endothelin-1 secretion of human ECs.	Cyclophosphamide	0-16	endothelin 1	Homo sapiens	46-58
18772604-11	2008	As Fas/FasL signaling is reported to be essential for cyclophosphamide-induced diabetes model, we extracted RNA from lymphocytes of the inguinal lymph nodes of anti-FasL Ab-treated NOD mice and performed real-time PCR to determine expression of Rse gene.	Cyclophosphamide	54-70	Fas ligand (TNF superfamily, member 6)	Mus musculus	7-11
18390970-0	2008	Influence of activation state of ErbB-2 (HER-2) on response to adjuvant cyclophosphamide, doxorubicin, and fluorouracil for stage II, node-positive breast cancer: study 8541 from the Cancer and Leukemia Group B.	Cyclophosphamide	72-88	erb-b2 receptor tyrosine kinase 2	Homo sapiens	41-46
18390970-2	2008	Results from a previous study from the Cancer and Leukemia Group B (CALGB 8541) demonstrated an interaction between ErbB-2 and increasing dose of adjuvant cyclophosphamide, doxorubicin, and fluorouracil (CAF) chemotherapy.	Cyclophosphamide	155-171	erb-b2 receptor tyrosine kinase 2	Homo sapiens	116-122
18443965-1	2008	We report a case of a previously healthy 31 year old woman diagnosed with Stage IIIA follicular lymphoma treated with fludarabine in combination with cyclophosphamide and rituximab who presented seven years after the completion of therapy with CD4 count depression, panhypogammaglobulinema and a history of recurrent sinus infections.	Cyclophosphamide	150-166	CD4 molecule	Homo sapiens	244-247
18410892-2	2008	We show that treatment of mice with cyclophosphamide (Cy) followed by CD8(+) T cell-depleted allogeneic donor lymphocyte infusion (Cy + CD8(-) DLI) induces regression of established tumors with minimal toxicity in models of both hematologic and solid cancers, even though the donor cells are eventually rejected by the host immune system.	Cyclophosphamide	54-56	CD8a molecule	Homo sapiens	136-139
18451231-5	2008	Both letrozole alone and letrozole with cyclophosphamide resulted in a significant reduction of PI3K expression (P = 0.02 and P < 0.005, respectively) and phospho-mTOR expression (P = 0.0001 and P = 0.0001, respectively).	Cyclophosphamide	40-56	mechanistic target of rapamycin kinase	Homo sapiens	166-170
18388918-2	2008	One such vector, rRp450, is ICP6-deleted and expresses a prodrug enzyme for cyclophosphamide (CPA) (rat CYP2B1).	Cyclophosphamide	76-92	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	104-110
18473730-9	2008	D341 MED (4-HCR) also had a 20-fold increase in the expression of the aldo-keto reductase gene, AKR1B10, which may deactivate the reactive cyclophosphamide metabolite, aldophosphamide.	Cyclophosphamide	139-155	coiled-coil alpha-helical rod protein 1	Homo sapiens	12-15
18473730-9	2008	D341 MED (4-HCR) also had a 20-fold increase in the expression of the aldo-keto reductase gene, AKR1B10, which may deactivate the reactive cyclophosphamide metabolite, aldophosphamide.	Cyclophosphamide	139-155	aldo-keto reductase family 1 member B10	Homo sapiens	96-103
18177354-0	2008	Cyclophosphamide for anti-GAD antibody-positive refractory status epilepticus.	Cyclophosphamide	0-16	glutamate decarboxylase 1	Homo sapiens	26-29
18177354-4	2008	We report here for the first time on a patient with sudden onset of refractory status epilepticus in the presence of strong intrathecal anti-GAD antibody synthesis who was successfully treated with cyclophosphamide, and give an overview of available data on epilepsy associated with GAD autoimmunity.	Cyclophosphamide	198-214	glutamate decarboxylase 1	Homo sapiens	141-144
18375833-0	2008	Upregulation of macrophage migration inhibitory factor (MIF) and CD74, receptor for MIF, in rat bladder during persistent cyclophosphamide-induced inflammation.	Cyclophosphamide	122-138	macrophage migration inhibitory factor	Rattus norvegicus	16-54
18375833-0	2008	Upregulation of macrophage migration inhibitory factor (MIF) and CD74, receptor for MIF, in rat bladder during persistent cyclophosphamide-induced inflammation.	Cyclophosphamide	122-138	macrophage migration inhibitory factor	Rattus norvegicus	56-59
18375833-0	2008	Upregulation of macrophage migration inhibitory factor (MIF) and CD74, receptor for MIF, in rat bladder during persistent cyclophosphamide-induced inflammation.	Cyclophosphamide	122-138	CD74 molecule	Rattus norvegicus	65-69
18375833-0	2008	Upregulation of macrophage migration inhibitory factor (MIF) and CD74, receptor for MIF, in rat bladder during persistent cyclophosphamide-induced inflammation.	Cyclophosphamide	122-138	macrophage migration inhibitory factor	Rattus norvegicus	84-87
18391755-7	2008	Induction of lymphopenia with Cy and Flu in combination with adoptive transfer of naive T cells and OVA peptide-pulsed DCs immunization led to an enhancement in the number of OVA specific, CD8 T cells that demonstrated specific cytotoxic activity, proliferation, and interferon-gamma production in response to the OVA expressing M05 melanoma.	Cyclophosphamide	30-32	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	175-178
18391755-7	2008	Induction of lymphopenia with Cy and Flu in combination with adoptive transfer of naive T cells and OVA peptide-pulsed DCs immunization led to an enhancement in the number of OVA specific, CD8 T cells that demonstrated specific cytotoxic activity, proliferation, and interferon-gamma production in response to the OVA expressing M05 melanoma.	Cyclophosphamide	30-32	interferon gamma	Mus musculus	267-283
18391755-7	2008	Induction of lymphopenia with Cy and Flu in combination with adoptive transfer of naive T cells and OVA peptide-pulsed DCs immunization led to an enhancement in the number of OVA specific, CD8 T cells that demonstrated specific cytotoxic activity, proliferation, and interferon-gamma production in response to the OVA expressing M05 melanoma.	Cyclophosphamide	30-32	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	175-178
18388918-2	2008	One such vector, rRp450, is ICP6-deleted and expresses a prodrug enzyme for cyclophosphamide (CPA) (rat CYP2B1).	Cyclophosphamide	94-97	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	104-110
18754430-0	2008	[Role of gonadotropin releasing hormone analogues for ovarian protection in systemic lupus erythematosus patients treated with cyclophosphamide].	Cyclophosphamide	127-143	gonadotropin releasing hormone 1	Homo sapiens	9-39
18754430-1	2008	OBJECTIVE: To evaluate the effectiveness of gonadotropin releasing hormone analogues (GnRH-a) in protection against premature ovarian failure during cyclophosphamide (CTX) therapy for systemic lupus erythematosus (SLE).	Cyclophosphamide	149-165	gonadotropin releasing hormone 1	Homo sapiens	44-74
18420078-5	2008	Following combined chemotherapy with rituximab and mini-CHOP (cyclophosphamide, adriamycin, oncovin and prednisone), complete remission was obtained rapidly, with no relapse at two years.	Cyclophosphamide	62-78	DNA damage inducible transcript 3	Homo sapiens	56-60
18712992-4	2008	The patient was treated with 6 courses of CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine, and prednisone).	Cyclophosphamide	61-77	DNA damage inducible transcript 3	Homo sapiens	42-46
18303033-1	2008	BACKGROUND: A prospective, single-arm, open-label, nonrandomized phase II combination chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) plus radioimmunotherapy trial was conducted to evaluate the efficacy and safety in untreated elderly diffuse large B-cell lymphoma (DLBCL) patients.	Cyclophosphamide	104-120	DNA damage inducible transcript 3	Homo sapiens	164-168
17874068-0	2008	Enhanced PON1 activity in the kidneys of cyclophosphamide treated rats may play a protective role as an antioxidant against cyclophosphamide induced oxidative stress.	Cyclophosphamide	41-57	paraoxonase 1	Rattus norvegicus	9-13
17874068-0	2008	Enhanced PON1 activity in the kidneys of cyclophosphamide treated rats may play a protective role as an antioxidant against cyclophosphamide induced oxidative stress.	Cyclophosphamide	124-140	paraoxonase 1	Rattus norvegicus	9-13
17874068-2	2008	A time course study was carried out in order to find out alterations in PON1 activity in cyclophosphamide (CYP) induced renal injury.	Cyclophosphamide	89-105	paraoxonase 1	Rattus norvegicus	72-76
17874068-9	2008	The present investigation shows for the first time that an increase in renal PON1 activity is an early biochemical event in cyclophosphamide induced renal damage.	Cyclophosphamide	124-140	paraoxonase 1	Rattus norvegicus	77-81
18171905-1	2008	CYP2B6 is a polymorphic human drug metabolizing cytochrome P450 with clinical relevance for several drug substrates including cyclophosphamide, bupropion, and efavirenz.	Cyclophosphamide	126-142	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	0-6
18212249-0	2008	Improvement of cyclophosphamide activation by CYP2B6 mutants: from in silico to ex vivo.	Cyclophosphamide	15-31	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	46-52
18212249-1	2008	Cyclophosphamide (CPA) is a chemotherapeutic agent that is primarily activated in the liver by cytochrome P4502B6 (CYP2B6) and then transported to the tumor via blood flow.	Cyclophosphamide	0-16	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	115-121
18212249-1	2008	Cyclophosphamide (CPA) is a chemotherapeutic agent that is primarily activated in the liver by cytochrome P4502B6 (CYP2B6) and then transported to the tumor via blood flow.	Cyclophosphamide	18-21	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	115-121
18212249-3	2008	Given the relatively low affinity of CYP2B6 for CPA, the aim of our work was to modify CYP2B6 to increase its catalytic efficiency (V(max)/K(m)) to metabolize CPA into 4"-OH CPA.	Cyclophosphamide	48-51	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	37-43
18212249-3	2008	Given the relatively low affinity of CYP2B6 for CPA, the aim of our work was to modify CYP2B6 to increase its catalytic efficiency (V(max)/K(m)) to metabolize CPA into 4"-OH CPA.	Cyclophosphamide	48-51	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	87-93
18212249-3	2008	Given the relatively low affinity of CYP2B6 for CPA, the aim of our work was to modify CYP2B6 to increase its catalytic efficiency (V(max)/K(m)) to metabolize CPA into 4"-OH CPA.	Cyclophosphamide	159-162	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	37-43
18212249-3	2008	Given the relatively low affinity of CYP2B6 for CPA, the aim of our work was to modify CYP2B6 to increase its catalytic efficiency (V(max)/K(m)) to metabolize CPA into 4"-OH CPA.	Cyclophosphamide	159-162	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	87-93
18212249-5	2008	Canine CYP2B11 exhibiting a particularly low K(m) to CPA, the amino acids exclusively present in the CYP2B11 substrate recognition sequences were substituted in human CYP2B6.	Cyclophosphamide	53-56	cytochrome P450 2B11	Canis lupus familiaris	7-14
18212249-5	2008	Canine CYP2B11 exhibiting a particularly low K(m) to CPA, the amino acids exclusively present in the CYP2B11 substrate recognition sequences were substituted in human CYP2B6.	Cyclophosphamide	53-56	cytochrome P450 2B11	Canis lupus familiaris	101-108
18212249-5	2008	Canine CYP2B11 exhibiting a particularly low K(m) to CPA, the amino acids exclusively present in the CYP2B11 substrate recognition sequences were substituted in human CYP2B6.	Cyclophosphamide	53-56	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	167-173
18212249-10	2008	Finally, expression of the CYP2B6 114V/477W double mutant, contrary to wt CYP2B6, allowed switching of a resistant human head and neck cancer cell line (A-253) into a sensitive cell line toward CPA.	Cyclophosphamide	194-197	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	27-33
18212249-11	2008	Thus, we were able to obtain a new efficient CYP2B6 mutant able to metabolize CPA, an important step in the GDEPT strategy for human cancer treatment.	Cyclophosphamide	78-81	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	45-51
18442331-2	2008	Five groups of mice were considered: young (Y) and aged (A) that were given intraperitoneally 10 doses of cyclophosphamide (CPX, 25mg/kg/bw) or CPX plus (150 mg/kg/bw) of the nutraceutical DTS (Denshichi-Tochiu-Sen), and control.	Cyclophosphamide	106-122	coproporphyrinogen oxidase	Mus musculus	124-127
18381103-3	2008	The addition of rituximab to cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy (R-CHOP regimen) improves the response rate, progression-free survival (PFS), and overall survival (OS) in diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	29-45	DNA damage inducible transcript 3	Homo sapiens	89-93
18211907-4	2008	A single iv administration of cyclophosphamide (CP, 5 mg/kg) induced an approximately 10-fold increase in blood MN-RET frequency, with the peak occurring 2 days after administration.	Cyclophosphamide	30-46	ret proto-oncogene	Macaca mulatta	115-118
18189308-0	2008	p75NTR expression in rat urinary bladder sensory neurons and spinal cord with cyclophosphamide-induced cystitis.	Cyclophosphamide	78-94	nerve growth factor receptor	Rattus norvegicus	0-6
18189308-3	2008	The present studies examine the expression and regulation of another receptor known to bind NGF, p75(NTR), after various durations of bladder inflammation induced by cyclophosphamide (CYP).	Cyclophosphamide	166-182	nerve growth factor	Rattus norvegicus	92-95
18189308-3	2008	The present studies examine the expression and regulation of another receptor known to bind NGF, p75(NTR), after various durations of bladder inflammation induced by cyclophosphamide (CYP).	Cyclophosphamide	166-182	nerve growth factor receptor	Rattus norvegicus	97-100
18349391-2	2008	PATIENTS AND METHODS: International Breast Cancer Study Group Trial VIII compared cyclophosphamide, methotrexate, and fluorouracil (CMF) chemotherapy for 6 cycles followed by endocrine therapy with goserelin with either modality alone in pre- and perimenopausal patients.	Cyclophosphamide	82-98	cytochrome c oxidase subunit 8A	Homo sapiens	68-72
18307678-4	2008	Indeed, the alpha(1)-adrenoceptor antagonist alfuzosin inhibits expression of the oncogene c-fos- a marker of nociceptive pathway activation - evoked by cyclophosphamide in rats.	Cyclophosphamide	153-169	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	91-96
18496131-10	2008	CONCLUSION: This study indicates that the presently evaluated variant alleles in the CYP2B6, CYP2C9, CYP2C19, CYP3A4, CYP3A5, GSTA1, GSTP1, ALDH1A1 and ALDH3A1 genes do not explain the interindividual variability in cyclophosphamide and 4-hydroxycyclophosphamide pharmacokinetics and are, probably, not the cause of the observed variability in toxicity.	Cyclophosphamide	216-232	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	85-91
18496131-10	2008	CONCLUSION: This study indicates that the presently evaluated variant alleles in the CYP2B6, CYP2C9, CYP2C19, CYP3A4, CYP3A5, GSTA1, GSTP1, ALDH1A1 and ALDH3A1 genes do not explain the interindividual variability in cyclophosphamide and 4-hydroxycyclophosphamide pharmacokinetics and are, probably, not the cause of the observed variability in toxicity.	Cyclophosphamide	216-232	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
18496131-10	2008	CONCLUSION: This study indicates that the presently evaluated variant alleles in the CYP2B6, CYP2C9, CYP2C19, CYP3A4, CYP3A5, GSTA1, GSTP1, ALDH1A1 and ALDH3A1 genes do not explain the interindividual variability in cyclophosphamide and 4-hydroxycyclophosphamide pharmacokinetics and are, probably, not the cause of the observed variability in toxicity.	Cyclophosphamide	216-232	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	101-108
18496131-10	2008	CONCLUSION: This study indicates that the presently evaluated variant alleles in the CYP2B6, CYP2C9, CYP2C19, CYP3A4, CYP3A5, GSTA1, GSTP1, ALDH1A1 and ALDH3A1 genes do not explain the interindividual variability in cyclophosphamide and 4-hydroxycyclophosphamide pharmacokinetics and are, probably, not the cause of the observed variability in toxicity.	Cyclophosphamide	216-232	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	110-116
18496131-10	2008	CONCLUSION: This study indicates that the presently evaluated variant alleles in the CYP2B6, CYP2C9, CYP2C19, CYP3A4, CYP3A5, GSTA1, GSTP1, ALDH1A1 and ALDH3A1 genes do not explain the interindividual variability in cyclophosphamide and 4-hydroxycyclophosphamide pharmacokinetics and are, probably, not the cause of the observed variability in toxicity.	Cyclophosphamide	216-232	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	118-124
18496131-10	2008	CONCLUSION: This study indicates that the presently evaluated variant alleles in the CYP2B6, CYP2C9, CYP2C19, CYP3A4, CYP3A5, GSTA1, GSTP1, ALDH1A1 and ALDH3A1 genes do not explain the interindividual variability in cyclophosphamide and 4-hydroxycyclophosphamide pharmacokinetics and are, probably, not the cause of the observed variability in toxicity.	Cyclophosphamide	216-232	aldehyde dehydrogenase 1 family member A1	Homo sapiens	140-147
18496131-10	2008	CONCLUSION: This study indicates that the presently evaluated variant alleles in the CYP2B6, CYP2C9, CYP2C19, CYP3A4, CYP3A5, GSTA1, GSTP1, ALDH1A1 and ALDH3A1 genes do not explain the interindividual variability in cyclophosphamide and 4-hydroxycyclophosphamide pharmacokinetics and are, probably, not the cause of the observed variability in toxicity.	Cyclophosphamide	216-232	aldehyde dehydrogenase 3 family member A1	Homo sapiens	152-159
18307678-6	2008	Involvement of the TRP cation channel, subfamily A, member 1 (TRPA1) has also been reported in models of neurogenic inflammation and nociception promoted by the cyclophosphamide metabolite, acrolein.	Cyclophosphamide	161-177	transient receptor potential cation channel, subfamily A, member 1	Rattus norvegicus	62-67
18316569-10	2008	CONCLUSION: Granulocyte macrophage colony-stimulating factor-secreting pancreatic cancer cell lines CG8020/CG2505 alone or in sequence with cyclophosphamide showed minimal treatment-related toxicity in patients with advanced pancreatic cancer.	Cyclophosphamide	140-156	colony stimulating factor 2	Homo sapiens	12-60
18032000-0	2008	Increased glutathione levels and activity of PON1 (phenyl acetate esterase) in the liver of rats after a single dose of cyclophosphamide: a defense mechanism?	Cyclophosphamide	120-136	paraoxonase 1	Rattus norvegicus	45-49
18296739-0	2008	Effects of poly(ADP-ribose) polymerase inhibition in bladder damage caused by cyclophosphamide in rats.	Cyclophosphamide	78-94	poly (ADP-ribose) polymerase 1	Rattus norvegicus	11-38
18296739-1	2008	It was previously shown that nitric oxide produced by inducible nitric oxide synthase (iNOS) and peroxynitrite are responsible for cyclophosphamide (CP)-induced cystitis.	Cyclophosphamide	131-147	nitric oxide synthase 2	Rattus norvegicus	54-85
18296739-1	2008	It was previously shown that nitric oxide produced by inducible nitric oxide synthase (iNOS) and peroxynitrite are responsible for cyclophosphamide (CP)-induced cystitis.	Cyclophosphamide	131-147	nitric oxide synthase 2	Rattus norvegicus	87-91
18388378-7	2008	The patient received five cycles of a cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) regimen which resulted in the regression in her skin lesions and constitutional symptoms.	Cyclophosphamide	38-54	DNA damage inducible transcript 3	Homo sapiens	97-101
18206168-2	2008	We report the heme oxygenase-1 mediated production of bilirubin and its cytoprotective roles in cyclophosphamide induced hemorrhagic cystitis in rats.	Cyclophosphamide	96-112	heme oxygenase 1	Rattus norvegicus	14-30
18206168-11	2008	The elevated expression of inducible nitric oxide synthase and interleukin-1beta in cyclophosphamide induced cystitis was significantly down-regulated by exogenously applied bilirubin.	Cyclophosphamide	84-100	interleukin 1 beta	Rattus norvegicus	63-80
18206168-13	2008	CONCLUSIONS: Cyclophosphamide induced hemorrhagic cystitis is accompanied by endogenous bilirubin production through heme oxygenase-1 induction in the bladder.	Cyclophosphamide	13-29	heme oxygenase 1	Rattus norvegicus	117-133
18619249-3	2008	METHODS: The immunity-deficiency model was induced by intraperitoneal injection of cyclophosphamide (CTX) at the dose of 100 mg/kg in mice; all the animals were divided into normal control group, immunity-deficiency model group, Part III treated group (300 mg/kg) and positive control group (TSPG, 300 mg/kg).	Cyclophosphamide	83-99	V-set and immunoglobulin domain containing 2	Mus musculus	101-104
18306483-2	2008	Shortness of breath developed following the 5th course of Rituximab-CHOP chemotherapy (cyclophosphamide, Vincristine, Doxorubicin, Prednisolone).	Cyclophosphamide	87-103	DNA damage inducible transcript 3	Homo sapiens	68-72
18226581-1	2008	BACKGROUND: Cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) is used to treat patients with non-Hodgkin lymphoma.	Cyclophosphamide	12-28	DNA damage inducible transcript 3	Homo sapiens	74-78
18085594-5	2008	After cyclophosphamide-induced bladder inflammation, fluorescence intensity of GFRalpha1-positive fibers increased within the dorsal horn, but there was no change in the GFRalpha2- or GFRalpha3-positive fibers.	Cyclophosphamide	6-22	GDNF family receptor alpha 1	Rattus norvegicus	79-88
18162120-1	2008	Immunochemotherapy with cyclophosphamide, adriamycin, vincristine, prednisone and rituximab (R-CHOP) is the standard treatment in non-immunosuppressed patients with diffuse large B-cell lymphoma (DLBCL), but its adequacy has not been definitively established in patients with human immunodeficiency virus (HIV)-related lymphoma.	Cyclophosphamide	24-40	DNA damage inducible transcript 3	Homo sapiens	95-99
18271922-6	2008	However, the overall survival of BL/BLL patients who received cyclophosphamide, doxorubicin, vincristine, and prednisolone-related therapy (22%) was significantly lower than that of DLBCL patients (P = 0.01).	Cyclophosphamide	62-78	mannose-binding lectin (protein C) 2	Mus musculus	33-35
18751869-0	2008	Anti-neutrophil cytoplasmic antibody (c-ANCA) positive recurrent eosinophilic fasciitis responsive to cyclophosphamide: a clinical pathology conference held by the Division of Rheumatology at Hospital for Special Surgery.	Cyclophosphamide	102-118	proteinase 3	Homo sapiens	38-44
18209092-1	2008	Costimulatory blockade with CTLA4Ig and anti-CD40L along with a single dose of cyclophosphamide induces remission of systemic lupus erythematosus nephritis in NZB/W F(1) mice.	Cyclophosphamide	79-95	TP53 regulated inhibitor of apoptosis 1	Mus musculus	163-169
18688165-0	2008	MIR in atypical idiopathic inflammatory demyelinating disease treated with methylprednisolone and cyclophosphamide.	Cyclophosphamide	98-114	membrane associated ring-CH-type finger 8	Homo sapiens	0-3
18281474-10	2008	Furthermore, we found that hypoxia-induced chemoresistance to cyclophosphamide was partially blocked by a combination of FAS inhibitor and cyclophosphamide.	Cyclophosphamide	62-78	fatty acid synthase	Homo sapiens	121-124
18258986-1	2008	PURPOSE: National Surgical Adjuvant Breast and Bowel Project (NSABP) Protocol B-18 was designed to determine whether four cycles of doxorubicin and cyclophosphamide (AC) administered preoperatively improved breast cancer disease-free survival (DFS) and overall survival (OS) compared with AC administered postoperatively.	Cyclophosphamide	148-164	NADH:ubiquinone oxidoreductase subunit B7	Homo sapiens	78-82
17875191-0	2008	Serious haematological toxicity of cyclophosphamide in relation to CYP2B6, GSTA1 and GSTP1 polymorphisms.	Cyclophosphamide	35-51	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	67-73
17875191-0	2008	Serious haematological toxicity of cyclophosphamide in relation to CYP2B6, GSTA1 and GSTP1 polymorphisms.	Cyclophosphamide	35-51	glutathione S-transferase alpha 1	Homo sapiens	75-80
17875191-0	2008	Serious haematological toxicity of cyclophosphamide in relation to CYP2B6, GSTA1 and GSTP1 polymorphisms.	Cyclophosphamide	35-51	glutathione S-transferase pi 1	Homo sapiens	85-90
17851116-9	2008	The foregoing findings are consistent with the hypothesis that malaria-caused attenuation of genotoxicity arose from a down modulation of CYP isoforms that convert CPA (CYP2B) and DMBA (CYP1A) into their active metabolites.	Cyclophosphamide	164-167	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	169-174
18254005-14	2008	Cyclosporin was as effective as cyclophosphamide (RR 1.07, 95% CI 0.48 to 2.35) and chlorambucil (RR 0.82, 95% CI 0.44 to 1.53) and levamisole (RR 0.43, 95% CI 0.27 to 0.68) was more effective than steroids alone but the effects were not sustained once treatment was stopped.	Cyclophosphamide	32-48	ribonucleotide reductase catalytic subunit M1	Homo sapiens	50-54
18079438-8	2008	The elevated expression of p65 nuclear localization in bladders treated with cyclophosphamide or cyclophosphamide with mecamylamine suggested nuclear factor-kappa B activation in the chronic inflammatory process.	Cyclophosphamide	97-113	RELA proto-oncogene, NF-kB subunit	Homo sapiens	27-30
18097780-1	2008	The aim of the study is to report the long-term outcome and secondary tumours of early breast cancer patients of adjuvant CNF (cyclophosphamide, mitoxantrone, and 5-fluorouracil) chemotherapy.	Cyclophosphamide	127-143	NPHS1 adhesion molecule, nephrin	Homo sapiens	122-125
18611066-3	2008	In uncontrolled clinical trials from approximately 20 studies, rituximab--a mouse-human chimeric anti-CD20 monoclonal antibody that effectively depletes B cells--has been demonstrated to reduce disease activity and decrease serum autoantibodies, with a clinical response of 86% in a case series of approximately 400 SLE patients with refractory disease, with or without concomitant use of cyclophosphamide.	Cyclophosphamide	389-405	membrane-spanning 4-domains, subfamily A, member 1	Mus musculus	102-106
18079438-8	2008	The elevated expression of p65 nuclear localization in bladders treated with cyclophosphamide or cyclophosphamide with mecamylamine suggested nuclear factor-kappa B activation in the chronic inflammatory process.	Cyclophosphamide	77-93	RELA proto-oncogene, NF-kB subunit	Homo sapiens	27-30
18540827-1	2008	Cyclophosphamide (CTX) is an alkylating cytotoxic drug that primarily affects proliferating lymphocytes.	Cyclophosphamide	0-16	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	18-21
18608354-10	2008	CD34(+) count on the day of leukapheresis, prior chemotherapy with prednisone, cyclophosphamide, adriamycin and BCNU or melphalan, and stem cell mobilization regimen significantly influenced CD34(+) cell yield.	Cyclophosphamide	79-95	CD34 molecule	Homo sapiens	191-195
18190241-6	2008	OPG levels were found to increase after treatment with CHOP (Vincristini, Cyklofosfamid, Adriamycin and Prednisol) and they decreased after administration of Leukeran (Chlorambucyl) and CMC (2CdA/Cladrybin, Mitoxanton and Cyklofosfamid).	Cyclophosphamide	74-87	TNF receptor superfamily member 11b	Homo sapiens	0-3
18196608-6	2008	Tumor-bearing mice treated with BBSKE showed an increase of life span with a comparable effect to cyclophosphamide (CTX).	Cyclophosphamide	98-114	V-set and immunoglobulin domain containing 2	Mus musculus	116-119
18036819-9	2008	With the 3-agent combination of CPA+VP-16 (ci)+VCR a significantly prolonged TtP was documented versus both single agent CPA (p=0.003) and the combination of CPA+VP-16 (dx5) (p=0.004).	Cyclophosphamide	32-35	ZFP36 ring finger protein	Homo sapiens	77-80
18036819-9	2008	With the 3-agent combination of CPA+VP-16 (ci)+VCR a significantly prolonged TtP was documented versus both single agent CPA (p=0.003) and the combination of CPA+VP-16 (dx5) (p=0.004).	Cyclophosphamide	32-35	host cell factor C1	Homo sapiens	162-167
18036819-11	2008	The addition of VP-16 (ci)+VCR to an already effective dosage of CPA further prolongs TtP.	Cyclophosphamide	65-68	host cell factor C1	Homo sapiens	16-21
18036819-11	2008	The addition of VP-16 (ci)+VCR to an already effective dosage of CPA further prolongs TtP.	Cyclophosphamide	65-68	ZFP36 ring finger protein	Homo sapiens	86-89
18202011-8	2008	The reduced tumor penetration of 4-OH-CPA was associated with a decrease in cyclophosphamide-induced tumor cell apoptosis and a block in the induction of the endogenous angiogenesis inhibitor thrombospondin-1 in tumor-associated host cells, which may contribute to the absence of tumor regression with the axitinib/cyclophosphamide combination.	Cyclophosphamide	315-331	thrombospondin 1	Rattus norvegicus	192-208
18190241-6	2008	OPG levels were found to increase after treatment with CHOP (Vincristini, Cyklofosfamid, Adriamycin and Prednisol) and they decreased after administration of Leukeran (Chlorambucyl) and CMC (2CdA/Cladrybin, Mitoxanton and Cyklofosfamid).	Cyclophosphamide	222-235	TNF receptor superfamily member 11b	Homo sapiens	0-3
19066630-0	2008	Cyclophosphamide-induced cystitis increases bladder CXCR4 expression and CXCR4-macrophage migration inhibitory factor association.	Cyclophosphamide	0-16	C-X-C motif chemokine receptor 4	Rattus norvegicus	52-57
19066630-0	2008	Cyclophosphamide-induced cystitis increases bladder CXCR4 expression and CXCR4-macrophage migration inhibitory factor association.	Cyclophosphamide	0-16	C-X-C motif chemokine receptor 4	Rattus norvegicus	73-78
19066630-0	2008	Cyclophosphamide-induced cystitis increases bladder CXCR4 expression and CXCR4-macrophage migration inhibitory factor association.	Cyclophosphamide	0-16	macrophage migration inhibitory factor	Rattus norvegicus	79-117
19066630-10	2008	Cyclophosphamide treatment caused: 1) significant redistribution of CXCR4 immunostaining to all urothelial layers (especially apical surface of superficial cells) and increased bladder CXCR4 expression; 2) increased urine MIF with decreased bladder MIF; 3) increased bladder SDF-1; 4) increased CXCR4-MIF associations.	Cyclophosphamide	0-16	C-X-C motif chemokine receptor 4	Rattus norvegicus	68-73
19066630-10	2008	Cyclophosphamide treatment caused: 1) significant redistribution of CXCR4 immunostaining to all urothelial layers (especially apical surface of superficial cells) and increased bladder CXCR4 expression; 2) increased urine MIF with decreased bladder MIF; 3) increased bladder SDF-1; 4) increased CXCR4-MIF associations.	Cyclophosphamide	0-16	C-X-C motif chemokine receptor 4	Rattus norvegicus	185-190
19066630-10	2008	Cyclophosphamide treatment caused: 1) significant redistribution of CXCR4 immunostaining to all urothelial layers (especially apical surface of superficial cells) and increased bladder CXCR4 expression; 2) increased urine MIF with decreased bladder MIF; 3) increased bladder SDF-1; 4) increased CXCR4-MIF associations.	Cyclophosphamide	0-16	macrophage migration inhibitory factor	Rattus norvegicus	222-225
19066630-10	2008	Cyclophosphamide treatment caused: 1) significant redistribution of CXCR4 immunostaining to all urothelial layers (especially apical surface of superficial cells) and increased bladder CXCR4 expression; 2) increased urine MIF with decreased bladder MIF; 3) increased bladder SDF-1; 4) increased CXCR4-MIF associations.	Cyclophosphamide	0-16	C-X-C motif chemokine ligand 12	Rattus norvegicus	275-280
19066630-10	2008	Cyclophosphamide treatment caused: 1) significant redistribution of CXCR4 immunostaining to all urothelial layers (especially apical surface of superficial cells) and increased bladder CXCR4 expression; 2) increased urine MIF with decreased bladder MIF; 3) increased bladder SDF-1; 4) increased CXCR4-MIF associations.	Cyclophosphamide	0-16	C-X-C motif chemokine receptor 4	Rattus norvegicus	185-190
19066630-10	2008	Cyclophosphamide treatment caused: 1) significant redistribution of CXCR4 immunostaining to all urothelial layers (especially apical surface of superficial cells) and increased bladder CXCR4 expression; 2) increased urine MIF with decreased bladder MIF; 3) increased bladder SDF-1; 4) increased CXCR4-MIF associations.	Cyclophosphamide	0-16	macrophage migration inhibitory factor	Rattus norvegicus	249-252
18161930-3	2007	The staphylococcal protein A (SPA) rosette test was utilized for measuring the ratio of T-lymphocyte subsets from peripheral blood in a cyclophosphamide-treated murine model.	Cyclophosphamide	136-152	surfactant associated protein A1	Mus musculus	30-33
18208780-8	2008	Chemotherapy using cyclophosphamide, vincristine and dexamethasone (COP modified) led to a dramatic response of the tumor and a complete resolution of compressive symptoms.	Cyclophosphamide	19-35	caspase recruitment domain family member 16	Homo sapiens	68-71
18751946-0	2008	Application of cyclophosphamide-induced tolerance in alpha1,3-galactosyltransferase knockout mice presensitized with Gal alpha 1-3Gal beta-4-GlcNAc antigens.	Cyclophosphamide	15-31	glycoprotein galactosyltransferase alpha 1, 3	Mus musculus	121-147
18284716-1	2007	Among the strategies developed to improve results in patients with diffuse large B-cell lymphoma, increasing the dose of CHOP (cyclophosphamide/doxorubicin/vincristine/prednisone) regimen (dose-intense regimen) and decreasing the duration of cycles (dose-dense regimen) or doing both had been proposed before the rituximab era.	Cyclophosphamide	127-143	DNA damage inducible transcript 3	Homo sapiens	121-125
17979934-0	2007	Protective effects of heme oxygenase-1 against cyclophosphamide-induced haemorrhagic cystitis in rats.	Cyclophosphamide	47-63	heme oxygenase 1	Rattus norvegicus	22-38
17979934-1	2007	OBJECTIVE: To investigate the expression profiles and protective roles of the inducible isoform of heme oxygenase-1 (HO-1) in cyclophosphamide (CYP)-induced cystitis, as the HO system is involved in heme degradation and plays an important role in cellular homeostasis but its characterization is still unknown in urinary tract diseases.	Cyclophosphamide	126-142	heme oxygenase 1	Rattus norvegicus	99-115
17979934-1	2007	OBJECTIVE: To investigate the expression profiles and protective roles of the inducible isoform of heme oxygenase-1 (HO-1) in cyclophosphamide (CYP)-induced cystitis, as the HO system is involved in heme degradation and plays an important role in cellular homeostasis but its characterization is still unknown in urinary tract diseases.	Cyclophosphamide	126-142	heme oxygenase 1	Rattus norvegicus	117-121
17979934-1	2007	OBJECTIVE: To investigate the expression profiles and protective roles of the inducible isoform of heme oxygenase-1 (HO-1) in cyclophosphamide (CYP)-induced cystitis, as the HO system is involved in heme degradation and plays an important role in cellular homeostasis but its characterization is still unknown in urinary tract diseases.	Cyclophosphamide	144-147	heme oxygenase 1	Rattus norvegicus	99-115
17979934-1	2007	OBJECTIVE: To investigate the expression profiles and protective roles of the inducible isoform of heme oxygenase-1 (HO-1) in cyclophosphamide (CYP)-induced cystitis, as the HO system is involved in heme degradation and plays an important role in cellular homeostasis but its characterization is still unknown in urinary tract diseases.	Cyclophosphamide	144-147	heme oxygenase 1	Rattus norvegicus	117-121
17516128-0	2007	Steady improvement of prothrombin levels after cyclophosphamide therapy in pediatric lupus anticoagulant hypoprothrombinemia syndrome (LAHPS).	Cyclophosphamide	47-63	coagulation factor II, thrombin	Homo sapiens	22-33
18396625-8	2007	Glucocorticoid combined with cyclophosphamide (CTX) was fundamentally effective treatment for NS post-HSCT.	Cyclophosphamide	29-45	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	47-50
17853921-3	2007	In mice bearing 9L gliosarcomas expressing the CPA 4-hydroxylase P450 2B6, enhanced tumor apoptosis was observed 48 h after CPA treatment; however, intratumoral 4-OH-CPA levels were indistinguishable from those of P450-deficient tumors, indicating that the bulk of activated CPA is derived from hepatic metabolism.	Cyclophosphamide	124-127	carboxypeptidase A4	Mus musculus	47-52
17956583-0	2007	Increase of CD4+ CD25+ regulatory T cells in the peripheral blood of patients with metastatic carcinoma: a Phase I clinical trial using cyclophosphamide and immunotherapy to eliminate CD4+ CD25+ T lymphocytes.	Cyclophosphamide	136-152	CD4 molecule	Homo sapiens	12-15
17956583-0	2007	Increase of CD4+ CD25+ regulatory T cells in the peripheral blood of patients with metastatic carcinoma: a Phase I clinical trial using cyclophosphamide and immunotherapy to eliminate CD4+ CD25+ T lymphocytes.	Cyclophosphamide	136-152	interleukin 2 receptor subunit alpha	Homo sapiens	17-21
17659340-2	2007	We measured TCL-1 protein in CLL cells from 51 patients who then received pentostatin, cyclophosphamide, and rituximab.	Cyclophosphamide	87-103	TCL1 family AKT coactivator A	Homo sapiens	12-17
17872895-4	2007	We assessed the impact of paternal cyclophosphamide exposure on phosphorylated H2AX (gammaH2AX) and poly(ADP-ribose) polymerase-1(PARP-1), biomarkers of DNA damage, to determine the capacity in the rat zygote to recognize genomic damage and initiate a response to DNA lesions.	Cyclophosphamide	35-51	poly (ADP-ribose) polymerase 1	Rattus norvegicus	100-129
17872895-4	2007	We assessed the impact of paternal cyclophosphamide exposure on phosphorylated H2AX (gammaH2AX) and poly(ADP-ribose) polymerase-1(PARP-1), biomarkers of DNA damage, to determine the capacity in the rat zygote to recognize genomic damage and initiate a response to DNA lesions.	Cyclophosphamide	35-51	poly (ADP-ribose) polymerase 1	Rattus norvegicus	130-136
17872895-6	2007	PARP-1 immunoreactivity was substantially elevated in both parental genomes, coincident with the second phase of gammaH2AX induction in embryos sired by cyclophosphamide-exposed spermatozoa.	Cyclophosphamide	153-169	poly (ADP-ribose) polymerase 1	Rattus norvegicus	0-6
17923867-0	2007	Intensified dose of cyclophosphamide with G-CSF support versus standard dose combined with platinum in first-line treatment of advanced ovarian cancer a randomised study from the GINECO group.	Cyclophosphamide	20-36	colony stimulating factor 3	Homo sapiens	42-47
18024297-0	2007	[Cyclophosphamide-induced rat ovarian damage and expression of gonadotropin-releasing hormone receptor in the damaged ovaries].	Cyclophosphamide	1-17	gonadotropin releasing hormone receptor	Rattus norvegicus	63-102
17980564-0	2007	WITHDRAWN: Increased glutathione levels and activity of PON(1) (phenyl acetate esterase) in the liver of rats after a single dose of cyclophosphamide; a defense mechanism?	Cyclophosphamide	133-149	paraoxonase 1	Rattus norvegicus	56-62
18024297-5	2007	Both the protein and mRNA expressions of GnRHR were detected in normal rat ovaries, but in rats exposed to cyclophosphamide, the expressions were significantly lowered in the ovaries (P<0.05).	Cyclophosphamide	107-123	gonadotropin releasing hormone receptor	Rattus norvegicus	41-46
18024297-6	2007	CONCLUSION: Low-level GnRHR expressions in the ovaries of rats with cyclophosphamide exposure suggest microenvironment disturbances in the damaged rat ovaries in advanced stage of chemotherapy.	Cyclophosphamide	68-84	gonadotropin releasing hormone receptor	Rattus norvegicus	22-27
17661091-0	2007	Protracted remission of proteinuria after combined therapy with plasmapheresis and anti-CD20 antibodies/cyclophosphamide in a child with oligoclonal IgM and glomerulosclerosis.	Cyclophosphamide	104-120	keratin 20	Homo sapiens	88-92
17876337-1	2007	In advanced breast cancers, TP53 mutation is highly predictive of complete response to high-dose epirubicin/cyclophosphamide chemotherapy.	Cyclophosphamide	108-124	tumor protein p53	Homo sapiens	28-32
17569821-3	2007	In the current study, we tested BDDpfVIII activity after nonmyeloablative conditioning with busulfan, cyclophosphamide, or fludarabine and immunosuppressive agents CTLA4-Ig + anti-CD40L or anti-(murine)thymocyte serum (ATS).	Cyclophosphamide	102-118	cytochrome c oxidase subunit 8A	Homo sapiens	32-41
17928597-2	2007	We hypothesized that HER2 positivity predicts a benefit from adjuvant doxorubicin doses above standard levels, from the addition of paclitaxel after adjuvant chemotherapy with doxorubicin plus cyclophosphamide, or from both.	Cyclophosphamide	193-209	erb-b2 receptor tyrosine kinase 2	Homo sapiens	21-25
17928597-10	2007	CONCLUSIONS: The expression or amplification, or both, of HER2 by a breast cancer is associated with a benefit from the addition of paclitaxel after adjuvant treatment with doxorubicin (<60 mg per square meter) plus cyclophosphamide in node-positive breast cancer, regardless of estrogen-receptor status.	Cyclophosphamide	219-235	erb-b2 receptor tyrosine kinase 2	Homo sapiens	58-62
17716984-8	2007	CONCLUSION: A dose-intense and dose-dense regimen of cyclophosphamide, epirubicin and 5-fluorouracil was delivered with G-CSF without apparent increase in acute toxicity.	Cyclophosphamide	53-69	colony stimulating factor 3	Homo sapiens	120-125
17440723-1	2007	Single administration of low dose cyclophosphamide (CTX) was previously reported to enhance the antitumor efficacy of immunotherapies.	Cyclophosphamide	34-50	V-set and immunoglobulin domain containing 2	Mus musculus	52-55
17908969-3	2007	EXPERIMENTAL DESIGN: Expression of a macrophage marker, CD68, was determined immunohistochemically from FL samples of 96 patients treated with rituximab and cyclophosphamide-Adriamycin-vincristine-prednisone regimen.	Cyclophosphamide	157-173	CD68 molecule	Homo sapiens	56-60
17854912-0	2007	High dose cyclophosphamide preferentially targets naive T (CD45/CD4/RA+) cells in CIDP and MS patients.	Cyclophosphamide	10-26	protein tyrosine phosphatase receptor type C	Homo sapiens	59-63
17854912-0	2007	High dose cyclophosphamide preferentially targets naive T (CD45/CD4/RA+) cells in CIDP and MS patients.	Cyclophosphamide	10-26	CD4 molecule	Homo sapiens	59-62
17881193-7	2007	EHF-irradiation of the skin before and after injection of CPA increased the staining of orexin-containing neurons, i.e. it prevented the redistribution of orexin.	Cyclophosphamide	58-61	hypocretin neuropeptide precursor	Rattus norvegicus	88-94
17959517-6	2007	There was a higher granulosa SCF, lower oocyte SCF and higher SCF mRNA level in the ovaries of the rats exposed to cyclophosphamide as compared with those in control rat ovaries (P <0.05).	Cyclophosphamide	115-131	KIT ligand	Rattus norvegicus	29-32
17959517-6	2007	There was a higher granulosa SCF, lower oocyte SCF and higher SCF mRNA level in the ovaries of the rats exposed to cyclophosphamide as compared with those in control rat ovaries (P <0.05).	Cyclophosphamide	115-131	KIT ligand	Rattus norvegicus	47-50
17959517-6	2007	There was a higher granulosa SCF, lower oocyte SCF and higher SCF mRNA level in the ovaries of the rats exposed to cyclophosphamide as compared with those in control rat ovaries (P <0.05).	Cyclophosphamide	115-131	KIT ligand	Rattus norvegicus	47-50
17959517-7	2007	CONCLUSION: Altered SCF expression in the ovaries of rats exposed to cyclophosphamide can be helpful for understanding the mechanisms for chemotherapeutic drug-induced ovarian damage.	Cyclophosphamide	69-85	KIT ligand	Rattus norvegicus	20-23
17881193-0	2007	Responses of hypothalamic orexin-containing neurons to cyclophosphamide, EHF-irradiation of the skin, and their combination in rats.	Cyclophosphamide	55-71	hypocretin neuropeptide precursor	Rattus norvegicus	26-32
17881193-2	2007	The aim of the present study was to clarify the responses of the hypothalamic orexin-containing neurons to an intraperitoneal injection of cyclophosphamide (CPA), extremely high frequency (EHF)-electromagnetic stimulation of skin, which is used to modulate side effects of cytostatics and their combination.	Cyclophosphamide	139-155	hypocretin neuropeptide precursor	Rattus norvegicus	78-84
17881193-4	2007	Injection of cyclophosphamide (40mg/kg) or EHF-irradiation of the skin decreased the staining of orexin-containing neurons, which was most pronounced in the subfornical region of the lateral hypothalamic area (LHAs).	Cyclophosphamide	13-29	hypocretin neuropeptide precursor	Rattus norvegicus	97-103
17881193-6	2007	c-Fos protein was expressed in most neurons with minimum content of orexin, i.e. activation of these neurons correlated with the redistribution of orexins caused by skin EHF-irradiation and injection of cyclophosphamide (CPA).	Cyclophosphamide	203-219	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
17881193-6	2007	c-Fos protein was expressed in most neurons with minimum content of orexin, i.e. activation of these neurons correlated with the redistribution of orexins caused by skin EHF-irradiation and injection of cyclophosphamide (CPA).	Cyclophosphamide	203-219	hypocretin neuropeptide precursor	Rattus norvegicus	68-74
17881193-6	2007	c-Fos protein was expressed in most neurons with minimum content of orexin, i.e. activation of these neurons correlated with the redistribution of orexins caused by skin EHF-irradiation and injection of cyclophosphamide (CPA).	Cyclophosphamide	221-224	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
17881193-6	2007	c-Fos protein was expressed in most neurons with minimum content of orexin, i.e. activation of these neurons correlated with the redistribution of orexins caused by skin EHF-irradiation and injection of cyclophosphamide (CPA).	Cyclophosphamide	221-224	hypocretin neuropeptide precursor	Rattus norvegicus	68-74
17647266-1	2007	BACKGROUND: A previously published prospective randomized phase 3 trial showed that administration of 24 weeks of primary systemic chemotherapy (PST) with paclitaxel and FEC(75) (fluorouracil, epirubicin, cyclophosphamide) concurrently with trastuzumab in patients with HER2-positive primary breast cancer resulted in a 60% pathologic complete response rate (PCR) with no associated severe cardiac toxicity.	Cyclophosphamide	205-221	erb-b2 receptor tyrosine kinase 2	Homo sapiens	270-274
17586065-5	2007	Here, we show that high VEGF mRNA and protein levels are concomitant with reparative angiogenesis that occurs dramatically during regeneration following acute involution induced by cyclophosphamide (CY) in the rat thymus.	Cyclophosphamide	181-197	vascular endothelial growth factor A	Rattus norvegicus	24-28
17586065-5	2007	Here, we show that high VEGF mRNA and protein levels are concomitant with reparative angiogenesis that occurs dramatically during regeneration following acute involution induced by cyclophosphamide (CY) in the rat thymus.	Cyclophosphamide	199-201	vascular endothelial growth factor A	Rattus norvegicus	24-28
17240043-9	2007	Finally, cyclophosphamide increased c-fos expression in the rat lumbar spinal cord.	Cyclophosphamide	9-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
17939339-5	2007	A CT scan performed following three cycles of chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) showed that the mass had nearly disappeared.	Cyclophosphamide	64-80	DNA damage inducible transcript 3	Homo sapiens	126-130
17475930-9	2007	Interestingly, cyclophosphamide selectively induced numerous changes in cell defense and detoxification proteins, most notably, in all known forms of the antioxidant enzyme glutathione peroxidase 4, in addition to an uncharacterized 54-kDa form; an overall increase in glutathione peroxidase 4 immunoreactivity was observed in the nuclear matrix extracts from cyclophosphamide-exposed spermatozoa.	Cyclophosphamide	15-31	glutathione peroxidase 4	Rattus norvegicus	173-197
17475930-9	2007	Interestingly, cyclophosphamide selectively induced numerous changes in cell defense and detoxification proteins, most notably, in all known forms of the antioxidant enzyme glutathione peroxidase 4, in addition to an uncharacterized 54-kDa form; an overall increase in glutathione peroxidase 4 immunoreactivity was observed in the nuclear matrix extracts from cyclophosphamide-exposed spermatozoa.	Cyclophosphamide	15-31	glutathione peroxidase 4	Rattus norvegicus	269-293
17297610-0	2007	Low LATS2 mRNA level can predict favorable response to epirubicin plus cyclophosphamide, but not to docetaxel, in breast cancers.	Cyclophosphamide	71-87	large tumor suppressor kinase 2	Homo sapiens	4-9
17297610-2	2007	This study investigated possible correlations of intra-tumoral LATS1 and LATS2 mRNA levels with response to epirubicin plus cyclophosphamide (EC) or docetaxel (DOC) treatment.	Cyclophosphamide	124-140	large tumor suppressor kinase 2	Homo sapiens	73-78
17681724-5	2007	Mice that received intra-colonic capsaicin (0.3%, 50 microl/animal) or intraperitoneal injection of cyclophosphamide (400 mg/kg) manifested spontaneous nociceptive behaviors or crises, which were significantly suppressed in animal groups treated with red sap (200 and 400 mg/kg, p.o.)	Cyclophosphamide	100-116	SH2 domain containing 1A	Mus musculus	255-258
17567945-4	2007	Of note, new knowledge has recently been generated on the mechanisms of action of some chemotherapeutic agents, such as cyclophosphamide (CTX), on cells of the immune system, whose effects can now be exploited for the design of more effective combination therapies.	Cyclophosphamide	120-136	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	138-141
18019678-4	2007	Cyclophosphamide was administered twice to streptozocin-induced diabetic females NOD-TGF-beta1 Tg or their female littermates after islet transplantation.	Cyclophosphamide	0-16	transforming growth factor, beta 1	Mus musculus	85-94
18019678-6	2007	Hyperglycemia was induced in all littermates, but three out of four NOD-TGF-beta1 Tg, which were STZ-induced diabetic female mice, remained normoglycemic in response to the administration of cyclophosphamide after islet transplantation.	Cyclophosphamide	191-207	transforming growth factor, beta 1	Mus musculus	72-81
17657277-9	2007	Immunosuppressive therapy with steroids, cyclophosphamide (CTX) is required for relief.	Cyclophosphamide	41-57	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	59-62
17537839-0	2007	Expression of cyclooxygenase-2 in urinary bladder in rats with cyclophosphamide-induced cystitis.	Cyclophosphamide	63-79	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	14-30
17537839-1	2007	These studies examined the expression of cyclooxygenase-2 (COX-2) expression in the urothelium and suburothelial space and detrusor from rats treated with cyclophosphamide (CYP) to induce acute (4 h), intermediate (48 h), or chronic (10-day) cystitis.	Cyclophosphamide	155-171	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	41-57
17537839-1	2007	These studies examined the expression of cyclooxygenase-2 (COX-2) expression in the urothelium and suburothelial space and detrusor from rats treated with cyclophosphamide (CYP) to induce acute (4 h), intermediate (48 h), or chronic (10-day) cystitis.	Cyclophosphamide	155-171	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	59-64
17485251-0	2007	Role of MGMT in protecting against cyclophosphamide-induced toxicity in cells and animals.	Cyclophosphamide	35-51	methylated-DNA--protein-cysteine methyltransferase	Cricetulus griseus	8-12
17485251-4	2007	Here, we demonstrate that Chinese hamster ovary cells transfected with MGMT are protected against cytotoxicity following treatment with chloroacetaldehyde (CAA), a neuro- and nephrotoxic metabolite of cyclophosphamide and ifosfamide.	Cyclophosphamide	201-217	methylated-DNA--protein-cysteine methyltransferase	Cricetulus griseus	71-75
17660247-0	2007	p53 regulates cyclophosphamide teratogenesis by controlling caspases 3, 8, 9 activation and NF-kappaB DNA binding.	Cyclophosphamide	14-30	transformation related protein 53, pseudogene	Mus musculus	0-3
17881193-7	2007	EHF-irradiation of the skin before and after injection of CPA increased the staining of orexin-containing neurons, i.e. it prevented the redistribution of orexin.	Cyclophosphamide	58-61	hypocretin neuropeptide precursor	Rattus norvegicus	155-161
17660247-0	2007	p53 regulates cyclophosphamide teratogenesis by controlling caspases 3, 8, 9 activation and NF-kappaB DNA binding.	Cyclophosphamide	14-30	caspase 8	Mus musculus	60-68
17660247-0	2007	p53 regulates cyclophosphamide teratogenesis by controlling caspases 3, 8, 9 activation and NF-kappaB DNA binding.	Cyclophosphamide	14-30	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	92-101
17983495-1	2007	OBJECTIVE: To investigate the effects of gonadotropin releasing hormone agonist (GnRH-a) and antagonist (GnRH-ant) on cyclophosphamide (CTX)-induced ovarian damage in rats.	Cyclophosphamide	118-134	gonadotropin releasing hormone 1	Rattus norvegicus	81-85
17983495-1	2007	OBJECTIVE: To investigate the effects of gonadotropin releasing hormone agonist (GnRH-a) and antagonist (GnRH-ant) on cyclophosphamide (CTX)-induced ovarian damage in rats.	Cyclophosphamide	118-134	gonadotropin releasing hormone 1	Rattus norvegicus	105-109
17063267-8	2007	The results of a multivariate logistic regression analysis revealed a significant association of the response to doxorubicin plus cyclophosphamide therapy with the DFI (P = 0.02); human epidermal receptor type 2 (HER2) status also tended to affect the response rate, however the association was not statistically significant (P = 0.06).	Cyclophosphamide	130-146	erb-b2 receptor tyrosine kinase 2	Homo sapiens	213-217
17634551-0	2007	The effect of repeated administration of cyclophosphamide on cytochrome P450 2B in rats.	Cyclophosphamide	41-57	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	61-76
17634551-1	2007	PURPOSE: The prodrug cyclophosphamide (CPA) is activated by cytochrome P450 (CYP) enzymes.	Cyclophosphamide	21-37	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	60-75
17634551-1	2007	PURPOSE: The prodrug cyclophosphamide (CPA) is activated by cytochrome P450 (CYP) enzymes.	Cyclophosphamide	21-37	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	77-80
17634551-1	2007	PURPOSE: The prodrug cyclophosphamide (CPA) is activated by cytochrome P450 (CYP) enzymes.	Cyclophosphamide	39-42	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	60-75
17634551-1	2007	PURPOSE: The prodrug cyclophosphamide (CPA) is activated by cytochrome P450 (CYP) enzymes.	Cyclophosphamide	39-42	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	77-80
17580253-2	2007	Fluconazole inhibits cytochrome P450 2C9, which is involved with the activation of CY, and so might provide protection from CY-related toxicities.	Cyclophosphamide	83-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-40
17580253-2	2007	Fluconazole inhibits cytochrome P450 2C9, which is involved with the activation of CY, and so might provide protection from CY-related toxicities.	Cyclophosphamide	124-126	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	21-40
17580253-8	2007	These data support the hypothesis that fluconazole, when coadministered with CY, decreases CY-related toxicities by inhibiting cytochrome P450 2C9 metabolism.	Cyclophosphamide	77-79	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	127-146
17606729-11	2007	Notably, mitigating immune tolerance by inhibiting regulatory T cell activity with cyclophosphamide revealed DC101-mediated augmentation of antitumor responses in vaccinated neu-N mice.	Cyclophosphamide	83-99	erb-b2 receptor tyrosine kinase 2	Mus musculus	174-177
17476281-6	2007	However, when analysis was carried out according to the primary neoplasia involved, a significant association was observed between the MTHFR haplotype (single nucleotide polymorphisms 677 and 1298) and the risk of developing t-MDS/AML in the breast cancer patients group (P=0.016) and cyclophosphamide-treated hematological disease group (P=0.005).	Cyclophosphamide	285-301	methylenetetrahydrofolate reductase	Homo sapiens	135-140
17446263-6	2007	Cyclophosphamide inhibited the mOscp1-mediated PAH uptake.	Cyclophosphamide	0-16	organic solute carrier partner 1	Mus musculus	31-37
17409468-1	2007	Chemotherapy of non-Hodgkin lymphoma (NHL) with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) is associated with significant gonadal damage.	Cyclophosphamide	48-64	DNA-damage inducible transcript 3	Rattus norvegicus	108-112
17548941-1	2007	We examined whether low dose radiation (LDR) exposure (75 mGy) could increase the therapeutic efficacy of cyclophosphamide (CTX) by comparing the effects of tumor suppression, tumor cell apoptosis, cell cycle and proliferation of bone marrow in vivo.	Cyclophosphamide	106-122	V-set and immunoglobulin domain containing 2	Mus musculus	124-127
17825150-3	2007	The CD34(+) cells were mobilized with cytoxan (CTX) + granulocyte-colony stimulating factor (G-CSF) and selected by clinical magnetic activated cell sorting (CliniMACS).	Cyclophosphamide	38-45	CD34 molecule	Homo sapiens	4-8
17549346-3	2007	The present study was designed to assess the association between the activity of OPRT in the tumor, and the clinicopathological status and prognosis of human resectable pancreatic cancer, especially regarding its relevance to the efficacy of adjuvant chemotherapy with uracil and tegafur (UFT), cyclophosphamide (CPA) and/or gemcitabine (GEM).	Cyclophosphamide	295-311	uridine monophosphate synthetase	Homo sapiens	81-85
17549346-3	2007	The present study was designed to assess the association between the activity of OPRT in the tumor, and the clinicopathological status and prognosis of human resectable pancreatic cancer, especially regarding its relevance to the efficacy of adjuvant chemotherapy with uracil and tegafur (UFT), cyclophosphamide (CPA) and/or gemcitabine (GEM).	Cyclophosphamide	313-316	uridine monophosphate synthetase	Homo sapiens	81-85
17549346-8	2007	In the OPRT (+) group, the survival rate of the patients, who received adjuvant chemotherapy (ACT) with UFT, CPA or GEM, was significantly higher than that of the patients without ACT; however, in the OPRT (-) group, there was no difference in the survival between the ACT (+) and (-) groups.	Cyclophosphamide	109-112	uridine monophosphate synthetase	Homo sapiens	7-11
17549346-9	2007	Multivariate analyses demonstrated that for all patients, primary tumor, status of nodal involvement (pN), residual tumor, level of dissection and CPA were significant variables for the prognosis: in OPRT (+) groups, primary tumor, nodal involvement, GEM and CPA were significant variables.	Cyclophosphamide	147-150	uridine monophosphate synthetase	Homo sapiens	200-204
17558308-0	2007	Polymorphism of the DNA repair enzyme XRCC1 is associated with treatment prediction in anthracycline and cyclophosphamide/methotrexate/5-fluorouracil-based chemotherapy of patients with primary invasive breast cancer.	Cyclophosphamide	105-121	X-ray repair cross complementing 1	Homo sapiens	38-43
17558308-14	2007	CONCLUSION: The DNA repair enzyme XRCC1 is a potential treatment predictor for the outcome and survival of anthracycline and cyclophosphamide/methotrexate/5-fluorouracil-based chemotherapy of invasive breast cancer.	Cyclophosphamide	125-141	X-ray repair cross complementing 1	Homo sapiens	34-39
17591563-3	2007	Cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy has been the standard systemic therapy for this disease with a cure rate of 40% to 50%, although, more recently, the addition of rituximab has been shown in phase III trials to confer a significant survival benefit in both older and younger patients.	Cyclophosphamide	0-16	DNA damage inducible transcript 3	Homo sapiens	60-64
17449250-0	2007	The erbB2+ cluster of the intrinsic gene set predicts tumor response of breast cancer patients receiving neoadjuvant chemotherapy with docetaxel, doxorubicin and cyclophosphamide within the GEPARTRIO trial.	Cyclophosphamide	162-178	erb-b2 receptor tyrosine kinase 2	Homo sapiens	4-9
17575218-1	2007	PURPOSE: To evaluate 3"-deoxy-3"-[(18)F]fluorothymidine-positron emission tomography (FLT-PET) for early monitoring response of high-grade non-Hodgkin"s lymphoma to treatment with cyclophosphamide-adriamycin-vincristine-prednisone chemotherapy with or without rituximab immunotherapy (R-CHOP/CHOP).	Cyclophosphamide	180-196	fms related receptor tyrosine kinase 1	Homo sapiens	86-89
17316840-3	2007	The present study describes the expression of NGF during thymus regeneration following acute involution induced by cyclophosphamide in the rat.	Cyclophosphamide	115-131	nerve growth factor	Rattus norvegicus	46-49
17763583-14	2007	CONCLUSIONS: Sufficient CD34+ cells can be mobilized by low dose of cyclophosphamide and rhG-CSF.	Cyclophosphamide	68-84	CD34 molecule	Homo sapiens	24-28
17545523-6	2007	CK18 levels were determined in serum from 61 breast cancer patients during docetaxel or cyclophosphamide/epirubicin/5-fluorouracil (CEF) therapy.	Cyclophosphamide	88-104	keratin 18	Homo sapiens	0-4
17361405-2	2007	Six cycles of cyclophosphamide, doxorubicin, vincristine, and prednisone-21 (CHOP-21) with rituximab (R-CHOP-21) achieved an event free survival after 3 years of > 90% in patients with a very good prognosis (IPI 0, without bulk).	Cyclophosphamide	14-30	DNA damage inducible transcript 3	Homo sapiens	77-81
17562513-5	2007	We present multidetector CT (MDCT) findings in a case of Hodgkin disease status one month post-chemotherapy (CHOP protocol; cyclophosphamide, doxorubicin, vincristine, prednisone) that presented with acute lower GIS bleeding.	Cyclophosphamide	124-140	DNA damage inducible transcript 3	Homo sapiens	109-113
17346282-7	2007	However, whereas the frequency and activity of CD4(+) CD25(+) CD45RB(low) regulatory T cells and the expression of cytotoxic T-lymphocyte antigen 4 (CTLA-4) in CD4(+) cells were up-regulated by hCDR1 treatment, they were minimally affected following treatment with CYC.	Cyclophosphamide	265-268	cytotoxic T-lymphocyte-associated protein 4	Mus musculus	115-147
17346282-7	2007	However, whereas the frequency and activity of CD4(+) CD25(+) CD45RB(low) regulatory T cells and the expression of cytotoxic T-lymphocyte antigen 4 (CTLA-4) in CD4(+) cells were up-regulated by hCDR1 treatment, they were minimally affected following treatment with CYC.	Cyclophosphamide	265-268	cytotoxic T-lymphocyte-associated protein 4	Mus musculus	149-155
17562616-8	2007	ET-1 results for the entire group of patients showed a significant difference between baseline ET-1 values and ET-1 values determined 8 hours after high-dose cyclophosphamide administration (P = .004).	Cyclophosphamide	158-174	endothelin 1	Homo sapiens	0-4
17562616-11	2007	In conclusion, the significant neurohumoral activation of heart failure occurring after high-dose cyclophosphamide treatment is manifested by an increase in BNP and ET-1 levels, yet without concomitant cardiomyocyte necrosis.	Cyclophosphamide	98-114	natriuretic peptide B	Homo sapiens	157-160
17562616-11	2007	In conclusion, the significant neurohumoral activation of heart failure occurring after high-dose cyclophosphamide treatment is manifested by an increase in BNP and ET-1 levels, yet without concomitant cardiomyocyte necrosis.	Cyclophosphamide	98-114	endothelin 1	Homo sapiens	165-169
17722867-0	2007	Alpha 2 macroglobulin activity in rats infected with Typanosoma lewisi and treated with cyclophosphamide and its effect on the malignancy of the disease.	Cyclophosphamide	88-104	alpha-2-macroglobulin	Rattus norvegicus	0-21
17502835-0	2007	Genetic polymorphisms of CYP2B6 affect the pharmacokinetics/pharmacodynamics of cyclophosphamide in Japanese cancer patients.	Cyclophosphamide	80-96	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	25-31
17502835-7	2007	We found that the homozygotes of CYP2B6*6 (Q172H and K262R) showed significantly (P<0.05) higher clearance and shorter half-life of cyclophosphamide than heterozygotes and homozygotes of CYP2B6*1.	Cyclophosphamide	135-151	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	33-39
17502835-12	2007	CONCLUSIONS: We clarified that the single nucleotide polymorphisms in the promoter region or introns in the CYP2B6 affect the potency of cyclophosphamide activation to 4-hydroxycyclophosphamide.	Cyclophosphamide	137-153	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	108-114
17874631-3	2007	As a result of the progress in RA therapy in the recent years, including introduction of anti - TNF alpha therapy, the importance of cyclophosphamide significantly decreased.	Cyclophosphamide	133-149	tumor necrosis factor	Homo sapiens	96-105
17488991-5	2007	However, response rate is usually lower in elderly patients compared with young patients, even if the patients are treated with the cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) regimen.	Cyclophosphamide	132-148	DNA damage inducible transcript 3	Homo sapiens	192-196
16960692-0	2007	Metronomic cyclophosphamide regimen selectively depletes CD4+CD25+ regulatory T cells and restores T and NK effector functions in end stage cancer patients.	Cyclophosphamide	11-27	CD4 molecule	Homo sapiens	57-60
16997373-10	2007	The patient was treated with six cycles of cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP).	Cyclophosphamide	43-59	DNA damage inducible transcript 3	Homo sapiens	102-106
17498006-0	2007	A case report of plasmapheresis and cyclophosphamide for steroid-resistant focal segmental glomerulosclerosis: recovery of renal function after five months on dialysis.	Cyclophosphamide	36-52	actinin alpha 4	Homo sapiens	75-109
17498006-5	2007	This is the first report of late rescue from apparent ESRD due to FSGS with combined plasmapheresis and low dose oral cyclophosphamide.	Cyclophosphamide	118-134	actinin alpha 4	Homo sapiens	66-70
17918443-2	2007	METHODS: The immunity-deficiency model was induced by intraperitoneal injection (ip) of cyclophosphamide (CTX) at the dose of 100 mg/ kg in mice which were randomly divided into normal control group, immunity-deficiency model group, SKC treated group (250 mg/kg, 500 mg/kg) and positive control group (500 mg/kg).	Cyclophosphamide	88-104	V-set and immunoglobulin domain containing 2	Mus musculus	106-109
17530014-5	2007	A combination of rituximab plus chemotherapy, rituximab+cyclophosphamide+doxorubicin+vincristine+prednisolone (R-CHOP), has the highest efficacy ever described with any chemotherapy in DLBCL and FL.	Cyclophosphamide	56-72	DNA damage inducible transcript 3	Homo sapiens	113-117
17116724-2	2007	Using Mgmt-/- mice, we examined MGMT"s role in protecting from in vivo mutations induced by three different alkylating agents, temozolomide (TMZ), 1,3-bis (2-chloroethyl)-1-nitrosourea (BCNU) and cyclophosphamide.	Cyclophosphamide	196-212	O-6-methylguanine-DNA methyltransferase	Mus musculus	32-36
17116724-8	2007	Following cyclophosphamide, mutation frequencies significantly increased from 1.8 x 10(-6) in control-treated mice to 12.9 x 10(-6) in Mgmt+/+ and 18.1 x 10(-6) in Mgmt-/- mice, although the difference in Mgmt-/- compared with Mgmt+/+ was not significant.	Cyclophosphamide	10-26	O-6-methylguanine-DNA methyltransferase	Mus musculus	135-139
17116724-8	2007	Following cyclophosphamide, mutation frequencies significantly increased from 1.8 x 10(-6) in control-treated mice to 12.9 x 10(-6) in Mgmt+/+ and 18.1 x 10(-6) in Mgmt-/- mice, although the difference in Mgmt-/- compared with Mgmt+/+ was not significant.	Cyclophosphamide	10-26	O-6-methylguanine-DNA methyltransferase	Mus musculus	164-168
17116724-8	2007	Following cyclophosphamide, mutation frequencies significantly increased from 1.8 x 10(-6) in control-treated mice to 12.9 x 10(-6) in Mgmt+/+ and 18.1 x 10(-6) in Mgmt-/- mice, although the difference in Mgmt-/- compared with Mgmt+/+ was not significant.	Cyclophosphamide	10-26	O-6-methylguanine-DNA methyltransferase	Mus musculus	164-168
17116724-8	2007	Following cyclophosphamide, mutation frequencies significantly increased from 1.8 x 10(-6) in control-treated mice to 12.9 x 10(-6) in Mgmt+/+ and 18.1 x 10(-6) in Mgmt-/- mice, although the difference in Mgmt-/- compared with Mgmt+/+ was not significant.	Cyclophosphamide	10-26	O-6-methylguanine-DNA methyltransferase	Mus musculus	164-168
17257903-4	2007	Acetyl 11-keto beta-boswellic acids (10 mg/kg/d) inhibited the Matrigel+bFGF-induced angiogenesis significantly (P<0.01) in contrast to anti-inflammatory agent indomethacin (10 mg/kg/d) and alkylating agent cyclophosphamide (10 mg/kg/d).	Cyclophosphamide	210-226	fibroblast growth factor 2	Mus musculus	72-76
17498486-1	2007	OBJECTIVE: To observe the effect of high-dose Astragalus injection and cyclophosphamide (CTX) on infection, urine protein and immune function of the patients with lupus nephritis.	Cyclophosphamide	71-87	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	89-92
17430582-0	2007	Prognostic significance of bcl-2 expression in stage III breast cancer patients who had received doxorubicin and cyclophosphamide followed by paclitaxel as adjuvant chemotherapy.	Cyclophosphamide	113-129	BCL2 apoptosis regulator	Homo sapiens	27-32
17296975-0	2007	Phase II study of neoadjuvant docetaxel, vinorelbine, and trastuzumab followed by surgery and adjuvant doxorubicin plus cyclophosphamide in women with human epidermal growth factor receptor 2-overexpressing locally advanced breast cancer.	Cyclophosphamide	120-136	erb-b2 receptor tyrosine kinase 2	Homo sapiens	157-191
17218484-0	2007	A mouse model with liver-specific deletion and global suppression of the NADPH-cytochrome P450 reductase gene: characterization and utility for in vivo studies of cyclophosphamide disposition.	Cyclophosphamide	163-179	cytochrome p450 oxidoreductase	Mus musculus	73-104
17218484-6	2007	injection of CPA at 100 mg/kg, the t1/2 and the area under the concentration-time curve for plasma CPA were significantly increased in mice deficient in liver CPR compared with wild-type controls, indicating a lower rate of metabolism, with the effects greater in CL-LCN mice than in LCN mice.	Cyclophosphamide	13-16	cytochrome p450 oxidoreductase	Mus musculus	159-162
17218484-6	2007	injection of CPA at 100 mg/kg, the t1/2 and the area under the concentration-time curve for plasma CPA were significantly increased in mice deficient in liver CPR compared with wild-type controls, indicating a lower rate of metabolism, with the effects greater in CL-LCN mice than in LCN mice.	Cyclophosphamide	99-102	cytochrome p450 oxidoreductase	Mus musculus	159-162
17382773-0	2007	Cyclophosphamide induced cystitis: role of nitric oxide synthase, cyclooxygenase-1 and 2, and NK(1) receptors.	Cyclophosphamide	0-16	prostaglandin-endoperoxide synthase 1	Rattus norvegicus	66-88
17382773-4	2007	RESULTS: Cyclophosphamide produced inflammatory and cytotoxic changes in the bladder, accompanied by increased nitric oxide metabolites, urinary prostaglandins, myeloperoxidase and inducible nitric oxide synthase activity.	Cyclophosphamide	9-25	myeloperoxidase	Rattus norvegicus	161-176
17382773-4	2007	RESULTS: Cyclophosphamide produced inflammatory and cytotoxic changes in the bladder, accompanied by increased nitric oxide metabolites, urinary prostaglandins, myeloperoxidase and inducible nitric oxide synthase activity.	Cyclophosphamide	9-25	nitric oxide synthase 2	Rattus norvegicus	181-212
17407229-0	2007	Cytochrome P450 polymorphism as a predictor of ovarian toxicity to pulse cyclophosphamide in systemic lupus erythematosus.	Cyclophosphamide	73-89	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	0-15
17407229-12	2007	CONCLUSION: Presence of the variant allele CYP2C19*2 is associated with lower risk of ovarian toxicity in Indian patients treated with CYC.	Cyclophosphamide	135-138	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	43-50
17462476-8	2007	Fos proteins present in spinal cord neurons have been shown to be upregulated in animals that have undergone cyclophosphamide-induced chemical cystitis.	Cyclophosphamide	109-125	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	0-3
17296974-10	2007	CONCLUSION: The addition of oblimersen to fludarabine plus cyclophosphamide significantly increases the CR/nPR rate in patients with relapsed or refractory CLL (particularly fludarabine-sensitive patients), as well as response duration among patients who achieve CR/nPR.	Cyclophosphamide	59-75	neuronal pentraxin receptor	Homo sapiens	104-110
17254689-0	2007	EPO receptor, Bax and Bcl-x(L) expressions in murine erythropoiesis after cyclophosphamide treatment.	Cyclophosphamide	74-90	erythropoietin	Mus musculus	0-3
17254689-0	2007	EPO receptor, Bax and Bcl-x(L) expressions in murine erythropoiesis after cyclophosphamide treatment.	Cyclophosphamide	74-90	BCL2-like 1	Mus musculus	22-30
17254689-7	2007	During spontaneous recovery post-CY; EPO-R was expressed between 4 and 5 days.	Cyclophosphamide	33-35	erythropoietin receptor	Mus musculus	37-42
17110531-0	2007	Region-specific changes in the phosphorylation of ERK1/2 and ERK5 in rat micturition pathways following cyclophosphamide-induced cystitis.	Cyclophosphamide	104-120	mitogen activated protein kinase 3	Rattus norvegicus	50-56
17110531-0	2007	Region-specific changes in the phosphorylation of ERK1/2 and ERK5 in rat micturition pathways following cyclophosphamide-induced cystitis.	Cyclophosphamide	104-120	mitogen-activated protein kinase 7	Rattus norvegicus	61-65
17110531-3	2007	In the present studies, we characterized and compared the activation of two ERK isoforms, ERK1/2 and ERK5, in micturition pathways, including the urinary bladder, lumbosacral dorsal root ganglia (DRG), and spinal cord in adult female and male rats before and after cyclophosphamide (CYP)-induced bladder inflammation.	Cyclophosphamide	265-281	Eph receptor B1	Rattus norvegicus	76-79
17110531-3	2007	In the present studies, we characterized and compared the activation of two ERK isoforms, ERK1/2 and ERK5, in micturition pathways, including the urinary bladder, lumbosacral dorsal root ganglia (DRG), and spinal cord in adult female and male rats before and after cyclophosphamide (CYP)-induced bladder inflammation.	Cyclophosphamide	265-281	mitogen activated protein kinase 3	Rattus norvegicus	90-96
16437363-1	2007	We describe the case of a 75-year-old Italian woman affected by dermatomyositis (DM) treated with steroid, high-dose intravenous immunoglobulins (IVIgs) and cyclophosphamide (CPX), taken orally.	Cyclophosphamide	157-173	T-box transcription factor 22	Homo sapiens	175-178
17425746-3	2007	We assessed whether the clinical outcomes, including acute graft-vs.-host disease, of 61 patients with hematological malignancies, following HLA-matched sibling allogeneic stem cell transplantation using busulfan/cyclophosphamide conditioning are altered by glutathione S-transferase A1 genotypes.	Cyclophosphamide	213-229	glutathione S-transferase alpha 1	Homo sapiens	258-286
17425746-11	2007	We conclude that the GSTA1*A/*A diplotype is an independent protective factor against acute graft-vs.-host disease, especially for skin graft-vs.-host disease, and probably for hepatic graft-vs.-host disease, in patients using busulfan/cyclophosphamide conditioning.	Cyclophosphamide	236-252	glutathione S-transferase alpha 1	Homo sapiens	21-26
17200359-1	2007	PURPOSE: Findings from our previously published phase III randomized trial showed a high pathologic complete remission (CR) rate in patients with human epidermal growth factor receptor 2-positive breast cancer after the concurrent administration of trastuzumab and paclitaxel, followed by concurrent trastuzumab and 5-fluorouracil, epirubicin, and cyclophosphamide (FEC) preoperative chemotherapy.	Cyclophosphamide	348-364	erb-b2 receptor tyrosine kinase 2	Homo sapiens	152-186
17383157-5	2007	Using the model of cyclophosphamide-accelerated diabetes in non-obese diabetic (CAD-NOD) mice, we report that recombinant adenovirus mediated PDX-1 gene therapy, ameliorates hyperglycemia in CAD-NOD mice.	Cyclophosphamide	19-35	pancreatic and duodenal homeobox 1	Mus musculus	142-147
17010609-0	2007	Gene expression profiling of breast cancer patients treated with docetaxel, doxorubicin, and cyclophosphamide within the GEPARTRIO trial: HER-2, but not topoisomerase II alpha and microtubule-associated protein tau, is highly predictive of tumor response.	Cyclophosphamide	93-109	erb-b2 receptor tyrosine kinase 2	Homo sapiens	138-143
17258079-2	2007	Since the proliferation and migration of leukocytes represent a necessary and important step in response to the inflammatory insult, we have investigated whether Gal-1 affects the mobilization of hematopoietic progenitor cells (HPC) induced by cyclophosphamide (CY) and granulocyte colony-stimulating factor (G-CSF).	Cyclophosphamide	244-260	galectin 1	Homo sapiens	162-167
17258079-2	2007	Since the proliferation and migration of leukocytes represent a necessary and important step in response to the inflammatory insult, we have investigated whether Gal-1 affects the mobilization of hematopoietic progenitor cells (HPC) induced by cyclophosphamide (CY) and granulocyte colony-stimulating factor (G-CSF).	Cyclophosphamide	262-264	galectin 1	Homo sapiens	162-167
17255288-8	2007	Optimal therapeutic responses to the transfer of immune cells were associated with the cyclophosphamide-mediated induction of a "cytokine storm" [including granulocyte macrophage colony-stimulating factor, interleukin (IL)-1beta, IL-7, IL-15, IL-2, IL-21, and IFN-gamma], occurring during the "rebound phase" after drug-induced lymphodepletion.	Cyclophosphamide	87-103	interleukin 7	Mus musculus	230-234
17255288-8	2007	Optimal therapeutic responses to the transfer of immune cells were associated with the cyclophosphamide-mediated induction of a "cytokine storm" [including granulocyte macrophage colony-stimulating factor, interleukin (IL)-1beta, IL-7, IL-15, IL-2, IL-21, and IFN-gamma], occurring during the "rebound phase" after drug-induced lymphodepletion.	Cyclophosphamide	87-103	interleukin 15	Mus musculus	236-241
17255288-8	2007	Optimal therapeutic responses to the transfer of immune cells were associated with the cyclophosphamide-mediated induction of a "cytokine storm" [including granulocyte macrophage colony-stimulating factor, interleukin (IL)-1beta, IL-7, IL-15, IL-2, IL-21, and IFN-gamma], occurring during the "rebound phase" after drug-induced lymphodepletion.	Cyclophosphamide	87-103	interleukin 2	Mus musculus	243-247
17255288-8	2007	Optimal therapeutic responses to the transfer of immune cells were associated with the cyclophosphamide-mediated induction of a "cytokine storm" [including granulocyte macrophage colony-stimulating factor, interleukin (IL)-1beta, IL-7, IL-15, IL-2, IL-21, and IFN-gamma], occurring during the "rebound phase" after drug-induced lymphodepletion.	Cyclophosphamide	87-103	interleukin 21	Mus musculus	249-254
17255288-8	2007	Optimal therapeutic responses to the transfer of immune cells were associated with the cyclophosphamide-mediated induction of a "cytokine storm" [including granulocyte macrophage colony-stimulating factor, interleukin (IL)-1beta, IL-7, IL-15, IL-2, IL-21, and IFN-gamma], occurring during the "rebound phase" after drug-induced lymphodepletion.	Cyclophosphamide	87-103	interferon gamma	Mus musculus	260-269
17453364-2	2007	A toxicity-based dosing schedule for individually tailored treatment with granulocyte colony-stimulating factor (G-CSF) supported 5-fluorouracil (F), epirubicin (E) and cyclophosphamide (C) (dFEC) was developed and studied in patients with metastatic breast cancer with the purpose to determine its efficiency and toxicity.	Cyclophosphamide	169-185	colony stimulating factor 3	Homo sapiens	113-118
17388661-0	2007	Exquisite sensitivity of TP53 mutant and basal breast cancers to a dose-dense epirubicin-cyclophosphamide regimen.	Cyclophosphamide	89-105	tumor protein p53	Homo sapiens	25-29
17388661-16	2007	CONCLUSIONS: This study demonstrates that, in noninflammatory breast cancers, TP53 status is a key predictive factor for response to this dose-dense epirubicin-cyclophosphamide regimen and further suggests that the basal subtype is exquisitely sensitive to this association.	Cyclophosphamide	160-176	tumor protein p53	Homo sapiens	78-82
17284714-8	2007	Use of G-CSF and GM-CSF was associated with more recent diagnosis, younger age, urban residence, fewer comorbidities, receipt of radiation therapy, positive lymph nodes, and cyclophosphamide treatment.	Cyclophosphamide	174-190	colony stimulating factor 3	Homo sapiens	7-12
17284714-8	2007	Use of G-CSF and GM-CSF was associated with more recent diagnosis, younger age, urban residence, fewer comorbidities, receipt of radiation therapy, positive lymph nodes, and cyclophosphamide treatment.	Cyclophosphamide	174-190	colony stimulating factor 2	Homo sapiens	17-23
16733672-0	2007	Low-dose cyclophosphamide modulates galectin-1 expression and function in an experimental rat lymphoma model.	Cyclophosphamide	9-25	galectin 1	Rattus norvegicus	36-46
16733672-4	2007	Here we show that administration of a single low-dose cyclophosphamide (Cy), which is capable of restraining metastasis in the rat lymphoma model L-TACB, can also influence Gal-1 expression in primary tumor, metastasis, and spleen cells and modulate the effects of this protein on T cell survival.	Cyclophosphamide	54-70	galectin 1	Rattus norvegicus	173-178
16733672-4	2007	Here we show that administration of a single low-dose cyclophosphamide (Cy), which is capable of restraining metastasis in the rat lymphoma model L-TACB, can also influence Gal-1 expression in primary tumor, metastasis, and spleen cells and modulate the effects of this protein on T cell survival.	Cyclophosphamide	72-74	galectin 1	Rattus norvegicus	173-178
16733672-7	2007	Interestingly, cyclophosphamide treatment was capable of restoring the basal levels of Gal-1 expression in primary tumors and spleens.	Cyclophosphamide	15-31	galectin 1	Rattus norvegicus	87-92
16733672-9	2007	Our results suggest that, in addition to other well-known functions of cyclophosphamide, this immunomodulatory agent may also modulate Gal-1 expression and function during tumor growth and metastasis with critical implications for tumor-immune escape and immunotherapy.	Cyclophosphamide	71-87	galectin 1	Rattus norvegicus	135-140
17660958-4	2007	A humanized antibody to HER2/neu, trastuzumab, is now FDA approved for the treatment of early stage, HER2/neu overexpressing breast cancer sequenced with chemotherapy including doxorubicin, cyclophosphamide, and paclitaxel.	Cyclophosphamide	190-206	erb-b2 receptor tyrosine kinase 2	Homo sapiens	24-28
17660958-4	2007	A humanized antibody to HER2/neu, trastuzumab, is now FDA approved for the treatment of early stage, HER2/neu overexpressing breast cancer sequenced with chemotherapy including doxorubicin, cyclophosphamide, and paclitaxel.	Cyclophosphamide	190-206	erb-b2 receptor tyrosine kinase 2	Homo sapiens	29-32
17660958-4	2007	A humanized antibody to HER2/neu, trastuzumab, is now FDA approved for the treatment of early stage, HER2/neu overexpressing breast cancer sequenced with chemotherapy including doxorubicin, cyclophosphamide, and paclitaxel.	Cyclophosphamide	190-206	erb-b2 receptor tyrosine kinase 2	Homo sapiens	24-32
17354532-3	2007	Among novel developments based on biologicals, the anti-CD20 monoclonal antibody rituximab (anti-B cells) appears encouraging in open studies, in association or not with cyclophosphamide, and is generally well tolerated.	Cyclophosphamide	170-186	keratin 20	Homo sapiens	56-60
18086299-0	2007	CD40 signaling predicts response to preoperative trastuzumab and concomitant paclitaxel followed by 5-fluorouracil, epirubicin, and cyclophosphamide in HER-2-overexpressing breast cancer.	Cyclophosphamide	132-148	CD40 molecule	Homo sapiens	0-4
18086299-0	2007	CD40 signaling predicts response to preoperative trastuzumab and concomitant paclitaxel followed by 5-fluorouracil, epirubicin, and cyclophosphamide in HER-2-overexpressing breast cancer.	Cyclophosphamide	132-148	erb-b2 receptor tyrosine kinase 2	Homo sapiens	152-157
16614850-1	2007	PURPOSE: Aldehyde dehydrogenases class-1A1 (ALDH1A1) and class-3A1 (ALDH3A1) have been associated with resistance to cyclophosphamide (CP) and its derivatives.	Cyclophosphamide	117-133	aldehyde dehydrogenase 1 family member A1	Homo sapiens	9-42
16614850-1	2007	PURPOSE: Aldehyde dehydrogenases class-1A1 (ALDH1A1) and class-3A1 (ALDH3A1) have been associated with resistance to cyclophosphamide (CP) and its derivatives.	Cyclophosphamide	117-133	aldehyde dehydrogenase 1 family member A1	Homo sapiens	44-51
16614850-1	2007	PURPOSE: Aldehyde dehydrogenases class-1A1 (ALDH1A1) and class-3A1 (ALDH3A1) have been associated with resistance to cyclophosphamide (CP) and its derivatives.	Cyclophosphamide	117-133	aldehyde dehydrogenase 3 family member A1	Homo sapiens	68-75
17082249-1	2007	BACKGROUND: CYP2B6 is a highly variable and polymorphic cytochrome P450 (CYP) enzyme involved in the biotransformation of an increasing number of drugs, including cyclophosphamide, bupropion, and the nonnucleosidic reverse transcriptase inhibitor efavirenz.	Cyclophosphamide	163-179	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	12-18
17082249-1	2007	BACKGROUND: CYP2B6 is a highly variable and polymorphic cytochrome P450 (CYP) enzyme involved in the biotransformation of an increasing number of drugs, including cyclophosphamide, bupropion, and the nonnucleosidic reverse transcriptase inhibitor efavirenz.	Cyclophosphamide	163-179	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	56-71
17082249-1	2007	BACKGROUND: CYP2B6 is a highly variable and polymorphic cytochrome P450 (CYP) enzyme involved in the biotransformation of an increasing number of drugs, including cyclophosphamide, bupropion, and the nonnucleosidic reverse transcriptase inhibitor efavirenz.	Cyclophosphamide	163-179	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	12-15
16636934-0	2007	T-889C IL-1alpha promoter polymorphism influences the response to oral cyclophosphamide in scleroderma patients with alveolitis.	Cyclophosphamide	71-87	interleukin 1 alpha	Homo sapiens	7-16
17375983-7	2007	The body surface area, peak concentrations of etoposide, urinary recovery of dechloroethylcyclophosphamide (formed by cytochrome P450 [CYP] 3A4) relative to the cyclophosphamide dose and number of cycles had a significant effect on toxicity.	Cyclophosphamide	90-106	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	118-143
17495446-1	2007	BACKGROUND: Cyclophosphamide and high-dose steroids have been used as limited induction therapy in progressive IgA nephropathy (IgAN) to reduce the loss of renal function and proteinuria.	Cyclophosphamide	12-28	IGAN1	Homo sapiens	111-126
17495446-1	2007	BACKGROUND: Cyclophosphamide and high-dose steroids have been used as limited induction therapy in progressive IgA nephropathy (IgAN) to reduce the loss of renal function and proteinuria.	Cyclophosphamide	12-28	IGAN1	Homo sapiens	128-132
17212724-5	2007	In this study, we present four patients with acquired FVIII inhibitor titres >100 BU who were resistant to initial therapy with cyclophosphamide, vincristine and prednisone.	Cyclophosphamide	131-147	coagulation factor VIII	Homo sapiens	54-59
17206641-10	2007	CONCLUSIONS: Quantification of mucosal TNF-alpha transcripts prior to therapy allows identification of patients achieving long-term remission upon immunosuppression with infliximab or cyclophosphamide.	Cyclophosphamide	184-200	tumor necrosis factor	Homo sapiens	39-48
17143493-6	2007	The TS activity was decreased by NAC with UFT, and the addition of CPA resulted in an increased inhibition of TS activity.	Cyclophosphamide	67-70	thymidylate synthetase	Homo sapiens	110-112
17198082-0	2007	Defining the ability of cyclophosphamide preconditioning to enhance the antigen-specific CD8+ T-cell response to peptide vaccination: creation of a beneficial host microenvironment involving type I IFNs and myeloid cells.	Cyclophosphamide	24-40	CD8a molecule	Homo sapiens	89-92
17198082-1	2007	Although cyclophosphamide (CTX) has been clearly shown to enhance active specific and adoptive immunotherapies, the mechanism(s) underlying these beneficial effects have not been clearly defined.	Cyclophosphamide	9-25	V-set and immunoglobulin domain containing 2	Mus musculus	27-30
17932452-10	2007	CONCLUSION: We concluded that high concentrations of cyclophosphamide(CPA) might be able to inhibit cell growth through down-regulation of HER-2 protein level in breast cancer cell lines.	Cyclophosphamide	53-69	erb-b2 receptor tyrosine kinase 2	Homo sapiens	139-144
17917084-10	2007	Each oligo combined with Cytoxan significantly inhibited: MR1 by 51.0, MR2 by 55.0, MR4 by 58.0; MR12 by 56.0; MR21 by 61.1, MR24 by 65.5 and MR42 by 66.0%.	Cyclophosphamide	25-32	major histocompatibility complex, class I-related	Homo sapiens	58-61
17917084-12	2007	Each oligo combined with Cytoxan significantly inhibited: MR1 by 49.0, MR2 by 50.0, MR4 by 53.0; MR12 by 52.0; MR21 by 58.6, MR24 by 53.9 and MR42 by 58.0%.	Cyclophosphamide	25-32	major histocompatibility complex, class I-related	Homo sapiens	58-61
17143493-0	2007	Cyclophosphamide augments the anti-tumor efficacy of uracil and tegafur by inhibiting dihydropyrimidine dehydrogenase.	Cyclophosphamide	0-16	dihydropyrimidine dehydrogenase	Homo sapiens	86-117
17507877-2	2007	We demonstrated that LF accelerated reconstitution of the immune system function after administration of a sublethal dose cyclophosphamide (CP) and normalized the ratio of major blood cell types in that model.	Cyclophosphamide	122-138	lactotransferrin	Rattus norvegicus	21-23
21794392-1	2007	OBJECTIVE: In patients with proliferative lupus nephritis treated with IV cyclophosphamide, analyze urinary tract infection (UTI) as a cause of treatment delay and renal relapses, compared with lupus nephritis patients without infection.	Cyclophosphamide	74-90	alpha-1-microglobulin/bikunin precursor	Homo sapiens	125-128
17668812-9	2007	The patient was treated with R-COP regiment (six cycles rituximab + COP- cyclophosphamid, vincristin, prednisolon).	Cyclophosphamide	73-88	caspase recruitment domain family member 16	Homo sapiens	68-71
17143493-7	2007	In contrast, DPD activity was increased by NAC with UFT administration, but its increased activity was significantly inhibited by the addition of CPA.	Cyclophosphamide	146-149	dihydropyrimidine dehydrogenase	Homo sapiens	13-16
17143493-8	2007	Multiple regression analyses demonstrated that the total dose of UFT was a significant variable for inhibiting TS activity, and that CPA was a significant variable for inhibiting DPD activity.	Cyclophosphamide	133-136	dihydropyrimidine dehydrogenase	Homo sapiens	179-182
17143493-9	2007	The DPD activity increased by UFT can be inhibited by CPA, and this may represent one of the possible mechanisms responsible for the anti-tumor activity of 5-FU or its derivatives as enhanced by CPA.	Cyclophosphamide	54-57	dihydropyrimidine dehydrogenase	Homo sapiens	4-7
17143493-9	2007	The DPD activity increased by UFT can be inhibited by CPA, and this may represent one of the possible mechanisms responsible for the anti-tumor activity of 5-FU or its derivatives as enhanced by CPA.	Cyclophosphamide	195-198	dihydropyrimidine dehydrogenase	Homo sapiens	4-7
17802794-0	2007	[Prognostic significance of immunoglobulin variable region gene mutations in B-CLL patients treated with combination therapy fludarabine plus cyclophosphamide].	Cyclophosphamide	142-158	immunoglobulin heavy variable 4-38-2-like	Homo sapiens	28-58
17802794-14	2007	CONCLUSION: Our data show that mutational status of immunoglobulin variable region genes remains a significant prognostic factor in patients receiving combined therapy with cyclophosphamide and fludarabine.	Cyclophosphamide	173-189	immunoglobulin heavy variable 4-38-2-like	Homo sapiens	52-82
17156807-0	2007	Cyclophosphamide as a potent inhibitor of tumor thioredoxin reductase in vivo.	Cyclophosphamide	0-16	peroxiredoxin 5	Mus musculus	48-69
17156807-1	2007	Cyclophosphamide (CTX) is in the nitrogen mustard group of alkylating antineoplastic chemotherapeutic agents.	Cyclophosphamide	0-16	V-set and immunoglobulin domain containing 2	Mus musculus	18-21
17114213-5	2006	RESULTS: When analyzed as a continuous log-transformed variable, increasing TIMP-1 levels were significantly associated with lack of response to cyclophosphamide/methotrexate/5-fluorouracil and anthracycline-based chemotherapy (P = 0.01; odds ratio, 2.0; 95% confidence interval, 1.1-3.3).	Cyclophosphamide	145-161	TIMP metallopeptidase inhibitor 1	Homo sapiens	76-82
17114213-8	2006	By using TIMP-1, we identified a group of patients with metastatic breast cancer, which hardly respond to the most frequently used chemotherapy regimes (i.e., cyclophosphamide/methotrexate/5-fluorouracil and anthracyclines).	Cyclophosphamide	159-175	TIMP metallopeptidase inhibitor 1	Homo sapiens	9-15
17130511-3	2006	Previously, we used linkage analysis of NOD crossed to the nonobese diabetes-resistant (NOR) strain and NOD congenic strains to map susceptibility to both spontaneous and cyclophosphamide-accelerated type 1 diabetes to the Idd4 locus on chromosome 11 that displayed a sex-specific effect on diabetes susceptibility.	Cyclophosphamide	171-187	insulin dependent diabetes susceptibility 4	Mus musculus	223-227
17177909-1	2006	The routine use of granulocyte-colony stimulating factor (G-CSF) for 10 days during full-dose cyclophosphamide-doxorubicin-vincristine-prednisone (CHOP) chemotherapy in HIV-associated diffuse non-Hodgkin"s lymphoma (NHL) patients is very expensive in developing countries.	Cyclophosphamide	94-110	colony stimulating factor 3	Homo sapiens	19-56
17069538-0	2006	Targeting the CYP2B 1/cyclophosphamide suicide system to fibroblast growth factor receptors results in a potent antitumoral response in pancreatic cancer models.	Cyclophosphamide	22-38	cytochrome P450 family 2 subfamily B member 7, pseudogene	Homo sapiens	14-19
17085516-4	2006	The management of patients with AIDS-related NHL with either infusional chemotherapy or CHOP-like regimens (cyclophosphamide, doxorubicin, vincristine and prednisolone) achieves response and survival rates approaching those observed in the general population.	Cyclophosphamide	108-124	DNA damage inducible transcript 3	Homo sapiens	88-92
17164692-3	2006	Because roxithromycin inhibits cytochrome P450 (CYP) 3A4 and P-glycoprotein, the patient may have been exposed to higher cyclophosphamide and/or cyclophosphamide metabolite concentrations.	Cyclophosphamide	121-137	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	31-56
17164692-3	2006	Because roxithromycin inhibits cytochrome P450 (CYP) 3A4 and P-glycoprotein, the patient may have been exposed to higher cyclophosphamide and/or cyclophosphamide metabolite concentrations.	Cyclophosphamide	121-137	ATP binding cassette subfamily B member 1	Homo sapiens	61-75
17164692-7	2006	Although roxithromycin did not favor the generation of toxic metabolites from cyclophosphamide, it led to cyclophosphamide accumulation due to inhibition of both CYP3A4 and CYP2B6.	Cyclophosphamide	106-122	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	162-168
17164692-9	2006	In the presence of roxithromycin (500 micromol/L), cyclophosphamide (500 micromol/L) induced apoptosis in endothelial cells (34.3 +/- 10.4% apoptotic cells [in % of total cells] for the combination of cyclophosphamide and roxithromycin, 0.7 +/- 0.25% for cyclophosphamide alone, 0% for roxithromycin alone; P < 0.0001) most probably by mitochondrial membrane permeability transition and release of cytochrome c.	Cyclophosphamide	51-67	cytochrome c, somatic	Homo sapiens	401-413
17082572-0	2006	Cyclophosphamide-induced type-1 diabetes in the NOD mouse is associated with a reduction of CD4+CD25+Foxp3+ regulatory T cells.	Cyclophosphamide	0-16	forkhead box P3	Mus musculus	101-106
17082572-5	2006	We demonstrate in this study that CY targets CD4+CD25+Foxp3+ Tregs in vivo.	Cyclophosphamide	34-36	forkhead box P3	Mus musculus	54-59
17082572-10	2006	We conclude that acceleration of T1D by CY is associated with a reduction in CD4+CD25+Foxp3+ Tregs and can be prevented by transfer of CD4+CD25+ Tregs.	Cyclophosphamide	40-42	forkhead box P3	Mus musculus	86-91
17075808-0	2006	Hepatocyte growth factor and transforming growth factor beta1 ratio at baseline can predict early response to cyclophosphamide in systemic lupus erythematosus nephritis.	Cyclophosphamide	110-126	hepatocyte growth factor	Homo sapiens	0-24
17075808-0	2006	Hepatocyte growth factor and transforming growth factor beta1 ratio at baseline can predict early response to cyclophosphamide in systemic lupus erythematosus nephritis.	Cyclophosphamide	110-126	transforming growth factor beta 1	Homo sapiens	29-61
17075808-1	2006	OBJECTIVE: To determine whether the ratio of hepatocyte growth factor (HGF) to transforming growth factor beta1 (TGFbeta1) in systemic lupus erythematosus (SLE) nephritis could be a prognostic factor for response to therapy with cyclophosphamide (CYC) and steroids at 6 months, and to examine whether the molecular ratio of HGF to TGFbeta1 correlates with the activity index (AI) and chronicity index (CI) and has predictive value for remission at the sixth month.	Cyclophosphamide	229-245	hepatocyte growth factor	Homo sapiens	71-74
17075808-1	2006	OBJECTIVE: To determine whether the ratio of hepatocyte growth factor (HGF) to transforming growth factor beta1 (TGFbeta1) in systemic lupus erythematosus (SLE) nephritis could be a prognostic factor for response to therapy with cyclophosphamide (CYC) and steroids at 6 months, and to examine whether the molecular ratio of HGF to TGFbeta1 correlates with the activity index (AI) and chronicity index (CI) and has predictive value for remission at the sixth month.	Cyclophosphamide	247-250	hepatocyte growth factor	Homo sapiens	71-74
17075808-9	2006	CONCLUSION: These findings indicate that baseline expression of renal HGF and TGFbeta1 predicts short-term renal outcome after therapy with CYC and steroids.	Cyclophosphamide	140-143	hepatocyte growth factor	Homo sapiens	70-73
17075808-9	2006	CONCLUSION: These findings indicate that baseline expression of renal HGF and TGFbeta1 predicts short-term renal outcome after therapy with CYC and steroids.	Cyclophosphamide	140-143	transforming growth factor beta 1	Homo sapiens	78-86
17110316-5	2006	Immunosuppressive and cytotoxic drugs used in antirheumatic therapy, such as methotrexate, cyclophosphamide, azathioprine or anti-TNF biologicals may also lead to the development of such tumors.	Cyclophosphamide	91-107	tumor necrosis factor	Homo sapiens	130-133
17181940-3	2006	RESULTS: The ratio of the median of the intensity of MN-RET fluorescent signals to that of nucleated cell was low in the cyclophosphamide treated mouse, while the median was high in the colchicine treated mouse.	Cyclophosphamide	121-137	ret proto-oncogene	Mus musculus	56-59
17130538-0	2006	Immunolocalization of monocyte chemoattractant protein-1 in islets of NOD mice during cyclophosphamide administration.	Cyclophosphamide	86-102	chemokine (C-C motif) ligand 2	Mus musculus	22-56
17130538-4	2006	The aims of the present study were to employ immunohistochemical techniques to examine the expression of MCP-1 and quantify its cellular sources in islets of NOD mice both after cyclophosphamide (Cy) administration and in spontaneous diabetes.	Cyclophosphamide	178-194	chemokine (C-C motif) ligand 2	Mus musculus	105-110
17130538-7	2006	In the Cy group, a small number of peri-islet macrophages were immunopositive for MCP-1 at day 1 whereas at day 4, the number declined but increased subsequently at day 7.	Cyclophosphamide	7-9	chemokine (C-C motif) ligand 2	Mus musculus	82-87
17130538-14	2006	Thus, MCP-1 positive macrophages that migrate to the islet periphery during the early stages of Cy-induced diabetes and preceding spontaneous diabetes may augment insulitis by further attracting macrophages and T cells.	Cyclophosphamide	96-98	chemokine (C-C motif) ligand 2	Mus musculus	6-11
17250437-2	2006	Immunological and biochemical studies were here carried out to investigate protective effects of ethanolic extract of Andrographis paniculata against cyclophosphamide (CTX) induced toxicity in vivo.	Cyclophosphamide	150-166	V-set and immunoglobulin domain containing 2	Mus musculus	168-171
17020986-6	2006	RESULTS: Overexpression of caspase-3s variant in caspase-3-transfected cell lines significantly inhibits apoptosis induced by cyclophosphamide (P < 0.0001 for both cell lines).	Cyclophosphamide	126-142	caspase 3	Homo sapiens	27-36
17020986-6	2006	RESULTS: Overexpression of caspase-3s variant in caspase-3-transfected cell lines significantly inhibits apoptosis induced by cyclophosphamide (P < 0.0001 for both cell lines).	Cyclophosphamide	126-142	caspase 3	Homo sapiens	49-58
17020986-11	2006	CONCLUSIONS: The results agree with an antagonist function between the two transcripts of caspase-3 and show that their ratio of expression levels may define a subset of locally advanced breast cancer patients who are more likely to benefit from neoadjuvant cyclophosphamide-containing chemotherapy.	Cyclophosphamide	258-274	caspase 3	Homo sapiens	90-99
17073575-2	2006	For bupropion, cyclophosphamide, ifosfamide, pethidine, ketamine and propofol, these reactions represent major metabolic or activation pathways and for their kinetics CYP2B6 function is of considerable importance.	Cyclophosphamide	15-31	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	167-173
17050200-5	2006	In a retrospective cohort study, we used a methylation-specific polymerase chain reaction technique to analyze the methylation status of the promoter region of the MGMT gene in 116 DLBCL patients who received cyclophosphamide as part of multidrug combination chemotherapies.	Cyclophosphamide	209-225	O-6-methylguanine-DNA methyltransferase	Homo sapiens	164-168
17091317-2	2006	Both Idds are located on distal mouse Chromosome 6, and previous studies on NOD.C3H congenic strains have shown that C3H alleles at Idd20 can suppress the disease-promoting effects of C3H alleles at Idd19 in both spontaneous and cyclophosphamide-induced diabetes.	Cyclophosphamide	229-245	insulin dependent diabetes susceptibility 20	Mus musculus	132-137
17091317-2	2006	Both Idds are located on distal mouse Chromosome 6, and previous studies on NOD.C3H congenic strains have shown that C3H alleles at Idd20 can suppress the disease-promoting effects of C3H alleles at Idd19 in both spontaneous and cyclophosphamide-induced diabetes.	Cyclophosphamide	229-245	insulin dependent diabetes susceptibility 19	Mus musculus	199-204
16609067-1	2006	The precise mechanism of rituximab plus cyclophosphamide/doxorubicin/vincristine/prednisone (R-CHOP) therapy in diffuse large B-cell lymphoma (DLBCL) is not fully elucidated.	Cyclophosphamide	40-56	DNA damage inducible transcript 3	Homo sapiens	95-99
16995867-0	2006	Relationship of glutathione S-transferase genotypes with side-effects of pulsed cyclophosphamide therapy in patients with systemic lupus erythematosus.	Cyclophosphamide	80-96	glutathione S-transferase kappa 1	Homo sapiens	16-41
16995867-1	2006	AIMS: Cyclophosphamide (CTX) is an established treatment of severe systemic lupus erythematosus (SLE).	Cyclophosphamide	6-22	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	24-27
17033231-5	2006	CAF therapy consisted of CPA (100 mg/day) on days 1 to 14, followed by 2 weeks of rest, plus ADM (20 mg/m(2)/day) on days 1 and 8 and 5-FU (300 mg/m(2)/day) on days 1 and 8.	Cyclophosphamide	25-28	lysine acetyltransferase 2B	Homo sapiens	0-3
17010015-0	2006	Up-regulation of interleukin-6 gene expression in cyclophosphamide-induced cystitis in mice: An in situ hybridization histochemical study.	Cyclophosphamide	50-66	interleukin 6	Mus musculus	17-30
17177909-1	2006	The routine use of granulocyte-colony stimulating factor (G-CSF) for 10 days during full-dose cyclophosphamide-doxorubicin-vincristine-prednisone (CHOP) chemotherapy in HIV-associated diffuse non-Hodgkin"s lymphoma (NHL) patients is very expensive in developing countries.	Cyclophosphamide	94-110	colony stimulating factor 3	Homo sapiens	58-63
16797508-4	2006	Cyclophosphamide (CTX), one of the most widely prescribed antineoplastic drugs, could cause cystitis.	Cyclophosphamide	0-16	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	18-21
16788784-5	2006	The standard chemotherapy for aggressive non-Hodgkin"s lymphomas is the CHOP regimen consisting of cyclophosphamide, doxorubicin, vincristine, and prednisone.	Cyclophosphamide	99-115	DNA damage inducible transcript 3	Homo sapiens	72-76
16943530-2	2006	This conclusion is mainly derived from patients with mixed international prognostic index (IPI) risk profiles treated with CHOP-like therapy (cyclophosphamide, doxorubicin, vincristine, and prednisone).	Cyclophosphamide	142-158	DNA damage inducible transcript 3	Homo sapiens	123-127
16908838-5	2006	Pretreatment with CPA enhances HSV replication and oncolysis and reduces an HSV-mediated increase in CD68+ and CD163+ cells and intratumoral IFN-gamma.	Cyclophosphamide	18-21	Cd68 molecule	Rattus norvegicus	101-105
16908838-5	2006	Pretreatment with CPA enhances HSV replication and oncolysis and reduces an HSV-mediated increase in CD68+ and CD163+ cells and intratumoral IFN-gamma.	Cyclophosphamide	18-21	interferon gamma	Rattus norvegicus	141-150
16880627-4	2006	Serum albumin concentration was time-dependently decreased and correlated well with 3 major biologic determinants of drug clearance, hepatic blood flow (HBF), intrinsic clearance (CL(int)), and the unbound fraction of drugs in plasma (fp) after intravenous administration of cyclophosphamide, tolbutamide, zonisamide, and chlorzoxazone (as probe drugs for low hepatic extraction) and propranolol and lidocaine (as high-hepatic extraction drugs).	Cyclophosphamide	275-291	albumin	Rattus norvegicus	6-13
16879691-0	2006	Effects of intravesical instillation of cyclooxygenase-2 inhibitor on the expression of inducible nitric oxide synthase and nerve growth factor in cyclophosphamide-induced overactive bladder.	Cyclophosphamide	147-163	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	40-56
16879691-0	2006	Effects of intravesical instillation of cyclooxygenase-2 inhibitor on the expression of inducible nitric oxide synthase and nerve growth factor in cyclophosphamide-induced overactive bladder.	Cyclophosphamide	147-163	nitric oxide synthase 2	Rattus norvegicus	88-119
16879691-0	2006	Effects of intravesical instillation of cyclooxygenase-2 inhibitor on the expression of inducible nitric oxide synthase and nerve growth factor in cyclophosphamide-induced overactive bladder.	Cyclophosphamide	147-163	nerve growth factor	Rattus norvegicus	124-143
16879691-1	2006	OBJECTIVE: To examine the effects of intravesical cyclooxygenase-2 (COX-2) inhibitors on the expression of inducible nitric oxide synthase (iNOS) and nerve growth factor (NGF) in cyclophosphamide (CYP)-induced overactive bladder (OAB).	Cyclophosphamide	179-195	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	50-66
16879691-1	2006	OBJECTIVE: To examine the effects of intravesical cyclooxygenase-2 (COX-2) inhibitors on the expression of inducible nitric oxide synthase (iNOS) and nerve growth factor (NGF) in cyclophosphamide (CYP)-induced overactive bladder (OAB).	Cyclophosphamide	179-195	nitric oxide synthase 2	Rattus norvegicus	107-138
16543915-1	2006	Cytochrome P450 (CYP) enzyme 2B1 metabolizes the anticancer prodrug cyclophosphamide (CPA) to 4-hydroxy-CPA, which decomposes to the cytotoxic metabolites acrolein and phosphoramide mustard.	Cyclophosphamide	68-84	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	11-15
16543915-1	2006	Cytochrome P450 (CYP) enzyme 2B1 metabolizes the anticancer prodrug cyclophosphamide (CPA) to 4-hydroxy-CPA, which decomposes to the cytotoxic metabolites acrolein and phosphoramide mustard.	Cyclophosphamide	86-89	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	11-15
16939069-10	2006	CONCLUSIONS: This report demonstrates the useful role of cyclophosphamide in the treatment of steroid-resistant nephrotic syndrome due to FSGS with glomerular tip lesion.	Cyclophosphamide	57-73	actinin alpha 4	Homo sapiens	138-142
17027654-4	2006	Second, the discovery of a potential curative combination of drugs, including cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP), for use in advanced disease could eradicate micro-metastatic disease in patients with LD.	Cyclophosphamide	78-94	DNA damage inducible transcript 3	Homo sapiens	138-142
17217824-4	2006	The effects of 5-fluorouracil (5-FU), mitomycin C (MMC) and cyclophosphamide (CTX) on the transfected cells were detected by assaying the apoptotic rate and growth inhibition by methabenzthiazuron (MTT) assay and flow cytometry (FCM).	Cyclophosphamide	60-76	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	78-81
16985248-1	2006	BACKGROUND: Follicular lymphoma is considered incurable, although cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy can induce sequential remissions.	Cyclophosphamide	66-82	DNA damage inducible transcript 3	Homo sapiens	126-130
16978400-2	2006	We therefore tested the activity of the combination of Trastuzumab with metronomic, low dose chemotherapy with cyclophosphamide (CTX) and methotrexate (MTX) in metastatic breast cancer (MBC).	Cyclophosphamide	111-127	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	129-132
16614059-0	2006	Expression of corticotropin-releasing factor and CRF receptors in micturition pathways after cyclophosphamide-induced cystitis.	Cyclophosphamide	93-109	corticotropin releasing hormone	Rattus norvegicus	14-44
16622862-8	2006	MMW exposure caused upregulation in tumor necrosis factor-alpha (TNF-alpha) production in peritoneal macrophages suppressed by CPA administration.	Cyclophosphamide	127-130	tumor necrosis factor	Mus musculus	36-63
16622862-8	2006	MMW exposure caused upregulation in tumor necrosis factor-alpha (TNF-alpha) production in peritoneal macrophages suppressed by CPA administration.	Cyclophosphamide	127-130	tumor necrosis factor	Mus musculus	65-74
16926418-3	2006	In animals rendered temporarily neutropenic by cyclophosphamide treatment, the C. glabrata ace2 null mutant was confirmed as hypervirulent: it led to early terminal illness and kidney, brain, and lung fungal burdens substantially and significantly larger than those in controls.	Cyclophosphamide	47-63	DNA-binding transcription factor ACE2	Saccharomyces cerevisiae S288C	91-95
16925484-1	2006	For more than 25 years, the combination of cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) was considered the gold standard for the treatment of aggressive lymphomas, 90% of which are diffuse, large B-cell lymphomas (DLBCLs).	Cyclophosphamide	43-59	DNA damage inducible transcript 3	Homo sapiens	102-106
16760192-2	2006	METHODS: Cyclophosphamide-suppressed CD-1 mice were infected intracerebrally with conidia of Aspergillus fumigatus and treated for 10 days with suboptimal doses of Abelcet (4 mg/kg) plus micafungin (1 mg/kg), caspofungin (1 mg/kg), itraconazole (100 mg/kg) or voriconazole (40 mg/kg) and compared with monotherapy.	Cyclophosphamide	9-25	CD1 antigen complex	Mus musculus	37-41
16877730-6	2006	There was a significantly greater suppression of Ki67 and VEGF-A expression in the letrozole/cyclophosphamide-treated group than in the letrozole-treated group, leading to lower Ki67 and VEGF expression at post-treatment residual histology (P = .03 and P = .002, respectively).	Cyclophosphamide	93-109	vascular endothelial growth factor A	Homo sapiens	58-64
16877730-6	2006	There was a significantly greater suppression of Ki67 and VEGF-A expression in the letrozole/cyclophosphamide-treated group than in the letrozole-treated group, leading to lower Ki67 and VEGF expression at post-treatment residual histology (P = .03 and P = .002, respectively).	Cyclophosphamide	93-109	vascular endothelial growth factor A	Homo sapiens	58-62
16797508-0	2006	Cyclophosphamide suppresses thioredoxin reductase in bladder tissue and its adaptive response via inductions of thioredoxin reductase and glutathione peroxidase.	Cyclophosphamide	0-16	peroxiredoxin 5	Homo sapiens	28-49
16797508-0	2006	Cyclophosphamide suppresses thioredoxin reductase in bladder tissue and its adaptive response via inductions of thioredoxin reductase and glutathione peroxidase.	Cyclophosphamide	0-16	peroxiredoxin 5	Homo sapiens	112-133
16699765-3	2006	We wished to test (99m)Tc-HYNIC-C-tagged VEGF ((99m)Tc-HYNIC-VEGF) for the imaging of tumor vasculature before and after antiangiogenic (low continuous dosing, metronomic) and tumoricidal (high-dose) cyclophosphamide treatment.	Cyclophosphamide	200-216	vascular endothelial growth factor A	Mus musculus	41-45
16888188-4	2006	Using gene delivery to express VIP, we interfered in the immune process leading to diabetes in prone, cyclophosphamide-treated NOD mice.	Cyclophosphamide	102-118	vasoactive intestinal polypeptide	Mus musculus	31-34
16769988-0	2006	Does granulocyte colony-stimulating factor worsen anemia in early breast cancer patients treated with epirubicin and cyclophosphamide?	Cyclophosphamide	117-133	colony stimulating factor 3	Homo sapiens	5-42
16769988-1	2006	PURPOSE: We report on the effects of granulocyte colony-stimulating factor (G-CSF) on hemoglobin (Hb) value in early breast cancer patients receiving high-dose epirubicin and cyclophosphamide (EC) adjuvant treatment.	Cyclophosphamide	175-191	colony stimulating factor 3	Homo sapiens	37-74
16769988-1	2006	PURPOSE: We report on the effects of granulocyte colony-stimulating factor (G-CSF) on hemoglobin (Hb) value in early breast cancer patients receiving high-dose epirubicin and cyclophosphamide (EC) adjuvant treatment.	Cyclophosphamide	175-191	colony stimulating factor 3	Homo sapiens	76-81
16786137-1	2006	It is known that, besides its direct cytotoxic effect as an alkylating chemotherapeutic agent, cyclophosphamide also has immuno-modulatory effects, such as depletion of CD4+CD25+ regulatory T cells.	Cyclophosphamide	95-111	CD4 antigen	Mus musculus	169-172
17048204-0	2006	Mycophenolic acid therapy after cyclophosphamide pulses in progressive IgA nephropathy.	Cyclophosphamide	32-48	IGAN1	Homo sapiens	71-86
17048204-1	2006	BACKGROUND: In progressive IgA nephropathy (IgAN), cyclophosphamide or steroids have been used to reduce the loss of renal function, but disease progression may occur after the end of treatment.	Cyclophosphamide	51-67	IGAN1	Homo sapiens	27-42
17048204-1	2006	BACKGROUND: In progressive IgA nephropathy (IgAN), cyclophosphamide or steroids have been used to reduce the loss of renal function, but disease progression may occur after the end of treatment.	Cyclophosphamide	51-67	IGAN1	Homo sapiens	44-48
16786137-4	2006	Cyclophosphamide (20 mg/kg) decreased the numbers of splenocytes, CD4+ and CD8+ T cells by approximately 50%, while a decline in CD4+CD25+ T cell number was more profound, leading to the remarkably lower ratios of CD4+CD25+ T cells to CD4+ T cells.	Cyclophosphamide	0-16	CD4 antigen	Mus musculus	66-69
16786137-5	2006	In contrast, 200 mg/kg cyclophosphamide severely decreased the numbers of all the T cell subsets by > 90% although the decreased ratios of CD4+CD25+ T cells to CD4+ T cells were still observed.	Cyclophosphamide	23-39	CD4 antigen	Mus musculus	142-145
16786137-5	2006	In contrast, 200 mg/kg cyclophosphamide severely decreased the numbers of all the T cell subsets by > 90% although the decreased ratios of CD4+CD25+ T cells to CD4+ T cells were still observed.	Cyclophosphamide	23-39	CD4 antigen	Mus musculus	163-166
16786137-10	2006	Our data show that low-dose cyclophosphamide selectively depletes CD4+CD25+ T cells, leading to enhanced anti-tumor effects against pre-existing tumors, while the anti-tumor effect of high-dose cyclophosphamide is solely attributed to its direct cytotoxicity.	Cyclophosphamide	28-44	CD4 antigen	Mus musculus	66-69
16786137-10	2006	Our data show that low-dose cyclophosphamide selectively depletes CD4+CD25+ T cells, leading to enhanced anti-tumor effects against pre-existing tumors, while the anti-tumor effect of high-dose cyclophosphamide is solely attributed to its direct cytotoxicity.	Cyclophosphamide	194-210	CD4 antigen	Mus musculus	66-69
16909595-6	2006	RESULTS: The combined low-dose therapy with cyclophosphamide and paclitaxel was most effective for antagonizing tumor-associated angiogensis; the mice of this group had the lowest MVD and VEGF expression, compared to mice of other groups (P < 0.005).	Cyclophosphamide	44-60	vascular endothelial growth factor A	Mus musculus	188-192
16651033-0	2006	Expression of fractalkine and fractalkine receptor in urinary bladder after cyclophosphamide (CYP)-induced cystitis.	Cyclophosphamide	76-92	C-X3-C motif chemokine ligand 1	Rattus norvegicus	14-50
16651033-0	2006	Expression of fractalkine and fractalkine receptor in urinary bladder after cyclophosphamide (CYP)-induced cystitis.	Cyclophosphamide	94-97	C-X3-C motif chemokine ligand 1	Rattus norvegicus	14-50
16933209-0	2006	Differential teratogenic response of TNFalpha+/+ and TNFalpha-/- mice to cyclophosphamide: the possible role of NF-kappaB.	Cyclophosphamide	73-89	tumor necrosis factor	Mus musculus	37-45
16933209-0	2006	Differential teratogenic response of TNFalpha+/+ and TNFalpha-/- mice to cyclophosphamide: the possible role of NF-kappaB.	Cyclophosphamide	73-89	tumor necrosis factor	Mus musculus	53-61
16933209-1	2006	BACKGROUND: We observed previously that tumor necrosis factor alpha (TNFalpha)-knockout embryos are more sensitive to a cyclophosphamide (CP)-induced teratogenic insult than their TNFalpha-positive counterparts, implicating molecules acting in TNFalpha-activated antiapoptotic pathways in the mechanisms underlying this phenomenon.	Cyclophosphamide	120-136	tumor necrosis factor	Mus musculus	40-67
16933209-1	2006	BACKGROUND: We observed previously that tumor necrosis factor alpha (TNFalpha)-knockout embryos are more sensitive to a cyclophosphamide (CP)-induced teratogenic insult than their TNFalpha-positive counterparts, implicating molecules acting in TNFalpha-activated antiapoptotic pathways in the mechanisms underlying this phenomenon.	Cyclophosphamide	120-136	tumor necrosis factor	Mus musculus	69-77
16792147-0	2006	Prednisone/cyclophosphamide treatment in adult-onset autosomal dominant familial focal segmental glomerulosclerosis (FSGS 1).	Cyclophosphamide	11-27	actinin alpha 4	Homo sapiens	117-123
16731821-3	2006	Unexpectedly, the cytoplasmic antioxidants, MT and catalase, greatly accelerated diabetes after cyclophosphamide and accelerated spontaneous diabetes in male NOD mice.	Cyclophosphamide	96-112	catalase	Mus musculus	51-59
16769594-1	2006	We evaluated the combination of thalidomide, pulsed dexamethasone and weekly cyclophosphamide (CTD) for the treatment of patients with newly diagnosed, relapsed or VAD-refractory multiple myeloma.	Cyclophosphamide	77-93	CTD	Homo sapiens	95-98
16840195-1	2006	Recently, the cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) regimen plus rituximab (R-CHOP) have been used widely to treat patients with follicular lymphoma.	Cyclophosphamide	14-30	DNA damage inducible transcript 3	Homo sapiens	73-77
16764697-0	2006	Sequential analysis of anti-alpha Gal natural antibody-producing B cells in GalT knockout mice in cyclophosphamide-induced tolerance.	Cyclophosphamide	98-114	galanin and GMAP prepropeptide	Mus musculus	34-37
16764697-0	2006	Sequential analysis of anti-alpha Gal natural antibody-producing B cells in GalT knockout mice in cyclophosphamide-induced tolerance.	Cyclophosphamide	98-114	galactose-1-phosphate uridyl transferase	Mus musculus	76-80
16646004-15	2006	CONCLUSION: Data from the WGET, the first substantial reported experience of the combined use of etanercept and cyclophosphamide in the treatment of WG, indicate that the combination of TNF inhibition and cyclophosphamide may heighten the risk of cancer beyond that observed with cyclophosphamide alone.	Cyclophosphamide	112-128	tumor necrosis factor	Homo sapiens	186-189
16675587-0	2006	The combination of the proteasome inhibitor bortezomib and the bcl-2 antisense molecule oblimersen sensitizes human B-cell lymphomas to cyclophosphamide.	Cyclophosphamide	136-152	BCL2 apoptosis regulator	Homo sapiens	63-68
16675587-1	2006	PURPOSE: To determine whether the combination of the proteasome inhibitor bortezomib and the bcl-2 antisense molecule oblimersen can sensitize human lymphoma to cyclophosphamide.	Cyclophosphamide	161-177	BCL2 apoptosis regulator	Homo sapiens	93-98
17063385-0	2006	Immunohistochemical study of monocyte chemoattractant protein-1 in the pancreas of NOD mice following cyclophosphamide administration and during spontaneous diabetes.	Cyclophosphamide	102-118	chemokine (C-C motif) ligand 2	Mus musculus	29-63
16757436-3	2006	We investigated MGMT protein expression by immunohistochemical analysis of 63 DLBCL patients who received cyclophosphamide as part of multidrug regimens.	Cyclophosphamide	106-122	O-6-methylguanine-DNA methyltransferase	Homo sapiens	16-20
17063385-5	2006	We employed dual-label immunohistochemistry to examine the intra-islet expression, distribution and cellular source of MCP-1 in the NOD mouse following cyclophosphamide administration.	Cyclophosphamide	152-168	chemokine (C-C motif) ligand 2	Mus musculus	119-124
17063385-8	2006	In the cyclophosphamide group at day 0, MCP-1 immunolabelling was present in selective peri-islet macrophages but declined at day 4.	Cyclophosphamide	7-23	chemokine (C-C motif) ligand 2	Mus musculus	40-45
17063385-10	2006	The pattern of MCP-1 expression in macrophages was different over time in both the cyclophosphamide and control groups.	Cyclophosphamide	83-99	chemokine (C-C motif) ligand 2	Mus musculus	15-20
16636524-2	2006	During the administration of cyclophosphamide (60 mg/kg/day for 2 days) for mobilization and collection of CD34+ selected peripheral blood stem cells, he developed congestive heart failure.	Cyclophosphamide	29-45	CD34 molecule	Homo sapiens	107-111
16753869-3	2006	We used clinical information obtained during pretreatment evaluation to develop a predictive model for severe neutropenia in the first cycle of cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) chemotherapy.	Cyclophosphamide	144-160	DNA damage inducible transcript 3	Homo sapiens	203-207
16532434-2	2006	The authors report on their results from a regimen of ifosfamide, carboplatin, and etoposide (ICE) with cyclophosphamide, doxorubicin, and vincristine (CAV) dose intensification in patients with high-risk ESFT.	Cyclophosphamide	104-120	caveolin 2	Homo sapiens	152-155
16585551-3	2006	We found that intranasal vaccination of NOD mice with plasmid DNA encoding mouse proinsulin II-induced CD4+ T(reg) that suppressed diabetes development, both after adoptive cotransfer with "diabetogenic" spleen cells and after transfer into NOD mice given cyclophosphamide to accelerate diabetes onset.	Cyclophosphamide	256-272	insulin II	Mus musculus	81-91
16585551-3	2006	We found that intranasal vaccination of NOD mice with plasmid DNA encoding mouse proinsulin II-induced CD4+ T(reg) that suppressed diabetes development, both after adoptive cotransfer with "diabetogenic" spleen cells and after transfer into NOD mice given cyclophosphamide to accelerate diabetes onset.	Cyclophosphamide	256-272	CD4 antigen	Mus musculus	103-106
16609087-13	2006	CONCLUSION: Among patients with node-positive tumors, ER-negative breast cancer, biweekly doxorubicin/cyclophosphamide plus paclitaxel lowers the rate of recurrence and death by more than 50% in comparison with low-dose cyclophosphamide, doxorubicin, and fluorouracil as used in the first study.	Cyclophosphamide	102-118	estrogen receptor 1	Homo sapiens	54-56
16609087-13	2006	CONCLUSION: Among patients with node-positive tumors, ER-negative breast cancer, biweekly doxorubicin/cyclophosphamide plus paclitaxel lowers the rate of recurrence and death by more than 50% in comparison with low-dose cyclophosphamide, doxorubicin, and fluorouracil as used in the first study.	Cyclophosphamide	220-236	estrogen receptor 1	Homo sapiens	54-56
16416337-1	2006	The addition of rituximab to cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) has been shown to improve the outcome in all age groups with newly diagnosed diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	29-45	DNA damage inducible transcript 3	Homo sapiens	89-93
16595573-5	2006	DISCUSSION: Since roxithromycin inhibits CYP3A4, which is involved with cyclophosphamide metabolism, a drug-drug interaction could have been responsible.	Cyclophosphamide	72-88	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	41-47
16126793-6	2006	The frequency of RAG+ IgD+CD5+/- B cells was reduced during intravenous cyclophosphamide treatment.	Cyclophosphamide	72-88	CD5 molecule	Homo sapiens	26-29
16545732-11	2006	VP/Cy is able to induce CR1 in most patients with primary refractory AL with an acceptable toxicity profile.	Cyclophosphamide	3-5	complement C3b/C4b receptor 1 (Knops blood group)	Homo sapiens	24-27
16337237-2	2006	Previously, it was demonstrated that DNA-damaging agents such as irradiation, cyclophosphamide or 5-fluorouracil increase the expression of SDF-1 by osteoblasts in murine marrow.	Cyclophosphamide	78-94	chemokine (C-X-C motif) ligand 12	Mus musculus	140-145
15965646-0	2006	Importance of signaling via the IFN-alpha/beta receptor on host cells for the realization of the therapeutic benefits of cyclophosphamide for mice bearing a large MOPC-315 tumor.	Cyclophosphamide	121-137	interferon alpha	Mus musculus	32-41
16131469-1	2006	Recent evidence suggests that young women with estrogen receptor (ER)-positive breast cancer (BC) require additional treatment because of the inadequacy of cyclophosphamide, methotrexate fluorouracil (CMF) alone.	Cyclophosphamide	156-172	estrogen receptor 1	Homo sapiens	47-64
17152352-0	2006	Expression of the c-Fos gene in hypothalamic cells and cytotoxic activity of natural killer cells in the spleen of rats after treatment with Cytoxan.	Cyclophosphamide	141-148	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	18-23
17152352-2	2006	Administration of Cytoxan in a dose of 60 mg/kg increased the number of c-Fos-positive cells in the ventromedial hypothalamus and lateral hypothalamic area and reduced interferon-alpha-induced cytotoxic activity of natural killer cells.	Cyclophosphamide	18-25	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	72-77
16630220-3	2006	We report here a 50-year-old female with AMM/PMF, conditioned with busulfan and cyclophosphamide, who rejected a single locus (HLA-B) mismatched bone marrow transplant from her daughter, but recovered normal autologous hematopoiesis with disappearance of marrow fibrosis and extramedullary hematopoiesis.	Cyclophosphamide	80-96	major histocompatibility complex, class I, B	Homo sapiens	127-132
16740391-4	2006	IL-10-deficient NOD mice under such conditions were protected from spontaneous as well as cyclophosphamide-induced diabetes, but were susceptible to diabetes induced by adoptive transfer of splenocytes from spontaneously diabetic NOD mice.	Cyclophosphamide	90-106	interleukin 10	Mus musculus	0-5
16675587-10	2006	CONCLUSION: The use of Bcl-2-directed therapy and a proteasome inhibitor sensitizes human lymphoma cells to cytotoxic drugs like cyclophosphamide.	Cyclophosphamide	129-145	BCL2 apoptosis regulator	Homo sapiens	23-28
15965646-1	2006	Here we show that low-dose cyclophosphamide (CY), that depends for its therapeutic effectiveness on the immunopotentiating activity of the drug for T cell-mediated tumor-eradicating immunity, is curative for approximately 80% of wild-type (WT) mice bearing a large s.c. MOPC-315 tumor, but only for approximately 10% of IFN-alpha/betaR-/- mice bearing a large s.c. MOPC-315 tumor.	Cyclophosphamide	27-43	interferon alpha	Mus musculus	320-329
15965646-1	2006	Here we show that low-dose cyclophosphamide (CY), that depends for its therapeutic effectiveness on the immunopotentiating activity of the drug for T cell-mediated tumor-eradicating immunity, is curative for approximately 80% of wild-type (WT) mice bearing a large s.c. MOPC-315 tumor, but only for approximately 10% of IFN-alpha/betaR-/- mice bearing a large s.c. MOPC-315 tumor.	Cyclophosphamide	45-47	interferon alpha	Mus musculus	320-329
15965646-2	2006	Histopathological examination of the s.c. tumors of such mice on day 4 after the chemotherapy revealed that the low dose of CY led to accumulation of T lymphocytes in both the WT and the IFN-alpha/betaR-/- mice.	Cyclophosphamide	124-126	interferon alpha	Mus musculus	187-196
15965646-3	2006	However, in the CY treated tumor bearing WT mice the T lymphocytes were present throughout the tumor mass and in direct contact with tumor cells, but in the CY treated tumor bearing IFN-alpha/betaR-/- mice most of the T lymphocytes remained in blood vessels.	Cyclophosphamide	157-159	interferon alpha	Mus musculus	182-191
15965646-4	2006	In addition to being important for CY-induced transendothelial migration of T lymphocytes into the tumor mass, we show here that signaling via the IFN-alpha/betaR is also important for CY-induced control of metastatic tumor progression in the spleen and liver of the tumor bearing mice.	Cyclophosphamide	185-187	interferon (alpha and beta) receptor 1	Mus musculus	147-162
15965646-6	2006	Thus, signaling via the IFN-alpha/betaR on host cells in MOPC-315 tumor bearers is important for CY-induced: (a) transendothelial migration of T lymphocytes into the tumor mass and the eradication of the primary tumor, (b) control of metastatic tumor progression, and (c) resistance to a subsequent tumor challenge.	Cyclophosphamide	97-99	interferon (alpha and beta) receptor 1	Mus musculus	24-39
16453328-1	2006	BACKGROUND: Cyclophosphamide (CTX) and ifosfamide (IFX) are alkylating agents used to treat osteosarcoma (OS).	Cyclophosphamide	12-28	V-set and immunoglobulin domain containing 2	Mus musculus	30-33
16304055-6	2006	Exogenous KGF also accelerated thymic recovery after irradiation, cyclophosphamide, and dexamethasone treatment.	Cyclophosphamide	66-82	fibroblast growth factor 7	Mus musculus	10-13
16550168-6	2006	This includes also some anticancer drugs like tamoxifen and cyclophosphamide metabolized by CYP2D6, CYP2C19 and CYP2B6.	Cyclophosphamide	60-76	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	92-98
16550168-6	2006	This includes also some anticancer drugs like tamoxifen and cyclophosphamide metabolized by CYP2D6, CYP2C19 and CYP2B6.	Cyclophosphamide	60-76	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	100-107
16550168-6	2006	This includes also some anticancer drugs like tamoxifen and cyclophosphamide metabolized by CYP2D6, CYP2C19 and CYP2B6.	Cyclophosphamide	60-76	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	112-118
16488414-0	2006	Cyclophosphamide enhances TNF-alpha-induced apoptotic cell death in murine vascular endothelial cell.	Cyclophosphamide	0-16	tumor necrosis factor	Mus musculus	26-35
16488414-2	2006	In murine dermal endothelial cells (F-2), 4-hydroxycyclophosphamide (4-HC), which is active metabolite of CPA, enhanced TNF-alpha-induced DNA fragmentation.	Cyclophosphamide	106-109	tumor necrosis factor	Mus musculus	120-129
16488414-6	2006	These results suggest that CPA may sensitize endothelial cells to TNF-alpha-induced apoptosis through a mitochondria-dependent pathway and clinically may contribute to the limitation of inflammatory process.	Cyclophosphamide	27-30	tumor necrosis factor	Mus musculus	66-75
16860296-4	2006	Our results demonstrate that anti-CD25 treatment, like cyclophosphamide, partially blocks the efficacy of gene therapy for tolerance.	Cyclophosphamide	55-71	interleukin 2 receptor, alpha chain	Mus musculus	34-38
16522464-7	2006	There was also increased total and ovalbumin-specific serum IgE, increased IL-4 and IL-5 secretion by peritracheal lymph node cells, and reduced lung mRNA expression of IL-10 and TGF-beta in animals treated with cyclophosphamide.	Cyclophosphamide	212-228	interleukin 4	Mus musculus	75-79
16640819-3	2006	In this regard, we report an 80-year-old patient with follicular grade 3 non-Hodgkin"s lymphoma who developed a fatal interstitial pneumonitis related to treatment with a rituximab/CHOP (cyclophosphamide/doxorubicin/vincristine/prednisone) regimen.	Cyclophosphamide	187-203	DNA damage inducible transcript 3	Homo sapiens	181-185
16522464-7	2006	There was also increased total and ovalbumin-specific serum IgE, increased IL-4 and IL-5 secretion by peritracheal lymph node cells, and reduced lung mRNA expression of IL-10 and TGF-beta in animals treated with cyclophosphamide.	Cyclophosphamide	212-228	interleukin 5	Mus musculus	84-88
16522464-7	2006	There was also increased total and ovalbumin-specific serum IgE, increased IL-4 and IL-5 secretion by peritracheal lymph node cells, and reduced lung mRNA expression of IL-10 and TGF-beta in animals treated with cyclophosphamide.	Cyclophosphamide	212-228	interleukin 10	Mus musculus	169-174
16522464-7	2006	There was also increased total and ovalbumin-specific serum IgE, increased IL-4 and IL-5 secretion by peritracheal lymph node cells, and reduced lung mRNA expression of IL-10 and TGF-beta in animals treated with cyclophosphamide.	Cyclophosphamide	212-228	transforming growth factor, beta 1	Mus musculus	179-187
16522464-8	2006	The expression of FoxP3, a marker of regulatory T cells, was significantly reduced in lymphoid organs after the second injection of cyclophosphamide, and in the lung tissue after allergen challenge in cyclophosphamide-treated mice.	Cyclophosphamide	132-148	forkhead box P3	Mus musculus	18-23
16522464-8	2006	The expression of FoxP3, a marker of regulatory T cells, was significantly reduced in lymphoid organs after the second injection of cyclophosphamide, and in the lung tissue after allergen challenge in cyclophosphamide-treated mice.	Cyclophosphamide	201-217	forkhead box P3	Mus musculus	18-23
16522464-9	2006	Lung IL-10+CD4+ T cells and cytotoxic T lymphocyte-associated antigen 4+CD4+ T cells were reduced after allergen challenge in cyclophosphamide-treated mice.	Cyclophosphamide	126-142	interleukin 10	Mus musculus	5-10
16493027-3	2006	Cyclophosphamide could 1) abolish the suppressive function of CD4+CD25+Foxp3+ regulatory T cells, 2) markedly enhance the magnitude of secondary but not primary CTL responses induced by DEX vaccines, 3) synergize with DEX in therapy but not prophylaxis tumor models.	Cyclophosphamide	0-16	CD4 antigen	Mus musculus	62-65
16546968-1	2006	Gene therapy using the prodrug-activating enzyme P450 2B6 has shown substantial promise in preclinical and initial clinical studies with the P450 prodrugs cyclophosphamide and ifosfamide.	Cyclophosphamide	155-171	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	49-53
16546968-1	2006	Gene therapy using the prodrug-activating enzyme P450 2B6 has shown substantial promise in preclinical and initial clinical studies with the P450 prodrugs cyclophosphamide and ifosfamide.	Cyclophosphamide	155-171	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	141-145
16546968-2	2006	We sought to optimize this therapy using the canine P450 enzyme 2B11, which activates cyclophosphamide and ifosfamide with Km of 80 to 160 micromol/L, approximately 10- to 20-fold lower than the Km of P450 2B6.	Cyclophosphamide	86-102	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	52-56
16546968-3	2006	Retrovirus encoding a P450 2B11-internal ribosome entry signal-P450 reductase expression cassette induced marked cyclophosphamide and ifosfamide cytotoxicity toward 9L gliosarcoma cells and exhibited an impressive bystander killing effect at micromolar prodrug concentrations, where P450 2B6 displayed low activity.	Cyclophosphamide	113-129	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	22-26
16546968-3	2006	Retrovirus encoding a P450 2B11-internal ribosome entry signal-P450 reductase expression cassette induced marked cyclophosphamide and ifosfamide cytotoxicity toward 9L gliosarcoma cells and exhibited an impressive bystander killing effect at micromolar prodrug concentrations, where P450 2B6 displayed low activity.	Cyclophosphamide	113-129	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	63-67
16546968-3	2006	Retrovirus encoding a P450 2B11-internal ribosome entry signal-P450 reductase expression cassette induced marked cyclophosphamide and ifosfamide cytotoxicity toward 9L gliosarcoma cells and exhibited an impressive bystander killing effect at micromolar prodrug concentrations, where P450 2B6 displayed low activity.	Cyclophosphamide	113-129	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	63-67
16546968-4	2006	Adeno-2B11, a replication-defective, E1/E3 region-deleted adenovirus engineered to coexpress P450 2B11 and P450 reductase, dramatically increased tumor cell-catalyzed cyclophosphamide 4-hydroxylation and cytotoxicity compared with Adeno-2B6 and effected strong bystander killing at low (20 micromol/L) cyclophosphamide concentrations.	Cyclophosphamide	167-183	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	93-97
16546968-4	2006	Adeno-2B11, a replication-defective, E1/E3 region-deleted adenovirus engineered to coexpress P450 2B11 and P450 reductase, dramatically increased tumor cell-catalyzed cyclophosphamide 4-hydroxylation and cytotoxicity compared with Adeno-2B6 and effected strong bystander killing at low (20 micromol/L) cyclophosphamide concentrations.	Cyclophosphamide	167-183	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	107-111
16546968-4	2006	Adeno-2B11, a replication-defective, E1/E3 region-deleted adenovirus engineered to coexpress P450 2B11 and P450 reductase, dramatically increased tumor cell-catalyzed cyclophosphamide 4-hydroxylation and cytotoxicity compared with Adeno-2B6 and effected strong bystander killing at low (20 micromol/L) cyclophosphamide concentrations.	Cyclophosphamide	302-318	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	93-97
16546968-5	2006	Further increases in cyclophosphamide cytotoxicity were obtained in several human cancer cell lines, including a 4-hydroperoxycyclophosphamide-resistant MCF-7 breast cancer cell line, when Adeno-2B11 was combined with Onyx-017, an E1b-55-kDa gene-deleted, tumor cell-replicating adenovirus that coamplifies and facilitates tumor cell spread of Adeno-2B11.	Cyclophosphamide	21-37	branched chain keto acid dehydrogenase E1 subunit beta	Homo sapiens	231-234
16546968-9	2006	Thus, P450 gene-directed enzyme prodrug therapy can be greatly improved by using the low Km P450 enzyme 2B11, which catalyzes intratumoral activation of cyclophosphamide and ifosfamide at pharmacologically relevant drug concentrations.	Cyclophosphamide	153-169	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	6-10
16546968-9	2006	Thus, P450 gene-directed enzyme prodrug therapy can be greatly improved by using the low Km P450 enzyme 2B11, which catalyzes intratumoral activation of cyclophosphamide and ifosfamide at pharmacologically relevant drug concentrations.	Cyclophosphamide	153-169	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	92-96
16322118-1	2006	BACKGROUND: We previously demonstrated efficacy and impact on serum vascular endothelial growth factor (VEGF) for metronomic cyclophosphamide (C) and methotrexate (M) in patients with breast cancer.	Cyclophosphamide	125-141	vascular endothelial growth factor A	Homo sapiens	68-102
16322118-1	2006	BACKGROUND: We previously demonstrated efficacy and impact on serum vascular endothelial growth factor (VEGF) for metronomic cyclophosphamide (C) and methotrexate (M) in patients with breast cancer.	Cyclophosphamide	125-141	vascular endothelial growth factor A	Homo sapiens	104-108
16372153-8	2006	Adoptive transfer of spleen cells from normal mice into STAT6 knockout mice before tumor inoculation reduces both the immunogenicity and response to Cy plus IL-12 immunotherapy of 4T1 in the recipient mice.	Cyclophosphamide	149-151	signal transducer and activator of transcription 6	Mus musculus	56-61
16739330-3	2006	PATIENTS AND METHODS: Semi-quantitative syndecan-1 immunohistochemistry was performed in pre-chemotherapy breast cancer biopsies of 37 patients undergoing high-dose neoadjuvant treatment with cyclophosphamide and epirubicin.	Cyclophosphamide	192-208	syndecan 1	Homo sapiens	40-50
16331635-2	2006	Attempts to improve the results achieved with the combination of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) using second-generation or third-generation chemotherapy have failed.	Cyclophosphamide	65-81	DNA damage inducible transcript 3	Homo sapiens	125-129
16183265-3	2006	The pharmacokinetics of CPA and its active metabolite were related to the genotype of CYP2B6, CYP2C9 and CYP2C19.	Cyclophosphamide	24-27	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	86-92
16183265-3	2006	The pharmacokinetics of CPA and its active metabolite were related to the genotype of CYP2B6, CYP2C9 and CYP2C19.	Cyclophosphamide	24-27	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	94-100
16183265-3	2006	The pharmacokinetics of CPA and its active metabolite were related to the genotype of CYP2B6, CYP2C9 and CYP2C19.	Cyclophosphamide	24-27	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	105-112
16183265-13	2006	In the population analysis, the CYP2B6 G516T variant allele contribution to CPA clearance was about twice as the contribution from the wild type gene while the genotype of CYP2C9 and CYP2C19 did not influence clearance.	Cyclophosphamide	76-79	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	32-38
16116645-0	2006	High-dose cyclophosphamide in refractory myasthenia gravis with MuSK antibodies.	Cyclophosphamide	10-26	muscle associated receptor tyrosine kinase	Homo sapiens	64-68
16293390-1	2006	Cancer chemotherapeutic prodrugs, such as the oxazaphosphorines cyclophosphamide and ifosfamide, are metabolized by liver cytochrome P450 enzymes to yield therapeutically active, cytotoxic metabolites.	Cyclophosphamide	64-80	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	133-137
16219798-5	2006	All detectable HSCs from old, reconstituted, and cyclophosphamide/G-CSF-mobilized mice were CD150+ CD48-, just as in normal young bone marrow.	Cyclophosphamide	49-65	signaling lymphocytic activation molecule family member 1	Mus musculus	92-97
16219798-5	2006	All detectable HSCs from old, reconstituted, and cyclophosphamide/G-CSF-mobilized mice were CD150+ CD48-, just as in normal young bone marrow.	Cyclophosphamide	49-65	CD48 antigen	Mus musculus	99-103
16452226-7	2006	We found that LDM cyclophosphamide impairs the oxygenation of PC-3 xenografts even during relapse, coinciding with reduced microvessel density.	Cyclophosphamide	18-34	chromobox 8	Homo sapiens	62-66
16452226-8	2006	Combination of LDM cyclophosphamide with tirapazamine results in significantly improved tumor control in the PC-3, HT-29 colon adenocarcinoma, and MDA-MB-231 breast cancer human xenograft models without having a negative effect on the favorable toxicity profile of LDM cyclophosphamide.	Cyclophosphamide	19-35	chromobox 8	Homo sapiens	109-113
16475710-1	2006	The oxazaphosphorines cyclophosphamide (CP) and ifosfamide (IF) are alkylating agents that require bioactivation via cytochrome (CYP) P450 isoenzymes including CYP2C9 enzymes.	Cyclophosphamide	22-38	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	160-166
16831024-5	2006	The combination of rituximab with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) was cost effective as first-line therapy for advanced-stage diffuse large B-cell NHL compared with CHOP alone.	Cyclophosphamide	34-50	DNA damage inducible transcript 3	Homo sapiens	93-97
16429836-1	2006	AIMS: We herein report the results of intravenous pulse cyclophosphamide (IVCP) therapy of 5 patients with steroid-resistant focal segmental glomerulosclerosis (FSGS).	Cyclophosphamide	56-72	actinin alpha 4	Homo sapiens	161-165
16706552-5	2006	The combination of rituximab with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) was cost effective as first-line therapy for advanced-stage diffuse large B-cell NHL compared with CHOP alone.	Cyclophosphamide	34-50	DNA damage inducible transcript 3	Homo sapiens	93-97
16595331-0	2006	Effect of millimeter waves on cyclophosphamide induced NF-kappaB.	Cyclophosphamide	30-46	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	55-64
16595331-2	2006	The effect of millimeter waves (MMWs) on NF-kappaB activation induced by cyclophosphamide (CPA) was studied in the spleen of mice.	Cyclophosphamide	73-89	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	41-50
16595331-2	2006	The effect of millimeter waves (MMWs) on NF-kappaB activation induced by cyclophosphamide (CPA) was studied in the spleen of mice.	Cyclophosphamide	91-94	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	41-50
16595331-3	2006	CPA, an anticancer drug, caused a marked increase (58.9-fold) in NF-kappaB DNA-binding activity as compared to the control group.	Cyclophosphamide	0-3	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	65-74
16522464-9	2006	Lung IL-10+CD4+ T cells and cytotoxic T lymphocyte-associated antigen 4+CD4+ T cells were reduced after allergen challenge in cyclophosphamide-treated mice.	Cyclophosphamide	126-142	cytotoxic T-lymphocyte-associated protein 4	Mus musculus	28-75
16522464-11	2006	The reduced expression of FoxP3 and immunosuppressive cytokines by cyclophosphamide is consistent with the possibility that toxicity to regulatory T cells may contribute to the increased inflammation.	Cyclophosphamide	67-83	forkhead box P3	Mus musculus	26-31
16421623-6	2006	Western blotting revealed that CY significantly down-regulated the protein expression of vascular endothelial growth factor (VEGF), c-Myc and ornithine decarboxylase (ODC) in gastric mucosae but had no effect on epidermal growth factor (EGF) expression.	Cyclophosphamide	31-33	vascular endothelial growth factor A	Mus musculus	89-123
16421623-6	2006	Western blotting revealed that CY significantly down-regulated the protein expression of vascular endothelial growth factor (VEGF), c-Myc and ornithine decarboxylase (ODC) in gastric mucosae but had no effect on epidermal growth factor (EGF) expression.	Cyclophosphamide	31-33	vascular endothelial growth factor A	Mus musculus	125-129
16421623-6	2006	Western blotting revealed that CY significantly down-regulated the protein expression of vascular endothelial growth factor (VEGF), c-Myc and ornithine decarboxylase (ODC) in gastric mucosae but had no effect on epidermal growth factor (EGF) expression.	Cyclophosphamide	31-33	ornithine decarboxylase, structural 1	Mus musculus	142-165
16421623-6	2006	Western blotting revealed that CY significantly down-regulated the protein expression of vascular endothelial growth factor (VEGF), c-Myc and ornithine decarboxylase (ODC) in gastric mucosae but had no effect on epidermal growth factor (EGF) expression.	Cyclophosphamide	31-33	ornithine decarboxylase, structural 1	Mus musculus	167-170
16421623-7	2006	AP also reversed the dampening effect of CY on VEGF expression in the gastric mucosa.	Cyclophosphamide	41-43	vascular endothelial growth factor A	Mus musculus	47-51
17318948-6	2006	FAC (5 fluorouracil/doxorubicin/cyclophosphamide/methotrexate/5 fluorouracil), higher doses of epirubicin in FE(100)C are twice as high compared with FAC.	Cyclophosphamide	32-48	FA complementation group C	Homo sapiens	0-3
16719378-1	2006	The cytochrome P450 enzyme CYP2B6 plays an important role in the metabolism of structurally diverse drugs, including the anticancer drug cyclophosphamide, and may be an important determinant of clinical responses to these agents.	Cyclophosphamide	137-153	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	27-33
16686258-9	2006	Although overt POF with cyclophosphamide exposure is rare, it is a risk factor for significantly decreased ovarian reserve cSLE.	Cyclophosphamide	24-40	POF1B actin binding protein	Homo sapiens	15-18
16720917-4	2006	Neoadjuvant regimen consisted in 600 mg/m2 5-fluorouracil, 60 mg/m2 doxorubicin, and 600 mg/m2 cyclophosphamide (FAC).	Cyclophosphamide	95-111	FA complementation group C	Homo sapiens	113-116
16985290-4	2006	The levels of interferon-(IFN-)gamma, tumor necrosis factor-(TNF-)alpha, granulocyte-macrophage-colony stimulating factor (GM-CSF), interleukin-(IL-) 6 and IL-12p70 were significantly increased by SCG in CY-treated mice.	Cyclophosphamide	204-206	interferon gamma	Mus musculus	14-71
16518803-14	2006	Also, GSH, GSH-Px, and SOD enzyme activities were significantly increased in the cyclophosphamide and 5-fluorouracil groups, compared to the other two antineoplastic agent groups (P < 0.01).	Cyclophosphamide	81-97	glutathione peroxidase 1	Rattus norvegicus	11-17
16985290-5	2006	GM-CSF production in the splenocytes from the CY-treated mice was higher than that in normal mice regardless of SCG stimulation.	Cyclophosphamide	46-48	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	0-6
16985290-7	2006	The level of cytokine induction by SCG was regulated by the amount of endogenous GM-CSF produced in response to CY treatment in a dose-dependent manner.	Cyclophosphamide	112-114	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	81-87
16575475-1	2006	Authors conducted a one-year prospective study to determine whether CHOP regimen (cyclophosphamide, doxorubicin, vincristin, and prednisone), used in the treatment of aggressive non-Hodgkin s lymphoma, is associated with the presence of an early impairment of cardiac function.	Cyclophosphamide	82-98	DNA damage inducible transcript 3	Homo sapiens	68-72
16141461-1	2006	BACKGROUND: Here we compare the efficacy of cyclophosphamide (CYC) for treatment of crescentic nephritis (CGN) with the newer immunosuppressants 15-deoxyspergualin (DSG) and mycophenolate mofetil (MMF) in SCG/Kj mice, an inbred mouse strain that spontaneously develops CGN, systemic necrotizing vasculitis and antineutrophil cytoplasmic antibodies (ANCAs).	Cyclophosphamide	44-60	cingulin	Mus musculus	106-109
16141461-1	2006	BACKGROUND: Here we compare the efficacy of cyclophosphamide (CYC) for treatment of crescentic nephritis (CGN) with the newer immunosuppressants 15-deoxyspergualin (DSG) and mycophenolate mofetil (MMF) in SCG/Kj mice, an inbred mouse strain that spontaneously develops CGN, systemic necrotizing vasculitis and antineutrophil cytoplasmic antibodies (ANCAs).	Cyclophosphamide	62-65	cingulin	Mus musculus	106-109
15940386-1	2005	The aim of the present study was to evaluate the efficacy of the combination of cyclophosphamide (CTX) and interferon beta (IFN beta) in a group of relapsing remitting (RR) multiple sclerosis (MS) patients who experienced treatment failure during IFN beta therapy.	Cyclophosphamide	80-96	interferon beta 1	Homo sapiens	247-255
16837820-9	2006	CONCLUSIONS: These results indicate that the expression of the high-affinity concentrative nucleoside transporter hCNT1 has a prognostic value in determining disease-free survival and risk of relapse in breast cancer patients undergoing surgery followed by cyclophosphamide-methotrexate-5-fluorouracil chemotherapy.	Cyclophosphamide	257-273	solute carrier family 28 member 1	Homo sapiens	114-119
16339582-2	2005	Type 1 diabetes is considered to be a Th1-dominant autoimmune disease, and a suppressive effect of CXCL10 neutralization on diabetes development has been reported in a cyclophosphamide-induced accelerated diabetes model through induction of beta cell proliferation.	Cyclophosphamide	168-184	chemokine (C-X-C motif) ligand 10	Mus musculus	99-105
16123223-0	2005	Frontline therapy with rituximab added to the combination of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) significantly improves the outcome for patients with advanced-stage follicular lymphoma compared with therapy with CHOP alone: results of a prospective randomized study of the German Low-Grade Lymphoma Study Group.	Cyclophosphamide	61-77	DNA damage inducible transcript 3	Homo sapiens	121-125
16076520-10	2005	The enhanced lipid peroxidation and decreased catalase and superoxide dismutase activities found in lymphocytes, polymorphonuclear cells (PMN) and macrophages from cyclophosphamide treated rats were significantly ameliorated in mangiferin treated groups.	Cyclophosphamide	164-180	catalase	Rattus norvegicus	46-54
16291906-0	2005	Efficacy of TNF {alpha} blockade in cyclophosphamide resistant neuro-Behcet disease.	Cyclophosphamide	36-52	tumor necrosis factor	Homo sapiens	12-15
16132345-18	2005	Further studies are needed to explore the role of MRP4 in resistance, toxicity, and pharmacokinetics of CPTs and cyclophosphamide.	Cyclophosphamide	113-129	ATP binding cassette subfamily C member 4	Homo sapiens	50-54
16226702-3	2005	report that mice carrying a mutation in Nf1, the gene responsible for neurofibromatosis type 1, treated with radiation and/or cyclophosphamide, developed tumors similar to human SMNs at a significantly higher rate than did wild-type controls treated similarly.	Cyclophosphamide	126-142	neurofibromin 1	Mus musculus	40-43
16227744-8	2005	The antitumor effect in the MTD-administered group was the strongest of all of the tested anticancer drug groups (cyclophosphamide, mitomycin C, fluorouracil, cisplatin, doxorubicin).	Cyclophosphamide	114-130	metallothionein 1E	Homo sapiens	28-31
16142355-0	2005	Reduced radiosensitivity and increased CD40 expression in cyclophosphamide-resistant subclones established from human cervical squamous cell carcinoma cells.	Cyclophosphamide	58-74	CD40 molecule	Homo sapiens	39-43
16193896-0	2005	A randomized blinded trial of combination therapy with cyclophosphamide in patients-with active multiple sclerosis on interferon beta.	Cyclophosphamide	55-71	interferon beta 1	Homo sapiens	118-133
16193896-1	2005	OBJECTIVE: To evaluate the efficacy and safety of combination therapy with pulse cyclophosphamide given with methylprednisolone (MP) and interferon beta (IFNbeta)-Ia in multiple sclerosis (MS) patients with active disease during IFNbeta monotherapy.	Cyclophosphamide	81-97	interferon beta 1	Homo sapiens	137-152
16193896-1	2005	OBJECTIVE: To evaluate the efficacy and safety of combination therapy with pulse cyclophosphamide given with methylprednisolone (MP) and interferon beta (IFNbeta)-Ia in multiple sclerosis (MS) patients with active disease during IFNbeta monotherapy.	Cyclophosphamide	81-97	interferon beta 1	Homo sapiens	154-161
16142355-8	2005	Furthermore, CD40 activation signals may be associated with the multidrug- and radioresistance in these cyclophosphamide-resistant subclones.	Cyclophosphamide	104-120	CD40 molecule	Homo sapiens	13-17
16166447-6	2005	We found that multiple chemotherapy agents, cyclophosphamide (cytoxan), cisplatin, and docetaxel, induced endothelial CD95 in vitro and in vivo at low doses that failed to kill endothelial cells (cytoxan > cisplatin > docetaxel).	Cyclophosphamide	44-60	Fas (TNF receptor superfamily member 6)	Mus musculus	118-122
16305339-1	2005	Experimental evidence from previous studies supports the conclusion that orally administered lactoferrin (LF) restores the immune response in mice treated with a sublethal dose of cyclophosphamide (CP).	Cyclophosphamide	180-196	lactotransferrin	Mus musculus	93-104
16305339-1	2005	Experimental evidence from previous studies supports the conclusion that orally administered lactoferrin (LF) restores the immune response in mice treated with a sublethal dose of cyclophosphamide (CP).	Cyclophosphamide	180-196	lactotransferrin	Mus musculus	106-108
16166447-6	2005	We found that multiple chemotherapy agents, cyclophosphamide (cytoxan), cisplatin, and docetaxel, induced endothelial CD95 in vitro and in vivo at low doses that failed to kill endothelial cells (cytoxan > cisplatin > docetaxel).	Cyclophosphamide	62-69	Fas (TNF receptor superfamily member 6)	Mus musculus	118-122
16166447-6	2005	We found that multiple chemotherapy agents, cyclophosphamide (cytoxan), cisplatin, and docetaxel, induced endothelial CD95 in vitro and in vivo at low doses that failed to kill endothelial cells (cytoxan > cisplatin > docetaxel).	Cyclophosphamide	196-203	Fas (TNF receptor superfamily member 6)	Mus musculus	118-122
16142702-0	2005	Use of a gonadotropin-releasing hormone analog for protection against premature ovarian failure during cyclophosphamide therapy in women with severe lupus.	Cyclophosphamide	103-119	gonadotropin releasing hormone 1	Homo sapiens	9-39
16142702-1	2005	OBJECTIVE: Cyclophosphamide (CYC) therapy for systemic lupus erythematosus (SLE), a disease predominantly affecting women of childbearing age, causes an unacceptably high incidence of irreversible premature ovarian failure (POF).	Cyclophosphamide	11-27	POF1B actin binding protein	Homo sapiens	224-227
16142702-1	2005	OBJECTIVE: Cyclophosphamide (CYC) therapy for systemic lupus erythematosus (SLE), a disease predominantly affecting women of childbearing age, causes an unacceptably high incidence of irreversible premature ovarian failure (POF).	Cyclophosphamide	29-32	POF1B actin binding protein	Homo sapiens	224-227
15914552-1	2005	The addition of rituximab to cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy results in significant improvement in clinical outcome for individuals with non-HIV-associated aggressive B-cell lymphoma.	Cyclophosphamide	29-45	DNA damage inducible transcript 3	Homo sapiens	89-93
15919850-5	2005	Correspondingly, CYP3A4-expressing cells and cDNA-expressed CYP3A4 metabolized R-IFA to yield the active, 4-hydroxylated metabolite at a 2- to 3-fold higher rate than they metabolized S-IFA or CPA.	Cyclophosphamide	193-196	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	17-23
15919850-4	2005	Tumor cells expressing P450 enzyme CYP3A4 were the most sensitive to R-IFA cytotoxicity, whereas tumor cells expressing CYP2B1 or CYP2B6 were most sensitive to cyclophosphamide (CPA), an isomer of IFA.	Cyclophosphamide	160-176	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	130-136
15919850-4	2005	Tumor cells expressing P450 enzyme CYP3A4 were the most sensitive to R-IFA cytotoxicity, whereas tumor cells expressing CYP2B1 or CYP2B6 were most sensitive to cyclophosphamide (CPA), an isomer of IFA.	Cyclophosphamide	178-181	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	23-27
15919850-4	2005	Tumor cells expressing P450 enzyme CYP3A4 were the most sensitive to R-IFA cytotoxicity, whereas tumor cells expressing CYP2B1 or CYP2B6 were most sensitive to cyclophosphamide (CPA), an isomer of IFA.	Cyclophosphamide	178-181	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	130-136
16087946-5	2005	Patients having a variant genotype of cytochrome P450 3A4 displayed higher blood concentrations of parent (inactive) cyclophosphamide with the second and third doses (P = .024 and .028, respectively) in addition to slower cyclophosphamide activation over the three doses (P = .031).	Cyclophosphamide	117-133	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	38-57
16087946-5	2005	Patients having a variant genotype of cytochrome P450 3A4 displayed higher blood concentrations of parent (inactive) cyclophosphamide with the second and third doses (P = .024 and .028, respectively) in addition to slower cyclophosphamide activation over the three doses (P = .031).	Cyclophosphamide	222-238	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	38-57
16103104-0	2005	Cyclophosphamide inhibition of anti-CD40 monoclonal antibody-based therapy of B cell lymphoma is dependent on CD11b+ cells.	Cyclophosphamide	0-16	CD40 molecule	Homo sapiens	36-40
16103104-0	2005	Cyclophosphamide inhibition of anti-CD40 monoclonal antibody-based therapy of B cell lymphoma is dependent on CD11b+ cells.	Cyclophosphamide	0-16	integrin subunit alpha M	Homo sapiens	110-115
16103104-5	2005	Using the syngeneic tumor model, BCL1, we have shown that timing of cyclophosphamide relative to mAb is critical to therapeutic outcome.	Cyclophosphamide	68-84	cyclin D1	Homo sapiens	33-37
16103104-7	2005	Conversely, when anti-CD40 is given before cyclophosphamide, the level of tumor protection was moderately increased.	Cyclophosphamide	43-59	CD40 molecule	Homo sapiens	22-26
16103104-8	2005	In vivo tracking experiments reveal that pretreatment with cyclophosphamide leads to diminished CTL expansion, as well as an increased number of CD11b+ cells that display an activated phenotype.	Cyclophosphamide	59-75	integrin subunit alpha M	Homo sapiens	145-150
16137437-0	2005	HER2 overexpression as a predictive marker in a randomized trial comparing adjuvant cyclophosphamide/methotrexate/5-fluorouracil with epirubicin in patients with stage I/II breast cancer: long-term results.	Cyclophosphamide	84-100	erb-b2 receptor tyrosine kinase 2	Homo sapiens	0-4
15899580-0	2005	Cyclophosphamide decreases the number, percentage and the function of CD25+ CD4+ regulatory T cells, which suppress induction of contact hypersensitivity.	Cyclophosphamide	0-16	interleukin 2 receptor, alpha chain	Mus musculus	70-74
15899580-0	2005	Cyclophosphamide decreases the number, percentage and the function of CD25+ CD4+ regulatory T cells, which suppress induction of contact hypersensitivity.	Cyclophosphamide	0-16	CD4 antigen	Mus musculus	76-79
15899580-3	2005	OBJECTIVE: In order to examine whether the target cells of Cy in the immuno-augmentative effect are CD25(+) CD4(+) regulatory T cells or not, we investigated effect of Cy treatment on CD25(+) CD4(+) T cells.	Cyclophosphamide	168-170	interleukin 2 receptor, alpha chain	Mus musculus	184-188
15899580-4	2005	METHOD: We examined Cy-treated CD25(+) CD4(+) T cells by flow cytometer and by inhibition assay on proliferation of CD25(-) CD4(+) T cells.	Cyclophosphamide	20-22	interleukin 2 receptor, alpha chain	Mus musculus	31-35
15899580-4	2005	METHOD: We examined Cy-treated CD25(+) CD4(+) T cells by flow cytometer and by inhibition assay on proliferation of CD25(-) CD4(+) T cells.	Cyclophosphamide	20-22	CD4 antigen	Mus musculus	39-42
15899580-4	2005	METHOD: We examined Cy-treated CD25(+) CD4(+) T cells by flow cytometer and by inhibition assay on proliferation of CD25(-) CD4(+) T cells.	Cyclophosphamide	20-22	CD4 antigen	Mus musculus	124-127
15899580-5	2005	RESULTS: Cy treatment remarkably reduced the number and percentage of CD25(+) CD4(+) T cells in the spleen and lymph nodes 3 and 5 days later.	Cyclophosphamide	9-11	interleukin 2 receptor, alpha chain	Mus musculus	70-74
15899580-5	2005	RESULTS: Cy treatment remarkably reduced the number and percentage of CD25(+) CD4(+) T cells in the spleen and lymph nodes 3 and 5 days later.	Cyclophosphamide	9-11	CD4 antigen	Mus musculus	78-81
15899580-7	2005	Furthermore, transfer of CD25(+) CD4(+) T cells from untreated mice resulted in a significant decrease (p < 0.05) of the CH reactions enhanced by Cy treatment.	Cyclophosphamide	149-151	interleukin 2 receptor, alpha chain	Mus musculus	25-29
15899580-7	2005	Furthermore, transfer of CD25(+) CD4(+) T cells from untreated mice resulted in a significant decrease (p < 0.05) of the CH reactions enhanced by Cy treatment.	Cyclophosphamide	149-151	CD4 antigen	Mus musculus	33-36
15899580-8	2005	CONCLUSION: These results indicate that enhancement of the CH reactions to TNCB by Cy treatment is attributed to the decrease in the number, percentage and the function of CD25(+) CD4(+) regulatory T cells.	Cyclophosphamide	83-85	interleukin 2 receptor, alpha chain	Mus musculus	172-176
15899580-8	2005	CONCLUSION: These results indicate that enhancement of the CH reactions to TNCB by Cy treatment is attributed to the decrease in the number, percentage and the function of CD25(+) CD4(+) regulatory T cells.	Cyclophosphamide	83-85	CD4 antigen	Mus musculus	180-183
15712360-0	2005	A cytochrome P450 2B6 meditated gene therapy strategy to enhance the effects of radiation or cyclophosphamide when combined with the bioreductive drug AQ4N.	Cyclophosphamide	93-109	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	2-21
15712360-4	2005	We have therefore examined the potential of a CYP2B6-mediated GDEPT strategy to enhance the anti-tumour effect of the combination of AQ4N with radiation or cyclophosphamide (CPA).	Cyclophosphamide	156-172	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	46-52
15712360-4	2005	We have therefore examined the potential of a CYP2B6-mediated GDEPT strategy to enhance the anti-tumour effect of the combination of AQ4N with radiation or cyclophosphamide (CPA).	Cyclophosphamide	174-177	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	46-52
15712360-10	2005	AQ4N (100 mg/kg) and CPA (100 mg/kg) with CYP2B6 and CYPRED also enhanced tumour growth delay; this effect became significant when the schedule was repeated 14 days later (p = 0.0197).	Cyclophosphamide	21-24	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	42-48
16047061-12	2005	CONCLUSION: The MGMT promoter hypermethylation appears to be useful marker for predicting survival in patient with DLBCL treated with multi drug regimens including cyclophosphamide, at the same time the study shows that TMA technology is useful for immunohistochemical analysis of large lymphoma populations.	Cyclophosphamide	164-180	O-6-methylguanine-DNA methyltransferase	Homo sapiens	16-20
15958544-2	2005	It has been previously shown that cyclophosphamide augments the efficacy of antitumor immune responses by depleting CD4+ CD25+ T regulatory cells and increasing both T-lymphocyte proliferation and T memory cells.	Cyclophosphamide	34-50	CD4 antigen	Mus musculus	116-119
15958544-2	2005	It has been previously shown that cyclophosphamide augments the efficacy of antitumor immune responses by depleting CD4+ CD25+ T regulatory cells and increasing both T-lymphocyte proliferation and T memory cells.	Cyclophosphamide	34-50	interleukin 2 receptor, alpha chain	Mus musculus	121-125
15958544-6	2005	Moreover, combined application of cyclophosphamide with a novel, oral DNA vaccine targeting platelet-derived growth factor B (PDGF-B), overexpressed by proliferating endothelial cells in the tumor vasculature, not only completely inhibited the growth of different tumor types but also led to tumor rejections in mice.	Cyclophosphamide	34-50	platelet derived growth factor, B polypeptide	Mus musculus	126-132
15930421-1	2005	BACKGROUND: We compared docetaxel plus doxorubicin and cyclophosphamide (TAC) with fluorouracil plus doxorubicin and cyclophosphamide (FAC) as adjuvant chemotherapy for operable node-positive breast cancer.	Cyclophosphamide	117-133	FA complementation group C	Homo sapiens	135-138
15989703-1	2005	PURPOSE: The goal of this study was to evaluate the efficacy of the fludarabine/cyclophosphamide combination in patients with relapsed chronic lymphocytic lymphoma (CLL) and low-grade non-Hodgkin"s lymphoma (NHL) and to assess the impact of adding granulocyte-macrophage colony-stimulating factor (GM-CSF) to this regimen in a randomized fashion.	Cyclophosphamide	80-96	colony stimulating factor 2	Homo sapiens	248-296
15989703-1	2005	PURPOSE: The goal of this study was to evaluate the efficacy of the fludarabine/cyclophosphamide combination in patients with relapsed chronic lymphocytic lymphoma (CLL) and low-grade non-Hodgkin"s lymphoma (NHL) and to assess the impact of adding granulocyte-macrophage colony-stimulating factor (GM-CSF) to this regimen in a randomized fashion.	Cyclophosphamide	80-96	colony stimulating factor 2	Homo sapiens	298-304
15769884-1	2005	The polymorphic human cytochrome P450 (P450) 2B6 is primarily responsible for the metabolism of several clinically relevant drugs including bupropion, cyclophosphamide, propofol, and efavirenz.	Cyclophosphamide	151-167	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	22-48
15883172-3	2005	However, treatment of neu-N mice with vaccine and cyclophosphamide-containing chemotherapy resulted in tumor protection in a proportion of mice.	Cyclophosphamide	50-66	erb-b2 receptor tyrosine kinase 2	Mus musculus	22-25
15883172-7	2005	Cyclophosphamide seemed to inhibit regulatory T (T reg) cells by selectively depleting the cycling population of CD4(+)CD25(+) T cells in neu-N mice.	Cyclophosphamide	0-16	CD4 antigen	Mus musculus	113-116
15883172-7	2005	Cyclophosphamide seemed to inhibit regulatory T (T reg) cells by selectively depleting the cycling population of CD4(+)CD25(+) T cells in neu-N mice.	Cyclophosphamide	0-16	erb-b2 receptor tyrosine kinase 2	Mus musculus	138-141
15883172-8	2005	These findings demonstrate that neu-N mice possess latent pools of high-avidity neu-specific CD8(+) T cells that can be recruited to produce an effective antitumor response if T reg cells are blocked or removed by using approaches such as administration of cyclophosphamide before vaccination.	Cyclophosphamide	257-273	erb-b2 receptor tyrosine kinase 2	Mus musculus	32-35
15883172-8	2005	These findings demonstrate that neu-N mice possess latent pools of high-avidity neu-specific CD8(+) T cells that can be recruited to produce an effective antitumor response if T reg cells are blocked or removed by using approaches such as administration of cyclophosphamide before vaccination.	Cyclophosphamide	257-273	erb-b2 receptor tyrosine kinase 2	Mus musculus	80-83
16132345-14	2005	MRP4 also conferred resistance to cyclophosphamide and this was partially reversed by BSO.	Cyclophosphamide	34-50	ATP binding cassette subfamily C member 4	Homo sapiens	0-4
16132345-16	2005	CONCLUSIONS: Human MRP4 rendered significant resistance to cyclophosphamide, CPT, CPT-11, SN-38, rubitecan, and 10-OH-CPT.	Cyclophosphamide	59-75	ATP binding cassette subfamily C member 4	Homo sapiens	19-23
16209205-0	2005	[The changes of IGF-I in testis and epididymis on a rat model with oligozoospermia/azoospermia induced by cyclophosphamide].	Cyclophosphamide	106-122	insulin-like growth factor 1	Rattus norvegicus	16-21
16209205-1	2005	OBJECTIVE: To evaluate the effect of the levels of IGF-I in the epididymis and the expression of IGF-I in the testis of adult male rat after the administration of cyclophosphamide.	Cyclophosphamide	163-179	insulin-like growth factor 1	Rattus norvegicus	51-56
16209205-1	2005	OBJECTIVE: To evaluate the effect of the levels of IGF-I in the epididymis and the expression of IGF-I in the testis of adult male rat after the administration of cyclophosphamide.	Cyclophosphamide	163-179	insulin-like growth factor 1	Rattus norvegicus	97-102
16209205-9	2005	CONCLUSION: In the time of oligozoospermia/azoospermia induced by the administration of cyclophosphamide, the expression levels of IGF-I in the genetic system were significantly reduced.	Cyclophosphamide	88-104	insulin-like growth factor 1	Rattus norvegicus	131-136
16103078-13	2005	We also found that three other Flt1-expressing neuroblastoma cell lines show hypoxia-mediated drug resistance to etoposide, melphalan, doxorubicin, and cyclophosphamide.	Cyclophosphamide	152-168	fms related receptor tyrosine kinase 1	Homo sapiens	31-35
15955905-1	2005	PURPOSE: For more than two decades, cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) has been the standard therapy for diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	36-52	DNA damage inducible transcript 3	Homo sapiens	96-100
16156276-0	2005	[Impedance effects of interleukin-6 on cyclophosphamide-induced hematopoietic damnification in dogs].	Cyclophosphamide	39-55	interleukin 6	Canis lupus familiaris	22-35
16156276-1	2005	The aim of this study is to evaluate the effect of Interleukin-6 on cyclophosphamide-induced hematopoietic damnification.	Cyclophosphamide	68-84	interleukin 6	Canis lupus familiaris	51-64
16156276-2	2005	The doses of Interleukin-6 in 3 different regimens were hypodermally injected into dogs for 7 days respectively to establish the cyclophosphamide-induced hematopoietic damnification model.	Cyclophosphamide	129-145	interleukin 6	Canis lupus familiaris	13-26
16156276-6	2005	These suggest that the Interleukin-6 can significantly impede cyclophosphamide-induced hematopoietic damnification.	Cyclophosphamide	62-78	interleukin 6	Canis lupus familiaris	23-36
15917646-8	2005	Comparison of the in vivo responses of these mutants to the chemotherapeutic drug, cyclophosphamide (CY), has established a direct correlation between drug toxicity and the functional status of the CLOCK/BMAL1 transcriptional complex.	Cyclophosphamide	83-99	circadian locomotor output cycles kaput	Mus musculus	198-203
15917646-8	2005	Comparison of the in vivo responses of these mutants to the chemotherapeutic drug, cyclophosphamide (CY), has established a direct correlation between drug toxicity and the functional status of the CLOCK/BMAL1 transcriptional complex.	Cyclophosphamide	83-99	aryl hydrocarbon receptor nuclear translocator-like	Mus musculus	204-209
15917646-8	2005	Comparison of the in vivo responses of these mutants to the chemotherapeutic drug, cyclophosphamide (CY), has established a direct correlation between drug toxicity and the functional status of the CLOCK/BMAL1 transcriptional complex.	Cyclophosphamide	101-103	circadian locomotor output cycles kaput	Mus musculus	198-203
15917646-8	2005	Comparison of the in vivo responses of these mutants to the chemotherapeutic drug, cyclophosphamide (CY), has established a direct correlation between drug toxicity and the functional status of the CLOCK/BMAL1 transcriptional complex.	Cyclophosphamide	101-103	aryl hydrocarbon receptor nuclear translocator-like	Mus musculus	204-209
16006279-1	2005	Treatment of non-Hodgkin"s lymphoma with the CHOP regimen consists of intravenous cyclophosphamide 750 mg/m2 (day 1), intravenous doxorubicin 50 mg/m2 (day 1), intravenous vincristine 1.4 mg/m2 (day 1), and oral prednisone 100 mg (days 1-5).	Cyclophosphamide	82-98	DNA damage inducible transcript 3	Homo sapiens	45-49
16195169-4	2005	After many ineffective treatments, the use of pulse cyclophosphamide (CPX) resulted in complete remission of the disease that is still lasting after a 2-year follow-up.	Cyclophosphamide	52-68	T-box transcription factor 22	Homo sapiens	70-73
15914960-0	2005	Cyclophosphamide improves the function of post-infarct hearts by reducing old infarct area and accelerating the mobilization of CD34+ cells.	Cyclophosphamide	0-16	hematopoietic progenitor cell antigen CD34	Oryctolagus cuniculus	128-132
15914960-1	2005	BACKGROUND: Myelosuppressives such as cyclophosphamide (Cy) and 5-fluorouracil (5FU), which can increase circulating CD34+ cells, may have a beneficial effect in the post-infarct heart.	Cyclophosphamide	38-54	hematopoietic progenitor cell antigen CD34	Oryctolagus cuniculus	117-121
15914960-1	2005	BACKGROUND: Myelosuppressives such as cyclophosphamide (Cy) and 5-fluorouracil (5FU), which can increase circulating CD34+ cells, may have a beneficial effect in the post-infarct heart.	Cyclophosphamide	56-58	hematopoietic progenitor cell antigen CD34	Oryctolagus cuniculus	117-121
15914960-3	2005	Cy significantly improved cardiac function and remodeling and decreased the old infarct area 1 month after infarction, compared with those given S. The number of circulating CD34+ cells was higher and neovascularization and matrix metalloproteinase-1 was induced in the Cy group.	Cyclophosphamide	0-2	hematopoietic progenitor cell antigen CD34	Oryctolagus cuniculus	174-178
15914960-3	2005	Cy significantly improved cardiac function and remodeling and decreased the old infarct area 1 month after infarction, compared with those given S. The number of circulating CD34+ cells was higher and neovascularization and matrix metalloproteinase-1 was induced in the Cy group.	Cyclophosphamide	0-2	interstitial collagenase	Oryctolagus cuniculus	224-250
15914960-3	2005	Cy significantly improved cardiac function and remodeling and decreased the old infarct area 1 month after infarction, compared with those given S. The number of circulating CD34+ cells was higher and neovascularization and matrix metalloproteinase-1 was induced in the Cy group.	Cyclophosphamide	270-272	interstitial collagenase	Oryctolagus cuniculus	224-250
15844004-3	2005	Here, we describe the expression of RANKL during regeneration following acute involution induced by cyclophosphamide in the rat thymus.	Cyclophosphamide	100-116	TNF superfamily member 11	Rattus norvegicus	36-41
16158823-8	2005	We first treated the patient with fludarabine and then with the CHOP regimen (cyclophosphamide, hydroxydaunomycin, vincristine [Oncovin], and prednisone), but the disease was so refractory that the patient died of the disease 13 months after the splenectomy.	Cyclophosphamide	78-94	DNA damage inducible transcript 3	Homo sapiens	64-68
15918208-2	2005	The patient was successfully treated with a first generation therapy, CHOP modified regimen (cyclophosphamide 600 mg/m2 intravenously on d 1, epirubicin 55 mg/m2 intravenously on d 1, vincristine 1.2 mg/m2 intravenously on d 1, prednisone 60 mg/m2 on d 1-5), and a complete response was achieved.	Cyclophosphamide	93-109	DNA damage inducible transcript 3	Homo sapiens	70-74
15919850-5	2005	Correspondingly, CYP3A4-expressing cells and cDNA-expressed CYP3A4 metabolized R-IFA to yield the active, 4-hydroxylated metabolite at a 2- to 3-fold higher rate than they metabolized S-IFA or CPA.	Cyclophosphamide	193-196	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	60-66
15919850-6	2005	CYP2B cells and cDNA-expressed CYP2B enzymes metabolized CPA almost exclusively by 4-hydroxylation, whereas R-IFA and S-IFA were substantially converted to inactive, N-dechloroethylated metabolites.	Cyclophosphamide	57-60	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	0-5
15919850-6	2005	CYP2B cells and cDNA-expressed CYP2B enzymes metabolized CPA almost exclusively by 4-hydroxylation, whereas R-IFA and S-IFA were substantially converted to inactive, N-dechloroethylated metabolites.	Cyclophosphamide	57-60	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	31-36
15874908-4	2005	Treatment of rats with CPA decreases the activity of lymph cells in tumors, especially of CD4+ lymphocytes.	Cyclophosphamide	23-26	Cd4 molecule	Rattus norvegicus	90-93
15746946-2	2005	Our approach is a P450-based VDEPT that consists of using cyclophosphamide (CPA) as a prodrug and a Cytochrome P450 2B6/NADPH cytochrome P450 reductase fusion protein (CYP2B6/RED) as a prodrug-activating enzyme.	Cyclophosphamide	76-79	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	168-174
15746946-7	2005	After infection and treatment with CPA, in cell lines with low endogenous RED, the fusion protein mediated significantly higher CPA-induced cytotoxicity compared to cells expressing solely CYP2B6.	Cyclophosphamide	35-38	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	189-195
15921395-2	2005	In this study we found that HIV-infected patients with diffuse large B-cell lymphoma treated with cyclophosphamide, hydroxydoxorubicin, vincristine and prednisone (CHOP) and HAART showed a similar response rate to chemotherapy, disease-free survival and overall survival as those of HIV-negative patients receiving CHOP.	Cyclophosphamide	98-114	DNA damage inducible transcript 3	Homo sapiens	164-168
15872353-10	2005	RESULTS: After chemotherapy using gemcitabine and cyclophosphamide, the (99m)Tc-annexin V uptake (percentage injected dose per gram x kg [(%ID/g) x kg]; mean +/- SD) in tumor increased significantly (0.062 +/- 0.012 (%ID/g) x kg in the gemcitabine-treated group and 0.050 +/- 0.012 (%ID/g) x kg in the cyclophosphamide group vs. 0.031 +/- 0.005 (%ID/g) x kg in the control group; P < 0.01).	Cyclophosphamide	302-318	annexin A5	Rattus norvegicus	80-89
15872353-13	2005	In the gemcitabine and cyclophosphamide groups, the rate of TUNEL positively stained cells was significantly higher than that in the control group (10.2% +/- 1.7% and 8.0% +/- 1.5% vs. 5.2% +/- 1.5%; P < 0.01), whereas the GLUT-1 expression level showed no definite changes in histologic analyses.	Cyclophosphamide	23-39	solute carrier family 2 member 1	Rattus norvegicus	226-232
15821589-1	2005	PURPOSE: It was previously shown that nitric oxide (NO) produced by inducible NO synthase (iNOS) is responsible for cyclophosphamide (CP) induced cystitis.	Cyclophosphamide	116-132	nitric oxide synthase 2	Rattus norvegicus	68-89
15821589-1	2005	PURPOSE: It was previously shown that nitric oxide (NO) produced by inducible NO synthase (iNOS) is responsible for cyclophosphamide (CP) induced cystitis.	Cyclophosphamide	116-132	nitric oxide synthase 2	Rattus norvegicus	91-95
15874908-9	2005	In the thymus, CPA alone or in combination with sTAA repairs the inhibitor effect of a carcinogen on synthesis of CD4+ and CD8+ thymocytes.	Cyclophosphamide	15-18	Cd4 molecule	Rattus norvegicus	114-117
15791475-3	2005	The patient was treated for diffuse large B-cell non-Hodgkin"s lymphoma with CHOP therapy (doxorubicin, cyclophosphamide, vincristine, and prednisone).	Cyclophosphamide	104-120	DNA damage inducible transcript 3	Homo sapiens	77-81
15838423-9	2005	Cyclophosphamide-treated animals showed enhanced uptake of (99m)Tc-DMSA in the kidneys, a twofold enhanced uptake of (99m)Tc-DPD in all organs except the stomach, a decreased uptake of (99m)Tc-tin colloid in the lungs, spleen and kidneys and a significantly decreased uptake of (99m)Tc-MAA in the lungs.	Cyclophosphamide	0-16	dihydropyrimidine dehydrogenase	Rattus norvegicus	125-128
15809768-8	2005	The cytotoxity assay results demonstrated that cells overexpressing the Id-1 gene increased in their resistance to doxorubicin, paclitaxel and cyclophosphamide.	Cyclophosphamide	143-159	inhibitor of DNA binding 1, HLH protein	Homo sapiens	72-76
15829015-9	2005	Pretreatment with cyclophosphamide (CPA) decreased the number of neutrophils and eosinophils in BAL fluid of TiO2 treated-rats (p < 0.05), but affected neither the percentage of PAS (+) cells, nor IL-13 levels in the BAL fluids (p > 0.05).	Cyclophosphamide	18-34	interleukin 13	Rattus norvegicus	200-205
15824370-1	2005	A patient with thymoma-associated neuromyotonia and voltage-gated potassium channel (Kv1.2 and Kv1.6) antibodies by immunoprecipitation and rat brain immunolabeling was treated successfully with immunoadsorption and cyclophosphamide.	Cyclophosphamide	216-232	potassium voltage-gated channel subfamily A member 2	Homo sapiens	85-90
15829015-9	2005	Pretreatment with cyclophosphamide (CPA) decreased the number of neutrophils and eosinophils in BAL fluid of TiO2 treated-rats (p < 0.05), but affected neither the percentage of PAS (+) cells, nor IL-13 levels in the BAL fluids (p > 0.05).	Cyclophosphamide	36-39	interleukin 13	Rattus norvegicus	200-205
15591121-0	2005	Inhibition of CD4(+)25+ T regulatory cell function implicated in enhanced immune response by low-dose cyclophosphamide.	Cyclophosphamide	102-118	CD4 molecule	Homo sapiens	14-17
15824370-1	2005	A patient with thymoma-associated neuromyotonia and voltage-gated potassium channel (Kv1.2 and Kv1.6) antibodies by immunoprecipitation and rat brain immunolabeling was treated successfully with immunoadsorption and cyclophosphamide.	Cyclophosphamide	216-232	potassium voltage-gated channel subfamily A member 6	Homo sapiens	95-100
15591121-6	2005	Expression of GITR and FoxP3, which are involved in the suppressive activity of T(REGs), is down-regulated after CY administration, though the level of expression varies depending on the time studied.	Cyclophosphamide	113-115	TNF receptor superfamily member 18	Homo sapiens	14-18
15591121-6	2005	Expression of GITR and FoxP3, which are involved in the suppressive activity of T(REGs), is down-regulated after CY administration, though the level of expression varies depending on the time studied.	Cyclophosphamide	113-115	forkhead box P3	Homo sapiens	23-28
15870024-0	2005	IL-18 binding protein fusion construct delays the development of diabetes in adoptive transfer and cyclophosphamide-induced diabetes in NOD mouse.	Cyclophosphamide	99-115	interleukin 18	Mus musculus	0-5
15870024-3	2005	The data show that prolonged prophylactic treatment with IL-18bp:FcIg significantly reduced the cumulative incidence of diabetes induced in NOD mice either by adoptive transfer of diabetogenic cells or by injection with large doses of cyclophosphamide.	Cyclophosphamide	235-251	interleukin 18 binding protein	Mus musculus	57-64
15888259-3	2005	The combination of IFNbeta-1b with CY resulted in a statistically significant decrease in the production of interleukin-2 (IL-2) (P=0.003) and tumor necrosis factor alpha (TNF-alpha) (P=0.03).	Cyclophosphamide	35-37	interleukin 2	Homo sapiens	108-121
15888259-3	2005	The combination of IFNbeta-1b with CY resulted in a statistically significant decrease in the production of interleukin-2 (IL-2) (P=0.003) and tumor necrosis factor alpha (TNF-alpha) (P=0.03).	Cyclophosphamide	35-37	interleukin 2	Homo sapiens	123-127
15888259-3	2005	The combination of IFNbeta-1b with CY resulted in a statistically significant decrease in the production of interleukin-2 (IL-2) (P=0.003) and tumor necrosis factor alpha (TNF-alpha) (P=0.03).	Cyclophosphamide	35-37	tumor necrosis factor	Homo sapiens	143-170
15888259-3	2005	The combination of IFNbeta-1b with CY resulted in a statistically significant decrease in the production of interleukin-2 (IL-2) (P=0.003) and tumor necrosis factor alpha (TNF-alpha) (P=0.03).	Cyclophosphamide	35-37	tumor necrosis factor	Homo sapiens	172-181
15888259-6	2005	Our data show that CY was able to improve the effects of IFNbeta-1b on the ratio of Th1/Th2 cytokines.	Cyclophosphamide	19-21	negative elongation factor complex member C/D	Homo sapiens	84-87
16036801-6	2005	IL-6 levels returned to baseline following treatment of the patient with intravenous cyclophosphamide and plasma exchange and the patient experienced a significant and sustained recovery of function.	Cyclophosphamide	85-101	interleukin 6	Homo sapiens	0-4
17343335-2	2005	In this experiment we explored the combined effect between Cu(SalNEt(2))salicylate (Cu-Sal) complex and the widely used anticancer drugs carboplatin (CBDCA), cyclophosphamide (CTX) and paclitaxel (TXL) against T47D human breast cancer cells.	Cyclophosphamide	158-174	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	176-179
15666323-1	2005	BACKGROUND: The standard treatment for patients with aggressive non-Hodgkin lymphoma (NHL) is cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP).	Cyclophosphamide	94-110	DNA damage inducible transcript 3	Homo sapiens	154-158
15794864-2	2005	Cyclophosphamide/doxorubicin/vincristine/prednisone/rituximab (CHOP-R) is a stem cellsparing regimen that has been extensively evaluated in patients without WM or non-Hodgkin"s lymphoma.	Cyclophosphamide	0-16	DNA damage inducible transcript 3	Homo sapiens	63-67
15703814-10	2005	Interestingly, we found that patients who were on a chemotherapy regime which contained an anthracycline (a Pgp substrate) and subsequently developed recurrence, had a higher YB-1 score compared to patients on the Cyclophosphamide/Methotrexate/5-Fluorouracil regime (P=0.024).	Cyclophosphamide	214-230	ATP binding cassette subfamily B member 1	Homo sapiens	108-111
15934368-0	2005	[Hepatoprotectors prevent the toxic action of cyclophosphamide on the liver of rats with CCl4-induced hepatitis model].	Cyclophosphamide	46-62	C-C motif chemokine ligand 4	Rattus norvegicus	89-93
15934368-1	2005	The results of experiments on white rats with CCl4-induced hepatitis showed that the combined introduction of cyclophosphamide and hepatoprotectors of the plant origin (lochein, maksar, silimarin) leads to a decrease in acute toxicity and to less pronounced manifestations of hepatotoxicity of cyclophosphamide.	Cyclophosphamide	110-126	C-C motif chemokine ligand 4	Rattus norvegicus	46-50
15703814-10	2005	Interestingly, we found that patients who were on a chemotherapy regime which contained an anthracycline (a Pgp substrate) and subsequently developed recurrence, had a higher YB-1 score compared to patients on the Cyclophosphamide/Methotrexate/5-Fluorouracil regime (P=0.024).	Cyclophosphamide	214-230	Y-box binding protein 1	Homo sapiens	175-179
15621841-5	2005	The patient responded to chemotherapy with CHOP (doxorubicin, cyclophosphamide, vincristine and prednisone) therapy, with disappearance of the abnormal clone from the bone marrow.	Cyclophosphamide	62-78	DNA damage inducible transcript 3	Homo sapiens	43-47
15829405-0	2005	G-CSF treatment prevents cyclophosphamide acceleration of autoimmune diabetes in the NOD mouse.	Cyclophosphamide	25-41	peripheral blood stem cell response to granulocyte colony stimulating factor 1	Mus musculus	0-5
15829405-0	2005	G-CSF treatment prevents cyclophosphamide acceleration of autoimmune diabetes in the NOD mouse.	Cyclophosphamide	25-41	atrophin 1	Homo sapiens	85-88
15829405-1	2005	Cyclophosphamide (CY) accelerates autoimmune diabetes in the NOD mouse at different levels, including critical targeting of a regulatory T cell subset, exacerbation of pro-Th1 IFN-gamma production and promotion of inflammation in pancreatic islets.	Cyclophosphamide	0-16	atrophin 1	Homo sapiens	61-64
15829405-1	2005	Cyclophosphamide (CY) accelerates autoimmune diabetes in the NOD mouse at different levels, including critical targeting of a regulatory T cell subset, exacerbation of pro-Th1 IFN-gamma production and promotion of inflammation in pancreatic islets.	Cyclophosphamide	18-20	atrophin 1	Homo sapiens	61-64
15829405-2	2005	Here we evaluated the ability of G-CSF to antagonize the acceleration of the disease induced by CY.	Cyclophosphamide	96-98	peripheral blood stem cell response to granulocyte colony stimulating factor 1	Mus musculus	33-38
15829405-7	2005	G-CSF promoted only slight changes in the inflammatory effects of CY at the target tissue site, assessed by chemokine induction within the pancreas.	Cyclophosphamide	66-68	peripheral blood stem cell response to granulocyte colony stimulating factor 1	Mus musculus	0-5
15829405-8	2005	Thus the immunoregulatory properties of G-CSF were critical in the early control of the accelerating effects of CY on autoimmune diabetes in the NOD mouse.	Cyclophosphamide	112-114	peripheral blood stem cell response to granulocyte colony stimulating factor 1	Mus musculus	40-45
15829405-8	2005	Thus the immunoregulatory properties of G-CSF were critical in the early control of the accelerating effects of CY on autoimmune diabetes in the NOD mouse.	Cyclophosphamide	112-114	atrophin 1	Homo sapiens	145-148
15711368-2	2005	Studies were performed to determine the NGF dependence of cyclophosphamide (CYP) induced changes in bladder function using the recombinant NGF sequestering protein REN1820.	Cyclophosphamide	58-74	nerve growth factor	Rattus norvegicus	40-43
15656694-10	2005	Interactions with the alkylating agents cyclophosphamide and ifosfamide are complicated as a result of the involvement of the CYP3A4 and CYP2B6 isoenzymes in both the metabolic activation of these drugs and the generation of potentially neurotoxic metabolites.	Cyclophosphamide	40-56	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	126-132
15741301-1	2005	BACKGROUND: Expression of O(6)-methylguanine-DNA methyl transferase (MGMT), a DNA repair protein, has been associated with tumor resistance to alkylating agents such as cyclophosphamide.	Cyclophosphamide	169-185	O-6-methylguanine-DNA methyltransferase	Homo sapiens	26-67
15741301-1	2005	BACKGROUND: Expression of O(6)-methylguanine-DNA methyl transferase (MGMT), a DNA repair protein, has been associated with tumor resistance to alkylating agents such as cyclophosphamide.	Cyclophosphamide	169-185	O-6-methylguanine-DNA methyltransferase	Homo sapiens	69-73
15689397-0	2005	Circadian sensitivity to the chemotherapeutic agent cyclophosphamide depends on the functional status of the CLOCK/BMAL1 transactivation complex.	Cyclophosphamide	52-68	clock circadian regulator	Homo sapiens	109-114
15689397-0	2005	Circadian sensitivity to the chemotherapeutic agent cyclophosphamide depends on the functional status of the CLOCK/BMAL1 transactivation complex.	Cyclophosphamide	52-68	aryl hydrocarbon receptor nuclear translocator-like	Mus musculus	115-120
16019949-2	2005	After a single dose of CPA, mRNAs of CYPs 2B1, 2B2, 3A2, 2C11 were significantly induced up to 220-, 6.7-, 5.0- and 5.8-fold at the low dose CPA, and 4800-, 52-, 22- and 2.5-fold at the high dose.	Cyclophosphamide	23-26	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	37-50
16019949-2	2005	After a single dose of CPA, mRNAs of CYPs 2B1, 2B2, 3A2, 2C11 were significantly induced up to 220-, 6.7-, 5.0- and 5.8-fold at the low dose CPA, and 4800-, 52-, 22- and 2.5-fold at the high dose.	Cyclophosphamide	141-144	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	37-50
16019949-5	2005	Microsomal activities of CYP2B, CYP3A and 2C11 were increased by 2-, 1.8- and 1.3-fold at low dose CPA, and 3.2-, 1.7- and 1.6-fold at high dose.	Cyclophosphamide	99-102	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	32-46
16019949-7	2005	Acute induction effect on CYP2B1, 2B2, 2C11 and 3A2 and a substantial up regulation of CYP2B1 mRNA were observed after a single dose of CPA, auto induction was observed by repeated administration.	Cyclophosphamide	136-139	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	26-32
16019949-7	2005	Acute induction effect on CYP2B1, 2B2, 2C11 and 3A2 and a substantial up regulation of CYP2B1 mRNA were observed after a single dose of CPA, auto induction was observed by repeated administration.	Cyclophosphamide	136-139	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	87-93
16155834-4	2005	The tumor growth was markedly inhibited by cyclophosphamide (CTX) in model of S( 180) with IR of 70.7% and in model of HT-29 with IR of 67.1%, compared with control groups, both P< 0.01; apoptosis induced by CTX was markedly observed by in microscope examination.	Cyclophosphamide	43-59	V-set and immunoglobulin domain containing 2	Mus musculus	61-64
15746054-2	2005	Cytochrome P450 enzymes are primarily expressed in the liver and convert the prodrug cyclophosphamide to an active phosphoramide mustard and acrolein.	Cyclophosphamide	85-101	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	0-15
15667832-9	2005	Furthermore, downregulation of antiapoptotic Bcl-2 was observed in animals treated with CPA and CPA plus DOX when compared to untreated or DOX-treated groups.	Cyclophosphamide	88-91	B cell leukemia/lymphoma 2	Mus musculus	45-50
15667832-9	2005	Furthermore, downregulation of antiapoptotic Bcl-2 was observed in animals treated with CPA and CPA plus DOX when compared to untreated or DOX-treated groups.	Cyclophosphamide	96-99	B cell leukemia/lymphoma 2	Mus musculus	45-50
16393888-6	2005	Both CPA and IFO are prodrugs that require activation by hepatic cytochrome P450 (CYP)-catalyzed 4-hydroxylation, yielding cytotoxic nitrogen mustards capable of reacting with DNA molecules to form crosslinks and lead to cell apoptosis and/or necrosis.	Cyclophosphamide	5-8	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	65-80
16393888-6	2005	Both CPA and IFO are prodrugs that require activation by hepatic cytochrome P450 (CYP)-catalyzed 4-hydroxylation, yielding cytotoxic nitrogen mustards capable of reacting with DNA molecules to form crosslinks and lead to cell apoptosis and/or necrosis.	Cyclophosphamide	5-8	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	82-85
15621789-3	2005	Our very preliminary results revealed that mononuclear cell nuclear fraction from blood of patients responding to the used therapy, i.e., cladribine alone or its combination with mitoxantrone and cyclophosphamide indicates decrease (or even loss) of transition at 93 degrees C concomitant with increase of transition at 76 degrees C. A complementary study showed that in mononuclear cells of patients who appeared to be sensitive to chemotherapy the decrease of antiapoptotic Bcl-2 protein expression and signs of apoptotic morphology were observed.	Cyclophosphamide	196-212	BCL2 apoptosis regulator	Homo sapiens	476-481
16110137-7	2005	CONCLUSIONS: Because of the increase in dose and dose-density afforded by the administration of GM-CSF, the relative dose intensity was increased by twofold for cyclophosphamide (400 vs 200 mg/m2/wk) and etoposide (120 vs 60 mg/m2/wk), and by 1.3-fold for doxorubicin (16.7 vs 12.5 mg/m2/wk).	Cyclophosphamide	161-177	colony stimulating factor 2	Homo sapiens	96-102
16172536-1	2005	Bone marrow cells (BMC) obtained from normal and cyclophosphamide (CY)-treated mice were cultured in the presence of recombinant human granulocyte-colony stimulating factor (rhG-CSF) and their effector cell activities inhibiting growth of C. albicans were examined.	Cyclophosphamide	49-65	colony stimulating factor 3	Homo sapiens	135-172
16116487-0	2005	Association of cyclophosphamide pharmacokinetics to polymorphic cytochrome P450 2C19.	Cyclophosphamide	15-31	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	64-84
16116487-1	2005	Cyclophosphamide (CP), a widely used cytostatic, is metabolized by polymorphic drug metabolizing enzymes particularly cytochrome P450 (CYP) enzymes.	Cyclophosphamide	0-16	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	118-133
16116487-1	2005	Cyclophosphamide (CP), a widely used cytostatic, is metabolized by polymorphic drug metabolizing enzymes particularly cytochrome P450 (CYP) enzymes.	Cyclophosphamide	0-16	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	135-138
15550586-1	2004	BACKGROUND: We demonstrated that highly active antiretroviral therapy (HAART) increases the toxic effect of cyclophosphamide, vincristine, doxorubicin (DOX) and prednisone (CHOP) in HIV-patients with non-Hodgkin"s lymphoma (NHL).	Cyclophosphamide	108-124	DNA damage inducible transcript 3	Homo sapiens	173-177
15899616-5	2004	Conversely, two randomized trials have demonstrated that dose-dense scheduled chemotherapy with G-CSF support, containing an anthracycline, cyclophosphamide and paclitaxel, improves clinical outcomes compared with the same regimen administered every 3 weeks.	Cyclophosphamide	140-156	colony stimulating factor 3	Homo sapiens	96-101
15652242-2	2005	Previous studies demonstrated partial inhibition by thioTEPA of the cytochrome P4502B6 (CYP2B6)-catalyzed 4-hydroxylation of cyclophosphamide, which is required for its bioactivation.	Cyclophosphamide	125-141	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	88-94
15733095-3	2005	Here we studied the expression of phosphorylated extracellular signal-regulated kinases 1 and 2 (phosphoERK), the active form of these kinases, in spinal neurons following innocuous and noxious distension of non-inflamed and cyclophosphamide (CYP)-inflamed rat urinary bladders.	Cyclophosphamide	225-241	mitogen activated protein kinase 3	Rattus norvegicus	49-95
15643279-3	2005	MATERIALS AND METHODS: We examined the expression of PAR2 to 4 in bladder urothelium and detrusor muscle whole mounts in controls, female rats and those treated with cyclophosphamide (CYP) acutely (4 and 48 hours) or chronically (every third day for 10 days) using Western blot and immunohistochemical techniques.	Cyclophosphamide	166-182	F2R like trypsin receptor 1	Rattus norvegicus	53-57
15667832-8	2005	Additional analyses indicate that the tumor suppressor p53 and p53-regulated proapoptotic Bax were upregulated in vivo and in vitro following CPA treatment in combination with DOX, suggesting that upregulation of p53 may contribute to the enhancement of antitumor effect of CPA by DOX.	Cyclophosphamide	142-145	transformation related protein 53, pseudogene	Mus musculus	55-58
15667832-8	2005	Additional analyses indicate that the tumor suppressor p53 and p53-regulated proapoptotic Bax were upregulated in vivo and in vitro following CPA treatment in combination with DOX, suggesting that upregulation of p53 may contribute to the enhancement of antitumor effect of CPA by DOX.	Cyclophosphamide	142-145	transformation related protein 53, pseudogene	Mus musculus	63-66
15667832-8	2005	Additional analyses indicate that the tumor suppressor p53 and p53-regulated proapoptotic Bax were upregulated in vivo and in vitro following CPA treatment in combination with DOX, suggesting that upregulation of p53 may contribute to the enhancement of antitumor effect of CPA by DOX.	Cyclophosphamide	142-145	BCL2-associated X protein	Mus musculus	90-93
15667832-8	2005	Additional analyses indicate that the tumor suppressor p53 and p53-regulated proapoptotic Bax were upregulated in vivo and in vitro following CPA treatment in combination with DOX, suggesting that upregulation of p53 may contribute to the enhancement of antitumor effect of CPA by DOX.	Cyclophosphamide	142-145	transformation related protein 53, pseudogene	Mus musculus	63-66
15667832-8	2005	Additional analyses indicate that the tumor suppressor p53 and p53-regulated proapoptotic Bax were upregulated in vivo and in vitro following CPA treatment in combination with DOX, suggesting that upregulation of p53 may contribute to the enhancement of antitumor effect of CPA by DOX.	Cyclophosphamide	274-277	transformation related protein 53, pseudogene	Mus musculus	55-58
15667832-8	2005	Additional analyses indicate that the tumor suppressor p53 and p53-regulated proapoptotic Bax were upregulated in vivo and in vitro following CPA treatment in combination with DOX, suggesting that upregulation of p53 may contribute to the enhancement of antitumor effect of CPA by DOX.	Cyclophosphamide	274-277	transformation related protein 53, pseudogene	Mus musculus	63-66
15667832-8	2005	Additional analyses indicate that the tumor suppressor p53 and p53-regulated proapoptotic Bax were upregulated in vivo and in vitro following CPA treatment in combination with DOX, suggesting that upregulation of p53 may contribute to the enhancement of antitumor effect of CPA by DOX.	Cyclophosphamide	274-277	BCL2-associated X protein	Mus musculus	90-93
15667832-8	2005	Additional analyses indicate that the tumor suppressor p53 and p53-regulated proapoptotic Bax were upregulated in vivo and in vitro following CPA treatment in combination with DOX, suggesting that upregulation of p53 may contribute to the enhancement of antitumor effect of CPA by DOX.	Cyclophosphamide	274-277	transformation related protein 53, pseudogene	Mus musculus	63-66
15605409-14	2005	The level of CD69 expression, which represents a functional triggering molecule on activated NK cells, was increased in the CPA group at all the time points tested as compared to untreated mice.	Cyclophosphamide	124-127	CD69 antigen	Mus musculus	13-17
15605409-16	2005	A significant increase in TNF-alpha level was also observed on day 7 following CPA administration.	Cyclophosphamide	79-82	tumor necrosis factor	Mus musculus	26-35
15605409-18	2005	MMW irradiation of the CPA treated groups resulted in further enhancement of CD69 expression on NK cells, as well as in production of TNF-alpha.	Cyclophosphamide	23-26	CD69 antigen	Mus musculus	77-81
15605409-18	2005	MMW irradiation of the CPA treated groups resulted in further enhancement of CD69 expression on NK cells, as well as in production of TNF-alpha.	Cyclophosphamide	23-26	tumor necrosis factor	Mus musculus	134-143
15656694-10	2005	Interactions with the alkylating agents cyclophosphamide and ifosfamide are complicated as a result of the involvement of the CYP3A4 and CYP2B6 isoenzymes in both the metabolic activation of these drugs and the generation of potentially neurotoxic metabolites.	Cyclophosphamide	40-56	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	137-143
15645351-1	2004	Cyclophosphamide (CTX) is an alkylating agent related to nitrogen mustards whose anti-inflammatory and immunosuppressive effects have been utilised to treat selected cases of multiple sclerosis with a progressive and worsening course.	Cyclophosphamide	0-16	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	18-21
15585071-5	2004	Similarly, in the multicenter prospective Chemo N0 trial, administration of cyclophosphamide/methotrexate/5-fluorouracil-based chemotherapy led to a substantial reduction in risk of disease recurrence in patients with high uPA/PAI-1.	Cyclophosphamide	76-92	plasminogen activator, urokinase	Homo sapiens	223-226
15585071-5	2004	Similarly, in the multicenter prospective Chemo N0 trial, administration of cyclophosphamide/methotrexate/5-fluorouracil-based chemotherapy led to a substantial reduction in risk of disease recurrence in patients with high uPA/PAI-1.	Cyclophosphamide	76-92	serpin family E member 1	Homo sapiens	227-232
15755204-1	2004	A case of deep-vein thrombosis is reported in a female patient with multibacillary leprosy who received pulses of dexamethasone and cyclophosphamide for recurrent ENL that had not responded to prednisone and thalidomide.	Cyclophosphamide	132-148	MLLT1 super elongation complex subunit	Homo sapiens	163-166
15599402-6	2004	Induction of stromal cell-derived factor-1 production within the BM using low-dose irradiation or cyclophosphamide combined with IL-2 administration enhanced the homing of systemically delivered T bodies, resulting in decreased tumor growth and prostate-specific antigen secretion, prolongation of survival, and even cure of the treated mice.	Cyclophosphamide	98-114	chemokine (C-X-C motif) ligand 12	Mus musculus	13-42
15557199-4	2004	CXCL10 neutralization suppressed the occurrence of diabetes after administration with cyclophosphamide in NOD mice, although CXCL10 neutralization did not significantly inhibit insulitis and gave no influence on the trafficking of effector T cells into the islets.	Cyclophosphamide	86-102	chemokine (C-X-C motif) ligand 10	Mus musculus	0-6
15585485-9	2004	RESULTS: (99m)Tc-Annexin V accumulation in tumors significantly increased at 20 h (0.077 +/- 0.007 [%ID/g] x kg, where %ID/g = percentage injected dose per gram) but not at 4 or 12 h (0.048 +/- 0.008 and 0.052 +/- 0.014 [%ID/g] x kg, respectively) after cyclophosphamide treatment.	Cyclophosphamide	254-270	annexin A5	Rattus norvegicus	17-26
15585485-10	2004	(99m)Tc-Annexin V accumulation in tumors and the rate of apoptotic cells determined by caspase-3 immunostaining and TUNEL were significantly higher in treated rats 20 h after cyclophosphamide treatment as compared with control rats.	Cyclophosphamide	175-191	annexin A5	Rattus norvegicus	8-17
15585485-11	2004	CONCLUSION: The effective detection of apoptotic tumor response with (99m)Tc-annexin V required 20 h after cyclophosphamide treatment in an experimental model.	Cyclophosphamide	107-123	annexin A5	Rattus norvegicus	77-86
15538286-0	2004	Cyclophosphamide induced cystitis alters neurotrophin and receptor tyrosine kinase expression in pelvic ganglia and bladder.	Cyclophosphamide	0-16	erb-b2 receptor tyrosine kinase 4	Rattus norvegicus	58-82
15736418-1	2004	Our previous studies revealed that lactoferrin (LF) reconstitutes the cellular and humoral immune response in cyclophosphamide-treated mice.	Cyclophosphamide	110-126	lactotransferrin	Mus musculus	35-46
15685838-1	2004	This study was designed to evaluate the cardiac safety of the combined treatment of HER2-positive metastatic breast cancer patients with trastuzumab (Herceptin) plus epirubicin and cyclophosphamide (EC) in comparison with EC alone in HER2-negative metastatic breast cancer patients.	Cyclophosphamide	181-197	erb-b2 receptor tyrosine kinase 2	Homo sapiens	84-88
15736418-1	2004	Our previous studies revealed that lactoferrin (LF) reconstitutes the cellular and humoral immune response in cyclophosphamide-treated mice.	Cyclophosphamide	110-126	lactotransferrin	Mus musculus	48-50
15465593-6	2004	However, FS in combination with certain CY doses led to a further significant decrease in host responses compared to either CY or FS treatment alone, including decreased survival rate, increased weight loss, lowered leukocyte numbers, reduced cytokine production in vivo and in vitro, and decreased numbers of cytokine-producing cells (IL-12 and IFNgamma).	Cyclophosphamide	40-42	interferon gamma	Homo sapiens	346-354
15205203-2	2004	Recently, chemotherapy consisting of doxorubicin, cyclophosphamide, vincristine and prednisone (CHOP) has been reported as effective treatment for early-stage gastric DLBCL.	Cyclophosphamide	50-66	DNA damage inducible transcript 3	Homo sapiens	96-100
15358478-0	2004	A patient with granulocyte-colony stimulating factor-producing endometrial cancer who responded to high-dose cisplatin, cyclophosphamide and adriamycin.	Cyclophosphamide	120-136	colony stimulating factor 3	Homo sapiens	15-52
15258844-10	2004	CysC increased significantly after cisplatin, methotrexate, cyclophosphamide, ifosfamide, and multimodality treatment.	Cyclophosphamide	60-76	cystatin C	Homo sapiens	0-4
15142875-2	2004	Busulfan, as well as the metabolites of cyclophosphamide, are conjugated with glutathione (GSH), catalyzed by enzymes of the glutathione S-transferase (GST) family.	Cyclophosphamide	40-56	glutathione S-transferase kappa 1	Homo sapiens	125-150
15142875-2	2004	Busulfan, as well as the metabolites of cyclophosphamide, are conjugated with glutathione (GSH), catalyzed by enzymes of the glutathione S-transferase (GST) family.	Cyclophosphamide	40-56	glutathione S-transferase kappa 1	Homo sapiens	152-155
15342414-2	2004	Here, we show that Fas as a p53 target plays important role in the HF response to cyclophosphamide.	Cyclophosphamide	82-98	transformation related protein 53, pseudogene	Mus musculus	28-31
15626054-10	2004	Cyclophosphamide, doxorubicin, vincristine and prednisone, (CHOP) chemotherapy was given to 68.7% of the patients with complete remission rates of 55.6% for those who got a minimum of six courses of chemotherapy.	Cyclophosphamide	0-16	DNA damage inducible transcript 3	Homo sapiens	60-64
15251111-1	2004	Previous studies on cyclophosphamide (CP)-immunocompromised mice showed accelerated reconstitution of immune system function following oral treatment with lactoferrin (LF).	Cyclophosphamide	20-36	lactotransferrin	Mus musculus	155-166
15251111-1	2004	Previous studies on cyclophosphamide (CP)-immunocompromised mice showed accelerated reconstitution of immune system function following oral treatment with lactoferrin (LF).	Cyclophosphamide	20-36	lactotransferrin	Mus musculus	168-170
15261554-6	2004	In our studies of cyclophosphamide, we have found that although it is a general immunosuppressant that affects both T cell and B cell functions, cyclophosphamide has selective immune effects in MS by suppressing IL-12- and Th1-type responses and enhancing Th2/Th3 responses (IL-4, IL-10, TGF-beta; eosinophils in peripheral blood).	Cyclophosphamide	145-161	negative elongation factor complex member C/D	Homo sapiens	223-226
15261554-6	2004	In our studies of cyclophosphamide, we have found that although it is a general immunosuppressant that affects both T cell and B cell functions, cyclophosphamide has selective immune effects in MS by suppressing IL-12- and Th1-type responses and enhancing Th2/Th3 responses (IL-4, IL-10, TGF-beta; eosinophils in peripheral blood).	Cyclophosphamide	145-161	interleukin 4	Homo sapiens	275-279
15261554-6	2004	In our studies of cyclophosphamide, we have found that although it is a general immunosuppressant that affects both T cell and B cell functions, cyclophosphamide has selective immune effects in MS by suppressing IL-12- and Th1-type responses and enhancing Th2/Th3 responses (IL-4, IL-10, TGF-beta; eosinophils in peripheral blood).	Cyclophosphamide	145-161	interleukin 10	Homo sapiens	281-286
15261554-6	2004	In our studies of cyclophosphamide, we have found that although it is a general immunosuppressant that affects both T cell and B cell functions, cyclophosphamide has selective immune effects in MS by suppressing IL-12- and Th1-type responses and enhancing Th2/Th3 responses (IL-4, IL-10, TGF-beta; eosinophils in peripheral blood).	Cyclophosphamide	145-161	transforming growth factor beta 1	Homo sapiens	288-296
15261564-0	2004	A double blind, placebo-controlled, phase II, add-on study of cyclophosphamide (CTX) for 24 months in patients affected by multiple sclerosis on a background therapy with interferon-beta study denomination: CYCLIN.	Cyclophosphamide	62-78	interferon beta 1	Homo sapiens	171-186
15261565-0	2004	Preliminary analysis of a trial of pulse cyclophosphamide in IFN-beta-resistant active MS.	Cyclophosphamide	41-57	interferon beta 1	Homo sapiens	61-69
15261565-10	2004	Pulse cyclophosphamide decreases the number of Gd+ lesions in patients with active disease on IFN-beta compared to pulse methylprednisolone alone.	Cyclophosphamide	6-22	interferon beta 1	Homo sapiens	94-102
14982884-1	2004	The combination of cyclophosphamide, doxorubicin, vincristine, and prednisone, given every 3 weeks (CHOP-21) is standard chemotherapy for aggressive lymphomas.	Cyclophosphamide	19-35	DNA damage inducible transcript 3	Homo sapiens	100-104
15213720-4	2004	These studies had suggested that better 5-year survival with ET-2 over the earlier ET-1 was achieved by replacing cyclophosphamide by ifosfamide and increasing the dose of doxorubicin in a four-drug chemotherapy regimen.	Cyclophosphamide	114-130	endothelin 2	Homo sapiens	61-65
15213720-4	2004	These studies had suggested that better 5-year survival with ET-2 over the earlier ET-1 was achieved by replacing cyclophosphamide by ifosfamide and increasing the dose of doxorubicin in a four-drug chemotherapy regimen.	Cyclophosphamide	114-130	endothelin 1	Homo sapiens	83-87
15214939-8	2004	Their immunosuppressive activity can be prevented by treatment of TMf donors with cyclophosphamide or in vitro by anti-TGF-beta monoclonal antibody.	Cyclophosphamide	82-98	TATA element modulatory factor 1	Mus musculus	66-69
15662130-4	2004	demonstrated that low-dose cyclophosphamide inhibits tumor growth by upregulating the endogenous angiogenesis inhibitor thrombospondin-1 in tumor and perivascular cells.	Cyclophosphamide	27-43	thrombospondin 1	Homo sapiens	120-136
15662130-6	2004	It was also proposed that thrombospondin-1 levels might be used as a surrogate marker to monitor response to low-dose cyclophosphamide therapy in the clinic.	Cyclophosphamide	118-134	thrombospondin 1	Homo sapiens	26-42
15369444-5	2004	Agents such as luteinizing hormone releasing hormone (LHRH) agonists can suppress ovarian function in premenopausal patients and have been shown to be as effective and even better than chemotherapy (CMF--cyclophosphamide, methotrexate, fluorouracil-containing regimens) in certain patient populations.	Cyclophosphamide	204-220	gonadotropin releasing hormone 1	Homo sapiens	15-52
15367711-2	2004	We report here that Ad.Egr-TNF.11D is activated by the clinically important anticancer agents cisplatin, cyclophosphamide, doxorubicin, 5-fluorouracil, gemcitabine, and paclitaxel.	Cyclophosphamide	105-121	tumor necrosis factor	Homo sapiens	27-30
15276878-0	2004	Upregulation of corticotropin-releasing hormone gene expression in the paraventricular nucleus of cyclophosphamide-induced cystitis in male rats.	Cyclophosphamide	98-114	corticotropin releasing hormone	Rattus norvegicus	16-47
15276878-1	2004	We examined the effects of cyclophosphamide (CP)-induced cystitis on the expression of corticotropin-releasing hormone (CRH) mRNA in the paraventricular nucleus (PVN) and the serum levels of adrenocorticotropic hormone (ACTH) using in situ hybridization histochemistry and radioimmunoassay.	Cyclophosphamide	27-43	corticotropin releasing hormone	Rattus norvegicus	120-123
15100152-5	2004	Suboptimal doses of granulocyte colony-stimulating factor (G-CSF) or cyclophosphamide (CY) also resulted in enhanced HPC mobilization in alphaM-/- mice compared with alphaM+/+ controls, but this difference was overcome when standard doses of G-CSF or CY were administered.	Cyclophosphamide	69-85	colony stimulating factor 3 (granulocyte)	Mus musculus	242-247
15100152-5	2004	Suboptimal doses of granulocyte colony-stimulating factor (G-CSF) or cyclophosphamide (CY) also resulted in enhanced HPC mobilization in alphaM-/- mice compared with alphaM+/+ controls, but this difference was overcome when standard doses of G-CSF or CY were administered.	Cyclophosphamide	87-89	colony stimulating factor 3 (granulocyte)	Mus musculus	242-247
15016643-1	2004	Cyclophosphamide, doxorubicin, vincristine, and prednisone, given every 3 weeks (CHOP-21), is standard chemotherapy for aggressive lymphomas.	Cyclophosphamide	0-16	DNA damage inducible transcript 3	Homo sapiens	81-85
15034757-7	2004	Treatment with high-dose corticosteroids was initiated, with clinical improvement, and was immediately followed by therapy with cyclophosphamide, hydroxydaunomycin, vincristine, and prednisone (CHOP), which induced complete remission with a follow-up of 1 year.	Cyclophosphamide	128-144	DNA damage inducible transcript 3	Homo sapiens	194-198
15248218-0	2004	Cytochrome P450 pharmacogenetics as a predictor of toxicity and clinical response to pulse cyclophosphamide in lupus nephritis.	Cyclophosphamide	91-107	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	0-15
15248218-3	2004	Cyclophosphamide is a prodrug that requires activation by cytochrome P450 (CYP) enzymes.	Cyclophosphamide	0-16	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	58-73
15248218-3	2004	Cyclophosphamide is a prodrug that requires activation by cytochrome P450 (CYP) enzymes.	Cyclophosphamide	0-16	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	75-78
15248218-8	2004	Patients who were either heterozygous or homozygous for CYP2C19*2 had a significantly lower risk of developing premature ovarian failure (relative risk 0.10; 95% confidence interval 0.02-0.52), after adjustment for age and total number of cyclophosphamide pulses received.	Cyclophosphamide	239-255	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	56-63
15248218-10	2004	CONCLUSION: Determination of selected cytochrome P450 enzyme genotypes may be valuable for predicting the risk of premature ovarian failure in lupus nephritis patients treated with cyclophosphamide.	Cyclophosphamide	181-197	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	38-53
15359655-2	2004	After obtaining a partial remission with four cycles of fludarabine at standard dose, the patient underwent to high-dose Cytoxan in order to mobilize CD34+ hematopoietic progenitor cells.	Cyclophosphamide	121-128	CD34 molecule	Homo sapiens	150-154
15133484-8	2004	Cyclophosphamide alone is associated with impressive CD34(+) cell yields and clear antimyeloma activity.	Cyclophosphamide	0-16	CD34 molecule	Homo sapiens	53-57
15170171-4	2004	Monitoring of peripheral CD19+ and CD20+ B cells prior to and throughout the purging period showed that a treatment with Rituximab, Vincristine and Cyclophosphamide results in a profound depletion of B cells in peripheral blood.	Cyclophosphamide	148-164	CD19 molecule	Homo sapiens	25-29
15170171-4	2004	Monitoring of peripheral CD19+ and CD20+ B cells prior to and throughout the purging period showed that a treatment with Rituximab, Vincristine and Cyclophosphamide results in a profound depletion of B cells in peripheral blood.	Cyclophosphamide	148-164	keratin 20	Homo sapiens	35-39
15485083-1	2004	The aim of this study was to evaluate the prophylactic potential of hyperbaric oxygenation treatment and the timing of hyperbaric oxygen (HBO2) therapy for cyclophosphamide-(CYP) induced cystitis in rats.	Cyclophosphamide	156-172	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	174-177
15217956-0	2004	Mcl-1 is a novel therapeutic target for human sarcoma: synergistic inhibition of human sarcoma xenotransplants by a combination of mcl-1 antisense oligonucleotides with low-dose cyclophosphamide.	Cyclophosphamide	178-194	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	0-5
15217956-13	2004	CONCLUSION: A combination of Mcl-1 antisense oligonucleotides with low-dose cyclophosphamide provides a synergistic antitumor effect and might qualify as a promising strategy to overcome chemoresistance in human sarcoma.	Cyclophosphamide	76-92	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	29-34
15060745-2	2004	The risk is significantly evident in patients with aggressive lymphoma, which is highly responsive to standard chemotherapy with cyclophosphamide, hydroxydaunomycin, vincristine, and prednisone (CHOP) achieving a complete response rate of 60-80% and 5-year survival rate of 30-50% with only 1% of treatment-related mortality.	Cyclophosphamide	129-145	DNA damage inducible transcript 3	Homo sapiens	195-199
15164387-0	2004	Ablation of hemophilic FVIII inhibitors with FVIII priming, cyclophosphamide immune suppression, and rapid tapering of FVIII immune tolerance.	Cyclophosphamide	60-76	coagulation factor VIII	Homo sapiens	23-28
15164387-13	2004	Cyclophosphamide (1,400 mg/M2) administered after a priming dose of FVIII (80 U/kg) i.v.	Cyclophosphamide	0-16	coagulation factor VIII	Homo sapiens	68-73
15182437-9	2004	In the p53 wild-type group, we found a positive correlation for the following drugs: ADM (P < 0.02), ACNU (P < 0.007), CPA (P < 0.011), UFT (P < 0.012), and FT-207 (P < 0.02).	Cyclophosphamide	125-128	tumor protein p53	Homo sapiens	7-10
15182437-10	2004	In the p53 mutant group, only CPA (P < 0.003) showed a positive correlation.	Cyclophosphamide	30-33	tumor protein p53	Homo sapiens	7-10
15255968-8	2004	This might relate to only a partial suppression of PMN: CY has significantly reduced PMN influx into the lungs (P = 0.008) and suppressed their oxidative metabolism, but had no suppressive effect on degranulation (P = 0.227) and even induced MMP-9 activity (P = 0.0003).	Cyclophosphamide	56-58	matrix metallopeptidase 9	Mus musculus	242-247
15255968-9	2004	In CY-untreated animals, peak of CLP-induced ALI coincided with massive PMN influx (P = 0.013), their maximal degranulation (P = 0.014) and activation of lung MMP-9 (P = 0.002).	Cyclophosphamide	3-5	matrix metallopeptidase 9	Mus musculus	159-164
15205850-0	2004	Inducible nitric oxide synthase inhibition in cyclophosphamide induced hemorrhagic cystitis in rats.	Cyclophosphamide	46-62	nitric oxide synthase 2	Rattus norvegicus	0-31
15273668-0	2004	CD4+ T cells tumor specific response exists in L615 leukemia mice: adoptive transfer in combination with cyclophosphamide.	Cyclophosphamide	105-121	CD4 antigen	Mus musculus	0-3
15273668-11	2004	These CD4+ T cells can cure leukemia mice upon adoptive transfer in combination with cyclophosphamide pretreatment.	Cyclophosphamide	85-101	CD4 antigen	Mus musculus	6-9
15181605-5	2004	In patients with aggressive lymphoma who receive cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy, 40% to 70% of patients attain a complete remission, depending on risk factors such as age and extranodal involvement.	Cyclophosphamide	49-65	DNA damage inducible transcript 3	Homo sapiens	109-113
15060740-11	2004	Coadministration of cyclophosphamide had similar effects on thalidomide t(1/2) in C57Bl/6, TNF(-/-) and TNFR1(-/-) mice, while coadministration of DMXAA did not alter the t(1/2) or AUC in TNF(-/-) and TNFR1(-/-) mice.	Cyclophosphamide	20-36	tumor necrosis factor	Mus musculus	91-94
15274362-0	2004	Profile of cytokines produced in tumor tissue after administration of cyclophosphamide in a combination therapy with tumor necrosis factor.	Cyclophosphamide	70-86	tumor necrosis factor	Mus musculus	117-138
15274362-6	2004	CY significantly enhanced IL-12 (p40) mRNA compared to that by ONO-4007 alone.	Cyclophosphamide	0-2	interleukin 12b	Mus musculus	33-36
15274362-8	2004	CONCLUSION: The preadministration of CY enhances IL-12 production in tumor tissues and shifts the cytokine profile to the dominant Th1 type.	Cyclophosphamide	37-39	negative elongation factor complex member C/D, Th1l	Mus musculus	131-134
15060740-11	2004	Coadministration of cyclophosphamide had similar effects on thalidomide t(1/2) in C57Bl/6, TNF(-/-) and TNFR1(-/-) mice, while coadministration of DMXAA did not alter the t(1/2) or AUC in TNF(-/-) and TNFR1(-/-) mice.	Cyclophosphamide	20-36	tumor necrosis factor receptor superfamily, member 1b	Mus musculus	104-109
15060740-11	2004	Coadministration of cyclophosphamide had similar effects on thalidomide t(1/2) in C57Bl/6, TNF(-/-) and TNFR1(-/-) mice, while coadministration of DMXAA did not alter the t(1/2) or AUC in TNF(-/-) and TNFR1(-/-) mice.	Cyclophosphamide	20-36	tumor necrosis factor	Mus musculus	104-107
15100273-0	2004	In vivo cyclophosphamide and IL-2 treatment impedes self-antigen-induced effector CD4 cell tolerization: implications for adoptive immunotherapy.	Cyclophosphamide	8-24	CD4 antigen	Mus musculus	82-85
15168601-8	2004	In the setting of major ABO-incompatible NSCT, a fludarabine- and cyclophosphamide-based conditioning regimen may lead to prolonged PRCA.	Cyclophosphamide	66-82	ABO, alpha 1-3-N-acetylgalactosaminyltransferase and alpha 1-3-galactosyltransferase	Homo sapiens	24-27
14993510-4	2004	METHODS: We carried out a retrospective chart analysis of 46 patients with SDNS treated with CSA, after failure of cytotoxic treatment with cyclophosphamide (CPO).	Cyclophosphamide	158-161	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	93-96
15193230-1	2004	AIM: To detect the expression and status of extracellular regulatory kinase 1 and 2 (ERK1/2) and its upstream kinase MEK1/2 proteins in four breast cancer cell lines MCF-7, Bcap-37, SK-BR-3 and T47D and study the effects of cyclophosphamide and epirubicin on the growth of the cell lines and on the expression and status of the signaling molecules.	Cyclophosphamide	224-240	mitogen-activated protein kinase 3	Homo sapiens	85-91
15193230-8	2004	The inhibitory effect of cyclophosphamide and epirubicin on proliferation of the breast cancer cells may be by means of inhibiting expression and phosphorylation of MEK and ERK.	Cyclophosphamide	25-41	mitogen-activated protein kinase kinase 7	Homo sapiens	165-168
15193230-8	2004	The inhibitory effect of cyclophosphamide and epirubicin on proliferation of the breast cancer cells may be by means of inhibiting expression and phosphorylation of MEK and ERK.	Cyclophosphamide	25-41	mitogen-activated protein kinase 1	Homo sapiens	173-176
15078896-3	2004	Transgenic DCR3 protected mice from autoimmune and cyclophosphamide-induced diabetes in a dose-dependent manner and significantly reduced the severity of insulitis.	Cyclophosphamide	51-67	Dcr3	Mus musculus	11-15
15077271-11	2004	CONCLUSION: Switching cyclophosphamide to azathioprine after induction of remission in patients with PR3-ANCA-associated vasculitis who are still ANCA-positive at the time of treatment switch is associated with a high risk of relapse.	Cyclophosphamide	22-38	proteinase 3	Homo sapiens	101-104
15216955-0	2004	Effects of lactoferrin on IL-6 production by peritoneal and alveolar cells in cyclophosphamide-treated mice.	Cyclophosphamide	78-94	lactotransferrin	Mus musculus	11-22
15216955-0	2004	Effects of lactoferrin on IL-6 production by peritoneal and alveolar cells in cyclophosphamide-treated mice.	Cyclophosphamide	78-94	interleukin 6	Mus musculus	26-30
15216955-1	2004	Previous studies have shown that oral treatment with lactoferrin (LF) restores the immune response in cyclophosphamide (CP) immunocompromised mice.	Cyclophosphamide	102-118	lactotransferrin	Mus musculus	53-64
15216955-1	2004	Previous studies have shown that oral treatment with lactoferrin (LF) restores the immune response in cyclophosphamide (CP) immunocompromised mice.	Cyclophosphamide	102-118	lactotransferrin	Mus musculus	66-68
15160952-0	2004	High-dose topotecan, melphalan and cyclophosphamide (TMC) with stem cell support: a new regimen for the treatment of multiple myeloma.	Cyclophosphamide	35-51	STT3 oligosaccharyltransferase complex catalytic subunit A	Homo sapiens	53-56
15031341-2	2004	We evaluated the efficacy of methylprednisolone and urokinase pulse therapy combined with cyclophosphamide for patients with HSPN of at least grade IVb.	Cyclophosphamide	90-106	heat shock protein 90 alpha family class A member 1	Homo sapiens	125-129
15031341-9	2004	CONCLUSIONS: Our study suggests that methylprednisolone and urokinase pulse therapy combined with cyclophosphamide is useful for patients with severe HSPN.	Cyclophosphamide	98-114	heat shock protein 90 alpha family class A member 1	Homo sapiens	150-154
14679052-7	2003	During spontaneous and cyclophosphamide diabetes, it was observed in a higher proportion of islet infiltrating macrophages than in CD4 and CD8 cells.	Cyclophosphamide	23-39	CD4 antigen	Mus musculus	131-134
15154657-0	2004	Serum levels of HER2 ECD can determine the response rate to low dose oral cyclophosphamide and methotrexate in patients with advanced stage breast carcinoma.	Cyclophosphamide	74-90	erb-b2 receptor tyrosine kinase 2	Homo sapiens	16-20
15154657-4	2004	PATIENTS AND METHODS: HER2 ECD was determined in 39 patients with advanced breast cancer, treated with oral cyclophosphamide and methotrexate (CM) at low doses.	Cyclophosphamide	108-124	erb-b2 receptor tyrosine kinase 2	Homo sapiens	22-26
14996710-0	2004	Thrombospondin-1 associated with tumor microenvironment contributes to low-dose cyclophosphamide-mediated endothelial cell apoptosis and tumor growth suppression.	Cyclophosphamide	80-96	thrombospondin 1	Homo sapiens	0-16
15028885-3	2004	CY treatment induced B cell specific immunosuppression throughout the experiment confirmed by decreased bursal weight, intact lymphocyte mitogenetic activity stimulated by Con A and increased relative subpopulation of CD3-positive cells as measured by flow cytometry.	Cyclophosphamide	0-2	CD3d molecule	Gallus gallus	218-221
14767525-0	2004	Determination of the in vivo effects of cladribine alone and its combination with cyclophosphamide or cyclophosphamide and mitoxantrone on Bax and Bcl-2 protein expression in B-CLL cells.	Cyclophosphamide	102-118	BCL2 apoptosis regulator	Homo sapiens	147-152
14694538-1	2004	We examined the changes of two transcription factors, CREB and c-Jun, in dorsal root ganglia (DRG) after acute (8 or 48 hours) or chronic (10 days) cyclophosphamide (CYP)-induced cystitis.	Cyclophosphamide	148-164	cAMP responsive element binding protein 1	Homo sapiens	54-58
14694538-1	2004	We examined the changes of two transcription factors, CREB and c-Jun, in dorsal root ganglia (DRG) after acute (8 or 48 hours) or chronic (10 days) cyclophosphamide (CYP)-induced cystitis.	Cyclophosphamide	148-164	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	63-68
28140109-1	2004	In the past, CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine, prednisone) was considered the gold standard treatment for aggressive non-Hodgkin"s lymphoma (NHL).	Cyclophosphamide	32-48	DNA damage inducible transcript 3	Homo sapiens	13-17
14760101-14	2004	These data indicate that Fas/FasL may be involved in the cytotoxic pathway of CY.	Cyclophosphamide	78-80	Fas ligand	Homo sapiens	29-33
14688392-3	2004	We studied the surface expression of CXCR4 very late activation antigen (VLA)-4 and VLA-5 on myeloma cells mobilized with cyclophosphamide and GM-CSF in 12 multiple myeloma patients undergoing HSC mobilization for autologous transplantation.	Cyclophosphamide	122-138	C-X-C motif chemokine receptor 4	Homo sapiens	37-42
14695197-1	2003	The effect of cyclophosphamide (Cp) on the glycolytic rate of radiation-induced fibrosarcomas (RIF-1) was measured in vivo in C3H mice by following the production of [3-(13)C]lactate after tail vein infusion of labeled [1-(13)C]glucose.	Cyclophosphamide	14-30	replication timing regulatory factor 1	Mus musculus	95-100
14625575-4	2003	However, the mean of the median serum CsA concentration in patients (n=54) receiving the regimen containing cyclophosphamide (CY) (149.7 ng/ml; 95% confidence interval (CI): 132.1-167.4) was significantly (P<0.0001) lower than that in patients (n=49) receiving the non-CY regimen (217.3 ng/ml; 95% CI: 198.9-235.6).	Cyclophosphamide	108-124	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	38-41
14625575-4	2003	However, the mean of the median serum CsA concentration in patients (n=54) receiving the regimen containing cyclophosphamide (CY) (149.7 ng/ml; 95% confidence interval (CI): 132.1-167.4) was significantly (P<0.0001) lower than that in patients (n=49) receiving the non-CY regimen (217.3 ng/ml; 95% CI: 198.9-235.6).	Cyclophosphamide	126-128	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	38-41
14625575-5	2003	Longitudinal analysis and regression multivariate analysis showed that only administration of CY had a significant effect on the serum CsA concentration.	Cyclophosphamide	94-96	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	135-138
14625575-6	2003	Our results suggest that administration of CY during conditioning can reduce the effects on serum CsA concentrations during the 2 weeks following HSCT.	Cyclophosphamide	43-45	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	98-101
14679003-4	2003	We therefore investigated whether such metronomic therapy with the alkylating agent cyclophosphamide (CTX) could be effectively combined with immunotherapy eliciting tumor-reactive CTLs.	Cyclophosphamide	84-100	V-set and immunoglobulin domain containing 2	Mus musculus	102-105
14595707-6	2003	Among 17 patients referred because of resistant NB, favorable responses occurred in 6/12 treated with high-dose cyclophosphamide-based salvage therapy, including one patient who is in CR 170+ months after myeloablative consolidation and five patients who achieved CR/VGPR after 3F8/GM-CSF (n = 4) or 3F8/oral etoposide (n = 1).	Cyclophosphamide	112-128	colony stimulating factor 2	Homo sapiens	282-288
14679058-0	2003	Immunolocalization of caspase-3 in pancreatic islets of NOD mice during cyclophosphamide-accelerated diabetes.	Cyclophosphamide	72-88	caspase 3	Mus musculus	22-31
14679058-3	2003	Here, the intra-islet expression of caspase-3 in the NOD mouse was examined immunohistochemically following acceleration of the disease with cyclophosphamide.	Cyclophosphamide	141-157	caspase 3	Mus musculus	36-45
14679058-11	2003	We conclude that, during cyclophosphamide-accelerated diabetes, the predominant caspase-3 immunolabeling in intra- and extra-islet macrophages suggests that apoptosis of macrophages may be an important mechanism for their elimination.	Cyclophosphamide	25-41	caspase 3	Mus musculus	80-89
15228172-5	2004	The potential of applying pharmacogenetic screening before therapy in the treatment of cancer seems to be greatest for CYP2B6 (cyclophosphamide treatment), CYP2C8 (paclitaxel therapy), and CYP3A5; however, the drugs of interest still need to be identified for this latter enzyme.	Cyclophosphamide	127-143	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	119-125
14993808-1	2004	We evaluated the features of cell death induced by CDF (cyclophosphamide [CPA], doxorubicin [DOX], 5-fluorouracil [5-FU]) multi-drug administration in vitro using the human breast cancer cell line MCF-7.	Cyclophosphamide	56-72	LIF interleukin 6 family cytokine	Homo sapiens	51-54
14976460-0	2004	Normalization of peripheral blood cell composition by lactoferrin in cyclophosphamide-treated mice.	Cyclophosphamide	69-85	lactotransferrin	Mus musculus	54-65
15019293-1	2004	CD11b+Gr-1+ inhibitory macrophages (iMacs) were implicated in profound depression of T cell functions sometimes observed during cyclophosphamide treatments and overwhelming infections, through a secretion of nitric oxide (NO).	Cyclophosphamide	128-144	integrin alpha M	Mus musculus	0-5
14768038-0	2004	CD4+CD25+ regulatory T cells suppress tumor immunity but are sensitive to cyclophosphamide which allows immunotherapy of established tumors to be curative.	Cyclophosphamide	74-90	Cd4 molecule	Rattus norvegicus	0-3
14768038-6	2004	A single administration of cyclophosphamide depletes CD4(+)CD25(+) T cells in PROb tumor-bearing animals, delays the growth of PROb tumors, and cures rats bearing established PROb tumors when followed by an immunotherapy which has no curative effect when administered alone.	Cyclophosphamide	27-43	Cd4 molecule	Rattus norvegicus	53-56
14968341-5	2004	Studies showing an expansion of circulating tumor necrosis factor-(TNF-)alpha-producing Th1-type CD4(+)CD28(-) T-cell effector memory T-cells and their presence as Th1-type cytokine profile- driving cell population within granulomatous lesions provide the rationale for using TNF-alpha-blocking agents in Wegener"s granulomatosis refractory to standard induction therapy with cyclophosphamide and corticosteroids ("Fauci"s scheme").	Cyclophosphamide	376-392	tumor necrosis factor	Homo sapiens	67-77
14968341-5	2004	Studies showing an expansion of circulating tumor necrosis factor-(TNF-)alpha-producing Th1-type CD4(+)CD28(-) T-cell effector memory T-cells and their presence as Th1-type cytokine profile- driving cell population within granulomatous lesions provide the rationale for using TNF-alpha-blocking agents in Wegener"s granulomatosis refractory to standard induction therapy with cyclophosphamide and corticosteroids ("Fauci"s scheme").	Cyclophosphamide	376-392	negative elongation factor complex member C/D	Homo sapiens	164-167
14673513-0	2004	Protease-activated receptor-2-mediated contraction of urinary bladder is enhanced in cyclophosphamide-treated rats.	Cyclophosphamide	85-101	F2R like trypsin receptor 1	Rattus norvegicus	0-29
14673513-3	2004	In the present study, we investigated how the PAR-2-mediated responses are altered in rats with cyclophosphamide (CYP)-induced cystitis.	Cyclophosphamide	96-112	F2R like trypsin receptor 1	Rattus norvegicus	46-51
15042528-1	2004	In the past, CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine, prednisone) was considered the gold standard treatment for aggressive non-Hodgkin"s lymphoma (NHL).	Cyclophosphamide	32-48	DNA damage inducible transcript 3	Homo sapiens	13-17
15302998-0	2004	Angiogenesis inhibition by angiostatin, endostatin and TNP-470 prevents cyclophosphamide induced cystitis.	Cyclophosphamide	72-88	plasminogen	Mus musculus	27-38
15302998-0	2004	Angiogenesis inhibition by angiostatin, endostatin and TNP-470 prevents cyclophosphamide induced cystitis.	Cyclophosphamide	72-88	collagen, type XVIII, alpha 1	Mus musculus	40-50
15630257-5	2004	The increase of the GE activity is mainly favoured by the chemotherapy following the schemes FAC (5-fluorouracyl + doxorubicin + endoxan) and PAC (cisplatin + cyclofosfamide + pharmorubicin).	Cyclophosphamide	129-136	FA complementation group C	Homo sapiens	93-96
14726661-0	2004	A phase II study of topotecan and cyclophosphamide with G-CSF in patients with advanced small cell lung cancer.	Cyclophosphamide	34-50	colony stimulating factor 3	Homo sapiens	56-61
14729637-1	2004	Cytochrome P450 (CYP) gene transfer sensitizes tumor xenografts to anticancer prodrugs such as cyclophosphamide (CPA) without a detectable increase in host toxicity.	Cyclophosphamide	95-111	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	0-15
14729637-1	2004	Cytochrome P450 (CYP) gene transfer sensitizes tumor xenografts to anticancer prodrugs such as cyclophosphamide (CPA) without a detectable increase in host toxicity.	Cyclophosphamide	95-111	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	17-20
14729637-1	2004	Cytochrome P450 (CYP) gene transfer sensitizes tumor xenografts to anticancer prodrugs such as cyclophosphamide (CPA) without a detectable increase in host toxicity.	Cyclophosphamide	113-116	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	0-15
14729637-1	2004	Cytochrome P450 (CYP) gene transfer sensitizes tumor xenografts to anticancer prodrugs such as cyclophosphamide (CPA) without a detectable increase in host toxicity.	Cyclophosphamide	113-116	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	17-20
14729637-4	2004	Retrovirus encoding a CYP2B6-IRES-P450R expression cassette was shown to induce strong P450-dependent CPA cytotoxicity in a population of infected 9L gliosarcoma cells.	Cyclophosphamide	102-105	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	22-28
14729637-5	2004	Adeno-P450, a replication-defective, E1/E3 region-deleted adenovirus engineered to express CYP2B6-IRES-P450R, induced intracellular CPA 4-hydroxylation, and CPA cytotoxicity, in a broad range of human cancer cell lines.	Cyclophosphamide	132-135	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	91-97
14729649-6	2004	Moreover, adoptive transfer of TCR-transduced Th1 cells, but not mock-transduced Th1 cells, exhibited potent antitumor activity in vivo and, when combined with cyclophosphamide treatment, completely eradicated established tumor masses.	Cyclophosphamide	160-176	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	31-34
14752912-4	2004	Current chemotherapy of choice is CHOP [Cyclophosphamide, Hydroxydaunomycin (doxorubicin), Oncovin (vincristine sulfate) and Prednisone].	Cyclophosphamide	40-56	DNA damage inducible transcript 3	Homo sapiens	34-38
14712306-11	2004	RT-PCR analysis revealed that CPA administration resulted in impaired mRNA production by peripheral blood mononuclear cells (PBMCs) of several cytokines (interferons alpha/beta, interferon gamma, TNFalpha, IL-15, and IL-18) with anti-HSV function.	Cyclophosphamide	30-33	tumor necrosis factor	Homo sapiens	196-204
14712306-11	2004	RT-PCR analysis revealed that CPA administration resulted in impaired mRNA production by peripheral blood mononuclear cells (PBMCs) of several cytokines (interferons alpha/beta, interferon gamma, TNFalpha, IL-15, and IL-18) with anti-HSV function.	Cyclophosphamide	30-33	interleukin 15	Homo sapiens	206-211
14712306-11	2004	RT-PCR analysis revealed that CPA administration resulted in impaired mRNA production by peripheral blood mononuclear cells (PBMCs) of several cytokines (interferons alpha/beta, interferon gamma, TNFalpha, IL-15, and IL-18) with anti-HSV function.	Cyclophosphamide	30-33	interleukin 18	Homo sapiens	217-222
14979480-1	2004	The present study was performed to examine whether the expression of CD64 Fc gamma receptor type I (FcgammaRI) on both neutrophils and monocytes can be modulated by multiple daily administrations of granulocyte colony-stimulating factor (G-CSF) to patients with non-Hodgkin"s lymphoma in neutropenia caused by CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisone) chemotherapy.	Cyclophosphamide	316-332	Fc gamma receptor Ia	Homo sapiens	69-110
14979480-1	2004	The present study was performed to examine whether the expression of CD64 Fc gamma receptor type I (FcgammaRI) on both neutrophils and monocytes can be modulated by multiple daily administrations of granulocyte colony-stimulating factor (G-CSF) to patients with non-Hodgkin"s lymphoma in neutropenia caused by CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisone) chemotherapy.	Cyclophosphamide	316-332	colony stimulating factor 3	Homo sapiens	199-236
14979480-1	2004	The present study was performed to examine whether the expression of CD64 Fc gamma receptor type I (FcgammaRI) on both neutrophils and monocytes can be modulated by multiple daily administrations of granulocyte colony-stimulating factor (G-CSF) to patients with non-Hodgkin"s lymphoma in neutropenia caused by CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisone) chemotherapy.	Cyclophosphamide	316-332	colony stimulating factor 3	Homo sapiens	238-243
15648440-4	2004	As TNF-alpha has been shown to play a central pathogenic role in vasculitis as well as in crescentic glomerulonephritis, anti-TNF-alpha treatment in combination with cyclophosphamide has been found to be effective in therapy-resistant vasculitis.	Cyclophosphamide	166-182	tumor necrosis factor	Homo sapiens	3-12
15648440-4	2004	As TNF-alpha has been shown to play a central pathogenic role in vasculitis as well as in crescentic glomerulonephritis, anti-TNF-alpha treatment in combination with cyclophosphamide has been found to be effective in therapy-resistant vasculitis.	Cyclophosphamide	166-182	tumor necrosis factor	Homo sapiens	126-135
14698862-0	2004	Cyclophosphamide modulates CD4+ T cells into a T helper type 2 phenotype and reverses increased IFN-gamma production of CD8+ T cells in secondary progressive multiple sclerosis.	Cyclophosphamide	0-16	CD4 molecule	Homo sapiens	27-30
14698862-0	2004	Cyclophosphamide modulates CD4+ T cells into a T helper type 2 phenotype and reverses increased IFN-gamma production of CD8+ T cells in secondary progressive multiple sclerosis.	Cyclophosphamide	0-16	interferon gamma	Homo sapiens	96-105
14698862-0	2004	Cyclophosphamide modulates CD4+ T cells into a T helper type 2 phenotype and reverses increased IFN-gamma production of CD8+ T cells in secondary progressive multiple sclerosis.	Cyclophosphamide	0-16	CD8a molecule	Homo sapiens	120-123
14698862-9	2004	We report here that in patients with secondary progressive MS, cyclophosphamide induces a marked increase in the percentage of CCR4(+) T cells that produce high levels of IL-4 and reverses the increase in the percentages of IFN-gamma-producing CCR5(+) and CXCR3(+) CD8(+) T cells.	Cyclophosphamide	63-79	C-C motif chemokine receptor 4	Homo sapiens	127-131
14698862-9	2004	We report here that in patients with secondary progressive MS, cyclophosphamide induces a marked increase in the percentage of CCR4(+) T cells that produce high levels of IL-4 and reverses the increase in the percentages of IFN-gamma-producing CCR5(+) and CXCR3(+) CD8(+) T cells.	Cyclophosphamide	63-79	interleukin 4	Homo sapiens	171-175
14698862-9	2004	We report here that in patients with secondary progressive MS, cyclophosphamide induces a marked increase in the percentage of CCR4(+) T cells that produce high levels of IL-4 and reverses the increase in the percentages of IFN-gamma-producing CCR5(+) and CXCR3(+) CD8(+) T cells.	Cyclophosphamide	63-79	interferon gamma	Homo sapiens	224-233
14698862-9	2004	We report here that in patients with secondary progressive MS, cyclophosphamide induces a marked increase in the percentage of CCR4(+) T cells that produce high levels of IL-4 and reverses the increase in the percentages of IFN-gamma-producing CCR5(+) and CXCR3(+) CD8(+) T cells.	Cyclophosphamide	63-79	C-C motif chemokine receptor 5	Homo sapiens	244-248
14698862-9	2004	We report here that in patients with secondary progressive MS, cyclophosphamide induces a marked increase in the percentage of CCR4(+) T cells that produce high levels of IL-4 and reverses the increase in the percentages of IFN-gamma-producing CCR5(+) and CXCR3(+) CD8(+) T cells.	Cyclophosphamide	63-79	C-X-C motif chemokine receptor 3	Homo sapiens	256-261
14698862-9	2004	We report here that in patients with secondary progressive MS, cyclophosphamide induces a marked increase in the percentage of CCR4(+) T cells that produce high levels of IL-4 and reverses the increase in the percentages of IFN-gamma-producing CCR5(+) and CXCR3(+) CD8(+) T cells.	Cyclophosphamide	63-79	CD8a molecule	Homo sapiens	265-268
14698862-10	2004	Furthermore, therapy with cyclophosphamide increases IL-4-producing CD4(+) T cells and reverses the increase in IFN-gamma-producing CD8(+) T cells.	Cyclophosphamide	26-42	interleukin 4	Homo sapiens	53-57
14698862-10	2004	Furthermore, therapy with cyclophosphamide increases IL-4-producing CD4(+) T cells and reverses the increase in IFN-gamma-producing CD8(+) T cells.	Cyclophosphamide	26-42	CD4 molecule	Homo sapiens	68-71
14698862-10	2004	Furthermore, therapy with cyclophosphamide increases IL-4-producing CD4(+) T cells and reverses the increase in IFN-gamma-producing CD8(+) T cells.	Cyclophosphamide	26-42	interferon gamma	Homo sapiens	112-121
14698862-10	2004	Furthermore, therapy with cyclophosphamide increases IL-4-producing CD4(+) T cells and reverses the increase in IFN-gamma-producing CD8(+) T cells.	Cyclophosphamide	26-42	CD8a molecule	Homo sapiens	132-135
15579918-6	2004	A 1 d treatment of PC-3 cells with Cytoxan followed the next day with MR1 was significantly more effective (p <0.0001).	Cyclophosphamide	35-42	chromobox 8	Homo sapiens	19-23
15579918-6	2004	A 1 d treatment of PC-3 cells with Cytoxan followed the next day with MR1 was significantly more effective (p <0.0001).	Cyclophosphamide	35-42	major histocompatibility complex, class I-related	Homo sapiens	70-73
14506259-8	2003	When linked to a suboptimal phosphorylation site sequence (Lys+2 --> Pro) the Cy motif increases catalytic efficiency (kcat/Km) by increasing affinity without affecting turnover (kcat).	Cyclophosphamide	81-83	aminoadipate-semialdehyde dehydrogenase	Homo sapiens	59-64
14695163-5	2003	Recent studies using the cytochrome P-450 prodrug cyclophosphamide exemplify how the antiapoptotic, caspase-inhibitory baculovirus protein p35 can be combined with P-450 gene-directed enzyme prodrug therapy to prolong localized, intratumoral production of cytotoxic drug metabolites without inducing tumor cell drug resistance.	Cyclophosphamide	50-66	interleukin 12A	Homo sapiens	139-142
14693069-6	2003	In Group C, 60 patients received adjuvant chemotherapy with standard regimen [cyclophosphamide (CTX) 600 mg/m(2) d1+Adriamycin (ADM) 40 mg/m(2) d1 + cisplatin (DDP) 20 mg/m(2) d1-5).	Cyclophosphamide	78-94	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	96-99
14671431-5	2003	However, cisplatin, 5-FU and cyclophosphamide are not P-gp substrates, yet cisplatin, 5-FU and possibly cyclophosphamide are purported substrates for multidrug resistance proteins (MRPs) 1 and 2 (known to cause chemotherapy resistance).	Cyclophosphamide	104-120	ATP binding cassette subfamily B member 1	Homo sapiens	150-194
14578179-1	2003	Our effort to identify novel drug-resistant genes in cyclophosphamide-resistant EMT6 mouse mammary tumors led us to the identification of SPF45.	Cyclophosphamide	53-69	RNA binding motif protein 17	Homo sapiens	138-143
14679052-8	2003	In the cyclophosphamide group, Fas expression in intra-islet CD4 and CD8 cells showed an increase close to the onset of diabetes.	Cyclophosphamide	7-23	CD4 antigen	Mus musculus	61-64
12942200-3	2003	The alkylating agent cyclophosphamide (Cytoxan; CYC) has been used for many years to inhibit tumor-derived suppressor influences in rodents, and has been exploited for the same use in humans.	Cyclophosphamide	21-37	cytochrome c, somatic	Homo sapiens	48-51
12942200-3	2003	The alkylating agent cyclophosphamide (Cytoxan; CYC) has been used for many years to inhibit tumor-derived suppressor influences in rodents, and has been exploited for the same use in humans.	Cyclophosphamide	39-46	cytochrome c, somatic	Homo sapiens	48-51
12844214-6	2003	The expression of mdr1a, mdr1b, and CY3A2 mRNAs, and the levels of the corresponding proteins in the liver were increased after the CPA treatment.	Cyclophosphamide	132-135	ATP binding cassette subfamily B member 1A	Rattus norvegicus	18-23
14672398-0	2003	E2F1 expression is related with the poor survival of lymph node-positive breast cancer patients treated with fluorouracil, doxorubicin and cyclophosphamide.	Cyclophosphamide	139-155	E2F transcription factor 1	Homo sapiens	0-4
14556916-11	2003	Furthermore, since systematic dose reduction can impact on outcome, primary prophylactic use of G-CSF for all elderly patients receiving curative myelotoxic chemotherapy (cyclophosphamide, doxorubicin, vincristine and prednisolone (CHOP) or CHOP-like) is indicated and we suggest a risk-adapted strategy with primary prophylactic G-CSF administration in high-risk patients.	Cyclophosphamide	171-187	colony stimulating factor 3	Homo sapiens	96-101
12844214-6	2003	The expression of mdr1a, mdr1b, and CY3A2 mRNAs, and the levels of the corresponding proteins in the liver were increased after the CPA treatment.	Cyclophosphamide	132-135	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	25-30
12844214-8	2003	Thus, our results indicate that the decrease of blood CyA concentration induced is a consequence of the induction of P-glycoprotein and CYP3A in the liver by the CPA treatment, and these changes are reversed within 2 weeks after the transplantation.	Cyclophosphamide	162-165	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	136-141
12740217-6	2003	In further experiments, the addition of cyclophosphamide (which is known to cause severe injury to the alveolar epithelium in donor T cell-recipient mice) to the conditioning regimen prevented rHuKGF-induced upregulation of SP-A and suppression of lung inflammation in both SP-A(+/+) and SP-A(-/-) mice.	Cyclophosphamide	40-56	surfactant associated protein A1	Mus musculus	224-228
12946859-3	2003	The aim of this present study was to evaluate the effects of LF on humoral responses in mice treated with cyclophosphamide.	Cyclophosphamide	106-122	lactotransferrin	Mus musculus	61-63
14558094-10	2003	Successful cyclophosphamide treatment of CNS lupus resulted in significantly decreased levels of both proteins; levels of GFAP reached those observed in healthy subjects.	Cyclophosphamide	11-27	glial fibrillary acidic protein	Homo sapiens	122-126
14651772-10	2003	Patients treated with AC with intensified doses of cyclophosphamide requiring G-CSF support had increased rates of treatment-related AML/MDS, even though the incidence was slight relative to breast cancer relapse.	Cyclophosphamide	51-67	colony stimulating factor 3	Homo sapiens	78-83
14513044-1	2003	For the last decade, cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) has been the best available standard of care for aggressive non-Hodgkin"s lymphoma (NHL), based on equivalent therapeutic results with other multiagent chemotherapy accompanied by lower costs and lesser toxicity.	Cyclophosphamide	21-37	DNA damage inducible transcript 3	Homo sapiens	81-85
14515060-11	2003	The role of this allele should also be studied in other CYP2B6 substrates, including cyclophosphamide, halothane, mianserin, promethazine and propofol.	Cyclophosphamide	85-101	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	56-62
14598658-11	2003	Methylprednisolone pulse therapy followed by intravenous cyclophosphamide pulse therapy improved his clinical conditions such as pyrexia, cough, myalgia, episcleritis and respiratory symptoms with decreased titer of serum MPO-ANCA.	Cyclophosphamide	57-73	myeloperoxidase	Homo sapiens	222-225
14561896-4	2003	Increases in circulating TSP-1 were also detected in the plasma of human tumor-bearing severe combined immunodeficient mice treated with metronomic low-dose cyclophosphamide.	Cyclophosphamide	157-173	thrombospondin 1	Homo sapiens	25-30
14561896-5	2003	Most importantly, the antiangiogenic and antitumor effects of low-dose continuous cyclophosphamide were lost in TSP-1-null C57BL/6 mice, whereas, in contrast, these effects were retained by using a MTD schedule of the same drug.	Cyclophosphamide	82-98	tumor suppressor region 1	Mus musculus	112-117
14556668-8	2003	We also demonstrated that Th1-cell therapy is greatly augmented by combination therapy with cyclophosphamide treatment.	Cyclophosphamide	92-108	negative elongation factor complex member C/D, Th1l	Mus musculus	26-29
12740217-6	2003	In further experiments, the addition of cyclophosphamide (which is known to cause severe injury to the alveolar epithelium in donor T cell-recipient mice) to the conditioning regimen prevented rHuKGF-induced upregulation of SP-A and suppression of lung inflammation in both SP-A(+/+) and SP-A(-/-) mice.	Cyclophosphamide	40-56	surfactant associated protein A1	Mus musculus	274-278
12740217-6	2003	In further experiments, the addition of cyclophosphamide (which is known to cause severe injury to the alveolar epithelium in donor T cell-recipient mice) to the conditioning regimen prevented rHuKGF-induced upregulation of SP-A and suppression of lung inflammation in both SP-A(+/+) and SP-A(-/-) mice.	Cyclophosphamide	40-56	surfactant associated protein A1	Mus musculus	274-278
14581895-1	2003	BACKGROUND: Six to eight cycles of CHOP therapy (cyclophosphamide, doxorubicin, vincristine, and prednisone) is standard for intermediate-grade non-Hodgkin"s lymphoma (NHL) but is associated with toxicity that may cause premature termination of therapy.	Cyclophosphamide	49-65	DNA damage inducible transcript 3	Homo sapiens	35-39
14994920-6	2003	Using Carboplatin with G-CSF and Cyclophosphamide with G-CSF we collected respectively a median value of 6.75 and 7.3 x 10(6) CD34+ cells/kg.	Cyclophosphamide	33-49	colony stimulating factor 3	Homo sapiens	55-60
12915593-1	2003	PURPOSE: To investigate whether the relative dose-intensity of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy could be improved by prophylactic administration of granulocyte colony-stimulating factor (G-CSF) in elderly patients with aggressive non-Hodgkin"s lymphoma (NHL).	Cyclophosphamide	63-79	DNA damage inducible transcript 3	Homo sapiens	123-127
12966906-7	2003	Trastuzumab has significant activity against HER-2-positive breast cancer, especially in combination with paclitaxel or an anthracycline and cyclophosphamide.	Cyclophosphamide	141-157	erb-b2 receptor tyrosine kinase 2	Homo sapiens	45-50
12915593-1	2003	PURPOSE: To investigate whether the relative dose-intensity of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy could be improved by prophylactic administration of granulocyte colony-stimulating factor (G-CSF) in elderly patients with aggressive non-Hodgkin"s lymphoma (NHL).	Cyclophosphamide	63-79	colony stimulating factor 3	Homo sapiens	194-231
12907602-2	2003	Here we show that the administration of cyclophosphamide (CTX) at the maximum tolerable dose with 21-day breaks or at more frequent low-dose (metronomic) schedules have opposite effects on the mobilization and viability of circulating endothelial progenitors (CEPs) in immunodeficient mice bearing human lymphoma cells.	Cyclophosphamide	40-56	V-set and immunoglobulin domain containing 2	Mus musculus	58-61
12902896-4	2003	We report a patient with lymphoma refractory to treatment with cyclophosphamide, vincristine, and prednisone, who was successfully treated with rituximab, a CD-20 monoclonal antibody.	Cyclophosphamide	63-79	keratin 20	Homo sapiens	157-162
12951753-7	2003	Trastuzumab has significant activity against HER-2-positive breast cancer, especially in combination with paclitaxel or an anthracycline and cyclophosphamide.	Cyclophosphamide	141-157	erb-b2 receptor tyrosine kinase 2	Homo sapiens	45-50
12872138-0	2003	Sustained P450 expression and prodrug activation in bolus cyclophosphamide-treated cultured tumor cells.	Cyclophosphamide	58-74	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	10-14
12872138-2	2003	Cytochrome P450-based gene therapy can substantially increase the sensitivity of tumor cells to P450-activated cancer chemotherapeutic prodrugs such as cyclophosphamide (CPA) without increasing host toxicity.	Cyclophosphamide	152-168	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	11-15
12872138-2	2003	Cytochrome P450-based gene therapy can substantially increase the sensitivity of tumor cells to P450-activated cancer chemotherapeutic prodrugs such as cyclophosphamide (CPA) without increasing host toxicity.	Cyclophosphamide	152-168	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	96-100
12955576-4	2003	A recent European phase III study in elderly patients with untreated diffuse large B-cell lymphoma suggested that rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) chemotherapy is superior to CHOP chemotherapy alone in terms of complete response rate and event-free and overall survivals.	Cyclophosphamide	129-145	DNA damage inducible transcript 3	Homo sapiens	191-195
12872138-2	2003	Cytochrome P450-based gene therapy can substantially increase the sensitivity of tumor cells to P450-activated cancer chemotherapeutic prodrugs such as cyclophosphamide (CPA) without increasing host toxicity.	Cyclophosphamide	170-173	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	11-15
12872138-2	2003	Cytochrome P450-based gene therapy can substantially increase the sensitivity of tumor cells to P450-activated cancer chemotherapeutic prodrugs such as cyclophosphamide (CPA) without increasing host toxicity.	Cyclophosphamide	170-173	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	96-100
12872138-4	2003	The present study addresses this question and characterizes the impact of CPA dose and treatment schedule on the ability of P450-expressing tumor cells to sustain prodrug activation over time.	Cyclophosphamide	74-77	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	124-128
12872138-5	2003	9L gliosarcoma cells expressing human P450 2B6 and treated with CPA in a continuous manner exhibited a time- and CPA dose-dependent decrease in P450-catalyzed CPA 4-hydroxylase activity.	Cyclophosphamide	64-67	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	38-42
12872138-5	2003	9L gliosarcoma cells expressing human P450 2B6 and treated with CPA in a continuous manner exhibited a time- and CPA dose-dependent decrease in P450-catalyzed CPA 4-hydroxylase activity.	Cyclophosphamide	64-67	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	144-148
12872138-5	2003	9L gliosarcoma cells expressing human P450 2B6 and treated with CPA in a continuous manner exhibited a time- and CPA dose-dependent decrease in P450-catalyzed CPA 4-hydroxylase activity.	Cyclophosphamide	64-67	carboxypeptidase A4	Homo sapiens	159-164
12872138-5	2003	9L gliosarcoma cells expressing human P450 2B6 and treated with CPA in a continuous manner exhibited a time- and CPA dose-dependent decrease in P450-catalyzed CPA 4-hydroxylase activity.	Cyclophosphamide	113-116	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	38-42
12872138-5	2003	9L gliosarcoma cells expressing human P450 2B6 and treated with CPA in a continuous manner exhibited a time- and CPA dose-dependent decrease in P450-catalyzed CPA 4-hydroxylase activity.	Cyclophosphamide	113-116	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	144-148
12872138-5	2003	9L gliosarcoma cells expressing human P450 2B6 and treated with CPA in a continuous manner exhibited a time- and CPA dose-dependent decrease in P450-catalyzed CPA 4-hydroxylase activity.	Cyclophosphamide	113-116	carboxypeptidase A4	Homo sapiens	159-164
12872138-7	2003	By contrast, when the P450-expressing tumor cells were treated with CPA as a single 8 hours exposure, cellular CPA 4-hydroxylase activity and P450 protein expression were substantially prolonged when compared to continuous prodrug treatment.	Cyclophosphamide	68-71	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	22-26
12872138-7	2003	By contrast, when the P450-expressing tumor cells were treated with CPA as a single 8 hours exposure, cellular CPA 4-hydroxylase activity and P450 protein expression were substantially prolonged when compared to continuous prodrug treatment.	Cyclophosphamide	68-71	carboxypeptidase A4	Homo sapiens	111-116
12872138-7	2003	By contrast, when the P450-expressing tumor cells were treated with CPA as a single 8 hours exposure, cellular CPA 4-hydroxylase activity and P450 protein expression were substantially prolonged when compared to continuous prodrug treatment.	Cyclophosphamide	68-71	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	142-146
12872138-8	2003	This schedule-dependent effect of CPA was influenced by the level of P450 protein expressed in the tumor cells.	Cyclophosphamide	34-37	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	69-73
12872138-11	2003	These findings demonstrate the impact of CPA dose and treatment schedule on the efficacy of P450 gene-directed enzyme prodrug therapy, with bolus CPA treatment being compatible with sustained expression of P450 protein and maintenance of P450-dependent prodrug activation by the target tumor tissue.	Cyclophosphamide	41-44	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	92-96
12872138-11	2003	These findings demonstrate the impact of CPA dose and treatment schedule on the efficacy of P450 gene-directed enzyme prodrug therapy, with bolus CPA treatment being compatible with sustained expression of P450 protein and maintenance of P450-dependent prodrug activation by the target tumor tissue.	Cyclophosphamide	146-149	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	92-96
12872138-11	2003	These findings demonstrate the impact of CPA dose and treatment schedule on the efficacy of P450 gene-directed enzyme prodrug therapy, with bolus CPA treatment being compatible with sustained expression of P450 protein and maintenance of P450-dependent prodrug activation by the target tumor tissue.	Cyclophosphamide	146-149	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	206-210
12872138-11	2003	These findings demonstrate the impact of CPA dose and treatment schedule on the efficacy of P450 gene-directed enzyme prodrug therapy, with bolus CPA treatment being compatible with sustained expression of P450 protein and maintenance of P450-dependent prodrug activation by the target tumor tissue.	Cyclophosphamide	146-149	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	206-210
12879463-10	2003	Stratifying patients on the basis of the type of adjuvant therapy given, high syndecan-1 expression was associated with a higher risk of death only in patients treated with the cyclophosphamide-methotrexate-fluorouracil regimen (HR, 1.9; P = 0.09); at multivariate analysis for OS, this association proved to be of independent statistical significance (P = 0.03; HR, 2.15).	Cyclophosphamide	177-193	syndecan 1	Homo sapiens	78-88
12912950-6	2003	However, the variant (C) hMSH2 allele was significantly overrepresented in t-AML cases that had previously been treated with O(6)-guanine alkylating agents, including cyclophosphamide and procarbazine, compared with controls (odds ratio, 4.02; 95% confidence interval, 1.40-11.37).	Cyclophosphamide	167-183	mutS homolog 2	Homo sapiens	25-30
12882912-5	2003	TRAIL blockade exacerbates the onset of type 1 diabetes in NOD.Scid recipients of transferred diabetogenic T-cells and in cyclophosphamide-treated NOD mice.	Cyclophosphamide	122-138	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	0-5
12955576-4	2003	A recent European phase III study in elderly patients with untreated diffuse large B-cell lymphoma suggested that rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) chemotherapy is superior to CHOP chemotherapy alone in terms of complete response rate and event-free and overall survivals.	Cyclophosphamide	129-145	DNA damage inducible transcript 3	Homo sapiens	225-229
12906019-2	2003	The first-line treatment for diffuse large-B-cell non Hodgkin"s lymphoma, a highly malignant lymphoma, is CHOP chemotherapy (cyclophosphamide + doxorubicin + vincristine + prednisone).	Cyclophosphamide	125-141	DNA damage inducible transcript 3	Homo sapiens	106-110
12832108-4	2003	MP-1 enhances a decreased level of antibody production in cyclophosphamide (Cy)-treated mice, but does not influence the antibody formation in normal animals.	Cyclophosphamide	58-74	late endosomal/lysosomal adaptor, MAPK and MTOR activator 3	Mus musculus	0-4
12832108-4	2003	MP-1 enhances a decreased level of antibody production in cyclophosphamide (Cy)-treated mice, but does not influence the antibody formation in normal animals.	Cyclophosphamide	76-78	late endosomal/lysosomal adaptor, MAPK and MTOR activator 3	Mus musculus	0-4
12956443-10	2003	In this study, the t(11;16) was seen in 2 patients with previous lymphomas treated with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP).	Cyclophosphamide	88-104	DNA damage inducible transcript 3	Homo sapiens	148-152
12764549-9	2003	Cyclophosphamide, hydroxydaunomycin, vincristine, and prednisone (CHOP)-like chemotherapy with or without local irradiation led to 17% relapses in patients with localized aggressive lymphoma.	Cyclophosphamide	0-16	DNA damage inducible transcript 3	Homo sapiens	66-70
17472258-2	2003	PATIENTS AND METHODS: From January 1998 to December 2002, 10 heavily pretreated patients with CTCL, hospitalized at the Department of Dermatology in Wroclaw, were administered monotherapy with 2-CdA (6 patients) or FAMP plus CY combination chemotherapy (4 patients).	Cyclophosphamide	225-227	TSPY like 2	Homo sapiens	94-98
12820293-15	2003	This was further supported by our observation of a significant enhancement of tumor necrosis factor-alpha (TNF-alpha) production by peritoneal macrophage"s in CPA treated mice.	Cyclophosphamide	159-162	tumor necrosis factor	Mus musculus	78-105
12820293-15	2003	This was further supported by our observation of a significant enhancement of tumor necrosis factor-alpha (TNF-alpha) production by peritoneal macrophage"s in CPA treated mice.	Cyclophosphamide	159-162	tumor necrosis factor	Mus musculus	107-116
12817034-10	2003	These findings suggest that costimulatory blockade together with cyclophosphamide influence the activation state of renal CD11c-positive cells and therefore lead to less B and T cell infiltration and nephritis.	Cyclophosphamide	65-81	integrin subunit alpha X	Homo sapiens	122-127
14653077-5	2003	The CR rate and 5-year survival rate of patients who were treated by the scheme of doxorubicin, cyclophosphamide, vincristine and prednisone (CHOP) were higher than those treated by the scheme of cyclophosphamide, vincristine, prednisone and etoposide (COP + VP16) (P < 0.05).	Cyclophosphamide	96-112	DNA damage inducible transcript 3	Homo sapiens	142-146
12931670-4	2003	Prior to pathological diagnosis, CHOP therapy with cyclophosphamide, adriamycin, vincristine and prednisolone was performed under mechanical ventilation for the purpose of resuscitation.	Cyclophosphamide	51-67	DNA damage inducible transcript 3	Homo sapiens	33-37
12684728-2	2003	The aim of this study was to investigate the contribution of CYP2C9 and CYP2C19 and their polymorphisms to the variability of cyclophosphamide activation.	Cyclophosphamide	126-142	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
12684728-2	2003	The aim of this study was to investigate the contribution of CYP2C9 and CYP2C19 and their polymorphisms to the variability of cyclophosphamide activation.	Cyclophosphamide	126-142	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	72-79
12684728-4	2003	The kinetic data obtained in the yeast system revealed that the intrinsic clearance (V(max)/K(m)) of cyclophosphamide by CYP2C9.2 and CYP2C9.3 samples was approximately threefold lower than that by CYP2C9.1.	Cyclophosphamide	101-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	121-127
12684728-4	2003	The kinetic data obtained in the yeast system revealed that the intrinsic clearance (V(max)/K(m)) of cyclophosphamide by CYP2C9.2 and CYP2C9.3 samples was approximately threefold lower than that by CYP2C9.1.	Cyclophosphamide	101-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	134-140
12684728-4	2003	The kinetic data obtained in the yeast system revealed that the intrinsic clearance (V(max)/K(m)) of cyclophosphamide by CYP2C9.2 and CYP2C9.3 samples was approximately threefold lower than that by CYP2C9.1.	Cyclophosphamide	101-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	134-140
12684728-6	2003	We found a statistically significant correlation ( r(s)=0.65, P=0.003) between 4-hydroxylation of cyclophosphamide and 5"-hydroxylation of R-omeprazole, a measure of CYP2C19 activity in human liver microsomes ( n=19).	Cyclophosphamide	98-114	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	166-173
12684728-8	2003	In conclusion, based on the correlation with the formation of R-5"-hydroxyomeprazole, CYP2C19 may partly contribute to the bioactivation of cyclophosphamide in human liver microsomes, while the role of CYP2C9 appears minor.	Cyclophosphamide	140-156	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	86-93
12852361-0	2003	[A case of recurrent breast cancer with lung metastasis and overexpression of HER2 that responded to UFT and cyclophosphamide combination therapy after sequential treatments with epirubicin, taxanes, and trastuzumab].	Cyclophosphamide	109-125	erb-b2 receptor tyrosine kinase 2	Homo sapiens	78-82
12852361-6	2003	We regard combination therapy with oral UFT and cyclophosphamide to be useful for the management of metastatic breast cancer, even in heavily pretreated cases with overexpression of HER2.	Cyclophosphamide	48-64	erb-b2 receptor tyrosine kinase 2	Homo sapiens	182-186
12802593-0	2003	Immunohistochemical study of caspase-3-expressing cells within the pancreas of non-obese diabetic mice during cyclophosphamide-accelerated diabetes.	Cyclophosphamide	110-126	caspase 3	Mus musculus	29-38
12802593-4	2003	Here dual-label immunohistochemistry was employed to examine the intra-islet expression, distribution and cellular sources of active caspase-3 in the non-obese diabetic (NOD) mouse given cyclophosphamide to accelerate diabetes.	Cyclophosphamide	187-203	caspase 3	Mus musculus	133-142
12802593-18	2003	We conclude that during cyclophosphamide-accelerated diabetes in the NOD mouse, the predominant immunolabelling of caspase-3 in intra-islet macrophages suggests that apoptosis of macrophages may be an important mechanism for its elimination.	Cyclophosphamide	24-40	caspase 3	Mus musculus	115-124
14653077-5	2003	The CR rate and 5-year survival rate of patients who were treated by the scheme of doxorubicin, cyclophosphamide, vincristine and prednisone (CHOP) were higher than those treated by the scheme of cyclophosphamide, vincristine, prednisone and etoposide (COP + VP16) (P < 0.05).	Cyclophosphamide	96-112	caspase recruitment domain family member 16	Homo sapiens	253-256
12707721-2	2003	During pregnancy chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) stabilized the disease for 4 months before new manifestations appeared.	Cyclophosphamide	35-51	DNA damage inducible transcript 3	Homo sapiens	95-99
12531794-1	2003	This study was designed to test the hypothesis that administration of granulocyte colony-stimulating factor (G-CSF; filgrastim) during induction chemotherapy with CHOP (cyclophosphamide, vincristine, doxorubicin, prednisone) or CNOP (doxorubicin replaced with mitoxantrone) in elderly patients with aggressive non-Hodgkin lymphoma (NHL) improves time to treatment failure (TTF), complete remission (CR) rate, and overall survival (OS).	Cyclophosphamide	169-185	colony stimulating factor 3	Homo sapiens	70-107
12531794-1	2003	This study was designed to test the hypothesis that administration of granulocyte colony-stimulating factor (G-CSF; filgrastim) during induction chemotherapy with CHOP (cyclophosphamide, vincristine, doxorubicin, prednisone) or CNOP (doxorubicin replaced with mitoxantrone) in elderly patients with aggressive non-Hodgkin lymphoma (NHL) improves time to treatment failure (TTF), complete remission (CR) rate, and overall survival (OS).	Cyclophosphamide	169-185	colony stimulating factor 3	Homo sapiens	109-114
12732880-5	2003	However, in the stratum of patients who had previously received more than two lines of chemotherapy, CD34+cell peak (P=0.05) and percentage of successful mobilization (P=0.01) were higher when "cyclophosphamide plus G-CSF" was used.	Cyclophosphamide	194-210	CD34 molecule	Homo sapiens	101-105
12894554-5	2003	The response of xenografted ALL toward vincristine and cyclophosphamide was inversely correlated with the expression of P-gp, LRP and MRP1 (R2 = 0.71, 0.70 and 0.64 for vincristine and 0.44, 0.70 and 0.60 for cyclophosphamide).	Cyclophosphamide	55-71	phosphoglycolate phosphatase	Homo sapiens	120-124
12894554-5	2003	The response of xenografted ALL toward vincristine and cyclophosphamide was inversely correlated with the expression of P-gp, LRP and MRP1 (R2 = 0.71, 0.70 and 0.64 for vincristine and 0.44, 0.70 and 0.60 for cyclophosphamide).	Cyclophosphamide	55-71	major vault protein	Homo sapiens	126-129
12894554-5	2003	The response of xenografted ALL toward vincristine and cyclophosphamide was inversely correlated with the expression of P-gp, LRP and MRP1 (R2 = 0.71, 0.70 and 0.64 for vincristine and 0.44, 0.70 and 0.60 for cyclophosphamide).	Cyclophosphamide	55-71	ATP binding cassette subfamily C member 1	Homo sapiens	134-138
12894554-5	2003	The response of xenografted ALL toward vincristine and cyclophosphamide was inversely correlated with the expression of P-gp, LRP and MRP1 (R2 = 0.71, 0.70 and 0.64 for vincristine and 0.44, 0.70 and 0.60 for cyclophosphamide).	Cyclophosphamide	209-225	phosphoglycolate phosphatase	Homo sapiens	120-124
12894554-5	2003	The response of xenografted ALL toward vincristine and cyclophosphamide was inversely correlated with the expression of P-gp, LRP and MRP1 (R2 = 0.71, 0.70 and 0.64 for vincristine and 0.44, 0.70 and 0.60 for cyclophosphamide).	Cyclophosphamide	209-225	ATP binding cassette subfamily C member 1	Homo sapiens	134-138
12797528-5	2003	CY induced a conspicuous upregulation of intercellular adhesion molecule-1 (ICAM-1) expression in the vascular endothelial cells, splenic marginal zone and thymic cortex.	Cyclophosphamide	0-2	intercellular adhesion molecule 1	Rattus norvegicus	41-74
12839696-1	2003	OBJECTIVE: To evaluate the efficacy and safety of the oral combination chemotherapy of furtulon (FTL) and cyclophosphamide (CTX) for advanced breast cancer (ABC).	Cyclophosphamide	106-122	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	124-127
12571232-1	2003	CYP2B6 plays an important role in the metabolism of a variety of structurally unrelated xenobiotics, including the anticancer drugs cyclophosphamide and ifosfamide.	Cyclophosphamide	132-148	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	0-6
12797528-5	2003	CY induced a conspicuous upregulation of intercellular adhesion molecule-1 (ICAM-1) expression in the vascular endothelial cells, splenic marginal zone and thymic cortex.	Cyclophosphamide	0-2	intercellular adhesion molecule 1	Rattus norvegicus	76-82
12655514-8	2003	However, in the lymph node negative population, the benefit of one course of perioperative chemotherapy with cyclophosphamide, methotrexate, and 5-fluorouracil was confined exclusively to patients with tumors that showed reduced p27 immunoreactivity (P = 0.03; test for interaction).	Cyclophosphamide	109-125	zinc ribbon domain containing 2	Homo sapiens	229-232
12646859-6	2003	Next, we showed that an adenovirus expressing the human cytochrome P450 (CYP2B6) regulated by the OBHRE promoter delays tumour growth in response to the prodrug cyclophosphamide (CPA).	Cyclophosphamide	161-177	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	73-79
12655533-1	2003	BACKGROUND: The objective of this study was to determine whether HER-2 overexpression is associated with improved response to neoadjuvant chemotherapy with 5-fluorouracil, doxorubicin, cyclophosphamide (FAC) in patients with breast carcinoma.	Cyclophosphamide	185-201	erb-b2 receptor tyrosine kinase 2	Homo sapiens	65-70
12646859-6	2003	Next, we showed that an adenovirus expressing the human cytochrome P450 (CYP2B6) regulated by the OBHRE promoter delays tumour growth in response to the prodrug cyclophosphamide (CPA).	Cyclophosphamide	179-182	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	73-79
12713714-3	2003	Since erythropoietic depression was elicited by cyclophosphamide administration, which could have altered EPO production directly, the aim of the present investigation was to estimate hypoxia-stimulated EPO secretion in a mouse model of functional depressed erythropoiesis induced by exposure to normobaric hyperoxia.	Cyclophosphamide	48-64	erythropoietin	Mus musculus	106-109
12663705-9	2003	In patients receiving two or four cycles of C at 2,400 mg/m(2) with granulocyte colony-stimulating factor (G-CSF) support, cumulative incidence of AML/MDS at 5 years was 1.01% (95% confidence interval [CI], 0.63% to 1.62%), compared with 0.21% (95% CI, 0.11% to 0.41%) for patients treated with standard AC.	Cyclophosphamide	44-45	colony stimulating factor 3	Homo sapiens	68-105
12663705-9	2003	In patients receiving two or four cycles of C at 2,400 mg/m(2) with granulocyte colony-stimulating factor (G-CSF) support, cumulative incidence of AML/MDS at 5 years was 1.01% (95% confidence interval [CI], 0.63% to 1.62%), compared with 0.21% (95% CI, 0.11% to 0.41%) for patients treated with standard AC.	Cyclophosphamide	44-45	colony stimulating factor 3	Homo sapiens	107-112
12663705-11	2003	CONCLUSION: AC regimens employing intensified doses of cyclophosphamide requiring G-CSF support were characterized by increased rates of subsequent AML/MDS, although the incidence of AML/MDS was small relative to that of breast cancer relapse.	Cyclophosphamide	55-71	colony stimulating factor 3	Homo sapiens	82-87
12730951-2	2003	In the present study, the effects of cyclophosphamide (Cp, a widely used alkylating agent) were monitored in a murine radiation induced fibrosarcoma (RIF-1) using in vivo (1)H NMR spectroscopy and imaging to evaluate the potential of these techniques towards early detection of treatment response.	Cyclophosphamide	37-53	replication timing regulatory factor 1	Mus musculus	150-155
12739762-0	2003	Induction of cytochrome P450 2B6 and 3A4 expression by phenobarbital and cyclophosphamide in cultured human liver slices.	Cyclophosphamide	73-89	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	13-32
12739762-4	2003	Then we tested the effects of phenobarbital and cyclophosphamide on CYP expression in both models.	Cyclophosphamide	48-64	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	68-71
12739762-8	2003	CYP2B6 and 3A4 mRNA, apoprotein, and enzyme-related activities were induced by phenobarbital and cyclophosphamide, whereas CYP2C9 apoprotein was not.	Cyclophosphamide	97-113	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	0-6
12802404-1	2003	Antitumor effect of cyclophosphamide on LS and P388 tumors is realized via apoptosis and on HA-1 and Krebs-2 tumors resistant to apoptosis via necrosis of tumor cells.	Cyclophosphamide	20-36	Rho GTPase activating protein 45	Mus musculus	92-96
12844025-2	2003	CASE REPORT: This case report describes acute respiratory distress syndrome, due to diffuse pneumonitis, in a patient with malignant non-Hodgkin"s lymphoma being treated with combination chemotherapy which included doxorubicin, cyclophosphamide, bleomycin, vindesin and intrathecal methotrexate with G-CSF (filgrastine- Neupogen).	Cyclophosphamide	228-244	colony stimulating factor 3	Homo sapiens	300-305
12565197-4	2003	The present study was performed to investigate whether inhibition of CYP2B1 reactions by BI could lead to an attenuation of cyclophosphamide (CP)-induced embryotoxicity in the rat.	Cyclophosphamide	124-140	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	69-75
12648379-4	2003	Immunosuppressive therapy with steroids, cyclophosphamide and methotrexate was required for relief of clinical symptoms and cANCA negativity as an expression of disease remission.	Cyclophosphamide	41-57	proteinase 3	Homo sapiens	124-129
12651270-15	2003	INTERPRETATION AND CONCLUSIONS: CD34+/ASCT using BCNU, Cy and ATG as conditioning regimen has an acceptable toxicity and clearly reduces the progression of MS. Further follow-up is necessary to establish the real impact of this procedure on the long-term evolution of the disease.	Cyclophosphamide	55-57	CD34 molecule	Homo sapiens	32-36
12516103-2	2003	A recently described polymorphism alters hepatic expression of GSTA1, a GST with high activity in glutathione conjugation of metabolites of cyclophosphamide (CP).	Cyclophosphamide	140-156	glutathione S-transferase alpha 1	Homo sapiens	63-68
12516103-2	2003	A recently described polymorphism alters hepatic expression of GSTA1, a GST with high activity in glutathione conjugation of metabolites of cyclophosphamide (CP).	Cyclophosphamide	140-156	glutathione S-transferase kappa 1	Homo sapiens	63-66
12788306-5	2003	RESULTS: MIF-mRNA expression was markedly increased in splenic lymphocytes of spontaneously diabetic NOD mice as well as in 8-week-old NOD mice treated with cyclophosphamide compared with 2-week-old non-diabetic NOD and healthy C57BL/6 control mice.	Cyclophosphamide	157-173	macrophage migration inhibitory factor (glycosylation-inhibiting factor)	Mus musculus	9-12
12655533-0	2003	Correlation between HER-2 expression and response to neoadjuvant chemotherapy with 5-fluorouracil, doxorubicin, and cyclophosphamide in patients with breast carcinoma.	Cyclophosphamide	116-132	erb-b2 receptor tyrosine kinase 2	Homo sapiens	20-25
12788306-6	2003	Western blot analyses showed decreased lymphocytic MIF-protein content in diabetic as well as in cyclophosphamide-treated animals compared with 2-week-old non-diabetic NOD and healthy C57BL/6 mice, probably as a consequence of increased protein secretion.	Cyclophosphamide	97-113	macrophage migration inhibitory factor (glycosylation-inhibiting factor)	Mus musculus	51-54
12478666-7	2003	The EL-4 responsiveness to the B7RP-1-Fc treatment was enhanced, however, by pre-treatment of the mice with cyclophosphamide.	Cyclophosphamide	108-124	epilepsy 4	Mus musculus	4-8
12478666-7	2003	The EL-4 responsiveness to the B7RP-1-Fc treatment was enhanced, however, by pre-treatment of the mice with cyclophosphamide.	Cyclophosphamide	108-124	icos ligand	Mus musculus	31-37
12388444-0	2003	COX-2 and prostanoid expression in micturition pathways after cyclophosphamide-induced cystitis in the rat.	Cyclophosphamide	62-78	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	0-5
12388444-1	2003	The purpose of this study was to determine the role of cyclooxygenase-2 (COX-2) and its metabolites in lower urinary tract function after induction of acute (4 h), intermediate (48 h), or chronic (10 day) cyclophosphamide (CYP)-induced cystitis.	Cyclophosphamide	205-221	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	55-71
12746660-6	2003	Treatment with high-dose corticosteroids and cyclophosphamide resulted in restoration of euglycemia associated with resolution of circulating anti-insulin antibodies and parallel improvement in clinical and laboratory features of SLE.	Cyclophosphamide	45-61	insulin	Homo sapiens	147-154
12576456-8	2003	However, in the subgroup of patients treated with anthracycline-based chemotherapy (5-fluorouracil, Adriamycin/epirubicin, and cyclophosphamide), a correlation between response and the expression of BCRP and MRP1 (only PFS) was found, whereas such an association was not present in the cyclophosphamide, methotrexate, and 5-fluorouracil-treated group of patients.	Cyclophosphamide	127-143	BCR pseudogene 1	Homo sapiens	199-203
12576456-10	2003	For lung resistance-related protein, this association was limited to 5-fluorouracil, Adriamycin/epirubicin, and cyclophosphamide.	Cyclophosphamide	112-128	major vault protein	Homo sapiens	4-35
12576456-8	2003	However, in the subgroup of patients treated with anthracycline-based chemotherapy (5-fluorouracil, Adriamycin/epirubicin, and cyclophosphamide), a correlation between response and the expression of BCRP and MRP1 (only PFS) was found, whereas such an association was not present in the cyclophosphamide, methotrexate, and 5-fluorouracil-treated group of patients.	Cyclophosphamide	127-143	ATP binding cassette subfamily C member 1	Homo sapiens	208-212
12576456-8	2003	However, in the subgroup of patients treated with anthracycline-based chemotherapy (5-fluorouracil, Adriamycin/epirubicin, and cyclophosphamide), a correlation between response and the expression of BCRP and MRP1 (only PFS) was found, whereas such an association was not present in the cyclophosphamide, methotrexate, and 5-fluorouracil-treated group of patients.	Cyclophosphamide	286-302	BCR pseudogene 1	Homo sapiens	199-203
12604187-2	2003	Among these enzymes, aldehyde dehydrogenase 3 (ALDH3) is considered a mechanism by which tumour cells evade the cytotoxic effects exerted by cyclophosphamide and drugs acting by free radical generation.	Cyclophosphamide	141-157	aldehyde dehydrogenase 3 family member A1	Homo sapiens	21-45
12604187-2	2003	Among these enzymes, aldehyde dehydrogenase 3 (ALDH3) is considered a mechanism by which tumour cells evade the cytotoxic effects exerted by cyclophosphamide and drugs acting by free radical generation.	Cyclophosphamide	141-157	aldehyde dehydrogenase 3 family member A1	Homo sapiens	47-52
12521569-9	2003	For diffuse large B-cell lymphoma, the most frequently diagnosed subtype of non-Hodgkin"s lymphoma (NHL), the CHOP regimen (cyclophosphamide, doxorubicin, vincristine, and prednisone) is still the gold standard.	Cyclophosphamide	124-140	DNA damage inducible transcript 3	Homo sapiens	110-114
12586609-1	2003	High-dose cyclophosphamide (CTX) is commonly used in preparation for autologous and allogeneic stem cell transplantation.	Cyclophosphamide	10-26	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	28-31
12529092-11	2003	After treatment with rituximab and cyclophosphamide, the disease remitted, ADAMTS13 levels normalized, and the inhibitor was undetectable.	Cyclophosphamide	35-51	ADAM metallopeptidase with thrombospondin type 1 motif 13	Homo sapiens	75-83
12662436-12	2003	There was an eight-fold increase in the SCF mRNA level in the bone marrow 2 days after cyclophosphamide, corresponding with a high proliferation rate of CFU-S. No significant changes in mRNAs for Flt-3 ligand and MIP-1 alpha have been found.	Cyclophosphamide	87-103	kit ligand	Mus musculus	40-43
12853690-0	2003	Intermediate-dose cyclophosphamide and granulocyte colony-stimulating factor is a valid alternative to high-dose cyclophosphamide for mobilizing peripheral blood CD34+ cells in patients with multiple myeloma.	Cyclophosphamide	18-34	CD34 molecule	Homo sapiens	162-166
12853690-0	2003	Intermediate-dose cyclophosphamide and granulocyte colony-stimulating factor is a valid alternative to high-dose cyclophosphamide for mobilizing peripheral blood CD34+ cells in patients with multiple myeloma.	Cyclophosphamide	113-129	CD34 molecule	Homo sapiens	162-166
12853690-3	2003	Cyclophosphamide (CTX) is an effective drug in the treatment of MM which is capable of mobilizing PBSC if followed by growth factors, even though administration of high-dose CTX (7 g/m(2)) results in severe toxicity requiring hospitalization and increasing costs.	Cyclophosphamide	0-16	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	18-21
12853690-3	2003	Cyclophosphamide (CTX) is an effective drug in the treatment of MM which is capable of mobilizing PBSC if followed by growth factors, even though administration of high-dose CTX (7 g/m(2)) results in severe toxicity requiring hospitalization and increasing costs.	Cyclophosphamide	0-16	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	174-177
12464259-4	2003	A strong NADPH- and liver microsome-dependent increase in 9L cytotoxicity was observed for the CYP prodrugs cyclophosphamide, ifosfamide, and methoxymorpholinyl doxorubicin (MMDX) but not with three other CYP prodrugs, procarbazine, dacarbazine, and tamoxifen.	Cyclophosphamide	108-124	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	95-98
14569871-0	2003	[Activity and induction of CYP2B, CYP2C, and CYP3A in tissues of cyclophosphane-sensitive and resistant neoplasms and the liver of neoplasm-carrying mice].	Cyclophosphamide	65-79	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	27-32
14569871-0	2003	[Activity and induction of CYP2B, CYP2C, and CYP3A in tissues of cyclophosphane-sensitive and resistant neoplasms and the liver of neoplasm-carrying mice].	Cyclophosphamide	65-79	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	34-39
14569871-0	2003	[Activity and induction of CYP2B, CYP2C, and CYP3A in tissues of cyclophosphane-sensitive and resistant neoplasms and the liver of neoplasm-carrying mice].	Cyclophosphamide	65-79	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	45-50
14569871-1	2003	The activities of three cytochrome P450 families involved in metabolic transformation of cyclophosphamide (CP) (CYP2B and CYP2C responsible for metabolic activation of CP and CYP3A responsible for inactivation of CP) have been investigated in lymphosarcoma and liver microsomes of tumor-bearing CBA mice.	Cyclophosphamide	89-105	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	112-117
14569871-1	2003	The activities of three cytochrome P450 families involved in metabolic transformation of cyclophosphamide (CP) (CYP2B and CYP2C responsible for metabolic activation of CP and CYP3A responsible for inactivation of CP) have been investigated in lymphosarcoma and liver microsomes of tumor-bearing CBA mice.	Cyclophosphamide	89-105	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	122-127
14569871-1	2003	The activities of three cytochrome P450 families involved in metabolic transformation of cyclophosphamide (CP) (CYP2B and CYP2C responsible for metabolic activation of CP and CYP3A responsible for inactivation of CP) have been investigated in lymphosarcoma and liver microsomes of tumor-bearing CBA mice.	Cyclophosphamide	89-105	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	175-180
12621490-1	2003	Cyclophosphamide with granulocyte colony stimulating factor (G-CSF) is commonly used to mobilize stem cells in multiple myeloma.	Cyclophosphamide	0-16	colony stimulating factor 3	Homo sapiens	22-59
12542495-10	2003	In addition, G-CSF administration to five lymphoma patients after consecutive courses of CHOP (cyclophosphamide, doxorubicin, vincristine, prednisone) chemotherapy, resulted in telomere length preservation or elongation, as opposed to marked attrition in patients who did not receive growth factors.	Cyclophosphamide	95-111	colony stimulating factor 3	Homo sapiens	13-18
12621490-1	2003	Cyclophosphamide with granulocyte colony stimulating factor (G-CSF) is commonly used to mobilize stem cells in multiple myeloma.	Cyclophosphamide	0-16	colony stimulating factor 3	Homo sapiens	61-66
14988743-10	2003	Impressive results have been seen in combination with CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine and prednisone) in follicular and high-grade lymphomas.	Cyclophosphamide	73-89	DNA damage inducible transcript 3	Homo sapiens	54-58
14499667-0	2003	Immunohistochemical detection of apoptosis, proliferation and inducible nitric oxide synthase in rat urothelium damaged by cyclophosphamide treatment.	Cyclophosphamide	123-139	nitric oxide synthase 2	Rattus norvegicus	62-93
14499667-1	2003	The present study was conducted to investigate cell death, proliferation and inducible nitric oxide synthase (iNOS) immunoreactivity in rat urothelium within 24 h after a single intraperitoneal dose of cyclophosphamide (CP).	Cyclophosphamide	202-218	nitric oxide synthase 2	Rattus norvegicus	77-108
14499667-1	2003	The present study was conducted to investigate cell death, proliferation and inducible nitric oxide synthase (iNOS) immunoreactivity in rat urothelium within 24 h after a single intraperitoneal dose of cyclophosphamide (CP).	Cyclophosphamide	202-218	nitric oxide synthase 2	Rattus norvegicus	110-114
12506169-0	2003	Preoperative therapy with trastuzumab and paclitaxel followed by sequential adjuvant doxorubicin/cyclophosphamide for HER2 overexpressing stage II or III breast cancer: a pilot study.	Cyclophosphamide	97-113	erb-b2 receptor tyrosine kinase 2	Homo sapiens	118-122
12543110-0	2003	CD40 ligand-specific antibodies synergize with cyclophosphamide to promote long-term transplantation tolerance across MHC barriers but inhibit graft-vs-leukemia effects of transplanted cells.	Cyclophosphamide	47-63	CD40 molecule	Homo sapiens	0-4
12543110-4	2003	In this study we have tried to minimize the Cy dose by a concomitant blockade of CD40-CD40L interaction.	Cyclophosphamide	44-46	CD40 molecule	Homo sapiens	81-85
12543110-4	2003	In this study we have tried to minimize the Cy dose by a concomitant blockade of CD40-CD40L interaction.	Cyclophosphamide	44-46	CD40 ligand	Homo sapiens	86-91
12543110-9	2003	RESULTS: Blocking CD40-CD40L interaction with MR1 mAb allowed the reduction of a tolerance-generating Cy dose by 50%.	Cyclophosphamide	102-104	CD40 molecule	Homo sapiens	18-22
12543110-9	2003	RESULTS: Blocking CD40-CD40L interaction with MR1 mAb allowed the reduction of a tolerance-generating Cy dose by 50%.	Cyclophosphamide	102-104	CD40 ligand	Homo sapiens	23-28
12543110-9	2003	RESULTS: Blocking CD40-CD40L interaction with MR1 mAb allowed the reduction of a tolerance-generating Cy dose by 50%.	Cyclophosphamide	102-104	major histocompatibility complex, class I-related	Homo sapiens	46-49
12543110-12	2003	CONCLUSIONS: CD40L-specific antibodies synergize with Cy to induce bilateral transplantation tolerance.	Cyclophosphamide	54-56	CD40 ligand	Homo sapiens	13-18
12548406-2	2003	Here, we report upon an examination of the expression of the TrkA neurotrophin receptor, the high affinity receptor for nerve growth factor, during regeneration following acute involution induced by cyclophosphamide in the rat thymus.	Cyclophosphamide	199-215	neurotrophic receptor tyrosine kinase 1	Rattus norvegicus	61-87
12548406-2	2003	Here, we report upon an examination of the expression of the TrkA neurotrophin receptor, the high affinity receptor for nerve growth factor, during regeneration following acute involution induced by cyclophosphamide in the rat thymus.	Cyclophosphamide	199-215	nerve growth factor	Rattus norvegicus	120-139
12872149-0	2003	Phase II study of cyclophosphamide, interferon-alpha and betamethasone (CIB) as induction therapy for patients 60-75 years of age with multiple myeloma stages II and III.	Cyclophosphamide	18-34	calcium and integrin binding 1	Homo sapiens	72-75
12777061-0	2003	Reconstitution of the cellular immune response by lactoferrin in cyclophosphamide-treated mice is correlated with renewal of T cell compartment.	Cyclophosphamide	65-81	lactotransferrin	Mus musculus	50-61
12777061-3	2003	The aim of this study was to evaluate the effects of oral administration of lactoferrin (LF) on cellular responses and reconstruction of the lymphocyte pool in mice treated with cyclophosphamide (CP).	Cyclophosphamide	178-194	lactotransferrin	Mus musculus	76-87
12777061-3	2003	The aim of this study was to evaluate the effects of oral administration of lactoferrin (LF) on cellular responses and reconstruction of the lymphocyte pool in mice treated with cyclophosphamide (CP).	Cyclophosphamide	178-194	lactotransferrin	Mus musculus	89-91
12531874-0	2003	Disruption of the CXCR4/CXCL12 chemotactic interaction during hematopoietic stem cell mobilization induced by GCSF or cyclophosphamide.	Cyclophosphamide	118-134	chemokine (C-X-C motif) receptor 4	Mus musculus	18-23
12535195-8	2003	By Western blotting and immunohistochemistry, expression levels of the c-kit ligand, stem cell factor, in skin and epidermis are strongly increased after cyclophosphamide treatment.	Cyclophosphamide	154-170	kit ligand	Mus musculus	71-83
12535195-8	2003	By Western blotting and immunohistochemistry, expression levels of the c-kit ligand, stem cell factor, in skin and epidermis are strongly increased after cyclophosphamide treatment.	Cyclophosphamide	154-170	kit ligand	Mus musculus	85-101
12535195-9	2003	Cyclophosphamide-induced migration of the hair follicle melanocytes into epidermis is completely abrogated by administration of c-kit neutralizing antibody.	Cyclophosphamide	0-16	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	128-133
12515881-9	2003	RESULTS: Cyclophosphamide treatment significantly increased the tumor uptake (percentage activity of injected dose per gram of tissue after normalization to the animal"s weight [%ID/g/kg]) of (99m)Tc-annexin V (0.070 +/- 0.007 %ID/g/kg for treated rats and 0.046 +/- 0.009 %ID/g/kg for controls, P < 0.001).	Cyclophosphamide	9-25	annexin A5	Rattus norvegicus	200-209
12515881-13	2003	CONCLUSION: Tumor uptake of (99m)Tc-annexin V was significantly increased by a single dose of cyclophosphamide treatment, and the increase was concordant with the number of TUNEL-positive cells in the tumor.	Cyclophosphamide	94-110	annexin A5	Rattus norvegicus	36-45
12659664-1	2003	Either ribavirin (RBV) or cyclophosphamide (CY) can shift an immune response from Th2 toward a Th1 cytokine profile.	Cyclophosphamide	26-42	negative elongation factor complex member C/D	Homo sapiens	95-98
12659664-1	2003	Either ribavirin (RBV) or cyclophosphamide (CY) can shift an immune response from Th2 toward a Th1 cytokine profile.	Cyclophosphamide	44-46	negative elongation factor complex member C/D	Homo sapiens	95-98
14586142-1	2003	Ifosfamide (IF) and cyclophosphamide (CTX) are chemotherapeutic agents frequently used in the treatment of human malignancies.	Cyclophosphamide	20-36	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	38-41
12759581-2	2003	We conducted a prospective, uncontrolled trial to evaluate the effect of intravenous cyclophosphamide pulse (CyP) therapy on the course of advanced progressive IgAN.	Cyclophosphamide	85-101	IGAN1	Homo sapiens	160-164
12629583-0	2003	Role of polymorphic human CYP2B6 in cyclophosphamide bioactivation.	Cyclophosphamide	36-52	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	26-32
12531874-0	2003	Disruption of the CXCR4/CXCL12 chemotactic interaction during hematopoietic stem cell mobilization induced by GCSF or cyclophosphamide.	Cyclophosphamide	118-134	chemokine (C-X-C motif) ligand 12	Mus musculus	24-30
12629583-1	2003	The role of polymorphic CYP2B6 in cyclophosphamide (CPA) bioactivation was investigated in human liver microsomes.	Cyclophosphamide	34-50	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	24-30
20021155-6	2003	Intraperitoneal administration of cyclophosphamide was found to decrease the activity of the kidney"s antioxidative enzymes, such as superoxide dismutase, glutathione peroxidase, gluthatione reductase, and catalase.	Cyclophosphamide	34-50	catalase	Rattus norvegicus	206-214
12412144-1	2002	This study examined tyrosine kinase receptor (Trk) expression and phosphorylation in lumbosacral dorsal root ganglia (DRG) after acute (8 or 48 hours) or chronic (10 days) cyclophosphamide (CYP)-induced cystitis.	Cyclophosphamide	172-188	neurotrophic receptor tyrosine kinase 1	Rattus norvegicus	20-44
12683239-4	2003	Administration of cyclophosphane brought about the rise of activity of acid lipase as compared to control.	Cyclophosphamide	18-32	lipase, endothelial	Mus musculus	76-82
12683239-6	2003	It may be suggested that only arylsulfatase and acid lipase are involved in performance and(or) manifestation of the natural killer activity in splenocytes of the C3HA mice after their administration with cyclophosphane or 5-fluorouracyl.	Cyclophosphamide	205-219	lipase, endothelial	Mus musculus	53-59
12490805-7	2002	Eventually the patient responded to CHOP (cyclophosphamide, Oncovin [vincristine, Eli Lilly, Indianapolis, IN], prednisone, and doxorubicin) therapy.	Cyclophosphamide	42-58	DNA damage inducible transcript 3	Homo sapiens	36-40
12520742-1	2002	BACKGROUND & OBJECTIVE: It was reported that there was negative correlation between the over-expression of lung resistant-related protein (LRP) and the sensitivity of cisplatin and cyclophosphamide.	Cyclophosphamide	185-201	major vault protein	Homo sapiens	111-141
12520742-1	2002	BACKGROUND & OBJECTIVE: It was reported that there was negative correlation between the over-expression of lung resistant-related protein (LRP) and the sensitivity of cisplatin and cyclophosphamide.	Cyclophosphamide	185-201	major vault protein	Homo sapiens	143-146
12460909-1	2002	Cytochrome P450 gene-directed enzyme prodrug therapy substantially augments intratumoral activation of anticancer prodrugs, such as cyclophosphamide (CPA), leading to a strong increase in antitumor effect without a corresponding increase in host toxicity.	Cyclophosphamide	132-148	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	11-15
12460909-1	2002	Cytochrome P450 gene-directed enzyme prodrug therapy substantially augments intratumoral activation of anticancer prodrugs, such as cyclophosphamide (CPA), leading to a strong increase in antitumor effect without a corresponding increase in host toxicity.	Cyclophosphamide	150-153	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	11-15
12460909-3	2002	Moreover, tumor cell P450 activity declined during the course of apoptosis induced by P450-activated CPA, limiting the potential of the tumor cell for continued production of activated drug metabolites.	Cyclophosphamide	101-104	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	21-25
12460909-3	2002	Moreover, tumor cell P450 activity declined during the course of apoptosis induced by P450-activated CPA, limiting the potential of the tumor cell for continued production of activated drug metabolites.	Cyclophosphamide	101-104	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	86-90
12482500-10	2002	CONCLUSION: CF101 induced upregulation of the PI3K/NF-kappaB pathway leading to G-CSF production, resulting in myeloprotective effect in cyclophosphamide-treated mice.	Cyclophosphamide	137-153	colony stimulating factor 3 (granulocyte)	Mus musculus	80-85
12629583-1	2003	The role of polymorphic CYP2B6 in cyclophosphamide (CPA) bioactivation was investigated in human liver microsomes.	Cyclophosphamide	52-55	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	24-30
12629583-13	2003	Our results demonstrate that the polymorphic CYP2B6 is a major enzyme in the bioactivation of CPA.	Cyclophosphamide	94-97	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	45-51
12460408-1	2002	To minimize the adverse effects of high-dose administration of steroids and cyclophosphamide in patients with myeloperoxidase (MPO) antineutrophil cytoplasmic antibody (ANCA), granulocytapheresis (GCAP) or leukocytapheresis (LCAP) was performed to reduce inflammation.	Cyclophosphamide	76-92	myeloperoxidase	Homo sapiens	110-125
12460408-1	2002	To minimize the adverse effects of high-dose administration of steroids and cyclophosphamide in patients with myeloperoxidase (MPO) antineutrophil cytoplasmic antibody (ANCA), granulocytapheresis (GCAP) or leukocytapheresis (LCAP) was performed to reduce inflammation.	Cyclophosphamide	76-92	myeloperoxidase	Homo sapiens	127-130
12486762-0	2002	Role of caspases in murine limb bud cell death induced by 4-hydroperoxycyclophosphamide, an activated analog of cyclophosphamide.	Cyclophosphamide	71-87	caspase 8	Mus musculus	8-16
12421990-0	2002	DNA vaccination with heat shock protein 60 inhibits cyclophosphamide-accelerated diabetes.	Cyclophosphamide	52-68	heat shock protein 1 (chaperonin)	Mus musculus	21-42
12402145-1	2002	This pilot phase I/II study intended to determine the maximum tolerated dose of cyclophosphamide and thiotepa administered on four consecutive courses with peripheral blood progenitor cell and granulocyte-colony stimulating factor support, as first-line therapy for hormone-refractory metastatic breast cancer patients.	Cyclophosphamide	80-96	colony stimulating factor 3	Homo sapiens	193-230
12419756-12	2002	CONCLUSIONS: The recommended dose level of docetaxel 85 mg/m(2), epirubicin 90 mg/m(2) and cyclophosphamide 600 mg/m(2) with G-CSF support has a favorable toxicity profile and is suitable for further investigation in phase II and III trials.	Cyclophosphamide	91-107	colony stimulating factor 3	Homo sapiens	125-130
12710585-5	2002	The most significant of these strategies is the combination of rituximab and CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine and prednisone), which is proving a highly effective combination in the treatment of NHL.	Cyclophosphamide	96-112	DNA damage inducible transcript 3	Homo sapiens	77-81
12710590-1	2002	The standard therapy for patients with aggressive lymphoma is cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) chemotherapy, which achieves a complete response in more than 60% of patients but is curative in only about 40-50%.	Cyclophosphamide	62-78	DNA damage inducible transcript 3	Homo sapiens	121-125
12452453-0	2002	Bcl-2/bcl-xL bispecific antisense treatment sensitizes breast carcinoma cells to doxorubicin, paclitaxel and cyclophosphamide.	Cyclophosphamide	109-125	BCL2 apoptosis regulator	Homo sapiens	0-5
12452453-0	2002	Bcl-2/bcl-xL bispecific antisense treatment sensitizes breast carcinoma cells to doxorubicin, paclitaxel and cyclophosphamide.	Cyclophosphamide	109-125	BCL2 like 1	Homo sapiens	6-12
12642684-1	2002	Either ribavirin, RBV, or cyclophosphamide, CY, can shift an immune response from Th2 towards a Th1 cytokine profile.	Cyclophosphamide	26-42	negative elongation factor complex member C/D	Homo sapiens	96-99
12465396-3	2002	The metastases partially responded to 10 cycles of CAF (cyclophosphamide, adriamycin, 5-fluorouracil).	Cyclophosphamide	56-72	lysine acetyltransferase 2B	Homo sapiens	51-54
12370764-2	2002	The aims of this study were: i) to correlate tumor MGMT expression and patient and tumor characteristics in malignant breast carcinomas treated with induction chemotherapy including cyclophosphamide (CPM) and ii) to study the predictive and prognostic values of tumor MGMT gene expression.	Cyclophosphamide	182-198	O-6-methylguanine-DNA methyltransferase	Homo sapiens	51-55
12370764-2	2002	The aims of this study were: i) to correlate tumor MGMT expression and patient and tumor characteristics in malignant breast carcinomas treated with induction chemotherapy including cyclophosphamide (CPM) and ii) to study the predictive and prognostic values of tumor MGMT gene expression.	Cyclophosphamide	200-203	O-6-methylguanine-DNA methyltransferase	Homo sapiens	51-55
12483228-1	2002	Human cytochrome P450 (CYP) 2B6 activates the anticancer prodrug cyclophosphamide (CPA) by 4-hydroxylation.	Cyclophosphamide	65-81	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	6-31
12483228-1	2002	Human cytochrome P450 (CYP) 2B6 activates the anticancer prodrug cyclophosphamide (CPA) by 4-hydroxylation.	Cyclophosphamide	83-86	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	6-31
12533055-2	2002	A 43-year-old female with DLCL, who relapsed after first line chemotherapy (CHOP--cyclophosphamide, doxorubicin, vincristine, and prednisone) and progressed despite salvage chemotherapy (EPOCH-etoposide, prednisone, vincristine, cyclophosphamide, and doxorubicin), was treated effectively with 8 cycles of Rituximab.	Cyclophosphamide	82-98	DNA damage inducible transcript 3	Homo sapiens	76-80
12412144-1	2002	This study examined tyrosine kinase receptor (Trk) expression and phosphorylation in lumbosacral dorsal root ganglia (DRG) after acute (8 or 48 hours) or chronic (10 days) cyclophosphamide (CYP)-induced cystitis.	Cyclophosphamide	172-188	neurotrophic receptor tyrosine kinase 1	Rattus norvegicus	46-49
12324935-4	2002	Treatment with steroid and cyclophosphamide resulted in significant improvement in renal function and normalization of MPO-ANCA level.	Cyclophosphamide	27-43	myeloperoxidase	Homo sapiens	119-122
12384137-1	2002	We report a case of severe Churg-Strauss syndrome (CSS) with mediastinal eosinophilic lymphadenopathy, with relapse after standard therapy with steroids and cyclophosphamide, subsequently treated with interferon (IFN) alpha 2b.	Cyclophosphamide	157-173	interferon alpha 1	Homo sapiens	201-223
12435290-3	2002	In the Aberdeen study, 162 patients with large and locally advanced breast cancer underwent 4 cycles of CVAP (cyclophosphamide/vincristine/doxorubicin/prednisone) primary chemotherapy.	Cyclophosphamide	110-126	amyloid beta precursor protein	Homo sapiens	104-108
12447847-5	2002	The anti-CD20 monoclonal antibody rituximab also is effective in treating CLL and is being evaluated in combination with chemotherapeutic agents (cyclophosphamide) and fludarabine.	Cyclophosphamide	146-162	keratin 20	Homo sapiens	9-13
12402185-3	2002	CHO oxidation in Cy was higher in ET2 and ET3 than in ET1 (p < 0.05), was lower in ET3 than in ET2 (p < 0.05) and was higher in Cy than in Sed only in ET2 (p < 0.05).	Cyclophosphamide	17-19	endothelin 2	Homo sapiens	34-37
12402185-3	2002	CHO oxidation in Cy was higher in ET2 and ET3 than in ET1 (p < 0.05), was lower in ET3 than in ET2 (p < 0.05) and was higher in Cy than in Sed only in ET2 (p < 0.05).	Cyclophosphamide	17-19	endothelin 3	Homo sapiens	42-45
12402185-3	2002	CHO oxidation in Cy was higher in ET2 and ET3 than in ET1 (p < 0.05), was lower in ET3 than in ET2 (p < 0.05) and was higher in Cy than in Sed only in ET2 (p < 0.05).	Cyclophosphamide	17-19	endothelin 1	Homo sapiens	54-57
12402185-3	2002	CHO oxidation in Cy was higher in ET2 and ET3 than in ET1 (p < 0.05), was lower in ET3 than in ET2 (p < 0.05) and was higher in Cy than in Sed only in ET2 (p < 0.05).	Cyclophosphamide	17-19	endothelin 3	Homo sapiens	86-89
12176813-1	2002	OBJECTIVE: To investigate the effect of pulse cyclophosphamide treatment on hepatitis C virus (HCV) kinetics and quasispecies in interferon alpha (IFNalpha) resistant HCV related cryoglobulinaemic vasculitis.	Cyclophosphamide	46-62	interferon alpha 1	Homo sapiens	147-155
12196358-3	2002	With a fixed dose of doxorubicin 75 mg/m(2), cyclophosphamide (CTX) was started at a dose of 1750 mg/m(2) and increased by 250 mg/m(2) in consecutive cohorts of patients provided that no dose-limiting toxicity occurred.	Cyclophosphamide	45-61	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	63-66
12199790-0	2002	Plasminogen activator inhibitor-1 is an independent diagnostic marker as well as severity predictor of hepatic veno-occlusive disease after allogeneic bone marrow transplantation in adults conditioned with busulphan and cyclophosphamide.	Cyclophosphamide	220-236	serpin family E member 1	Homo sapiens	0-33
12209705-2	2002	rRp450 is a novel replication-conditional HSV-1 mutant that expresses both the endogenous herpes viral thymidine kinase gene and the rat p450 CYP2B1 transgene; p450 bioactivates such cancer prodrugs as cyclophosphamide.	Cyclophosphamide	202-218	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	2-6
12209705-7	2002	Assays developed to separate cytotoxicity mediated by viral replication from cytotoxicity mediated by chemotherapy confirmed that HSV-1 thymidine kinase bioactivates ganciclovir and CYP2B1 bioactivates cyclophosphamide in rRp450-infected cells.	Cyclophosphamide	202-218	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	182-188
12209705-16	2002	Activation of cyclophosphamide by the p450 transgene augmented the anti-neoplastic effects of rRp450 without simultaneously decreasing viral replication.	Cyclophosphamide	14-30	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	38-42
12352050-14	2002	In rats with cyclophosphamide-induced neutropenia, tumor necrosis factor-alpha concentrations in alveolar macrophage supernatants and lung homogenates were significantly decreased compared with rats without neutropenia.	Cyclophosphamide	13-29	tumor necrosis factor	Rattus norvegicus	51-78
12494865-6	2002	CPA sharply decreased the production of all lymphoid cells studied, especially of CD4+ lymphocytes.	Cyclophosphamide	0-3	Cd4 molecule	Rattus norvegicus	82-85
12226743-0	2002	A clinical protocol for treatment of canine mammary tumors using encapsulated, cytochrome P450 synthesizing cells activating cyclophosphamide: a phase I/II study.	Cyclophosphamide	125-141	Cytochrome P450 1A1	Canis lupus familiaris	79-94
12352634-17	2002	Cyclophosphamide is the treatment of choice for HCV-negative patients and can be used safely in most HCV-positive patients if they fail IFN or IFN-ribavirin therapy, or if they require more aggressive therapy during periods of rapid clinical progression.	Cyclophosphamide	0-16	interferon alpha 1	Homo sapiens	136-139
12352634-17	2002	Cyclophosphamide is the treatment of choice for HCV-negative patients and can be used safely in most HCV-positive patients if they fail IFN or IFN-ribavirin therapy, or if they require more aggressive therapy during periods of rapid clinical progression.	Cyclophosphamide	0-16	interferon alpha 1	Homo sapiens	143-146
12436180-5	2002	Treatment with prednisone and/or cyclophosphamide controlled mucocutaneous and nail manifestations in all cases.	Cyclophosphamide	33-49	CD244 molecule	Homo sapiens	79-83
12195389-4	2002	CD-1 mice given cyclophosphamide to produce immunosuppression had continuous pancytopenia.	Cyclophosphamide	16-32	CD1 antigen complex	Mus musculus	0-4
12167460-0	2002	Effect of cyclophosphamide on gene expression of cytochromes p450 and beta-actin in the HL-60 cell line.	Cyclophosphamide	10-26	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	61-65
12167460-0	2002	Effect of cyclophosphamide on gene expression of cytochromes p450 and beta-actin in the HL-60 cell line.	Cyclophosphamide	10-26	POTE ankyrin domain family member F	Homo sapiens	70-80
12167460-1	2002	Many studies have demonstrated that cyclophosphamide (CPA) can affect hepatic cytochrome p450 (CYP) isoenzyme activity in animals.	Cyclophosphamide	36-52	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	78-93
12167460-1	2002	Many studies have demonstrated that cyclophosphamide (CPA) can affect hepatic cytochrome p450 (CYP) isoenzyme activity in animals.	Cyclophosphamide	36-52	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	95-98
12167460-1	2002	Many studies have demonstrated that cyclophosphamide (CPA) can affect hepatic cytochrome p450 (CYP) isoenzyme activity in animals.	Cyclophosphamide	54-57	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	78-93
12167460-1	2002	Many studies have demonstrated that cyclophosphamide (CPA) can affect hepatic cytochrome p450 (CYP) isoenzyme activity in animals.	Cyclophosphamide	54-57	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	95-98
12167460-2	2002	We have investigated the effect of CPA on gene expression of various CYP enzymes as well as beta-actin in the human acute promyelocytic leukemia cell line (HL-60S) and its multidrug-resistant (MDR) phenotype HL-60R.	Cyclophosphamide	35-38	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	69-72
12167460-4	2002	In determination of cytotoxicity and resistance factor (RF: IC(50) HL-60R/IC(50) HL-60S), concentrations of 100 and 500 micro g/ml CPA were selected to treat HL-60S and HL-60R up to 72 h. CYP gene expression in the cells prior to and after treatment with CPA was determined using semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR) and real-time PCR.	Cyclophosphamide	131-134	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	188-191
12173249-3	2002	Testicular oxidative stress in relation to cyclophosphamide treatment was monitored by the study of products of free radicals like conjugated dienes and malondialdehyde (MDA) as well as the activity of testicular antioxidant enzymes like peroxidase and catalase.	Cyclophosphamide	43-59	catalase	Rattus norvegicus	253-261
12167460-6	2002	However, CYP1B1-specific mRNA, which is predominantly expressed in HL-60 cell line, was suppressed after exposure to CPA in a concentration-dependent manner.	Cyclophosphamide	117-120	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	9-15
12167460-10	2002	Our study suggests that suppression of beta-actin gene expression contributes or is involved in the CPA cytotoxicity.	Cyclophosphamide	100-103	POTE ankyrin domain family member F	Homo sapiens	39-49
12173249-4	2002	Cyclophosphamide treatment at the dose of 5 mg/kg body weight/day for 28 days resulted a significant diminution in the activities of testicular delta 5, 3 beta-hydroxysteroid dehydrogenase (delta 5, 3 beta-HSD), 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) activities, plasma level of testosterone along with significant reduction in the number of germ cells at stage-VII of spermatogenesis.	Cyclophosphamide	0-16	aldo-keto reductase family 1, member C12	Rattus norvegicus	212-248
12173249-4	2002	Cyclophosphamide treatment at the dose of 5 mg/kg body weight/day for 28 days resulted a significant diminution in the activities of testicular delta 5, 3 beta-hydroxysteroid dehydrogenase (delta 5, 3 beta-HSD), 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) activities, plasma level of testosterone along with significant reduction in the number of germ cells at stage-VII of spermatogenesis.	Cyclophosphamide	0-16	hydroxysteroid (17-beta) dehydrogenase 3	Rattus norvegicus	250-261
12173249-5	2002	Levels of testicular MDA and conjugated dienes both were elevated whereas testicular peroxidase and catalase activities both were inhibited significantly in cyclophosphamide treated rats in comparison to control.	Cyclophosphamide	157-173	catalase	Rattus norvegicus	100-108
12173249-6	2002	After hCG co-administration at the dose of 5 I.U./kg body weight/day for 28 days in cyclophosphamide treated rats resulted a significant protection in the activities of testicular peroxidase and catalase along with significant decrease in the levels of MDA and conjugated dienes to the control level.	Cyclophosphamide	84-100	chorionic gonadotropin subunit beta 5	Homo sapiens	6-9
12173249-6	2002	After hCG co-administration at the dose of 5 I.U./kg body weight/day for 28 days in cyclophosphamide treated rats resulted a significant protection in the activities of testicular peroxidase and catalase along with significant decrease in the levels of MDA and conjugated dienes to the control level.	Cyclophosphamide	84-100	catalase	Rattus norvegicus	195-203
12173249-9	2002	Moreover, as restoration of plasma testosterone to the control level is noted in hCG co-treated cyclophosphamide treated rat, therefore, the results suggest that testosterone may be the key regulator for this correlation.	Cyclophosphamide	96-112	chorionic gonadotropin subunit beta 5	Homo sapiens	81-84
12060562-4	2002	Pretreatment with the selective EGFR tyrosine kinase inhibitor BIBX1522, cyclophosphamide (an inhibitor of bone marrow leukocyte mobilization), or a blocking antibody to IL-8 prevented CCSP staining.	Cyclophosphamide	73-89	secretoglobin family 1A member 1	Homo sapiens	185-189
12065440-0	2002	The effect of cyclophosphamide with and without dexamethasone on cytochrome P450 3A4 and 2B6 in human hepatocytes.	Cyclophosphamide	14-30	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	65-92
12176789-1	2002	BACKGROUND: Recent data suggest that chemotherapy with the cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) regimen is a highly effective treatment for localised primary gastric lymphoma of diffuse large B-cell histology (DLBCL).	Cyclophosphamide	59-75	DNA damage inducible transcript 3	Homo sapiens	118-122
12132673-11	2002	Interleukin-6 (IL-6) production of CY+SCG-treated peritoneal exdated cells (PECs), spleen cells and bone marrow cells (BMCs) were higher than that of the CY-treated group.	Cyclophosphamide	35-37	interleukin 6	Mus musculus	0-13
12132673-11	2002	Interleukin-6 (IL-6) production of CY+SCG-treated peritoneal exdated cells (PECs), spleen cells and bone marrow cells (BMCs) were higher than that of the CY-treated group.	Cyclophosphamide	35-37	interleukin 6	Mus musculus	15-19
12132673-12	2002	By in vitro culture of CY-treated PEC and spleen cells, IL-6 production was enhanced by the addition of SCG.	Cyclophosphamide	23-25	interleukin 6	Mus musculus	56-60
12470613-4	2002	After cyclophosphamide treatment, a massive splenic colonization of the spleens, but not lymph nodes, by immature myeloid progenitor (Ly-6G(+)CD11b(+))cells is observed.	Cyclophosphamide	6-22	lymphocyte antigen 6 complex, locus G	Mus musculus	134-139
12470613-4	2002	After cyclophosphamide treatment, a massive splenic colonization of the spleens, but not lymph nodes, by immature myeloid progenitor (Ly-6G(+)CD11b(+))cells is observed.	Cyclophosphamide	6-22	integrin subunit alpha M	Homo sapiens	142-147
12065440-1	2002	The purpose of this study was to characterize the concentration-response effects of cyclophosphamide (CPA) with and without dexamethasone (DEX; 10 microM) on the expression of CYP3A4 and CYP2B6 in cultured human hepatocytes at concentrations representative of standard- and high-dose CPA therapy (25 to 750 microM).	Cyclophosphamide	84-100	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	176-182
12065440-1	2002	The purpose of this study was to characterize the concentration-response effects of cyclophosphamide (CPA) with and without dexamethasone (DEX; 10 microM) on the expression of CYP3A4 and CYP2B6 in cultured human hepatocytes at concentrations representative of standard- and high-dose CPA therapy (25 to 750 microM).	Cyclophosphamide	84-100	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	187-193
12065440-1	2002	The purpose of this study was to characterize the concentration-response effects of cyclophosphamide (CPA) with and without dexamethasone (DEX; 10 microM) on the expression of CYP3A4 and CYP2B6 in cultured human hepatocytes at concentrations representative of standard- and high-dose CPA therapy (25 to 750 microM).	Cyclophosphamide	102-105	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	176-182
12065440-1	2002	The purpose of this study was to characterize the concentration-response effects of cyclophosphamide (CPA) with and without dexamethasone (DEX; 10 microM) on the expression of CYP3A4 and CYP2B6 in cultured human hepatocytes at concentrations representative of standard- and high-dose CPA therapy (25 to 750 microM).	Cyclophosphamide	102-105	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	187-193
12065440-1	2002	The purpose of this study was to characterize the concentration-response effects of cyclophosphamide (CPA) with and without dexamethasone (DEX; 10 microM) on the expression of CYP3A4 and CYP2B6 in cultured human hepatocytes at concentrations representative of standard- and high-dose CPA therapy (25 to 750 microM).	Cyclophosphamide	284-287	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	176-182
12065440-1	2002	The purpose of this study was to characterize the concentration-response effects of cyclophosphamide (CPA) with and without dexamethasone (DEX; 10 microM) on the expression of CYP3A4 and CYP2B6 in cultured human hepatocytes at concentrations representative of standard- and high-dose CPA therapy (25 to 750 microM).	Cyclophosphamide	284-287	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	187-193
12065440-2	2002	CPA produced concentration-dependent increases in CYP3A4 and CYP2B6 activity and immunoreactive protein that peaked at 250 and 125 microM, respectively, and declined thereafter.	Cyclophosphamide	0-3	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	50-56
12065440-2	2002	CPA produced concentration-dependent increases in CYP3A4 and CYP2B6 activity and immunoreactive protein that peaked at 250 and 125 microM, respectively, and declined thereafter.	Cyclophosphamide	0-3	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	61-67
12065440-3	2002	The inductive effect of CPA alone and in combination with DEX was greater in magnitude for CYP2B6 compared with CYP3A4.	Cyclophosphamide	24-27	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	91-97
12065440-3	2002	The inductive effect of CPA alone and in combination with DEX was greater in magnitude for CYP2B6 compared with CYP3A4.	Cyclophosphamide	24-27	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	112-118
12065440-7	2002	Induction index was highly correlated with CYP3A4 baseline activity for both CPA (r(2) = 0.75) and CPA plus DEX (r(2) = 0.85).	Cyclophosphamide	77-80	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	43-49
12065440-7	2002	Induction index was highly correlated with CYP3A4 baseline activity for both CPA (r(2) = 0.75) and CPA plus DEX (r(2) = 0.85).	Cyclophosphamide	99-102	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	43-49
12065440-8	2002	To investigate the potential mechanism for CPA-induced increases in CYP3A4 activity, the ability of CPA alone and in combination with DEX to activate pregnane X receptor (PXR) was explored using transient transfection assays.	Cyclophosphamide	43-46	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	68-74
12065440-8	2002	To investigate the potential mechanism for CPA-induced increases in CYP3A4 activity, the ability of CPA alone and in combination with DEX to activate pregnane X receptor (PXR) was explored using transient transfection assays.	Cyclophosphamide	100-103	nuclear receptor subfamily 1 group I member 2	Homo sapiens	150-169
12065440-8	2002	To investigate the potential mechanism for CPA-induced increases in CYP3A4 activity, the ability of CPA alone and in combination with DEX to activate pregnane X receptor (PXR) was explored using transient transfection assays.	Cyclophosphamide	100-103	nuclear receptor subfamily 1 group I member 2	Homo sapiens	171-174
12065440-9	2002	CPA produced a dose-dependent increase in PXR activation that was maximal at the highest CPA concentration studied (500 microM).	Cyclophosphamide	0-3	nuclear receptor subfamily 1 group I member 2	Homo sapiens	42-45
12065440-9	2002	CPA produced a dose-dependent increase in PXR activation that was maximal at the highest CPA concentration studied (500 microM).	Cyclophosphamide	89-92	nuclear receptor subfamily 1 group I member 2	Homo sapiens	42-45
12065440-10	2002	The addition of DEX to CPA resulted in a minor increase in PXR activation compared with CPA alone.	Cyclophosphamide	23-26	nuclear receptor subfamily 1 group I member 2	Homo sapiens	59-62
12065440-11	2002	These results indicate that CPA alone and in combination with DEX differentially induces the expression of CYP3A4 and 2B in a concentration-dependent manner, which may be mediated partially through activation of PXR.	Cyclophosphamide	28-31	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	107-120
12270059-23	2002	In conclusion, 2-CdA applied in monotherapy or in combination with prednisone or cyclophosphamide and mitoxantrone has therapeutic activity in some B-CLL patients in whom these drugs induced earlier complete or partial remission.	Cyclophosphamide	81-97	cytidine deaminase	Homo sapiens	17-20
12012107-5	2002	The therapeutic effect of CY followed by DNP-modified ATC vaccine was abrogated by depletion of CD4(+) or CD8(+) T-cells, illustrating the importance of both T-cell subsets for the anti-metastatic effect of this therapeutic protocol.	Cyclophosphamide	26-28	CD4 antigen	Mus musculus	96-99
12065440-11	2002	These results indicate that CPA alone and in combination with DEX differentially induces the expression of CYP3A4 and 2B in a concentration-dependent manner, which may be mediated partially through activation of PXR.	Cyclophosphamide	28-31	nuclear receptor subfamily 1 group I member 2	Homo sapiens	212-215
12382420-2	2002	The treatment with prednisolone and cyclophosphamide reduced his symptoms and laboratory data including serum C-ANCA.	Cyclophosphamide	36-52	proteinase 3	Homo sapiens	110-116
12080351-0	2002	Modulations of dose intensity of doxorubicin and cyclophosphamide in association with G-CSF and peripheral blood stem cells in adjuvant chemotherapy for breast cancer: comparative evaluation of completion and safety of three intensive regimens.	Cyclophosphamide	49-65	colony stimulating factor 3	Homo sapiens	86-91
12012107-6	2002	In addition, neutralizing anti-IFN-gamma monoclonal antibody (mAb), or neutralizing anti-tumor necrosis factor (TNF) mAb reduced the relapse-free survival of mice treated with CY followed by DNP-modified ATC vaccine, indicating the importance of both cytokines for the realization of the anti-metastatic effect of this therapeutic protocol.	Cyclophosphamide	176-178	interferon gamma	Mus musculus	31-40
12012107-6	2002	In addition, neutralizing anti-IFN-gamma monoclonal antibody (mAb), or neutralizing anti-tumor necrosis factor (TNF) mAb reduced the relapse-free survival of mice treated with CY followed by DNP-modified ATC vaccine, indicating the importance of both cytokines for the realization of the anti-metastatic effect of this therapeutic protocol.	Cyclophosphamide	176-178	tumor necrosis factor	Mus musculus	84-110
12012107-6	2002	In addition, neutralizing anti-IFN-gamma monoclonal antibody (mAb), or neutralizing anti-tumor necrosis factor (TNF) mAb reduced the relapse-free survival of mice treated with CY followed by DNP-modified ATC vaccine, indicating the importance of both cytokines for the realization of the anti-metastatic effect of this therapeutic protocol.	Cyclophosphamide	176-178	tumor necrosis factor	Mus musculus	112-115
12141952-8	2002	The triple combination of fludarabine/cyclophosphamide/mitoxantrone and fludarabine combinations with anti-CD20 (rituximab) or anti-CD52 (Campath-1H) antibody, might be even be more promising, since a relevant number of complete molecular remissions are achieved with these drugs.	Cyclophosphamide	38-54	keratin 20	Homo sapiens	107-111
12141952-8	2002	The triple combination of fludarabine/cyclophosphamide/mitoxantrone and fludarabine combinations with anti-CD20 (rituximab) or anti-CD52 (Campath-1H) antibody, might be even be more promising, since a relevant number of complete molecular remissions are achieved with these drugs.	Cyclophosphamide	38-54	CD52 molecule	Homo sapiens	132-136
12183838-3	2002	We found a significant increase of serum FL level at the WBC nadir after mobilization chemotherapy and a more dramatic increase at the WBC nadir post transplantation, consistent with a more profound BM aplasia after myeloablative chemotherapy as compared to high-dose cyclophosphamide used for mobilization.	Cyclophosphamide	268-284	fms related receptor tyrosine kinase 3 ligand	Homo sapiens	41-43
11992538-6	2002	In contrast, Apo2L/TRAIL-resistant cells were susceptible to Apo2L/TRAIL-mediated apoptosis in the presence of the anticancer drugs, Doxorubicin (DOX), Cisplatin (CDDP) and Etoposide (ETP) but not Methotrexate (MTX) or Cyclophosphamide (CPM).	Cyclophosphamide	219-235	TNF superfamily member 10	Homo sapiens	13-18
11992538-6	2002	In contrast, Apo2L/TRAIL-resistant cells were susceptible to Apo2L/TRAIL-mediated apoptosis in the presence of the anticancer drugs, Doxorubicin (DOX), Cisplatin (CDDP) and Etoposide (ETP) but not Methotrexate (MTX) or Cyclophosphamide (CPM).	Cyclophosphamide	219-235	TNF superfamily member 10	Homo sapiens	19-24
11992538-6	2002	In contrast, Apo2L/TRAIL-resistant cells were susceptible to Apo2L/TRAIL-mediated apoptosis in the presence of the anticancer drugs, Doxorubicin (DOX), Cisplatin (CDDP) and Etoposide (ETP) but not Methotrexate (MTX) or Cyclophosphamide (CPM).	Cyclophosphamide	219-235	TNF superfamily member 10	Homo sapiens	67-72
11992538-6	2002	In contrast, Apo2L/TRAIL-resistant cells were susceptible to Apo2L/TRAIL-mediated apoptosis in the presence of the anticancer drugs, Doxorubicin (DOX), Cisplatin (CDDP) and Etoposide (ETP) but not Methotrexate (MTX) or Cyclophosphamide (CPM).	Cyclophosphamide	237-240	TNF superfamily member 10	Homo sapiens	13-18
11992538-6	2002	In contrast, Apo2L/TRAIL-resistant cells were susceptible to Apo2L/TRAIL-mediated apoptosis in the presence of the anticancer drugs, Doxorubicin (DOX), Cisplatin (CDDP) and Etoposide (ETP) but not Methotrexate (MTX) or Cyclophosphamide (CPM).	Cyclophosphamide	237-240	TNF superfamily member 10	Homo sapiens	19-24
11992538-6	2002	In contrast, Apo2L/TRAIL-resistant cells were susceptible to Apo2L/TRAIL-mediated apoptosis in the presence of the anticancer drugs, Doxorubicin (DOX), Cisplatin (CDDP) and Etoposide (ETP) but not Methotrexate (MTX) or Cyclophosphamide (CPM).	Cyclophosphamide	237-240	TNF superfamily member 10	Homo sapiens	67-72
12040435-0	2002	Bax expression correlates with cellular drug sensitivity to doxorubicin, cyclophosphamide and chlorambucil but not fludarabine, cladribine or corticosteroids in B cell chronic lymphocytic leukemia.	Cyclophosphamide	73-89	BCL2 associated X, apoptosis regulator	Homo sapiens	0-3
12108896-4	2002	A trial conducted in the United Kingdom demonstrated that docetaxel sequential to CVAP (cyclophosphamide [Cytoxan, Neosar], vincristine, doxorubicin [Adriamycin], prednisolone) produced a higher overall clinical response rate (94% vs 66%, P = .001) and pathologic complete response rate (34% vs 18%) compared to additional cycles of CVAP as primary chemotherapy.	Cyclophosphamide	88-104	amyloid beta precursor protein	Homo sapiens	82-86
12015983-3	2002	Hence, tumors with p53 or INK4a/ARF mutations-but not those lacking ARF alone-respond poorly to cyclophosphamide therapy in vivo.	Cyclophosphamide	96-112	transformation related protein 53, pseudogene	Mus musculus	19-22
12513786-3	2002	Results showed that a retroviral vector was used to transduce full-length human ALDH1 cDNA into human hematopoietic cell line K562 that was then tested for resistance to 4-hydroxycyclophosphamide (4-HC), an active analogue of cyclophosphamide.	Cyclophosphamide	179-195	aldehyde dehydrogenase 1 family member A1	Homo sapiens	80-85
12513786-4	2002	Overexpression of the ALDH1 gene resulted in a significant increases in cyclophosphamide resistance in transduced K562 cells (50% inhibition concentration, IC50 = 10 micro mol/L).	Cyclophosphamide	72-88	aldehyde dehydrogenase 1 family member A1	Homo sapiens	22-27
12513786-5	2002	These findings indicate that ALDH1 overexpression is sufficient to induce cyclophosphamide resistance in vitro and provide a basis for testing the efficacy of ALDH1 gene transduction to protect bone marrow cells from high-dose cyclophosphamide in vivo.	Cyclophosphamide	74-90	aldehyde dehydrogenase 1 family member A1	Homo sapiens	29-34
12513786-5	2002	These findings indicate that ALDH1 overexpression is sufficient to induce cyclophosphamide resistance in vitro and provide a basis for testing the efficacy of ALDH1 gene transduction to protect bone marrow cells from high-dose cyclophosphamide in vivo.	Cyclophosphamide	227-243	aldehyde dehydrogenase 1 family member A1	Homo sapiens	29-34
12019144-5	2002	We tested one such drug, cyclophosphamide (CTX), in a protocol wherein the drug was administered to mice at low doses, of approximately 10-40 mg/kg on a daily basis through the drinking water.	Cyclophosphamide	25-41	V-set and immunoglobulin domain containing 2	Mus musculus	43-46
12031650-6	2002	RESULTS: Administration of either G-CSF or the myelosuppressive agent cyclophosphamide results in a sharp reduction of VCAM-1/CD106 expression in the bone marrow that coincides with the accumulation of granulocytic precursors and release of active neutrophil proteases neutrophil elastase and cathepsin G that directly cleave VCAM-1/CD106 in vitro.	Cyclophosphamide	70-86	vascular cell adhesion molecule 1	Mus musculus	119-125
12031650-6	2002	RESULTS: Administration of either G-CSF or the myelosuppressive agent cyclophosphamide results in a sharp reduction of VCAM-1/CD106 expression in the bone marrow that coincides with the accumulation of granulocytic precursors and release of active neutrophil proteases neutrophil elastase and cathepsin G that directly cleave VCAM-1/CD106 in vitro.	Cyclophosphamide	70-86	vascular cell adhesion molecule 1	Mus musculus	126-131
12031650-6	2002	RESULTS: Administration of either G-CSF or the myelosuppressive agent cyclophosphamide results in a sharp reduction of VCAM-1/CD106 expression in the bone marrow that coincides with the accumulation of granulocytic precursors and release of active neutrophil proteases neutrophil elastase and cathepsin G that directly cleave VCAM-1/CD106 in vitro.	Cyclophosphamide	70-86	cathepsin G	Mus musculus	293-304
12031650-6	2002	RESULTS: Administration of either G-CSF or the myelosuppressive agent cyclophosphamide results in a sharp reduction of VCAM-1/CD106 expression in the bone marrow that coincides with the accumulation of granulocytic precursors and release of active neutrophil proteases neutrophil elastase and cathepsin G that directly cleave VCAM-1/CD106 in vitro.	Cyclophosphamide	70-86	vascular cell adhesion molecule 1	Mus musculus	326-332
12031650-6	2002	RESULTS: Administration of either G-CSF or the myelosuppressive agent cyclophosphamide results in a sharp reduction of VCAM-1/CD106 expression in the bone marrow that coincides with the accumulation of granulocytic precursors and release of active neutrophil proteases neutrophil elastase and cathepsin G that directly cleave VCAM-1/CD106 in vitro.	Cyclophosphamide	70-86	vascular cell adhesion molecule 1	Mus musculus	333-338
12021842-4	2002	Quantitative RT-PCR analysis of pancreatic mRNA showed that cyclophosphamide induced the expression of Th1 cytokines (IFN-gamma and IL-12p40) in vehicle- or control plasmid-treated mice.	Cyclophosphamide	60-76	negative elongation factor complex member C/D, Th1l	Mus musculus	103-106
12021842-4	2002	Quantitative RT-PCR analysis of pancreatic mRNA showed that cyclophosphamide induced the expression of Th1 cytokines (IFN-gamma and IL-12p40) in vehicle- or control plasmid-treated mice.	Cyclophosphamide	60-76	interferon gamma	Mus musculus	118-127
12021842-4	2002	Quantitative RT-PCR analysis of pancreatic mRNA showed that cyclophosphamide induced the expression of Th1 cytokines (IFN-gamma and IL-12p40) in vehicle- or control plasmid-treated mice.	Cyclophosphamide	60-76	interleukin 12b	Mus musculus	132-140
11972091-3	2002	PATIENTS AND METHODS: The authors evaluated the activity of the combination of cyclophosphamide (500 mg/m2 per day for 5 days) and etoposide (100 mg/m2 per day for 5 days) given with granulocyte colony-stimulating factor (G-CSF) to children with osteosarcoma unresponsive to conventional treatment.	Cyclophosphamide	79-95	colony stimulating factor 3	Homo sapiens	183-220
12021086-9	2002	More importantly, the protective effect of gamma-GalCer in CY-accelerated T1D is abrogated by the in vivo blockade of IL-10 activity.	Cyclophosphamide	59-61	interleukin 10	Mus musculus	118-123
12021104-1	2002	The expression of IL-1beta in the NOD mouse pancreas was examined following disease acceleration with cyclophosphamide (Cy).	Cyclophosphamide	102-118	interleukin 1 beta	Mus musculus	18-26
12021104-1	2002	The expression of IL-1beta in the NOD mouse pancreas was examined following disease acceleration with cyclophosphamide (Cy).	Cyclophosphamide	120-122	interleukin 1 beta	Mus musculus	18-26
12021104-4	2002	At day 0 (Cy group), IL-1beta was expressed in selective intraislet macrophages but showed an increase from day 7 onwards in macrophages, a few beta cells, and somatostatin cells.	Cyclophosphamide	10-12	interleukin 1 beta	Mus musculus	21-29
12021104-6	2002	In the Cy group a proportion of macrophages coexpressed IL-1beta and inducible nitric oxide synthase (iNOS).	Cyclophosphamide	7-9	interleukin 1 beta	Mus musculus	56-64
12021104-6	2002	In the Cy group a proportion of macrophages coexpressed IL-1beta and inducible nitric oxide synthase (iNOS).	Cyclophosphamide	7-9	nitric oxide synthase 2, inducible	Mus musculus	69-100
12021104-6	2002	In the Cy group a proportion of macrophages coexpressed IL-1beta and inducible nitric oxide synthase (iNOS).	Cyclophosphamide	7-9	nitric oxide synthase 2, inducible	Mus musculus	102-106
11918545-0	2002	Factor VIII inhibitor in a patient with mild haemophilia A and an Asn618-->Ser mutation responsive to immune tolerance induction and cyclophosphamide.	Cyclophosphamide	136-152	cytochrome c oxidase subunit 8A	Homo sapiens	7-11
11918545-4	2002	Cyclophosphamide was administered and, after 8 months treatment, factor VIII levels increased to 0.20 U/ml and the inhibitor could no longer be detected.	Cyclophosphamide	0-16	cytochrome c oxidase subunit 8A	Homo sapiens	72-76
11918545-9	2002	Our findings suggest that immune tolerance therapy and cyclophosphamide were successful in eradicating inhibitory antibodies against a common epitope on factor VIII.	Cyclophosphamide	55-71	cytochrome c oxidase subunit 8A	Homo sapiens	160-164
12124655-5	2002	Cathepsin B is probably involved in apoptosis of tumor cells during chemotherapy of lymphosarcoma-LS with cyclophosphamide.	Cyclophosphamide	106-122	cathepsin B	Mus musculus	0-11
11965495-0	2002	Cyclin dependent kinase 5 and its interacting proteins in cell death induced in vivo by cyclophosphamide in developing mouse embryos.	Cyclophosphamide	88-104	cyclin-dependent kinase 5	Mus musculus	0-25
11891540-11	2002	CPA also sharply decreased the activity of all lymph cells studied, especially of CD4+ lymphocytes which could no longer be observed following this treatment.	Cyclophosphamide	0-3	Cd4 molecule	Rattus norvegicus	82-85
11891540-13	2002	Inhibition of mainly CD4+ lymphocyte synthesis of CPA was confirmed by the low CD4/CD8 ratio, which increased slightly after the combined treatment with CPA and sTAA.	Cyclophosphamide	50-53	Cd4 molecule	Rattus norvegicus	21-24
11891540-13	2002	Inhibition of mainly CD4+ lymphocyte synthesis of CPA was confirmed by the low CD4/CD8 ratio, which increased slightly after the combined treatment with CPA and sTAA.	Cyclophosphamide	50-53	Cd4 molecule	Rattus norvegicus	79-82
11891540-13	2002	Inhibition of mainly CD4+ lymphocyte synthesis of CPA was confirmed by the low CD4/CD8 ratio, which increased slightly after the combined treatment with CPA and sTAA.	Cyclophosphamide	153-156	Cd4 molecule	Rattus norvegicus	21-24
11891540-13	2002	Inhibition of mainly CD4+ lymphocyte synthesis of CPA was confirmed by the low CD4/CD8 ratio, which increased slightly after the combined treatment with CPA and sTAA.	Cyclophosphamide	153-156	Cd4 molecule	Rattus norvegicus	79-82
11886722-3	2002	Combined treatment with methylprednisolone and cyclophosphamide was successful in reducing serum IgE levels and IgE tissue deposits and in inducing the clinical manifestations of vasculitis into remission.	Cyclophosphamide	47-63	immunoglobulin heavy constant epsilon	Homo sapiens	97-100
11886722-3	2002	Combined treatment with methylprednisolone and cyclophosphamide was successful in reducing serum IgE levels and IgE tissue deposits and in inducing the clinical manifestations of vasculitis into remission.	Cyclophosphamide	47-63	immunoglobulin heavy constant epsilon	Homo sapiens	112-115
11999952-8	2002	In vivo localization of intravenously administered Tc 99m-annexin V has been demonstrated in numerous preclinical models of apoptosis, including anti-Fas-mediated hepatic apoptosis, rejection of allogeneic heterotopic cardiac allografts, cyclophosphamide treatment of murine lymphoma, cyclophosphamide-induced apoptosis in bone marrow, and leukocyte apoptosis associated with abscess formation.	Cyclophosphamide	238-254	annexin A11, opposite strand	Mus musculus	58-65
11999952-8	2002	In vivo localization of intravenously administered Tc 99m-annexin V has been demonstrated in numerous preclinical models of apoptosis, including anti-Fas-mediated hepatic apoptosis, rejection of allogeneic heterotopic cardiac allografts, cyclophosphamide treatment of murine lymphoma, cyclophosphamide-induced apoptosis in bone marrow, and leukocyte apoptosis associated with abscess formation.	Cyclophosphamide	285-301	annexin A11, opposite strand	Mus musculus	58-65
12070798-3	2002	A significant association between expression of c-erbB-2 mRNA und survival was obtained for the subgroup of patients who received a standard chemotherapy with carboplatin or cisplatin and cyclophosphamide (P = 0.0003).	Cyclophosphamide	188-204	erb-b2 receptor tyrosine kinase 2	Homo sapiens	48-56
12849064-4	2002	Paradoxically, the response to EGF immunization could be enhanced by an "immunosuppressive" treatment with cyclophosphamide, most probably by suppressing active control mechanisms.	Cyclophosphamide	107-123	epidermal growth factor	Homo sapiens	31-34
12006526-0	2002	HER-2 amplification and topoisomerase IIalpha gene aberrations as predictive markers in node-positive breast cancer patients randomly treated either with an anthracycline-based therapy or with cyclophosphamide, methotrexate, and 5-fluorouracil.	Cyclophosphamide	193-209	erb-b2 receptor tyrosine kinase 2	Homo sapiens	0-5
11950782-0	2002	Triethylenethiophosphoramide is a specific inhibitor of cytochrome P450 2B6: implications for cyclophosphamide metabolism.	Cyclophosphamide	94-110	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	56-75
11950782-4	2002	Studies suggest that CYP2B6 plays an important role in the 4-hydroxylation of cyclophosphamide and that this reaction can be inhibited by triethylenethiophosphoramide (thioTEPA).	Cyclophosphamide	78-94	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	21-27
11950782-10	2002	We conclude that thioTEPA is a potent and specific inhibitor of CYP2B6 and that this is the likely mechanism by which thioTEPA inhibits the activation of cyclophosphamide.	Cyclophosphamide	154-170	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	64-70
12164395-5	2002	Here, we report the outcomes of 15 patients with haematological disease or solid tumours who underwent an SCT in the University Hospital Maastricht after a non-myeloablative fludarabine/cyclophosphamide conditioning regimen.	Cyclophosphamide	186-202	secretin	Homo sapiens	106-109
11921026-0	2002	Acquired factor VIII inhibitor treated with cyclophosphamide, vincristine, and prednisone.	Cyclophosphamide	44-60	cytochrome c oxidase subunit 8A	Homo sapiens	16-20
11921026-3	2002	Since 1993 we treated 6 non-hemophilic patients with factor VIII inhibitor with cyclophosphamide, vincristine, and prednisone (CVP) every 3-4 weeks.	Cyclophosphamide	80-96	cytochrome c oxidase subunit 8A	Homo sapiens	60-64
11914911-0	2002	Cellular levels of aldehyde dehydrogenases (ALDH1A1 and ALDH3A1) as predictors of therapeutic responses to cyclophosphamide-based chemotherapy of breast cancer: a retrospective study.	Cyclophosphamide	107-123	aldehyde dehydrogenase 1 family member A1	Homo sapiens	44-51
11914911-0	2002	Cellular levels of aldehyde dehydrogenases (ALDH1A1 and ALDH3A1) as predictors of therapeutic responses to cyclophosphamide-based chemotherapy of breast cancer: a retrospective study.	Cyclophosphamide	107-123	aldehyde dehydrogenase 3 family member A1	Homo sapiens	56-63
11914911-2	2002	PURPOSE: In preclinical models, established molecular determinants of cellular sensitivity to cyclophosphamide, long a mainstay of chemotherapeutic regimens used to treat breast cancers, include the aldehyde dehydrogenases that catalyze the detoxification of this agent, namely, ALDH1A1 and ALDH3A1.	Cyclophosphamide	94-110	aldehyde dehydrogenase 1 family member A1	Homo sapiens	279-286
11914911-2	2002	PURPOSE: In preclinical models, established molecular determinants of cellular sensitivity to cyclophosphamide, long a mainstay of chemotherapeutic regimens used to treat breast cancers, include the aldehyde dehydrogenases that catalyze the detoxification of this agent, namely, ALDH1A1 and ALDH3A1.	Cyclophosphamide	94-110	aldehyde dehydrogenase 3 family member A1	Homo sapiens	291-298
11914911-8	2002	The premise that cellular levels of ALDH1A1 and/or ALDH3A1 predict clinical responses to cyclophosphamide-based chemotherapeutic regimens was submitted to statistical analysis.	Cyclophosphamide	89-105	aldehyde dehydrogenase 1 family member A1	Homo sapiens	36-43
11914911-8	2002	The premise that cellular levels of ALDH1A1 and/or ALDH3A1 predict clinical responses to cyclophosphamide-based chemotherapeutic regimens was submitted to statistical analysis.	Cyclophosphamide	89-105	aldehyde dehydrogenase 3 family member A1	Homo sapiens	51-58
11914911-11	2002	Retrospective analysis indicated that cellular levels of ALDH1A1, but not those of ALDH3A1, were (1) significantly higher in metastatic tumor cells that had survived exposure to cyclophosphamide than in those that had not been exposed to this drug, and (2) significantly higher in metastatic tumors that did not respond (tumor size did not decrease or even increased) to subsequent treatment with cyclophosphamide-based chemotherapeutic regimens than in those that did respond (tumor size decreased) to such regimens.	Cyclophosphamide	178-194	aldehyde dehydrogenase 1 family member A1	Homo sapiens	57-64
11914911-11	2002	Retrospective analysis indicated that cellular levels of ALDH1A1, but not those of ALDH3A1, were (1) significantly higher in metastatic tumor cells that had survived exposure to cyclophosphamide than in those that had not been exposed to this drug, and (2) significantly higher in metastatic tumors that did not respond (tumor size did not decrease or even increased) to subsequent treatment with cyclophosphamide-based chemotherapeutic regimens than in those that did respond (tumor size decreased) to such regimens.	Cyclophosphamide	397-413	aldehyde dehydrogenase 1 family member A1	Homo sapiens	57-64
11914911-12	2002	The therapeutic outcome of cyclophosphamide-based chemotherapy corresponded to cellular ALDH1A1 levels in 77% of cases.	Cyclophosphamide	27-43	aldehyde dehydrogenase 1 family member A1	Homo sapiens	88-95
11914911-14	2002	Thus, partial or complete responses to cyclophosphamide-based chemotherapy occurred 2.3 times more often when the ALDH1A1 level was low than when it was high.	Cyclophosphamide	39-55	aldehyde dehydrogenase 1 family member A1	Homo sapiens	114-121
11914911-16	2002	Failure to observe the expected inverse relationship between clinical responses to cyclophosphamide-based chemotherapeutic regimens and ALDH3A1 levels was probably because even the highest breast tumor tissue ALDH3A1 level thus far reported appears to be below the threshold level at which ALDH3A1-catalyzed detoxification of oxazaphosphorines becomes pharmacologically meaningful.	Cyclophosphamide	83-99	aldehyde dehydrogenase 3 family member A1	Homo sapiens	136-143
11914911-16	2002	Failure to observe the expected inverse relationship between clinical responses to cyclophosphamide-based chemotherapeutic regimens and ALDH3A1 levels was probably because even the highest breast tumor tissue ALDH3A1 level thus far reported appears to be below the threshold level at which ALDH3A1-catalyzed detoxification of oxazaphosphorines becomes pharmacologically meaningful.	Cyclophosphamide	83-99	aldehyde dehydrogenase 3 family member A1	Homo sapiens	209-216
11914911-16	2002	Failure to observe the expected inverse relationship between clinical responses to cyclophosphamide-based chemotherapeutic regimens and ALDH3A1 levels was probably because even the highest breast tumor tissue ALDH3A1 level thus far reported appears to be below the threshold level at which ALDH3A1-catalyzed detoxification of oxazaphosphorines becomes pharmacologically meaningful.	Cyclophosphamide	83-99	aldehyde dehydrogenase 3 family member A1	Homo sapiens	209-216
11982607-0	2002	Elevated monocytic IL-12 and TNF-alpha production in Wegener"s granulomatosis is normalized by cyclophosphamide and corticosteroid therapy.	Cyclophosphamide	95-111	tumor necrosis factor	Homo sapiens	29-38
11990872-4	2002	Although a general immunosuppressant that affects both T- and B-cell function, cyclophosphamide has selective immune effects in MS by suppressing IL-12 and Th1-type responses and enhancing Th2/Th3 responses (IL-4, IL-10, TGF-beta; eosinophils in peripheral blood).	Cyclophosphamide	79-95	negative elongation factor complex member C/D	Homo sapiens	156-159
11990872-4	2002	Although a general immunosuppressant that affects both T- and B-cell function, cyclophosphamide has selective immune effects in MS by suppressing IL-12 and Th1-type responses and enhancing Th2/Th3 responses (IL-4, IL-10, TGF-beta; eosinophils in peripheral blood).	Cyclophosphamide	79-95	interleukin 4	Homo sapiens	208-212
11990872-4	2002	Although a general immunosuppressant that affects both T- and B-cell function, cyclophosphamide has selective immune effects in MS by suppressing IL-12 and Th1-type responses and enhancing Th2/Th3 responses (IL-4, IL-10, TGF-beta; eosinophils in peripheral blood).	Cyclophosphamide	79-95	interleukin 10	Homo sapiens	214-219
11990872-4	2002	Although a general immunosuppressant that affects both T- and B-cell function, cyclophosphamide has selective immune effects in MS by suppressing IL-12 and Th1-type responses and enhancing Th2/Th3 responses (IL-4, IL-10, TGF-beta; eosinophils in peripheral blood).	Cyclophosphamide	79-95	transforming growth factor beta 1	Homo sapiens	221-229
11916544-3	2002	Moreover, recent findings pointed out that the methylenetetrahydrofolate reductase (MTHFR) C677T mutation might change patient susceptibility to the toxic effects of the cyclophosphamide, methotrexate, 5-fluorouracil (CMF) regimen and raltitrexed.	Cyclophosphamide	170-186	methylenetetrahydrofolate reductase	Homo sapiens	47-82
11916544-3	2002	Moreover, recent findings pointed out that the methylenetetrahydrofolate reductase (MTHFR) C677T mutation might change patient susceptibility to the toxic effects of the cyclophosphamide, methotrexate, 5-fluorouracil (CMF) regimen and raltitrexed.	Cyclophosphamide	170-186	methylenetetrahydrofolate reductase	Homo sapiens	84-89
11836638-6	2002	CPA decreased the size and cell content of follicles, splenic areas related to the production of B cells, of the marginal zone and to a lesser extent of the periarterial lymph sheath, and decreased the number of CD4(+) and, at a lower rate, of CD8(+ )T cells in the spleen.	Cyclophosphamide	0-3	Cd4 molecule	Rattus norvegicus	212-215
11935300-6	2002	RESULTS: Ex vivo chemosensitivity testing showed that tumors with p53 mutations were significantly more resistant to the cyclophosphamide/etoposide/epirubicin regimen than with normal p53 gene ( P = 0.012).	Cyclophosphamide	121-137	tumor protein p53	Homo sapiens	66-69
12113067-2	2002	However, older EMP-based combination chemotherapies with vinblastine, vinorelbine, doxorubicin or cyclophosphamide showed relatively low PSA response rate (25-58%) accompanied with high toxicities.	Cyclophosphamide	98-114	aminopeptidase puromycin sensitive	Homo sapiens	137-140
12015983-3	2002	Hence, tumors with p53 or INK4a/ARF mutations-but not those lacking ARF alone-respond poorly to cyclophosphamide therapy in vivo.	Cyclophosphamide	96-112	cyclin dependent kinase inhibitor 2A	Mus musculus	26-31
11773279-3	2002	METHODS: In a retrospective cohort study, we used methylation-specific polymerase chain reaction to analyze the MGMT promoter methylation status in tumor DNA of B-DLCL patients receiving cyclophosphamide as part of multidrug regimens.	Cyclophosphamide	187-203	O-6-methylguanine-DNA methyltransferase	Homo sapiens	112-116
11812172-10	2002	CAF chemotherapy (cyclophosphamide, adriamycin, and 5-fluorouracil) is predicted to be more effective than CMF (cyclophosphamide, methotrexate, and 5-fluorouracil).	Cyclophosphamide	18-34	lysine acetyltransferase 2B	Homo sapiens	0-3
11812172-10	2002	CAF chemotherapy (cyclophosphamide, adriamycin, and 5-fluorouracil) is predicted to be more effective than CMF (cyclophosphamide, methotrexate, and 5-fluorouracil).	Cyclophosphamide	112-128	lysine acetyltransferase 2B	Homo sapiens	0-3
11807147-1	2002	BACKGROUND: The standard treatment for patients with diffuse large-B-cell lymphoma is cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP).	Cyclophosphamide	86-102	DNA damage inducible transcript 3	Homo sapiens	146-150
11773279-11	2002	CONCLUSION: MGMT promoter hypermethylation appears to be a useful marker for predicting survival in patients with B-DLCL treated with multidrug regimens including cyclophosphamide.	Cyclophosphamide	163-179	O-6-methylguanine-DNA methyltransferase	Homo sapiens	12-16
11863115-0	2002	Low-dose oral methotrexate and cyclophosphamide in metastatic breast cancer: antitumor activity and correlation with vascular endothelial growth factor levels.	Cyclophosphamide	31-47	vascular endothelial growth factor A	Homo sapiens	117-151
11899748-7	2002	cyclophosphamide and scleroderma renal crisis with ACE inhibitors and haemodialysis, respectively.	Cyclophosphamide	0-16	angiotensin I converting enzyme	Homo sapiens	51-54
11863115-2	2002	Alternative mechanisms of efficacy have been ascribed to several common anticancer agents, including cyclophosphamide (CTX), methotrexate (MTX), anthracyclines and taxanes, postulating an antiangiogenic activity.	Cyclophosphamide	101-117	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	119-122
12479593-3	2002	The gold standard for primary treatment of aggressive NHL is combination chemotherapy with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP).	Cyclophosphamide	91-107	DNA damage inducible transcript 3	Homo sapiens	150-154
11893254-0	2002	NF-kappa B DNA-binding activity in embryos responding to a teratogen, cyclophosphamide.	Cyclophosphamide	70-86	nuclear factor kappa B subunit 1	Homo sapiens	0-10
11893254-4	2002	Fot this, we evaluated how NF-KappaB DNA binding activity in embryonic organs demonstrating differential sensitivity to a reference teratogen, cyclophosphamide, correlates with dysmorphic events induced by the teratogen at the cellular level (excessive apoptosis) and at the organ level (structural anomalies).	Cyclophosphamide	143-159	nuclear factor kappa B subunit 1	Homo sapiens	27-36
11893254-6	2002	We observed that the Cyclophosphamide-induced excessive apoptosis in the brain, followed by the formation of severe craniofacial structural anomalies, was accompanied by suppression of NF-kappaB DNA-binding activity as well as by a significant and lasting increase in the activity of caspases 3 and 8.	Cyclophosphamide	21-37	nuclear factor kappa B subunit 1	Homo sapiens	185-194
12196722-8	2002	The antitumor spectrum of UCN-01 was different from that of other conventional agents such as doxorubicin and cyclophosphamide which were ineffective against Br-10 but were active against MX-1.	Cyclophosphamide	110-126	MX dynamin like GTPase 1	Homo sapiens	188-192
11807622-5	2002	A shift from immunosuppression to immunopotentiation induced by low-dose Cy treatment was mainly mediated by a decrease in IL-10 production.	Cyclophosphamide	73-75	interleukin 10	Rattus norvegicus	123-128
11807623-0	2002	The antimetastatic effect of a single low dose of cyclophosphamide involves modulation of galectin-1 and Bcl-2 expression.	Cyclophosphamide	50-66	galectin 1	Rattus norvegicus	90-100
11807623-0	2002	The antimetastatic effect of a single low dose of cyclophosphamide involves modulation of galectin-1 and Bcl-2 expression.	Cyclophosphamide	50-66	BCL2, apoptosis regulator	Rattus norvegicus	105-110
11807623-3	2002	Since galectin-1 is expressed by highly metastatic tumors, in the present study we investigated the participation of this beta-galactoside-binding protein in cyclophosphamide-induced immunomodulation.	Cyclophosphamide	158-174	galectin 1	Rattus norvegicus	6-16
11807623-8	2002	Expression of galectin-1 was significantly decreased in tumors from cyclophosphamide-treated rats compared to non-treated rats.	Cyclophosphamide	68-84	galectin 1	Rattus norvegicus	14-24
11807623-12	2002	Our results suggest that a single low dose of cyclophosphamide modulates the expression of galectin-1 and Bcl-2 by tumors, which could in turn influence the apoptotic threshold of spleen mononuclear cells.	Cyclophosphamide	46-62	galectin 1	Rattus norvegicus	91-101
11807623-12	2002	Our results suggest that a single low dose of cyclophosphamide modulates the expression of galectin-1 and Bcl-2 by tumors, which could in turn influence the apoptotic threshold of spleen mononuclear cells.	Cyclophosphamide	46-62	BCL2, apoptosis regulator	Rattus norvegicus	106-111
12052216-1	2002	Several commonly used cancer chemotherapeutic prodrugs, including cyclophosphamide and ifosfamide, are metabolized in the liver by a cytochrome P450 (CYP)-catalyzed prodrug activation reaction that is required for therapeutic activity.	Cyclophosphamide	66-82	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	133-148
12052216-1	2002	Several commonly used cancer chemotherapeutic prodrugs, including cyclophosphamide and ifosfamide, are metabolized in the liver by a cytochrome P450 (CYP)-catalyzed prodrug activation reaction that is required for therapeutic activity.	Cyclophosphamide	66-82	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	150-153
12751907-5	2002	Intraperitoneal administration of cyclophosphamide was found to decrease the activity of liver antioxidative enzymes, i.e. superoxide dismutase, glutathione peroxidase and glutathione reductase, and to increase catalase activity.	Cyclophosphamide	34-50	glutathione-disulfide reductase	Rattus norvegicus	172-193
12751907-5	2002	Intraperitoneal administration of cyclophosphamide was found to decrease the activity of liver antioxidative enzymes, i.e. superoxide dismutase, glutathione peroxidase and glutathione reductase, and to increase catalase activity.	Cyclophosphamide	34-50	catalase	Rattus norvegicus	211-219
12751907-7	2002	Co-administration of cyclophosphamide and amifostine nearly prevented changes in activities of superoxide dismutase, glutathione reductase and catalase, as well as to a high degree of glutathione peroxidase.	Cyclophosphamide	21-37	glutathione-disulfide reductase	Rattus norvegicus	117-138
12479594-9	2002	Beneficial responses to granulocyte colony-stimulating factor (G-CSF; filgrastim) in elderly patients have been found in aggressive non-Hodgkin"s lymphoma with standard cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) therapy and acute myeloid leukaemia (AML) during induction and consolidation chemotherapy.	Cyclophosphamide	169-185	colony stimulating factor 3	Homo sapiens	24-61
12479594-9	2002	Beneficial responses to granulocyte colony-stimulating factor (G-CSF; filgrastim) in elderly patients have been found in aggressive non-Hodgkin"s lymphoma with standard cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) therapy and acute myeloid leukaemia (AML) during induction and consolidation chemotherapy.	Cyclophosphamide	169-185	colony stimulating factor 3	Homo sapiens	63-68
11823031-6	2002	We treated him with G-CSF-mobilized stem cells from his heterozygote, human leukocyte antigen-matched brother after RIC with fludarabine and cyclophosphamide.	Cyclophosphamide	141-157	colony stimulating factor 3	Homo sapiens	20-25
12751907-7	2002	Co-administration of cyclophosphamide and amifostine nearly prevented changes in activities of superoxide dismutase, glutathione reductase and catalase, as well as to a high degree of glutathione peroxidase.	Cyclophosphamide	21-37	catalase	Rattus norvegicus	143-151
11810040-1	2002	PURPOSE: To define the cyclophosphamide (CTX) maximal tolerated dose when combined with fixed doses of gemcitabine, fluorouracil (5-FU) and folinic acid (leucovorin, LFA) in metastatic breast cancer patients pretreated with anthracyclines and taxanes.	Cyclophosphamide	23-39	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	41-44
11751995-0	2002	ICA69(null) nonobese diabetic mice develop diabetes, but resist disease acceleration by cyclophosphamide.	Cyclophosphamide	88-104	islet cell autoantigen 1	Mus musculus	0-5
11751995-9	2002	Unexpectedly, ICA69(null) NOD mice were resistant to cyclophosphamide (CY)-accelerated diabetes.	Cyclophosphamide	53-69	islet cell autoantigen 1	Mus musculus	14-19
11751995-9	2002	Unexpectedly, ICA69(null) NOD mice were resistant to cyclophosphamide (CY)-accelerated diabetes.	Cyclophosphamide	71-73	islet cell autoantigen 1	Mus musculus	14-19
11751995-11	2002	CY-accelerated diabetes involves not only ablation of lymphoid cells, but ICA69-dependent drug toxicity in beta cells that boosts autoreactivity in the regenerating lymphoid system.	Cyclophosphamide	0-2	islet cell autoantigen 1	Mus musculus	74-79
12091638-20	2002	The CHOP regimen is cyclophosphamide, doxorubicine, vincristine and prednisone.	Cyclophosphamide	20-36	DNA damage inducible transcript 3	Homo sapiens	4-8
12365794-11	2002	In cyclophosphamide-treated mice, the proportion of Fas-positive intra-islet CD4 and CD8 T cells at day 14 (with and without diabetes) was considerably higher than at days 0, 4, 7 and 11.	Cyclophosphamide	3-19	CD4 antigen	Mus musculus	77-80
11748447-7	2002	In contrast, a correlation between the response to a cyclophosphamide + methotrexate + 5-FU regimen and overexpression of HER-2 is not certain.	Cyclophosphamide	53-69	erb-b2 receptor tyrosine kinase 2	Homo sapiens	122-127
11723074-6	2001	The Idd5.1 locus protected against both spontaneous and cyclophosphamide-induced diabetes, but it did not prevent inflammatory infiltration of the islets of Langerhans.	Cyclophosphamide	56-72	insulin dependent diabetes susceptibility 5.1	Mus musculus	4-10
11749812-1	2001	AIM: To observe polysaccharide of Spirulina platensis (PSp) on the hematopoietic system of mouse and dogs which were damaged by injection of cyclophosphamide (CTX) and 60Co-gamma irradiation.	Cyclophosphamide	141-157	persephin	Mus musculus	55-58
11804275-4	2001	This is achieved because CYP2B6 converts the inactive produg form cyclophosphamide into the active cytotoxic drug.	Cyclophosphamide	66-82	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	25-31
11723234-8	2001	Although Bcl-2 thus blocked the cytotoxic effects of activated CPA, it did not inhibit the drug"s cytostatic effects.	Cyclophosphamide	63-66	BCL2 apoptosis regulator	Homo sapiens	9-14
11745470-5	2001	Second, phosphorylation of CYP2B1 in intact hepatocytes reduced by up to 75% toxification of CPA to mutagenic metabolites (totally dependent on the same preferentially CYP2B-catalyzed 4-hydroxylation of CPA as is the generation of highly cytotoxic species).	Cyclophosphamide	93-96	cytochrome P450 family 2 subfamily B member 7, pseudogene	Homo sapiens	27-32
11745470-5	2001	Second, phosphorylation of CYP2B1 in intact hepatocytes reduced by up to 75% toxification of CPA to mutagenic metabolites (totally dependent on the same preferentially CYP2B-catalyzed 4-hydroxylation of CPA as is the generation of highly cytotoxic species).	Cyclophosphamide	203-206	cytochrome P450 family 2 subfamily B member 7, pseudogene	Homo sapiens	27-32
11723234-0	2001	Cyclophosphamide induces caspase 9-dependent apoptosis in 9L tumor cells.	Cyclophosphamide	0-16	caspase 9	Homo sapiens	25-34
11770832-8	2001	CONCLUSION: Comparing IC50 values with plasma concentrations present during antineoplastic therapy, the agents cyclophosphamide, ifosfamide, vinblastine, teniposide and docetaxel could possibly cause clinical drug interactions by inhibition of CYP3A4.	Cyclophosphamide	111-127	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	244-250
11723234-9	2001	CPA induced S-phase cell cycle arrest followed by conversion to an apoptotic pre-G1 state in wild-type 9L cells; by contrast, Bcl-2-expressing 9L cells accumulated in G2/M in response to CPA treatment.	Cyclophosphamide	187-190	BCL2 apoptosis regulator	Homo sapiens	126-131
11723234-10	2001	Intratumoral expression of Bcl-2 and related family members, including both apoptotic and antiapoptotic factors, is thus an important determinant of the responsiveness of tumor cells to CPA and ifosfamide, both in the context of conventional chemotherapy and in patients sensitized to these oxazaphosphorine drugs by the use of cytochrome P450-based gene therapy.	Cyclophosphamide	186-189	BCL2 apoptosis regulator	Homo sapiens	27-32
11691788-0	2001	Quantitative T1rho magnetic resonance imaging of RIF-1 tumors in vivo: detection of early response to cyclophosphamide therapy.	Cyclophosphamide	102-118	replication timing regulatory factor 1	Mus musculus	49-54
12578576-1	2001	The life span of NS-1 myeloma-bearing mice was observed after treating with KRN7000 and combined with cyclophosphamide (CTX).	Cyclophosphamide	102-118	V-set and immunoglobulin domain containing 2	Mus musculus	120-123
11745183-15	2001	CONCLUSIONS: Treatment with two cycles of mitoxantrone 25 mg/m2 and cyclophosphamide 4000 mg/m2 with G-CSF but without stem cell support was well tolerated.	Cyclophosphamide	68-84	colony stimulating factor 3	Homo sapiens	101-106
11723234-2	2001	Tumor cells transduced with the human cytochrome P450 gene CYP2B6 are greatly sensitized to CPA, however, the pathway of CPA-induced cell death is unknown.	Cyclophosphamide	92-95	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	59-65
11723234-2	2001	Tumor cells transduced with the human cytochrome P450 gene CYP2B6 are greatly sensitized to CPA, however, the pathway of CPA-induced cell death is unknown.	Cyclophosphamide	121-124	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	59-65
11723234-3	2001	The present study investigates the cytotoxic events induced by CPA in 9L gliosarcoma cells retrovirally transduced with CYP2B6, or induced in wild-type 9L cells treated with mafosfamide (MFA) or 4-hydroperoxyifosfamide (4OOH-IFA), chemically activated forms of CPA and its isomer ifosfamide.	Cyclophosphamide	63-66	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	120-126
11723234-4	2001	CPA and MFA were both shown to effect tumor cell death by stimulating apoptosis, as evidenced by the induction of plasma membrane blebbing, DNA fragmentation, and cleavage of the caspase 3 and caspase 7 substrate poly(ADP-ribose) polymerase (PARP) in drug-treated cells.	Cyclophosphamide	0-3	caspase 3	Homo sapiens	179-188
11723234-4	2001	CPA and MFA were both shown to effect tumor cell death by stimulating apoptosis, as evidenced by the induction of plasma membrane blebbing, DNA fragmentation, and cleavage of the caspase 3 and caspase 7 substrate poly(ADP-ribose) polymerase (PARP) in drug-treated cells.	Cyclophosphamide	0-3	caspase 7	Homo sapiens	193-202
11723234-4	2001	CPA and MFA were both shown to effect tumor cell death by stimulating apoptosis, as evidenced by the induction of plasma membrane blebbing, DNA fragmentation, and cleavage of the caspase 3 and caspase 7 substrate poly(ADP-ribose) polymerase (PARP) in drug-treated cells.	Cyclophosphamide	0-3	poly(ADP-ribose) polymerase 1	Homo sapiens	213-240
11723234-4	2001	CPA and MFA were both shown to effect tumor cell death by stimulating apoptosis, as evidenced by the induction of plasma membrane blebbing, DNA fragmentation, and cleavage of the caspase 3 and caspase 7 substrate poly(ADP-ribose) polymerase (PARP) in drug-treated cells.	Cyclophosphamide	0-3	poly(ADP-ribose) polymerase 1	Homo sapiens	242-246
11723234-5	2001	Caspase 9 was identified as the regulatory upstream caspase activated in 9L cells treated with CPA, MFA, or 4OOH-IFA, implicating the mitochondrial apoptotic pathway in oxazaphosphorine-induced tumor cell death.	Cyclophosphamide	95-98	caspase 9	Homo sapiens	0-9
11685103-10	2001	KGF prevented the decrease in lung GSH after TBI+Cy and decreased lung MDA after both TBI and TBI+Cy.	Cyclophosphamide	49-51	fibroblast growth factor 7	Mus musculus	0-3
11703364-5	2001	Following transplantation of cyclophosphamide-treated C57BL/6 with T-depleted C3H bone marrow cells, or for the EL4 tumour, immunization of C57BL/6 mice with tumour cells transfected with a vector encoding the co-stimulatory molecule CD80 (EL4-CD80), mice resist growth of tumour challenge.	Cyclophosphamide	29-45	CD80 antigen	Mus musculus	234-238
11703364-5	2001	Following transplantation of cyclophosphamide-treated C57BL/6 with T-depleted C3H bone marrow cells, or for the EL4 tumour, immunization of C57BL/6 mice with tumour cells transfected with a vector encoding the co-stimulatory molecule CD80 (EL4-CD80), mice resist growth of tumour challenge.	Cyclophosphamide	29-45	CD80 antigen	Mus musculus	240-248
11685103-10	2001	KGF prevented the decrease in lung GSH after TBI+Cy and decreased lung MDA after both TBI and TBI+Cy.	Cyclophosphamide	98-100	fibroblast growth factor 7	Mus musculus	0-3
11685103-11	2001	KGF increased liver GSH levels and GSH Eh after TBI and GSH Eh after TBI+Cy.	Cyclophosphamide	73-75	fibroblast growth factor 7	Mus musculus	0-3
11685103-14	2001	KGF treatment attenuates the Cy-induced decrease in lung GSH, decreases post-BMT lung lipid peroxidation, and improves liver GSH redox indices.	Cyclophosphamide	29-31	fibroblast growth factor 7	Mus musculus	0-3
11759828-2	2001	It was the purpose of this in vitro study to define the association between HER-2/neu overexpression and the sensitivity to the chemotherapeutic drug combinations of cyclophosphamide, methotrexate and 5-fluorouracil (CMF) and 5-fluorouracil, epirubicin and cyclophosphamide (FEC) of breast cancer cells derived from 140 chemotherapy-naive patients at the time of primary surgery.	Cyclophosphamide	166-182	erb-b2 receptor tyrosine kinase 2	Homo sapiens	82-85
11520135-0	2001	High-dose topotecan, melphalan, and cyclophosphamide (TMC) with stem cell support: a new regimen for the treatment of advanced ovarian cancer.	Cyclophosphamide	36-52	STT3 oligosaccharyltransferase complex catalytic subunit A	Homo sapiens	54-57
11583189-0	2001	HER-2 and topo-isomerase IIalpha as predictive markers in a population of node-positive breast cancer patients randomly treated with adjuvant CMF or epirubicin plus cyclophosphamide.	Cyclophosphamide	165-181	erb-b2 receptor tyrosine kinase 2	Homo sapiens	0-32
11878581-1	2001	PURPOSE: The authors report the use of a cyclophosphamide, hydroxydaunorubicin, vincristine, and prednisone (CHOP)-based chemotherapy regimen in treating six children with posttransplantation lymphoproliferative disorder (PTLD) that developed after solid organ transplantation.	Cyclophosphamide	41-57	DNA damage inducible transcript 3	Homo sapiens	109-113
11759828-2	2001	It was the purpose of this in vitro study to define the association between HER-2/neu overexpression and the sensitivity to the chemotherapeutic drug combinations of cyclophosphamide, methotrexate and 5-fluorouracil (CMF) and 5-fluorouracil, epirubicin and cyclophosphamide (FEC) of breast cancer cells derived from 140 chemotherapy-naive patients at the time of primary surgery.	Cyclophosphamide	257-273	erb-b2 receptor tyrosine kinase 2	Homo sapiens	82-85
11532345-1	2001	OBJECTIVE: Primitive hematopoietic stem cell function was assessed after cyclophosphamide with granulocyte-macrophage colony-stimulating factor (GM-CSF), with or without preadministration of interleukin-1, using competitive repopulation.	Cyclophosphamide	73-89	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	145-151
11562071-3	2001	(2) The protective effect of PSK was significantly decreased in mice treated with cyclophosphamide or carrageenan, or in mice treated previously with anti-tumor necrosis factor-alpha (TNF-alpha) antibody.	Cyclophosphamide	82-98	TAO kinase 2	Mus musculus	29-32
11591119-6	2001	Administration of cyclophosphamide caused a progression to severe islet destruction in ICAM-1(+/+) NOD mice within 10 days.	Cyclophosphamide	18-34	intercellular adhesion molecule 1	Mus musculus	87-93
11511721-1	2001	The effects of combined treatment with cyclophosphamide (CTX) and interferon-beta (IFN-beta) are described in selected patients with "rapidly transitional" multiple sclerosis.	Cyclophosphamide	39-55	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	57-60
11534764-3	2001	Sequencing revealed two contiguous open reading frames (ORF1 and ORF2) on the same strand and based on amino acid sequence homology, they were designated as astA and dsbA, respectively.	Cyclophosphamide	157-161	hypothetical protein	Citrobacter freundii	56-60
11511291-4	2001	Intraperitoneal administration of the agonist PTH(1-34) or the antagonists PTH(7-34) and PTHrP(7-34) significantly altered the follicular response to cyclophosphamide in vivo.	Cyclophosphamide	150-166	parathyroid hormone	Homo sapiens	46-49
11534764-3	2001	Sequencing revealed two contiguous open reading frames (ORF1 and ORF2) on the same strand and based on amino acid sequence homology, they were designated as astA and dsbA, respectively.	Cyclophosphamide	157-161	hypothetical protein	Citrobacter freundii	65-69
11511291-4	2001	Intraperitoneal administration of the agonist PTH(1-34) or the antagonists PTH(7-34) and PTHrP(7-34) significantly altered the follicular response to cyclophosphamide in vivo.	Cyclophosphamide	150-166	parathyroid hormone	Homo sapiens	75-78
11511291-4	2001	Intraperitoneal administration of the agonist PTH(1-34) or the antagonists PTH(7-34) and PTHrP(7-34) significantly altered the follicular response to cyclophosphamide in vivo.	Cyclophosphamide	150-166	parathyroid hormone like hormone	Homo sapiens	89-94
11502862-10	2001	In vivo treatment with PTX or ROL prevented iNOS protein expression in the islets of NOD mice with cyclophosphamide-accelerated disease.	Cyclophosphamide	99-115	nitric oxide synthase 2, inducible	Mus musculus	44-48
11584710-9	2001	Standard treatment of advanced aggressive NHL is polychemotherapy with cyclophosphamide, adriamycin, vincristine and prednisone (CHOP).	Cyclophosphamide	71-87	DNA damage inducible transcript 3	Homo sapiens	129-133
11389879-3	2001	In this study, a Chinese hamster ovary cell line expressing human cytochrome P450 CYP1B1 was used to evaluate the cytotoxic profile of several anticancer drugs (docetaxel, paclitaxel, cyclophosphamide, doxorubicin, 5-fluorouracil, cisplatin, and carboplatin) commonly used clinically in the treatment of cancer.	Cyclophosphamide	184-200	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	82-88
11466674-8	2001	CONCLUSIONS: T/N(d) ratios determined by (99m)Tc-MIBI scintigraphy are useful in the prediction of response to chemotherapy with epirubicin and cyclophosphamide or docetaxel as well as in the in vivo evaluation of P-gp expression status in tumors in patients with locally advanced or recurrent breast carcinoma.	Cyclophosphamide	144-160	phosphoglycolate phosphatase	Homo sapiens	214-218
11509931-0	2001	Dexamethasone, paclitaxel, etoposide, cyclophosphamide (d-TEC) and G-CSF for stem cell mobilisation in multiple myeloma.	Cyclophosphamide	38-54	tec protein tyrosine kinase	Homo sapiens	58-61
11498768-1	2001	Human cytochrome P450 2B6 (CYP2B6) metabolizes the prodrug cyclophosphamide (CPA) to produce phosphoramide mustard that cross-links DNA leading to cell death.	Cyclophosphamide	59-75	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	6-25
11466671-1	2001	BACKGROUND: To address the feasibility and outcome of moderate dose intensification with granulocyte-colony stimulating factor (G-CSF) for patients with aggressive non-Hodgkin lymphoma (NHL), the Cancer and Leukemia Group B (CALGB) conducted two studies evaluating dose-escalated cyclophosphamide and etoposide in the cyclophosphamide, doxorubicin, vincristine, prednisone, etoposide (CHOPE) regimen.	Cyclophosphamide	280-296	colony stimulating factor 3	Homo sapiens	128-133
11498768-1	2001	Human cytochrome P450 2B6 (CYP2B6) metabolizes the prodrug cyclophosphamide (CPA) to produce phosphoramide mustard that cross-links DNA leading to cell death.	Cyclophosphamide	59-75	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	27-33
11466671-1	2001	BACKGROUND: To address the feasibility and outcome of moderate dose intensification with granulocyte-colony stimulating factor (G-CSF) for patients with aggressive non-Hodgkin lymphoma (NHL), the Cancer and Leukemia Group B (CALGB) conducted two studies evaluating dose-escalated cyclophosphamide and etoposide in the cyclophosphamide, doxorubicin, vincristine, prednisone, etoposide (CHOPE) regimen.	Cyclophosphamide	318-334	colony stimulating factor 3	Homo sapiens	128-133
11899785-0	2001	Meta-analysis of adjuvant cyclophosphamide/methotrexate/5-fluorouracil chemotherapy in postmenopausal women with estrogen receptor-positive, node-positive breast cancer.	Cyclophosphamide	26-42	estrogen receptor 1	Homo sapiens	113-130
11899785-1	2001	Conflicting results have been published regarding the efficacy of adjuvant cyclophosphamide/methotrexate/5-fluorouracil (CMF)-type chemotherapy in postmenopausal, estrogen receptor (ER)-positive women.	Cyclophosphamide	75-91	estrogen receptor 1	Homo sapiens	163-180
11899785-1	2001	Conflicting results have been published regarding the efficacy of adjuvant cyclophosphamide/methotrexate/5-fluorouracil (CMF)-type chemotherapy in postmenopausal, estrogen receptor (ER)-positive women.	Cyclophosphamide	75-91	estrogen receptor 1	Homo sapiens	182-184
11406337-9	2001	In CPA-treated animals, NK1R-positive areas and staining intensity within the dorsal spinal cord were significantly increased in the L5 to S2 spinal cord areas, especially in the L6 and S1 segments.	Cyclophosphamide	3-6	tachykinin receptor 1	Rattus norvegicus	24-28
11508269-2	2001	We analysed temporal changes in ART2.2 expression in unmanipulated and cyclophosphamide-treated NOD/Lt mice compared with diabetes-resistant control strains.	Cyclophosphamide	71-87	ADP-ribosyltransferase 2b	Mus musculus	32-38
11508269-8	2001	This pattern was reproduced in cyclophosphamide-accelerated diabetes in young NOD/Lt males, wherein a retarded repopulation of ART2.2 T cells in spleen and islets correlated with development of heavy insulitis and diabetes.	Cyclophosphamide	31-47	ADP-ribosyltransferase 2b	Mus musculus	127-133
11406337-10	2001	In the L6 spinal segment, CPA-treatment enhanced NK1R immunostaining in the medial and the lateral dorsal horn, as well as in the lateral laminae including the sacral parasympathetic nucleus to a lesser extent.	Cyclophosphamide	26-29	tachykinin receptor 1	Rattus norvegicus	49-53
11406337-11	2001	In CPA-treated animals, substance P staining intensity increased in the same regions in which NK1R immunoreactivity was increased.	Cyclophosphamide	3-6	tachykinin receptor 1	Rattus norvegicus	94-98
11350799-9	2001	The concentrations of interleukin-8, granulocyte colony-stimulating factor, monocyte chemoattractant protein-1, and granulocyte-macrophage colony-stimulating factor significantly increased in response to cyclophosphamide.	Cyclophosphamide	204-220	C-X-C motif chemokine ligand 8	Homo sapiens	22-35
11677846-9	2001	The authors indicate that the location found in the present case--at the laryngeal-pharyngeal region boundary--is important for the clinical history, histopathological data and response to specific therapy (cyclophosphamide and desamethasone) for a diagnosis of localized Wegener granulomatosis, even when c-ANCA do not test positive.	Cyclophosphamide	207-223	proteinase 3	Homo sapiens	306-312
11350799-10	2001	These data suggest that lung fibroblasts may modulate inflammatory cell recruitment into the lung by releasing NCA and MCA in response to cyclophosphamide.	Cyclophosphamide	138-154	CEA cell adhesion molecule 4	Homo sapiens	111-114
11758808-0	2001	Immunoexpression of interleukin-1beta in pancreatic islets of NOD mice during cyclophosphamide-accelerated diabetes: co-localization in macrophages and endocrine cells and its attenuation with oral nicotinamide.	Cyclophosphamide	78-94	interleukin 1 beta	Mus musculus	20-37
11389073-1	2001	Transduction of tumor cells with a cyclophosphamide (CPA)-activating cytochrome P-450 (P450) gene provides the capacity for localized prodrug activation and greatly sensitizes solid tumors to CPA treatment in vivo.	Cyclophosphamide	35-51	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	69-91
11389073-1	2001	Transduction of tumor cells with a cyclophosphamide (CPA)-activating cytochrome P-450 (P450) gene provides the capacity for localized prodrug activation and greatly sensitizes solid tumors to CPA treatment in vivo.	Cyclophosphamide	53-56	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	69-91
11389073-1	2001	Transduction of tumor cells with a cyclophosphamide (CPA)-activating cytochrome P-450 (P450) gene provides the capacity for localized prodrug activation and greatly sensitizes solid tumors to CPA treatment in vivo.	Cyclophosphamide	192-195	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	69-91
11498765-0	2001	Modulation of cyclophosphamide-based cytochrome P450 gene therapy using liver P450 inhibitors.	Cyclophosphamide	14-30	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	37-52
11498765-1	2001	The sensitivity of tumors to cyclophosphamide (CPA) and other anticancer prodrugs can be substantially enhanced by transduction of tumors with a prodrug-activating mammalian cytochrome P450 (CYP) enzyme in combination with the flavoenzyme P450 reductase.	Cyclophosphamide	29-45	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	174-189
11498765-1	2001	The sensitivity of tumors to cyclophosphamide (CPA) and other anticancer prodrugs can be substantially enhanced by transduction of tumors with a prodrug-activating mammalian cytochrome P450 (CYP) enzyme in combination with the flavoenzyme P450 reductase.	Cyclophosphamide	29-45	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	191-194
11498765-1	2001	The sensitivity of tumors to cyclophosphamide (CPA) and other anticancer prodrugs can be substantially enhanced by transduction of tumors with a prodrug-activating mammalian cytochrome P450 (CYP) enzyme in combination with the flavoenzyme P450 reductase.	Cyclophosphamide	47-50	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	174-189
11498765-1	2001	The sensitivity of tumors to cyclophosphamide (CPA) and other anticancer prodrugs can be substantially enhanced by transduction of tumors with a prodrug-activating mammalian cytochrome P450 (CYP) enzyme in combination with the flavoenzyme P450 reductase.	Cyclophosphamide	47-50	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	191-194
11437491-0	2001	In vivo blockade of the Fas-Fas ligand pathway inhibits cyclophosphamide-induced diabetes in NOD mice.	Cyclophosphamide	56-72	Fas ligand (TNF superfamily, member 6)	Mus musculus	24-38
11437491-3	2001	Here we took advantage of the cyclophosphamide-induced model of accelerated diabetes in NOD mice to explore the physiopathological role of the Fas-Fas Ligand pathway.	Cyclophosphamide	30-46	Fas ligand (TNF superfamily, member 6)	Mus musculus	143-157
11359814-9	2001	Cy-treated mice develop splenic early myeloid (CD11b, Gr-1, CD31 (ER-MP12), ER-MP20, ER-MP54) cells producing large amounts of NO upon T cell-derived signals (IFN-gamma plus CD40 ligation) able to inhibit tumor cell growth in vitro.	Cyclophosphamide	0-2	integrin alpha M	Mus musculus	47-52
11359814-9	2001	Cy-treated mice develop splenic early myeloid (CD11b, Gr-1, CD31 (ER-MP12), ER-MP20, ER-MP54) cells producing large amounts of NO upon T cell-derived signals (IFN-gamma plus CD40 ligation) able to inhibit tumor cell growth in vitro.	Cyclophosphamide	0-2	glutathione reductase	Mus musculus	54-58
11359814-9	2001	Cy-treated mice develop splenic early myeloid (CD11b, Gr-1, CD31 (ER-MP12), ER-MP20, ER-MP54) cells producing large amounts of NO upon T cell-derived signals (IFN-gamma plus CD40 ligation) able to inhibit tumor cell growth in vitro.	Cyclophosphamide	0-2	platelet/endothelial cell adhesion molecule 1	Mus musculus	60-64
11359814-9	2001	Cy-treated mice develop splenic early myeloid (CD11b, Gr-1, CD31 (ER-MP12), ER-MP20, ER-MP54) cells producing large amounts of NO upon T cell-derived signals (IFN-gamma plus CD40 ligation) able to inhibit tumor cell growth in vitro.	Cyclophosphamide	0-2	interferon gamma	Mus musculus	159-168
11359814-9	2001	Cy-treated mice develop splenic early myeloid (CD11b, Gr-1, CD31 (ER-MP12), ER-MP20, ER-MP54) cells producing large amounts of NO upon T cell-derived signals (IFN-gamma plus CD40 ligation) able to inhibit tumor cell growth in vitro.	Cyclophosphamide	0-2	CD40 antigen	Mus musculus	174-178
11468938-0	2001	A mechanism-based pharmacokinetic model for the cytochrome P450 drug-drug interaction between cyclophosphamide and thioTEPA and the autoinduction of cyclophosphamide.	Cyclophosphamide	94-110	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	48-63
11468938-0	2001	A mechanism-based pharmacokinetic model for the cytochrome P450 drug-drug interaction between cyclophosphamide and thioTEPA and the autoinduction of cyclophosphamide.	Cyclophosphamide	149-165	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	48-63
11377097-9	2001	These results show the metabolic activation of APAP, CPA and BA by the specific CYP subtypes expressed in the transformants and demonstrate the usefulness of these transformants for in vitro metabolic and toxicological studies in human liver.	Cyclophosphamide	53-56	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	80-83
11510034-1	2001	We sought to define the recommended dose of cyclophosphamide (CTX) for subsequent phase II assessment when combined with fixed doses of gemcitabine (Gemzar; Eli Lilly and Company, Indianapolis, IN) and 5-fluorouracil/folinic acid in metastatic breast cancer patients previously treated with anthracyclines and taxanes.	Cyclophosphamide	44-60	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	62-65
11436102-0	2001	High-dose melphalan with G-CSF-stimulated whole blood rescue followed by stem cell harvesting and busulphan/cyclophosphamide with autologous stem cell transplantation in multiple myeloma.	Cyclophosphamide	108-124	colony stimulating factor 3	Homo sapiens	25-30
11379783-6	2001	Based on amino acid sequence homology, ORF1 and ORF2 are designated as astA and dsbA, respectively.	Cyclophosphamide	71-75	hypothetical protein	Salmonella enterica subsp. enterica serovar Typhimurium	39-43
11379783-6	2001	Based on amino acid sequence homology, ORF1 and ORF2 are designated as astA and dsbA, respectively.	Cyclophosphamide	71-75	hypothetical protein	Salmonella enterica subsp. enterica serovar Typhimurium	48-52
11290588-6	2001	Next, LT-HSC from mice previously treated with a single dose of CY, which kills cycling cells, and 3 daily doses of G-CSF, were nearly all killed by a second dose of CY, suggesting that CY/G-CSF causes virtually all LT-HSC to cycle.	Cyclophosphamide	64-66	colony stimulating factor 3 (granulocyte)	Mus musculus	189-194
11325840-0	2001	Cyclophosphamide, doxorubicin, and paclitaxel enhance the antitumor immune response of granulocyte/macrophage-colony stimulating factor-secreting whole-cell vaccines in HER-2/neu tolerized mice.	Cyclophosphamide	0-16	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	87-135
11325840-0	2001	Cyclophosphamide, doxorubicin, and paclitaxel enhance the antitumor immune response of granulocyte/macrophage-colony stimulating factor-secreting whole-cell vaccines in HER-2/neu tolerized mice.	Cyclophosphamide	0-16	erb-b2 receptor tyrosine kinase 2	Mus musculus	169-178
11325840-6	2001	We found that cyclophosphamide, paclitaxel, and doxorubicin, when given in a defined sequence with a GM-CSF-secreting, neu-expressing whole-cell vaccine, enhanced the vaccine"s potential to delay tumor growth in neu transgenic mice.	Cyclophosphamide	14-30	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	101-107
11325840-6	2001	We found that cyclophosphamide, paclitaxel, and doxorubicin, when given in a defined sequence with a GM-CSF-secreting, neu-expressing whole-cell vaccine, enhanced the vaccine"s potential to delay tumor growth in neu transgenic mice.	Cyclophosphamide	14-30	erb-b2 receptor tyrosine kinase 2	Mus musculus	119-122
11325840-6	2001	We found that cyclophosphamide, paclitaxel, and doxorubicin, when given in a defined sequence with a GM-CSF-secreting, neu-expressing whole-cell vaccine, enhanced the vaccine"s potential to delay tumor growth in neu transgenic mice.	Cyclophosphamide	14-30	erb-b2 receptor tyrosine kinase 2	Mus musculus	212-215
11325840-8	2001	Furthermore, paclitaxel and cyclophosphamide appear to amplify the T helper 1 neu-specific T-cell response.	Cyclophosphamide	28-44	erb-b2 receptor tyrosine kinase 2	Mus musculus	78-81
11409710-7	2001	NOD/LtJ and NOD/Bom mice were found significantly to upregulate pancreatic IL-12p40 and IL-18 expression after cyclophosphamide treatment, followed by an increase in IFN-gamma mRNA levels.	Cyclophosphamide	111-127	interleukin 12b	Mus musculus	75-83
11409710-7	2001	NOD/LtJ and NOD/Bom mice were found significantly to upregulate pancreatic IL-12p40 and IL-18 expression after cyclophosphamide treatment, followed by an increase in IFN-gamma mRNA levels.	Cyclophosphamide	111-127	interleukin 18	Mus musculus	88-93
11409710-9	2001	The two strains sharing MHC haplotype H-2g7 expression with NOD did respond to cyclophosphamide with IL-12p40/IL-18 gene expression.	Cyclophosphamide	79-95	interleukin 12b	Mus musculus	101-109
11409710-9	2001	The two strains sharing MHC haplotype H-2g7 expression with NOD did respond to cyclophosphamide with IL-12p40/IL-18 gene expression.	Cyclophosphamide	79-95	interleukin 18	Mus musculus	110-115
11317283-1	2001	We used cycles of plasma exchange and intravenous cyclophosphamide to treat a patient who had chronic inflammatory demyelinating polyneuropathy with anti-myelin-associated glycoprotein/sulfoglucuronylparagloboside IgM antibody.	Cyclophosphamide	50-66	myelin associated glycoprotein	Homo sapiens	154-184
11346706-10	2001	Compared to EPI-TAX, mobilization with CY required the overall processing of 30 percent less whole-blood volume to reach the target yield of > or = 10 x 10(6) CD34+ cells per kg of body weight.	Cyclophosphamide	39-41	CD34 molecule	Homo sapiens	162-166
11290588-6	2001	Next, LT-HSC from mice previously treated with a single dose of CY, which kills cycling cells, and 3 daily doses of G-CSF, were nearly all killed by a second dose of CY, suggesting that CY/G-CSF causes virtually all LT-HSC to cycle.	Cyclophosphamide	166-168	colony stimulating factor 3 (granulocyte)	Mus musculus	189-194
11385964-1	2001	PURPOSE: Somatostatin, prolactin, retinoids, melatonin and ACTH have been shown to influence the lymphatic growth, and the action of the cyclophosphamide in lymphoproliferative disorders is well known.	Cyclophosphamide	137-153	proopiomelanocortin	Homo sapiens	59-63
11304774-1	2001	PURPOSE: To evaluate whether an accelerated-intensified cyclophosphamide, epirubicin, and fluorouracil (CEF) chemotherapy regimen with the support of granulocyte colony-stimulating factor (G-CSF) induces a higher activity and efficacy compared with standard CEF in metastatic breast cancer patients.	Cyclophosphamide	56-72	colony stimulating factor 3	Homo sapiens	150-187
11286477-1	2001	Dexrazoxane combined with doxorubicin (+ 5-fluorouracil + cyclophosphamide - the FAC regime) leads to a significant decrease in doxorubicin cardiotoxicity and a significant increase in median survival time for patients with advanced breast cancer responsive to FAC.	Cyclophosphamide	58-74	FA complementation group C	Homo sapiens	81-84
11498768-1	2001	Human cytochrome P450 2B6 (CYP2B6) metabolizes the prodrug cyclophosphamide (CPA) to produce phosphoramide mustard that cross-links DNA leading to cell death.	Cyclophosphamide	77-80	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	6-25
11498768-1	2001	Human cytochrome P450 2B6 (CYP2B6) metabolizes the prodrug cyclophosphamide (CPA) to produce phosphoramide mustard that cross-links DNA leading to cell death.	Cyclophosphamide	77-80	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	27-33
11282106-6	2001	To explore the mechanism by which cyclophosphamide increases the expression of inducible NOS (iNOS), primary cultures of rat bladder smooth muscle were developed.	Cyclophosphamide	34-50	nitric oxide synthase 2	Rattus norvegicus	79-92
11276342-6	2001	The patient was treated with combination chemotherapy, including cyclophosphamide, doxorubicin, vincristine and prednisolone (CHOP), which resulted in complete clinical remission after two courses.	Cyclophosphamide	65-81	DNA damage inducible transcript 3	Homo sapiens	126-130
11282106-6	2001	To explore the mechanism by which cyclophosphamide increases the expression of inducible NOS (iNOS), primary cultures of rat bladder smooth muscle were developed.	Cyclophosphamide	34-50	nitric oxide synthase 2	Rattus norvegicus	94-98
11282106-9	2001	On the other hand, incubation of primary cell cultures with plasma from rats treated with cyclophosphamide (150 mg/kg, 12 h) produced a marked increase in iNOS expression and NO production.	Cyclophosphamide	90-106	nitric oxide synthase 2	Rattus norvegicus	155-159
11282106-10	2001	Taken together, our results indicate that NO plays an important role in the pathogenesis of cyclophosphamide-induced cystitis in rats, and some factors may be released in cyclophosphamide-treated rat plasma which stimulate iNOS expression in primary culture of rat bladder smooth muscle cells.	Cyclophosphamide	92-108	nitric oxide synthase 2	Rattus norvegicus	223-227
11282106-10	2001	Taken together, our results indicate that NO plays an important role in the pathogenesis of cyclophosphamide-induced cystitis in rats, and some factors may be released in cyclophosphamide-treated rat plasma which stimulate iNOS expression in primary culture of rat bladder smooth muscle cells.	Cyclophosphamide	171-187	nitric oxide synthase 2	Rattus norvegicus	223-227
11269797-6	2001	Cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) therapy was given, and the patient became asymptomatic with normal blood tests and was thought to be in remission.	Cyclophosphamide	0-16	DNA damage inducible transcript 3	Homo sapiens	60-64
11332152-2	2001	The in situ bioactivation of cyclophosphamide by cytochrome p450-2B1 and subsequent p53 delivery were examined.	Cyclophosphamide	29-45	tumor protein p53	Homo sapiens	84-87
11230885-1	2001	BACKGROUND: A limited number cycles of cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) chemotherapy followed by involved field radiotherapy is the treatment of choice for Ann Arbor stage I intermediate or high grade non-Hodgkin"s lymphomas (NHL).	Cyclophosphamide	39-55	DNA damage inducible transcript 3	Homo sapiens	98-102
11320670-3	2001	Preclinical models indicate that cellular sensitivity to cyclophosphamide and other oxazaphosphorines, e.g., ifosfamide, is inversely related to the cellular content of two aldehyde dehydrogenases, viz ALDH1A1 and ALDH3A1, and glutathione.	Cyclophosphamide	57-73	aldehyde dehydrogenase 1 family member A1	Homo sapiens	202-209
11320670-3	2001	Preclinical models indicate that cellular sensitivity to cyclophosphamide and other oxazaphosphorines, e.g., ifosfamide, is inversely related to the cellular content of two aldehyde dehydrogenases, viz ALDH1A1 and ALDH3A1, and glutathione.	Cyclophosphamide	57-73	aldehyde dehydrogenase 3 family member A1	Homo sapiens	214-221
11312054-1	2001	These studies examined changes in the expression of calcitonin gene-related peptide (CGRP) and substance P (SP) in lumbosacral (L6-S1) micturition reflex pathways, following chronic cystitis induced by cyclophosphamide (CYP).	Cyclophosphamide	202-218	calcitonin-related polypeptide alpha	Rattus norvegicus	52-83
11207247-2	2001	Furthermore, NOD mice given tolerogenic doses of GAD65(524--543) are protected from spontaneous and cyclophosphamide-induced diabetes.	Cyclophosphamide	100-116	glutamic acid decarboxylase 2	Mus musculus	49-54
11360931-0	2001	Down regulation of T-cell-derived IL-10 production by low-dose cyclophosphamide treatment in tumor-bearing rats restores in vitro normal lymphoproliferative response.	Cyclophosphamide	63-79	interleukin 10	Rattus norvegicus	34-39
11297880-2	2001	A significant reduction in plasma levels of LH and E2 along with significant diminution in the activities of ovarian Delta5,3beta -HSD and 17beta- HSD were observed following cyclophosphamide treatment for 28 days without any change in the plasma level of FSH.	Cyclophosphamide	175-191	hydroxysteroid (17-beta) dehydrogenase 3	Rattus norvegicus	139-150
11245434-0	2001	Erythropoietin restores the anemia-induced reduction in cyclophosphamide cytotoxicity in rat tumors.	Cyclophosphamide	56-72	erythropoietin	Rattus norvegicus	0-14
11245434-1	2001	The aim of this study was to examine the impact of anemia prevention by recombinant human erythropoietin (rHuEPO) treatment on the cytotoxicity of cyclophosphamide in solid experimental tumors.	Cyclophosphamide	147-163	erythropoietin	Homo sapiens	90-104
11360931-8	2001	Moreover, our results suggest that the shift from immunosuppression to immunopotentiation induced by treatment of tumor-bearing rats with a single low-dose of Cy is mediated by a reduction in T-cell derived IL-10 production, which would account, to some extent, for the antimetastatic effect of Cy treatment.	Cyclophosphamide	159-161	interleukin 10	Rattus norvegicus	207-212
11360931-8	2001	Moreover, our results suggest that the shift from immunosuppression to immunopotentiation induced by treatment of tumor-bearing rats with a single low-dose of Cy is mediated by a reduction in T-cell derived IL-10 production, which would account, to some extent, for the antimetastatic effect of Cy treatment.	Cyclophosphamide	295-297	interleukin 10	Rattus norvegicus	207-212
11426529-1	2001	UNLABELLED: Recent data from GELF (Groupe d"Etude des Lymphomes Folliculaires) have shown that the addition of interferon alfa-2b (IFN) to a doxorubicin-containing regimen (CHVP: cyclophosphamide, doxorubicin, teniposide and prednisone) prolongs both progression-free survival and overall survival in high-tumor-burden follicular non-Hodgkin"s lymphoma.	Cyclophosphamide	179-195	interferon alpha 1	Homo sapiens	131-134
11221993-0	2001	Oral administration of insulin to neonates suppresses spontaneous and cyclophosphamide induced diabetes in the NOD mouse.	Cyclophosphamide	70-86	insulin	Homo sapiens	23-30
11221993-7	2001	Neonatal administration of insulin B-chain peptide also suppressed cyclophosphamide induced diabetes in the NOD whereas oral insulin administration to 4-week-old NOD mice had no effect, suggesting that the mechanism of disease suppression in the neonate involved anergy or deletion.	Cyclophosphamide	67-83	insulin	Homo sapiens	27-34
11216531-0	2001	Imaging cyclophosphamide-induced intramedullary apoptosis in rats using 99mTc-radiolabeled annexin V.	Cyclophosphamide	8-24	annexin A5	Rattus norvegicus	91-100
11216531-5	2001	RESULTS: Intravenously administered radiolabeled annexin V localized preferentially in the femur, pelvis, vertebrae, and spleen; increased uptake in these organs was easily visualized as early as 8 h after injection of 100 mg/kg cyclophosphamide in 8- to 10-wk-old animals.	Cyclophosphamide	229-245	annexin A5	Rattus norvegicus	49-58
11216531-6	2001	Higher doses of cyclophosphamide (150 mg/kg) in animals of the same age increased annexin V uptake in the bone marrow and splenic tissue and delayed recovery of these organs as seen histologically compared with lower doses.	Cyclophosphamide	16-32	annexin A5	Rattus norvegicus	82-91
11477443-0	2001	HER-2 expression is a prognostic factor in patients with metastatic breast cancer treated with a combination of high-dose cyclophosphamide, mitoxantrone, paclitaxel and autologous blood stem cell support.	Cyclophosphamide	122-138	erb-b2 receptor tyrosine kinase 2	Homo sapiens	0-5
11306046-5	2001	It has been demonstrated that cytosolic ALDH3 is important in determining the resistance of tumor cells to antitumor drugs, such as cyclophosphamide.	Cyclophosphamide	132-148	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	40-45
11133503-7	2001	Pretreatment with an inhibitor of leukocytes in the bone marrow (cyclophosphamide) or with a blocking antibody to IL-8 prevented both IL-13-induced leukocyte recruitment and GC metaplasia.	Cyclophosphamide	65-81	interleukin 13	Homo sapiens	134-139
12577395-2	2001	METHODS: Influence of 3A on T-lymphocyte subsets, IgG production of B cells, interferon-gamma (IFN-gamma) mRNA expression in cyclophosphamide (Cy)-treated mice, tumor bearing mice and senescence accelerated mouse-prone/8 (SAMP8) were assessed in vivo and in vitro.	Cyclophosphamide	143-145	interferon gamma	Mus musculus	77-93
12577395-2	2001	METHODS: Influence of 3A on T-lymphocyte subsets, IgG production of B cells, interferon-gamma (IFN-gamma) mRNA expression in cyclophosphamide (Cy)-treated mice, tumor bearing mice and senescence accelerated mouse-prone/8 (SAMP8) were assessed in vivo and in vitro.	Cyclophosphamide	143-145	interferon gamma	Mus musculus	95-104
12577395-3	2001	RESULTS: Oral administration of 3A could elevate the decreased T-lymphocyte subsets in all model mice, it also could promote the IgG secretion of splenic cells in SAMP8 and increase IFN-gamma mRNA expression in Cy-treated mice.	Cyclophosphamide	211-213	interferon gamma	Mus musculus	182-191
11208823-0	2001	Response to cyclophosphamide, methotrexate, and fluorouracil in lymph node-positive breast cancer according to HER2 overexpression and other tumor biologic variables.	Cyclophosphamide	12-28	erb-b2 receptor tyrosine kinase 2	Homo sapiens	111-115
11208823-3	2001	However, the significance of HER2 overexpression in responsiveness to cyclophosphamide, methotrexate, and fluorouracil (CMF) has remained unclear.	Cyclophosphamide	70-86	erb-b2 receptor tyrosine kinase 2	Homo sapiens	29-33
11521718-7	2001	Furthermore, a number of studies have found that a HER2-positive status is associated with a relative resistance to CMF (cyclophosphamide.	Cyclophosphamide	121-137	erb-b2 receptor tyrosine kinase 2	Homo sapiens	51-55
11281378-10	2001	In conclusion, the administration of two cycles of high-dose mitoxantrone and cyclophosphamide with G-CSF support is safe and feasible.	Cyclophosphamide	78-94	colony stimulating factor 3	Homo sapiens	100-105
11787527-4	2001	Our laboratory has recently established a cyclophosphamide (CTX) plus thymic irradiation (TI)-based nonmyeloablative conditioning protocol for the treatment of hematologic malignancies.	Cyclophosphamide	42-58	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	60-63
11141334-1	2001	Systemic administration of human lymphotoxin-alpha (hLT-alpha) made NOD mice resistant not only to spontaneous autoimmune type 1 diabetes mellitus but also to cyclophosphamide (CY)-induced diabetes and diabetes transfer by diabetic NOD spleen cells (triple resistance).	Cyclophosphamide	177-179	lymphotoxin alpha	Homo sapiens	52-61
11141334-1	2001	Systemic administration of human lymphotoxin-alpha (hLT-alpha) made NOD mice resistant not only to spontaneous autoimmune type 1 diabetes mellitus but also to cyclophosphamide (CY)-induced diabetes and diabetes transfer by diabetic NOD spleen cells (triple resistance).	Cyclophosphamide	159-175	lymphotoxin alpha	Homo sapiens	33-50
11141334-1	2001	Systemic administration of human lymphotoxin-alpha (hLT-alpha) made NOD mice resistant not only to spontaneous autoimmune type 1 diabetes mellitus but also to cyclophosphamide (CY)-induced diabetes and diabetes transfer by diabetic NOD spleen cells (triple resistance).	Cyclophosphamide	159-175	lymphotoxin alpha	Homo sapiens	52-61
11141334-1	2001	Systemic administration of human lymphotoxin-alpha (hLT-alpha) made NOD mice resistant not only to spontaneous autoimmune type 1 diabetes mellitus but also to cyclophosphamide (CY)-induced diabetes and diabetes transfer by diabetic NOD spleen cells (triple resistance).	Cyclophosphamide	159-175	atrophin 1	Homo sapiens	68-71
11141334-1	2001	Systemic administration of human lymphotoxin-alpha (hLT-alpha) made NOD mice resistant not only to spontaneous autoimmune type 1 diabetes mellitus but also to cyclophosphamide (CY)-induced diabetes and diabetes transfer by diabetic NOD spleen cells (triple resistance).	Cyclophosphamide	177-179	lymphotoxin alpha	Homo sapiens	33-50
11211144-11	2001	Thus, the immunization with murine muc-1 reduced the tumor incidence in only cyclophosphamide-treated mice and led to strong muc-1 antibody production and to cellular responses.	Cyclophosphamide	77-93	mucin 1, transmembrane	Mus musculus	35-40
11787881-3	2001	Following treatment with ACE inhibitor, prednisolone and cyclophosphamide complete remission was achieved with minimal brain damage and normal kidney function.	Cyclophosphamide	57-73	angiotensin I converting enzyme	Homo sapiens	25-28
11280213-6	2001	Finally, RTA improved with prednisolon and short term cyclophosphamide treatment without supplemental potassium and alkali therapy.	Cyclophosphamide	54-70	MAS related GPR family member F	Homo sapiens	9-12
11306049-1	2001	ALDH3A1 catalyzes the detoxification of cyclophosphamide, mafosfamide, 4-hydroperoxycyclophosphamide and other oxazaphosphorines.	Cyclophosphamide	40-56	aldehyde dehydrogenase 3 family member A1	Homo sapiens	0-7
11467420-13	2001	The protective diets suppress Cy-induced intra-islet immune cell influx and iNOS expression.	Cyclophosphamide	30-32	nitric oxide synthase 2, inducible	Mus musculus	76-80
11141334-1	2001	Systemic administration of human lymphotoxin-alpha (hLT-alpha) made NOD mice resistant not only to spontaneous autoimmune type 1 diabetes mellitus but also to cyclophosphamide (CY)-induced diabetes and diabetes transfer by diabetic NOD spleen cells (triple resistance).	Cyclophosphamide	177-179	atrophin 1	Homo sapiens	68-71
11141334-2	2001	In this study we analyzed the mechanisms of hLT-alpha-induced resistance, focusing on (1) hLT-alpha-induced resistance in the pancreatic beta cell, (2) CY-resistant suppressor cells, (3) suppression of induction or function of effector cells for beta cell destruction, or (4) others.	Cyclophosphamide	152-154	lymphotoxin alpha	Homo sapiens	44-53
11121461-2	2000	This has led some clinicians to propose that HER2 should be used as a predictive marker in choosing between anthracycline-based regimens and combination chemotherapy with cyclophosphamide, methotrexate, and 5-fluorouracil (CMF).	Cyclophosphamide	171-187	erb-b2 receptor tyrosine kinase 2	Homo sapiens	45-49
10991840-12	2000	H2C9 cells mediated a bystander killing effect for CYP2C9-negative PPC-1 cells, reducing the IC(50) of CPA from about 14 to 3.62+/-0.73 mM in PPC-1 cells when they were cocultured with H2C9 cells.	Cyclophosphamide	103-106	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	51-57
11694791-5	2001	It has not yet been demonstrated conclusively that HER2 positivity increases resistance to adjuvant cyclophosphamide, methotrexate, 5-FU (CMF), but there are indications that HER2-positive patients benefit more from adequately dosed anthracyclines than from CMF.	Cyclophosphamide	100-116	erb-b2 receptor tyrosine kinase 2	Homo sapiens	51-55
11087342-12	2000	Cyclophosphamide-induced apoptosis in vivo could be imaged with [(99m)Tc]annexin V-117.	Cyclophosphamide	0-16	annexin A5	Mus musculus	73-82
11097380-0	2000	Cytotoxicity of cyclophosphamide, paclitaxel, and docetaxel for tumor cell lines in vitro: effects of concentration, time and cytochrome P450-catalyzed metabolism.	Cyclophosphamide	16-32	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	126-141
11097380-1	2000	Cytotoxic effects of cyclophosphamide (CPA), paclitaxel (PCT), and docetaxel (DTX) and their modulation by cytochrome P450 (CYP) metabolism were studied by incubating cell lines L929 and P388D1 with or without rat liver microsomes.	Cyclophosphamide	21-37	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	124-127
11097380-1	2000	Cytotoxic effects of cyclophosphamide (CPA), paclitaxel (PCT), and docetaxel (DTX) and their modulation by cytochrome P450 (CYP) metabolism were studied by incubating cell lines L929 and P388D1 with or without rat liver microsomes.	Cyclophosphamide	39-42	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	107-122
11097380-4	2000	CYP2B1-, CYP3A-, and CYP2E1-induced microsomes effectively oxidized the prodrug CPA to cytotoxic products in 2-h incubation periods.	Cyclophosphamide	80-83	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	9-14
11097380-4	2000	CYP2B1-, CYP3A-, and CYP2E1-induced microsomes effectively oxidized the prodrug CPA to cytotoxic products in 2-h incubation periods.	Cyclophosphamide	80-83	cytochrome P450, family 2, subfamily e, polypeptide 1	Mus musculus	21-27
11006039-0	2000	Cisplatin-paclitaxel-cyclophosphamide with G-CSF in primary advanced epithelial ovarian cancer.	Cyclophosphamide	21-37	colony stimulating factor 3	Homo sapiens	43-48
10992475-5	2000	Sequence analysis of the toxin coding region revealed that astA is completely embedded within a 1,209-bp open reading frame (ORF1), whose coding sequence is on the same strand but in the -1 reading frame in reference to the toxin gene.	Cyclophosphamide	59-63	hypothetical protein	Escherichia coli	125-129
10982843-6	2000	Bacterially expressed SSeCKS-CY bound cyclins D1 and E, whereas K-->S mutations within either CY motif ablated binding.	Cyclophosphamide	29-31	A kinase (PRKA) anchor protein (gravin) 12	Mus musculus	22-28
15959941-5	2000	An ongoing German study is evaluating epirubicin/cyclophosphamide in combination with trastuzumab as first-line therapy of metastatic breast cancer in patients whose tumors overexpress HER2/neu protein.	Cyclophosphamide	49-65	erb-b2 receptor tyrosine kinase 2	Homo sapiens	185-193
11016005-3	2000	After three courses of CAF therapy (cyclophosphamide, doxorubicin (DXR), 5-FU), the primary tumor was decreased by 56% and the liver metastases had disappeared.	Cyclophosphamide	36-52	lysine acetyltransferase 2B	Homo sapiens	23-26
10884587-13	2000	In the MC38 tumor model, combination treatment of established tumors with BCH-1393 and Cy (CTX) at 50 mg/kg resulted in a significant delay in tumor growth compared to CTX treatment alone.	Cyclophosphamide	87-89	V-set and immunoglobulin domain containing 2	Mus musculus	91-94
10884587-13	2000	In the MC38 tumor model, combination treatment of established tumors with BCH-1393 and Cy (CTX) at 50 mg/kg resulted in a significant delay in tumor growth compared to CTX treatment alone.	Cyclophosphamide	87-89	V-set and immunoglobulin domain containing 2	Mus musculus	168-171
10884587-14	2000	The observed concomitant anti-tumor activity of BCH-1393 with cyclophosphamide warrants further investigation of this immunomodulator as an adjunctive treatment of cancer.	Cyclophosphamide	62-78	chimerin 2	Mus musculus	48-51
10954901-3	2000	In this context, we have previously reported that glutathione S-transferase-pi (GST-pi) gene-transduced human CD34(+) cells showed resistance in vitro against 4-hydroperoxicyclophosphamide, an active form of cyclophosphamide (CY).	Cyclophosphamide	172-188	CD34 molecule	Homo sapiens	110-114
10954901-3	2000	In this context, we have previously reported that glutathione S-transferase-pi (GST-pi) gene-transduced human CD34(+) cells showed resistance in vitro against 4-hydroperoxicyclophosphamide, an active form of cyclophosphamide (CY).	Cyclophosphamide	226-228	CD34 molecule	Homo sapiens	110-114
10856427-2	2000	Since resistance to oxazaphosphorines can be produced in mammalian cells by transfecting them with the gene for human ALDH isozyme 3 (hALDH3), it seems possible that patients receiving therapy for solid tumors with cyclophosphamide might be protected from myelosuppression by their prior transplantation with autologous bone marrow that has been transduced with a retroviral vector causing overexpression of hALDH3.	Cyclophosphamide	215-231	aldehyde dehydrogenase 3 family member A1	Homo sapiens	134-140
10856427-2	2000	Since resistance to oxazaphosphorines can be produced in mammalian cells by transfecting them with the gene for human ALDH isozyme 3 (hALDH3), it seems possible that patients receiving therapy for solid tumors with cyclophosphamide might be protected from myelosuppression by their prior transplantation with autologous bone marrow that has been transduced with a retroviral vector causing overexpression of hALDH3.	Cyclophosphamide	215-231	aldehyde dehydrogenase 3 family member A1	Homo sapiens	408-414
11006010-3	2000	CY pretreatment 2 days before sensitization enhanced expression of IL-4 mRNA in the regional lymph node cells more strongly than expressions of both IL-2 and IFN-gamma mRNA on day 13.	Cyclophosphamide	0-2	interleukin 4	Mus musculus	67-71
11006010-7	2000	When immune lymph node cells prepared on day 13 were stimulated with hapten-modified cells in vitro, the level of IL-4 secreted in the culture supernatant was enhanced by CY pretreatment, but that of IL-2 was not.	Cyclophosphamide	171-173	interleukin 4	Mus musculus	114-118
10917206-1	2000	The effect of the antithyroid drug methimazole (MMI) on cytochrome P450/P450 reductase-dependent activation of the anti-cancer prodrug cyclophosphamide (CPA) was investigated in a rat model of P450 prodrug activation-based cancer gene therapy.	Cyclophosphamide	135-151	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	56-86
10917206-1	2000	The effect of the antithyroid drug methimazole (MMI) on cytochrome P450/P450 reductase-dependent activation of the anti-cancer prodrug cyclophosphamide (CPA) was investigated in a rat model of P450 prodrug activation-based cancer gene therapy.	Cyclophosphamide	153-156	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	56-86
11142168-0	2000	[A case of breast cancer with multiple organ metastases responding remarkably to combination therapy of CAF (cyclophosphamide, adriamycin and 5-FU), 5"-DFUR and MPA (medroxyprogesterone acetate)].	Cyclophosphamide	109-125	lysine acetyltransferase 2B	Homo sapiens	104-107
11104786-4	2000	Conditioning with DNA-damaging agents (ionizing irradiation, cyclophosphamide, and 5-fluorouracil) caused an increase in SDF-1 expression and in CXCR4-dependent homing and repopulation by human stem cells transplanted into NOD/SCID mice.	Cyclophosphamide	61-77	C-X-C motif chemokine ligand 12	Homo sapiens	121-126
11104786-4	2000	Conditioning with DNA-damaging agents (ionizing irradiation, cyclophosphamide, and 5-fluorouracil) caused an increase in SDF-1 expression and in CXCR4-dependent homing and repopulation by human stem cells transplanted into NOD/SCID mice.	Cyclophosphamide	61-77	C-X-C motif chemokine receptor 4	Homo sapiens	145-150
11104786-4	2000	Conditioning with DNA-damaging agents (ionizing irradiation, cyclophosphamide, and 5-fluorouracil) caused an increase in SDF-1 expression and in CXCR4-dependent homing and repopulation by human stem cells transplanted into NOD/SCID mice.	Cyclophosphamide	61-77	atrophin 1	Homo sapiens	223-226
11236028-3	2000	Chemotherapy trials have supported an interaction between HER-2 overexpression and chemotherapy sensitivity (cyclophosphamide/methotrexate/5-fluorouracil resistance and doxorubicin sensitivity) which is compelling.	Cyclophosphamide	109-125	erb-b2 receptor tyrosine kinase 2	Homo sapiens	58-63
11132240-4	2000	We hypothesized that ifosfamide is metabolized by cytochrome P450 (CYP) enzymes located in the renal tubular cell to the toxic metabolite chloroacetaldehyde; and, that the higher production of chloroacetaldehyde from ifosfamide than from cyclophosphamide explains the clinical differences in nephrotoxicity.	Cyclophosphamide	238-254	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	50-65
11132240-4	2000	We hypothesized that ifosfamide is metabolized by cytochrome P450 (CYP) enzymes located in the renal tubular cell to the toxic metabolite chloroacetaldehyde; and, that the higher production of chloroacetaldehyde from ifosfamide than from cyclophosphamide explains the clinical differences in nephrotoxicity.	Cyclophosphamide	238-254	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	67-70
11056294-9	2000	Dramatic increases in the transcripts for selected members of the nucleotide excision repair family (XPC, XPE and PCNA), mismatch repair family (PMS1), and recombination repair family (RAD50) were found in 1-cell stage embryos sired by cyclophosphamide-treated males compared to controls, while decreases in the expression of base excision repair family members (UNG1, UNG2, and XRCC1) and in recombination repair transcripts (RAD54) were observed.	Cyclophosphamide	236-252	XPC complex subunit, DNA damage recognition and repair factor	Rattus norvegicus	101-104
11056294-9	2000	Dramatic increases in the transcripts for selected members of the nucleotide excision repair family (XPC, XPE and PCNA), mismatch repair family (PMS1), and recombination repair family (RAD50) were found in 1-cell stage embryos sired by cyclophosphamide-treated males compared to controls, while decreases in the expression of base excision repair family members (UNG1, UNG2, and XRCC1) and in recombination repair transcripts (RAD54) were observed.	Cyclophosphamide	236-252	RAD50 double strand break repair protein	Rattus norvegicus	185-190
11069830-0	2000	Cyclophosphamide prevents systemic keratinocyte growth factor-induced up-regulation of surfactant protein A after allogeneic transplant in mice.	Cyclophosphamide	0-16	surfactant associated protein A1	Mus musculus	87-107
11069830-1	2000	We reported that systemic keratinocyte growth factor (KGF) given before bone marrow transplantation (BMT) prevents allogeneic T cell-dependent lung inflammation assessed on Day 7 post-BMT, but the antiinflammatory effects of KGF were impaired in mice injected with both T cells and conditioning regimen of cyclophosphamide (Cy).	Cyclophosphamide	306-322	fibroblast growth factor 7	Mus musculus	54-57
11069830-1	2000	We reported that systemic keratinocyte growth factor (KGF) given before bone marrow transplantation (BMT) prevents allogeneic T cell-dependent lung inflammation assessed on Day 7 post-BMT, but the antiinflammatory effects of KGF were impaired in mice injected with both T cells and conditioning regimen of cyclophosphamide (Cy).	Cyclophosphamide	324-326	fibroblast growth factor 7	Mus musculus	54-57
11069830-3	2000	We hypothesized that systemic KGF up-regulates SP-A after allogeneic BMT, and the addition of Cy may interfere with the ability of KGF to enhance SP-A production.	Cyclophosphamide	94-96	fibroblast growth factor 7	Mus musculus	131-134
11069830-3	2000	We hypothesized that systemic KGF up-regulates SP-A after allogeneic BMT, and the addition of Cy may interfere with the ability of KGF to enhance SP-A production.	Cyclophosphamide	94-96	surfactant associated protein A1	Mus musculus	146-150
11046124-11	2000	In summary, NK(1) receptors and iNOS play a role in NO formation and on cyclophosphamide-induced cystitis.	Cyclophosphamide	72-88	nitric oxide synthase 2	Rattus norvegicus	32-36
11032587-2	2000	We examine a possible interaction between HER-2/neu or p53 expression and tamoxifen effectiveness in patients with ER-positive, node-positive disease treated with cyclophosphamide, doxorubicin, and fluorouracil in a large adjuvant chemotherapy trial (Cancer and Leukemia Group B [CALGB] 8541).	Cyclophosphamide	163-179	erb-b2 receptor tyrosine kinase 2	Homo sapiens	42-51
10991840-0	2000	Cytochrome P-450 2C9 sensitizes human prostate tumor cells to cyclophosphamide via a bystander effect.	Cyclophosphamide	62-78	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-20
10991840-1	2000	The goal of the present study was to examine the ability of cytochrome P450-2C9 (CYP2C9) to activate cyclophosphamide (CPA) and elicit tumor cell death.	Cyclophosphamide	101-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-79
10991840-1	2000	The goal of the present study was to examine the ability of cytochrome P450-2C9 (CYP2C9) to activate cyclophosphamide (CPA) and elicit tumor cell death.	Cyclophosphamide	101-117	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-87
10991840-1	2000	The goal of the present study was to examine the ability of cytochrome P450-2C9 (CYP2C9) to activate cyclophosphamide (CPA) and elicit tumor cell death.	Cyclophosphamide	119-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-79
10991840-1	2000	The goal of the present study was to examine the ability of cytochrome P450-2C9 (CYP2C9) to activate cyclophosphamide (CPA) and elicit tumor cell death.	Cyclophosphamide	119-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	81-87
11092698-0	2000	Dual-label immunohistochemical study of interleukin-4-and interferon-gamma-expressing cells within the pancreas of the NOD mouse during disease acceleration with cyclophosphamide.	Cyclophosphamide	162-178	interleukin 4	Mus musculus	40-53
11092698-0	2000	Dual-label immunohistochemical study of interleukin-4-and interferon-gamma-expressing cells within the pancreas of the NOD mouse during disease acceleration with cyclophosphamide.	Cyclophosphamide	162-178	interferon gamma	Mus musculus	58-74
11092698-14	2000	Our results demonstrate that during Cy-induced diabetes, there is increasing expression of both IL-4 and IFN-gamma in specific immune cells within the inflamed islets in the late prediabetic stage and at onset of diabetes.	Cyclophosphamide	36-38	interleukin 4	Mus musculus	96-100
11092698-14	2000	Our results demonstrate that during Cy-induced diabetes, there is increasing expression of both IL-4 and IFN-gamma in specific immune cells within the inflamed islets in the late prediabetic stage and at onset of diabetes.	Cyclophosphamide	36-38	interferon gamma	Mus musculus	105-114
10970695-11	2000	There was a weak, inverse relationship between the expression levels of LRP and sensitivity to cisplatin and cyclophosphamide (r = -0.44 and -0.45), but not to doxorubicin.	Cyclophosphamide	109-125	LDL receptor related protein 1	Homo sapiens	72-75
11025602-1	2000	We describe a 65-year old woman who developed a t(8;16)(p11;p13) positive acute myeloid leukemia (AML)-M4 without a prior myelodysplasia thirty-six months after a low-grade non-Hodgkin"s lymphoma treated with alkylating agents (chlorambucil and cyclophosphamide) and fludarabine, a purine analog with a significant activity in lymphoproliferative disorders.	Cyclophosphamide	245-261	endonuclease, poly(U) specific	Homo sapiens	56-59
11025602-1	2000	We describe a 65-year old woman who developed a t(8;16)(p11;p13) positive acute myeloid leukemia (AML)-M4 without a prior myelodysplasia thirty-six months after a low-grade non-Hodgkin"s lymphoma treated with alkylating agents (chlorambucil and cyclophosphamide) and fludarabine, a purine analog with a significant activity in lymphoproliferative disorders.	Cyclophosphamide	245-261	H3 histone pseudogene 6	Homo sapiens	60-63
11002232-2	2000	The Medical Research Council therefore conducted the current randomized trial to assess the impact on survival of postradiotherapy chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) in nonimmunocompromised adult patients with pathologically proven PCL.	Cyclophosphamide	149-165	DNA damage inducible transcript 3	Homo sapiens	209-213
11016618-2	2000	In a mouse model for chemotherapy-induced hair loss, we demonstrate that p53 is essential for this process: in contrast to wild-type mice, p53-deficient mice show neither hair loss nor apoptosis in the HF keratinocytes that maintained active proliferation after cyclophosphamide treatment.	Cyclophosphamide	262-278	transformation related protein 53, pseudogene	Mus musculus	73-76
10995003-6	2000	High-dose cyclophosphamide was given with G-CSF support (5 microg/kg/day days 3-12).	Cyclophosphamide	10-26	colony stimulating factor 3	Homo sapiens	42-47
10967571-8	2000	Although numbers were relatively small, a BNP >43 pmol/l was significantly associated with the inclusion of high-dose cyclophosphamide in the preparative regimen (P = 0.02).	Cyclophosphamide	121-137	natriuretic peptide B	Homo sapiens	42-45
10990075-10	2000	Cyclophosphamide treatment decreased IL-12, IL-1beta, IL-2, IFN-gamma and TNF-alpha gene expressions in mononuclear spleen cells but IL-4 gene expression increased.	Cyclophosphamide	0-16	interleukin 1 beta	Rattus norvegicus	44-52
10990075-10	2000	Cyclophosphamide treatment decreased IL-12, IL-1beta, IL-2, IFN-gamma and TNF-alpha gene expressions in mononuclear spleen cells but IL-4 gene expression increased.	Cyclophosphamide	0-16	interleukin 2	Rattus norvegicus	54-58
10990075-10	2000	Cyclophosphamide treatment decreased IL-12, IL-1beta, IL-2, IFN-gamma and TNF-alpha gene expressions in mononuclear spleen cells but IL-4 gene expression increased.	Cyclophosphamide	0-16	interferon gamma	Rattus norvegicus	60-69
10990075-10	2000	Cyclophosphamide treatment decreased IL-12, IL-1beta, IL-2, IFN-gamma and TNF-alpha gene expressions in mononuclear spleen cells but IL-4 gene expression increased.	Cyclophosphamide	0-16	tumor necrosis factor	Rattus norvegicus	74-83
10990075-10	2000	Cyclophosphamide treatment decreased IL-12, IL-1beta, IL-2, IFN-gamma and TNF-alpha gene expressions in mononuclear spleen cells but IL-4 gene expression increased.	Cyclophosphamide	0-16	interleukin 4	Rattus norvegicus	133-137
10982237-0	2000	Mobilization with etoposide and granulocyte colony-stimulating factor can replace bone marrow harvesting in patients with malignant lymphoma who previously failed to mobilize sufficient stem cells with cyclophosphamide and G-CSF.	Cyclophosphamide	202-218	colony stimulating factor 3	Homo sapiens	32-69
10861484-0	2000	Cyclophosphamide enhances anti-tumor effect of wild-type p53-specific CTL.	Cyclophosphamide	0-16	transformation related protein 53, pseudogene	Mus musculus	57-60
10861484-7	2000	We show here that CY acts synergistically with adoptively transferred wtp53-specific CTL in controlling the growth of an aggressive mutant p53-induced and overexpressing tumor.	Cyclophosphamide	18-20	transformation related protein 53, pseudogene	Mus musculus	72-75
10933104-4	2000	The ASTA Medica multi-dose dry powder inhaler (AM-MDPI) has been designed to offer low resistance on inhalation, so that asthmatic patients can achieve inhaled flow rates of approximately 90 L x min(-1).	Cyclophosphamide	4-8	CD59 molecule (CD59 blood group)	Homo sapiens	195-201
10896769-0	2000	IL-10 deficiency does not inhibit insulitis and accelerates cyclophosphamide-induced diabetes in the nonobese diabetic mouse.	Cyclophosphamide	60-76	interleukin 10	Mus musculus	0-5
10915175-1	2000	Liver allograft survival rates of 50% to 60% are reported in blood group A, group B, group O (ABO)-incompatible mismatched grafts even when aggressive immunosuppressive protocols, including plasmapheresis, OKT(3), cyclophosphamide, cyclosporine, prostaglandin E(1), and steroids, are used.	Cyclophosphamide	214-230	ABO, alpha 1-3-N-acetylgalactosaminyltransferase and alpha 1-3-galactosyltransferase	Homo sapiens	94-97
10896769-5	2000	On the other hand, IL-10-deficient NOD mice developed accelerated disease following cyclophosphamide (CYP) injection.	Cyclophosphamide	84-100	interleukin 10	Mus musculus	19-24
10807765-2	2000	HPC mobilization by granulocyte colony-stimulating factor (G-CSF), cyclophosphamide (CY), or interleukin-8 but not flt-3 ligand is markedly impaired in G-CSF receptor-deficient (G-CSFR-deficient) mice.	Cyclophosphamide	67-83	colony stimulating factor 3 (granulocyte)	Mus musculus	152-157
10799737-5	2000	Our results suggest that hGSTP1-1 polymorphism may be an important factor in differential susceptibility of individuals to the toxic effects of acrolein, which is a widely spread environmental pollutant and generated endogenously during metabolic activation of anticancer drug cyclophosphamide.	Cyclophosphamide	277-293	glutathione S-transferase pi 1	Homo sapiens	25-33
12515139-3	2000	The results showed the infiltration of cells was inhibited in the "Chinese herbs combined with prednisone" group, the infiltration of cells, TGF-beta expression and interstitial fibrosis were all inhibited in the cyclophosphamide and prednisone" group.	Cyclophosphamide	213-229	transforming growth factor beta 1	Homo sapiens	141-149
11031727-1	2000	Recombinant human granulocyte colony-stimulating factor (rhG-CSF) was evaluated for its effects on granulopoiesis recovery in mice pretreated with cyclophosphamide.	Cyclophosphamide	147-163	colony stimulating factor 3	Homo sapiens	18-55
11032370-4	2000	Human G-CSF from transgenic goat milk increased the total number of white blood cells in C57BL/6N mice with leucopenia induced by cyclophosphamide (CPA).	Cyclophosphamide	130-146	colony stimulating factor 3	Homo sapiens	6-11
11032370-4	2000	Human G-CSF from transgenic goat milk increased the total number of white blood cells in C57BL/6N mice with leucopenia induced by cyclophosphamide (CPA).	Cyclophosphamide	148-151	colony stimulating factor 3	Homo sapiens	6-11
10807765-5	2000	Mobilization studies in these chimeras demonstrated that expression of the G-CSFR on transplantable hematopoietic cells but not stromal cells is required for CY- or G-CSF-induced mobilization.	Cyclophosphamide	158-160	colony stimulating factor 3 receptor (granulocyte)	Mus musculus	75-81
10807765-5	2000	Mobilization studies in these chimeras demonstrated that expression of the G-CSFR on transplantable hematopoietic cells but not stromal cells is required for CY- or G-CSF-induced mobilization.	Cyclophosphamide	158-160	colony stimulating factor 3 (granulocyte)	Mus musculus	75-80
10754506-1	2000	These studies examined changes in the expression of pituitary adenylate cyclase-activating polypeptide (PACAP) in micturition reflex pathways after chronic cystitis induced by cyclophosphamide (CYP).	Cyclophosphamide	176-192	adenylate cyclase activating polypeptide 1	Rattus norvegicus	52-102
10754506-1	2000	These studies examined changes in the expression of pituitary adenylate cyclase-activating polypeptide (PACAP) in micturition reflex pathways after chronic cystitis induced by cyclophosphamide (CYP).	Cyclophosphamide	176-192	adenylate cyclase activating polypeptide 1	Rattus norvegicus	104-109
10885612-6	2000	The restoration of spleen lymphoproliferative responses to normal levels when exposed to media conditioned by splenocytes from Cy-treated tumour-bearing rats, together with a decreased production of suppressive cytokines TGF-beta, IL-10 and NO, suggest an enhancement of host antimetastatic immunity triggered by single low-dose Cy treatment.	Cyclophosphamide	127-129	transforming growth factor, beta 1	Rattus norvegicus	221-229
10793033-5	2000	Therapy with oral prednisone and cyclophosphamide led to resolution of pulmonary hemorrhage and negativity of MPO-ANCA.	Cyclophosphamide	33-49	myeloperoxidase	Homo sapiens	110-113
10823419-2	2000	Cyclophosphamide injection temporarily abrogated the lung clearance activity of Yac-1 lymphoma cells, which is considered to be an index of NK activity in vivo.	Cyclophosphamide	0-16	ADP-ribosyltransferase 1	Mus musculus	80-85
10885612-6	2000	The restoration of spleen lymphoproliferative responses to normal levels when exposed to media conditioned by splenocytes from Cy-treated tumour-bearing rats, together with a decreased production of suppressive cytokines TGF-beta, IL-10 and NO, suggest an enhancement of host antimetastatic immunity triggered by single low-dose Cy treatment.	Cyclophosphamide	127-129	interleukin 10	Rattus norvegicus	231-236
10773007-1	2000	Previous studies in this laboratory showed that the overexpression of human aldehyde dehydrogenase class-1 (ALDH-1) with a retroviral vector resulted in increased resistance to 4-hydroperoxycyclophosphamide (4-HC), an active metabolite of cyclophosphamide.	Cyclophosphamide	190-206	aldehyde dehydrogenase 1 family member A1	Homo sapiens	76-106
10784622-14	2000	CONCLUSION: We report the first clinical trial that used a cross-over design showing that high-dose cyclophosphamide plus G-CSF results in mobilization of more progenitors then GM-CSF plus G-CSF when tested in the same patient regardless of sequence of administration, although the regimen is associated with greater morbidity.	Cyclophosphamide	100-116	colony stimulating factor 2	Homo sapiens	177-183
10784622-14	2000	CONCLUSION: We report the first clinical trial that used a cross-over design showing that high-dose cyclophosphamide plus G-CSF results in mobilization of more progenitors then GM-CSF plus G-CSF when tested in the same patient regardless of sequence of administration, although the regimen is associated with greater morbidity.	Cyclophosphamide	100-116	colony stimulating factor 3	Homo sapiens	189-194
10773007-1	2000	Previous studies in this laboratory showed that the overexpression of human aldehyde dehydrogenase class-1 (ALDH-1) with a retroviral vector resulted in increased resistance to 4-hydroperoxycyclophosphamide (4-HC), an active metabolite of cyclophosphamide.	Cyclophosphamide	190-206	aldehyde dehydrogenase 1 family member A1	Homo sapiens	108-114
10692561-0	2000	Role of human liver microsomal CYP3A4 and CYP2B6 in catalyzing N-dechloroethylation of cyclophosphamide and ifosfamide.	Cyclophosphamide	87-103	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	31-37
10775615-7	2000	Previously, we have shown that the immunosuppressive agent, cyclophosphamide (CPA), facilitates the in vivo propagation of an oncolytic HSV, delivered intravascularly, within infected multiple intracerebral masses, by inhibition of both innate and elicited anti-HSV neutralizing antibody response (K. Ikeda et al., Nat.	Cyclophosphamide	60-76	bromodomain containing 2	Homo sapiens	315-318
10775615-7	2000	Previously, we have shown that the immunosuppressive agent, cyclophosphamide (CPA), facilitates the in vivo propagation of an oncolytic HSV, delivered intravascularly, within infected multiple intracerebral masses, by inhibition of both innate and elicited anti-HSV neutralizing antibody response (K. Ikeda et al., Nat.	Cyclophosphamide	78-81	bromodomain containing 2	Homo sapiens	315-318
10692561-0	2000	Role of human liver microsomal CYP3A4 and CYP2B6 in catalyzing N-dechloroethylation of cyclophosphamide and ifosfamide.	Cyclophosphamide	87-103	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	42-48
10692561-3	2000	Analysis of a panel of fifteen human P450 cDNAs in the baculovirus expression system ("Supersomes") demonstrated that CYP3A4 exhibited the highest N-dechloroethylation activity toward both CPA and IFA, whereas CYP2B6 displayed high N-dechloroethylation activity toward IFA, but not CPA.	Cyclophosphamide	189-192	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	118-124
10692561-3	2000	Analysis of a panel of fifteen human P450 cDNAs in the baculovirus expression system ("Supersomes") demonstrated that CYP3A4 exhibited the highest N-dechloroethylation activity toward both CPA and IFA, whereas CYP2B6 displayed high N-dechloroethylation activity toward IFA, but not CPA.	Cyclophosphamide	282-285	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	118-124
10692561-5	2000	With CPA as substrate, CYP3A4 was shown to catalyze >/=95% of liver microsomal N-dechloroethylation, whereas with IFA as substrate, CYP3A4 catalyzed an average of approximately 70% of liver microsomal N-dechloroethylation (range = 40-90%), with the balance of this activity catalyzed by CYP2B6 (range = 10-70%, dependent on the CYP2B6 content of the liver).	Cyclophosphamide	5-8	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	23-29
10749792-1	2000	These studies examined Fos protein expression in spinal cord neurons synaptically activated by stimulation of bladder afferent pathways after cyclophosphamide (CYP)-induced bladder inflammation.	Cyclophosphamide	142-158	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	23-26
10706870-0	2000	Cyclophosphamide induces type I interferon and augments the number of CD44(hi) T lymphocytes in mice: implications for strategies of chemoimmunotherapy of cancer.	Cyclophosphamide	0-16	CD44 antigen	Mus musculus	70-74
10766175-6	2000	This antiangiogenic effect was more pronounced in p53-null mice in which the apoptosis of p53-null endothelial cells induced by cyclophosphamide was so vigorous that drug-resistant tumors comprising 4.5% of body weight were eradicated.	Cyclophosphamide	128-144	transformation related protein 53, pseudogene	Mus musculus	50-53
10766175-6	2000	This antiangiogenic effect was more pronounced in p53-null mice in which the apoptosis of p53-null endothelial cells induced by cyclophosphamide was so vigorous that drug-resistant tumors comprising 4.5% of body weight were eradicated.	Cyclophosphamide	128-144	transformation related protein 53, pseudogene	Mus musculus	90-93
10897619-2	2000	This study aimed at evaluating MDR1 expression in NS sensitive(S) and resistant(R) to therapy (steroids/S/, cyclophosphamide/C/, CsA) patients.	Cyclophosphamide	108-124	ATP binding cassette subfamily B member 1	Homo sapiens	31-35
10811509-0	2000	MTHFR gene polymorphism and severe toxicity during adjuvant treatment of early breast cancer with cyclophosphamide, methotrexate, and fluorouracil (CMF)	Cyclophosphamide	98-114	methylenetetrahydrofolate reductase	Homo sapiens	0-5
12849612-12	2000	It is also possible that HER2-overexpressing patients may respond better to dose-intense anthracycline therapy and worse to cyclophosphamide/methotrexate/5-fluorouracil than non-overexpressing patients.	Cyclophosphamide	124-140	erb-b2 receptor tyrosine kinase 2	Homo sapiens	25-29
10713624-4	2000	In previous clinical studies of total body irradiation, etoposide, cyclophosphamide (TBI-VP-16-Cy) in adult allogeneic bone marrow transplantation, there has been a high incidence of severe regimen-related toxicity.	Cyclophosphamide	67-83	host cell factor C1	Homo sapiens	89-94
11776651-8	2000	once every three werks in combination with cisplatin (PDD) 60 mg/m2 and cyclophosphamide (CTX) 60 mg/d.	Cyclophosphamide	72-88	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	90-93
10684711-12	2000	Glutathione reductase activity, however, showed a weak, inverse relation with the efficacy of cisplatin and cyclophosphamide (r values of -0.55 and -0.58, respectively).	Cyclophosphamide	108-124	glutathione-disulfide reductase	Homo sapiens	0-21
10683293-9	2000	Significant increases in urinary bladder neurotrophic factor mRNA levels of comparable magnitude were demonstrated following either acute or chronic cyclophosphamide-induced cystitis.	Cyclophosphamide	149-165	neurotrophin 3	Rattus norvegicus	41-60
10666167-8	2000	In our group of 14 patients, those with higher disease activity (measured by the SLAM) at onset of TM were treated more aggressively (for example, with plasmapheresis and intravenous pulse cyclophosphamide).	Cyclophosphamide	189-205	signaling lymphocytic activation molecule family member 1	Homo sapiens	81-85
10645906-6	2000	Pretreatment with tumor necrosis factor-alpha neutralizing antibody or pretreatment with cyclophosphamide abolished plug-induced EGFR protein expression and goblet cell metaplasia.	Cyclophosphamide	89-105	epidermal growth factor receptor	Rattus norvegicus	129-133
11268383-8	2000	The seasonal effects of rotational stress, and the reduction of the effects of cyclophosphamide caused by rotational stress, are accompanied by corresponding variations in the number of CD3+ and CD4+ splenic T-lymphocyte subsets and in the CD4+/CD8+ ratio, respectively.	Cyclophosphamide	79-95	CD3 antigen, epsilon polypeptide	Mus musculus	186-189
11268383-8	2000	The seasonal effects of rotational stress, and the reduction of the effects of cyclophosphamide caused by rotational stress, are accompanied by corresponding variations in the number of CD3+ and CD4+ splenic T-lymphocyte subsets and in the CD4+/CD8+ ratio, respectively.	Cyclophosphamide	79-95	CD4 antigen	Mus musculus	195-198
11268383-8	2000	The seasonal effects of rotational stress, and the reduction of the effects of cyclophosphamide caused by rotational stress, are accompanied by corresponding variations in the number of CD3+ and CD4+ splenic T-lymphocyte subsets and in the CD4+/CD8+ ratio, respectively.	Cyclophosphamide	79-95	CD4 antigen	Mus musculus	240-243
10623878-6	2000	HER2 overexpression is associated with breast cancer patient responsiveness to doxorubicin, to cyclophosphamide, methotrexate, and fluorouracil (CMF), and to paclitaxel, whereas tamoxifen was found to be ineffective and even detrimental in patients with HER2-positive tumors.	Cyclophosphamide	95-111	erb-b2 receptor tyrosine kinase 2	Homo sapiens	0-4
10771466-0	2000	Influence of adjuvant chemotherapy with cyclophosphamide, methotrexate and 5-fluorouracil on plasma insulin-like growth factor-I and chosen hormones in breast cancer pre-menopausal patients.	Cyclophosphamide	40-56	insulin like growth factor 1	Homo sapiens	100-128
10602717-2	2000	In C. albicans-infected mice which had been immunosuppressed with cyclophosphamide, treatment with hM-CSF at a daily dose of 8 x 10(5) units/kg of body weight or greater slightly but significantly prolonged survival.	Cyclophosphamide	66-82	colony stimulating factor 1	Homo sapiens	99-105
10607705-0	2000	Nitric oxide-producing CD11b(+)Ly-6G(Gr-1)(+)CD31(ER-MP12)(+) cells in the spleen of cyclophosphamide-treated mice: implications for T-cell responses in immunosuppressed mice.	Cyclophosphamide	85-101	integrin alpha M	Mus musculus	23-28
10607705-0	2000	Nitric oxide-producing CD11b(+)Ly-6G(Gr-1)(+)CD31(ER-MP12)(+) cells in the spleen of cyclophosphamide-treated mice: implications for T-cell responses in immunosuppressed mice.	Cyclophosphamide	85-101	lymphocyte antigen 6 complex, locus G	Mus musculus	31-36
10607705-0	2000	Nitric oxide-producing CD11b(+)Ly-6G(Gr-1)(+)CD31(ER-MP12)(+) cells in the spleen of cyclophosphamide-treated mice: implications for T-cell responses in immunosuppressed mice.	Cyclophosphamide	85-101	platelet/endothelial cell adhesion molecule 1	Mus musculus	45-49
10607705-1	2000	During recovery from intensive chemotherapy with cyclophosphamide (CTX), mice suffer a severe but transitory impairment in spleen cell proliferation to T-cell mitogens (Con A or anti-CD3 plus IL-2).	Cyclophosphamide	49-65	interleukin 2	Mus musculus	192-196
10661476-0	2000	Combination therapy using prednisolone and cyclophosphamide slows the progression of moderately advanced IgA nephropathy.	Cyclophosphamide	43-59	IGAN1	Homo sapiens	105-120
10661476-1	2000	AIM: We retrospectively examined the effect of combination therapy using prednisolone (PSL) and cyclophosphamide (CPA) on the progression of IgA nephropathy (IgAN) in 45 patients with moderate to severe histological changes.	Cyclophosphamide	96-112	IGAN1	Homo sapiens	141-156
10661476-1	2000	AIM: We retrospectively examined the effect of combination therapy using prednisolone (PSL) and cyclophosphamide (CPA) on the progression of IgA nephropathy (IgAN) in 45 patients with moderate to severe histological changes.	Cyclophosphamide	96-112	IGAN1	Homo sapiens	158-162
10661476-1	2000	AIM: We retrospectively examined the effect of combination therapy using prednisolone (PSL) and cyclophosphamide (CPA) on the progression of IgA nephropathy (IgAN) in 45 patients with moderate to severe histological changes.	Cyclophosphamide	114-117	IGAN1	Homo sapiens	141-156
10661476-1	2000	AIM: We retrospectively examined the effect of combination therapy using prednisolone (PSL) and cyclophosphamide (CPA) on the progression of IgA nephropathy (IgAN) in 45 patients with moderate to severe histological changes.	Cyclophosphamide	114-117	IGAN1	Homo sapiens	158-162
10661476-10	2000	Our results indicated that PSL+CPA combination therapy was effective in slowing the progression of moderately advanced IgAN.	Cyclophosphamide	31-34	IGAN1	Homo sapiens	119-123
10661476-11	2000	CONCLUSION: We suggest that the immunosuppressive treatment with CPA is sometimes necessary to preserve renal function in patients with histologically advanced IgAN.	Cyclophosphamide	65-68	IGAN1	Homo sapiens	160-164
11345042-15	2000	Effective treatment in all cases (especially with Ukrain or a combination of cyclophosphane plus Ukrain) induced a significant increase in cystatin C.	Cyclophosphamide	77-91	cystatin C	Mus musculus	139-149
10683293-15	2000	Retrogradely transported NGF may play a role in altered lower urinary tract function following spinal cord injury or cyclophosphamide-induced cystitis.	Cyclophosphamide	117-133	nerve growth factor	Mus musculus	25-28
10718156-5	2000	These studies demonstrate that the G-CSFR is required for mobilization in response to cyclophosphamide and IL-8, but not fit-3 ligand or IL-12, and suggest that the G-CSFR may play an important and previously unexpected role in HPC migration.	Cyclophosphamide	86-102	colony stimulating factor 3 receptor (granulocyte)	Mus musculus	35-41
11347331-10	2000	After methylprednisolone and cyclophosphamide application the suppressor/inducer CD8+ T-cells increased significantly in percentage (P < 0.05), while the values of B-lymphocytes decrease significantly (P < 0.05), in contrast to the results from the methylprednisolone-only treatment.	Cyclophosphamide	29-45	CD8a molecule	Homo sapiens	81-84
10637255-4	2000	Preliminary, nonrandomized feasibility studies showed that doxorubicin, cyclophosphamide, and etoposide (ACE) could be given every 2 (instead of the usual 3) weeks with granulocyte colony-stimulating factor (G-CSF) (lenograstim; Chugai-Rh?one-Poulenc, Tokyo, Japan) support.	Cyclophosphamide	72-88	colony stimulating factor 3	Homo sapiens	169-206
10637255-4	2000	Preliminary, nonrandomized feasibility studies showed that doxorubicin, cyclophosphamide, and etoposide (ACE) could be given every 2 (instead of the usual 3) weeks with granulocyte colony-stimulating factor (G-CSF) (lenograstim; Chugai-Rh?one-Poulenc, Tokyo, Japan) support.	Cyclophosphamide	72-88	colony stimulating factor 3	Homo sapiens	208-213
10674903-1	2000	A regimen which incorporates cyclophosphamide, doxorubicin, vincristine and prednisolone (CHOP) is the standard treatment for patients with non-Hodgkin"s lymphoma (NHL), but it has not been effective in patients with aggressive NHL who are at high risk.	Cyclophosphamide	29-45	DNA damage inducible transcript 3	Homo sapiens	90-94
10585754-0	1999	Acceleration of autoimmune diabetes by cyclophosphamide is associated with an enhanced IFN-gamma secretion pathway.	Cyclophosphamide	39-55	interferon gamma	Mus musculus	87-96
11007917-1	2000	CD34(+) cells and megakaryocyte progenitors were lower in marrow from patients after hematological recovery from the first cycle of 5-fluorouracil, leucovorin, adriamycin, cyclophosphamide (FLAC) chemotherapy plus PIXY321 (GM-CSF/interleukin 3; IL-3 hybrid) than in FLAC + GM-CSF or pre-FLAC marrows.	Cyclophosphamide	172-188	CD34 molecule	Homo sapiens	0-4
10983383-3	2000	The aim of the presented work is to asses the plasma GH levels in 24 pre-menopausal women after mastectomy for breast cancer on adjuvant chemotherapy with cyclophosphamide, methotrexate, 5-fluorouracil (CMF).	Cyclophosphamide	155-171	growth hormone 1	Homo sapiens	53-55
10585314-12	1999	Treatment with plasmapheresis plus cyclophosphamide can be effective in the control of FSGS relapse after renal transplantation.	Cyclophosphamide	35-51	actinin alpha 4	Homo sapiens	87-91
11345040-0	2000	Cystatin C in LS lymphosarcoma and HA-1 hepatoma treated with Ukrain and cyclophosphamide and involvement of apoptosis.	Cyclophosphamide	73-89	cystatin C	Mus musculus	0-10
11345040-0	2000	Cystatin C in LS lymphosarcoma and HA-1 hepatoma treated with Ukrain and cyclophosphamide and involvement of apoptosis.	Cyclophosphamide	73-89	Rho GTPase activating protein 45	Mus musculus	35-39
11345040-1	2000	The concentration of cystatin C, a cysteine proteinase inhibitor, was measured during the treatment of murine LS lymphosarcoma with cyclophosphamide and HA-1 murine hepatoma with the antitumor drug Ukrain.	Cyclophosphamide	132-148	cystatin C	Mus musculus	21-31
11345040-4	2000	At the same time, a marked increase in cathepsin B and cathepsin L activity in LS lymphosarcoma was found, indicating the involvement of apoptosis in the mechanism of antitumor action of cyclophosphamide.	Cyclophosphamide	187-203	cathepsin B	Mus musculus	39-50
11345040-4	2000	At the same time, a marked increase in cathepsin B and cathepsin L activity in LS lymphosarcoma was found, indicating the involvement of apoptosis in the mechanism of antitumor action of cyclophosphamide.	Cyclophosphamide	187-203	cathepsin L	Mus musculus	55-66
11345041-0	2000	Influence of Ukrain and cyclophosphamide administration on HA-1 murine hepatoma and LS lymphoma on aspartic proteinase cathepsin D.	Cyclophosphamide	24-40	cathepsin D	Mus musculus	119-130
11345041-2	2000	It was found that cyclophosphamide, as well as cyclophosphamide plus Ukrain, increased cathepsin D specific activity in mice with LS lymphosarcoma.	Cyclophosphamide	18-34	cathepsin D	Mus musculus	87-98
11345041-2	2000	It was found that cyclophosphamide, as well as cyclophosphamide plus Ukrain, increased cathepsin D specific activity in mice with LS lymphosarcoma.	Cyclophosphamide	47-63	cathepsin D	Mus musculus	87-98
11345042-8	2000	Cyclophosphane treatment of LS lymphosarcoma significantly increased the cystatin C concentration in serum.	Cyclophosphamide	0-14	cystatin C	Mus musculus	73-83
11345042-9	2000	Cyclophosphane treatment (50 mg/kg, single injection) increased cystatin C by up to 8-fold more in tumor issue.	Cyclophosphamide	0-14	cystatin C	Mus musculus	64-74
11345042-11	2000	In the group with LS lymphosarcoma Ukrain or cyclophosphane plus Ukrain treatment induced a significant increase in cystatin C concentration in liver.	Cyclophosphamide	45-59	cystatin C	Mus musculus	116-126
10585754-7	1999	We provide here evidence that IFN-gamma producers are relatively resistant to depletion by CY and that Th0 clones can be shifted towards Th1.	Cyclophosphamide	91-93	interferon gamma	Mus musculus	30-39
10585754-9	1999	Thus, the acceleration of diabetes by CY seems to be a complex event, which includes the relatively high resistance of IFN-gamma producers to the drug, their rapid reconstitution, and a Th1 shift of surviving T cell clones.	Cyclophosphamide	38-40	interferon gamma	Mus musculus	119-128
10585754-9	1999	Thus, the acceleration of diabetes by CY seems to be a complex event, which includes the relatively high resistance of IFN-gamma producers to the drug, their rapid reconstitution, and a Th1 shift of surviving T cell clones.	Cyclophosphamide	38-40	negative elongation factor complex member C/D, Th1l	Mus musculus	186-189
10703729-4	1999	Cyclophosphamide and irradiation caused a significant increase in acid phosphatase and N-acetyl-beta-D-glucosaminidase activity in the spleen of nonpregnant mice.	Cyclophosphamide	0-16	O-GlcNAcase	Mus musculus	87-118
10951848-3	1999	Mobilization with cyclophosphamide and granulocyte-colony stimulating factor was effective in terms of CD34+ cell shift to peripheral blood and the good quality autograft reliably led to haematopoetic recovery after megachemotherapy.	Cyclophosphamide	18-34	CD34 molecule	Homo sapiens	103-107
10536274-0	1999	Increased expression of growth-associated protein (GAP-43) in lower urinary tract pathways following cyclophosphamide (CYP)-induced cystitis.	Cyclophosphamide	101-117	growth associated protein 43	Homo sapiens	51-57
10536274-1	1999	Alterations in the expression of growth-associated protein 43 (GAP-43) were examined in lower urinary tract micturition reflex pathways in a chronic model of cyclophosphamide (CYP)-induced cystitis.	Cyclophosphamide	158-174	growth associated protein 43	Homo sapiens	33-61
10536274-1	1999	Alterations in the expression of growth-associated protein 43 (GAP-43) were examined in lower urinary tract micturition reflex pathways in a chronic model of cyclophosphamide (CYP)-induced cystitis.	Cyclophosphamide	158-174	growth associated protein 43	Homo sapiens	63-69
10536274-1	1999	Alterations in the expression of growth-associated protein 43 (GAP-43) were examined in lower urinary tract micturition reflex pathways in a chronic model of cyclophosphamide (CYP)-induced cystitis.	Cyclophosphamide	176-179	growth associated protein 43	Homo sapiens	33-61
10536274-1	1999	Alterations in the expression of growth-associated protein 43 (GAP-43) were examined in lower urinary tract micturition reflex pathways in a chronic model of cyclophosphamide (CYP)-induced cystitis.	Cyclophosphamide	176-179	growth associated protein 43	Homo sapiens	63-69
10534554-0	1999	Long-lasting remission and successful treatment of acquired factor VIII inhibitors using cyclophosphamide in a patient with systemic lupus erythematosus.	Cyclophosphamide	89-105	coagulation factor VIII	Homo sapiens	60-71
10463570-3	1999	It also expresses, in infected cells, the cyclophosphamide (CPA)-sensitive rat cytochrome P450 2B1 (CYP2B1) and the ganciclovir (GCV)-sensitive herpes simplex virus thymidine kinase (HSV-TK) transgenes.	Cyclophosphamide	42-58	cytochrome P450 2B1	Rattus norvegicus	79-98
10498854-0	1999	Pharmacological and molecular evidence for kinin B1 receptor expression in urinary bladder of cyclophosphamide-treated rats.	Cyclophosphamide	94-110	bradykinin receptor B1	Rattus norvegicus	43-60
10469060-8	1999	Maternal immunostimulation, while significantly decreasing the resorption rate in mice with CY-induced pregnancy loss, also strengthened CSF-1 mRNA expression at the fetomaternal interface and resulted in reconstitution in the number of CSF-1+ uterine leucocytes and metrial gland cells.	Cyclophosphamide	92-94	colony stimulating factor 1 (macrophage)	Mus musculus	137-142
10469060-8	1999	Maternal immunostimulation, while significantly decreasing the resorption rate in mice with CY-induced pregnancy loss, also strengthened CSF-1 mRNA expression at the fetomaternal interface and resulted in reconstitution in the number of CSF-1+ uterine leucocytes and metrial gland cells.	Cyclophosphamide	92-94	colony stimulating factor 1 (macrophage)	Mus musculus	237-242
10496187-1	1999	OBJECTIVE: To evaluate the response to cyclophosphamide (CTX) of five patients who failed an average three treatments with multiple other therapeutic agents, using serial monthly MRI measures.	Cyclophosphamide	39-55	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	57-60
10438709-12	1999	The addition of SCF to filgrastim after cyclophosphamide for PBPC mobilization resulted in a significant increase in CD34(+) cell yield and a concomitant reduction in the number of leukaphereses required to collect an optimal harvest of 5 x 10(6) CD34(+) cells/kg.	Cyclophosphamide	40-56	KIT ligand	Homo sapiens	16-19
10463570-3	1999	It also expresses, in infected cells, the cyclophosphamide (CPA)-sensitive rat cytochrome P450 2B1 (CYP2B1) and the ganciclovir (GCV)-sensitive herpes simplex virus thymidine kinase (HSV-TK) transgenes.	Cyclophosphamide	42-58	cytochrome P450 2B1	Rattus norvegicus	100-106
10463570-3	1999	It also expresses, in infected cells, the cyclophosphamide (CPA)-sensitive rat cytochrome P450 2B1 (CYP2B1) and the ganciclovir (GCV)-sensitive herpes simplex virus thymidine kinase (HSV-TK) transgenes.	Cyclophosphamide	60-63	cytochrome P450 2B1	Rattus norvegicus	79-98
10463570-3	1999	It also expresses, in infected cells, the cyclophosphamide (CPA)-sensitive rat cytochrome P450 2B1 (CYP2B1) and the ganciclovir (GCV)-sensitive herpes simplex virus thymidine kinase (HSV-TK) transgenes.	Cyclophosphamide	60-63	cytochrome P450 2B1	Rattus norvegicus	100-106
10476695-2	1999	METHOD OF STUDY: TGF beta 2 mRNA expression was evaluated in the uteroplacental units of mice with spontaneous (CBA/J x DBA/2J mouse combination) or cyclophosphamide (CP)-induced pregnancy loss.	Cyclophosphamide	149-165	transforming growth factor, beta 2	Mus musculus	17-27
10469894-1	1999	As judged by findings in preclinical models, determinants of cellular sensitivity to cyclophosphamide and other oxazaphosphorines include two cytosolic aldehyde dehydrogenases, viz., ALDH1A1 and ALDH3A1.	Cyclophosphamide	85-101	aldehyde dehydrogenase 1 family member A1	Homo sapiens	183-190
10509151-1	1999	BACKGROUND: To define a maximum tolerated dose (MTD) for the combination of epirubicin and cyclophosphamide with filgrastim (r-met-HuG-CSF) in patients with advanced solid tumors and non-Hodgkin"s lymphoma (NHL).	Cyclophosphamide	91-107	colony stimulating factor 2	Homo sapiens	135-138
10446877-0	1999	Granulocyte colony-stimulating factor treatment for cyclophosphamide-induced severe neutropenia in Wegener"s granulomatosis.	Cyclophosphamide	52-68	colony stimulating factor 3	Homo sapiens	0-37
10446877-1	1999	OBJECTIVE: To examine the efficacy and safety of recombinant human granulocyte colony-stimulating factor (rHuG-CSF) in the treatment of cyclophosphamide (CYC)-induced severe neutropenia (<1,000 neutrophils/microl) in patients with generalized Wegener"s granulomatosis (WG).	Cyclophosphamide	136-152	colony stimulating factor 3	Homo sapiens	67-104
10446877-1	1999	OBJECTIVE: To examine the efficacy and safety of recombinant human granulocyte colony-stimulating factor (rHuG-CSF) in the treatment of cyclophosphamide (CYC)-induced severe neutropenia (<1,000 neutrophils/microl) in patients with generalized Wegener"s granulomatosis (WG).	Cyclophosphamide	154-157	colony stimulating factor 3	Homo sapiens	67-104
10469894-1	1999	As judged by findings in preclinical models, determinants of cellular sensitivity to cyclophosphamide and other oxazaphosphorines include two cytosolic aldehyde dehydrogenases, viz., ALDH1A1 and ALDH3A1.	Cyclophosphamide	85-101	aldehyde dehydrogenase 3 family member A1	Homo sapiens	195-202
10402245-22	1999	Rapidly alternating or sequential cycles of epirubicin and cyclophosphamide with CSF support is a feasible strategy that allows a higher increase of dose-intensity of the single drugs.	Cyclophosphamide	59-75	colony stimulating factor 2	Homo sapiens	81-84
10457213-0	1999	Different effect of granulocyte colony-stimulating factor or bacterial infection on bone-marrow cells of cyclophosphamide-treated or irradiated mice.	Cyclophosphamide	105-121	colony stimulating factor 3 (granulocyte)	Mus musculus	20-57
10480343-7	1999	Despite the use of filgrastim, repeated cycles of CNF at doses of 2000 mg/m2 cyclophosphamide, 25 mg/m2 mitoxantrone, and 500 mg/m2 5-FU could not be given because of neutropenia and thrombopenia.	Cyclophosphamide	77-93	NPHS1 adhesion molecule, nephrin	Homo sapiens	50-53
10457213-5	1999	G-CSF administration to cyclophosphamide-treated mice increased the number of early blasts, myeloid blasts and granulocytic cells in the bone marrow, which indicates that this growth factor stimulates the proliferation of these cells in the bone marrow.	Cyclophosphamide	24-40	colony stimulating factor 3 (granulocyte)	Mus musculus	0-5
10457213-11	1999	Irradiation probably depletes the bone marrow from G-CSF-responsive cells, while cyclophosphamide spared G-CSF responsive cells, thus enabling the enhanced G-CSF-mediated recovery after cyclophosphamide treatment.	Cyclophosphamide	81-97	colony stimulating factor 3 (granulocyte)	Mus musculus	105-110
10457213-11	1999	Irradiation probably depletes the bone marrow from G-CSF-responsive cells, while cyclophosphamide spared G-CSF responsive cells, thus enabling the enhanced G-CSF-mediated recovery after cyclophosphamide treatment.	Cyclophosphamide	81-97	colony stimulating factor 3 (granulocyte)	Mus musculus	105-110
10478328-5	1999	Activities of GOT and GPT were elevated significantly in liver, kidney and serum after cyclophosphamide treatment, and were protected and restored to control level by ascorbic acid supplementation.	Cyclophosphamide	87-103	glutamic--pyruvic transaminase	Rattus norvegicus	22-25
10634173-0	1999	CD34+ cell dose requirements for rapid engraftment in a sequential high-dose chemotherapy regimen of paclitaxel, melphalan, and cyclophosphamide, thiotepa, and carboplatin (CTCb) with PBPC support in metastatic breast cancer.	Cyclophosphamide	128-144	CD34 molecule	Homo sapiens	0-4
10455355-1	1999	This report describes a patient with acute-type adult T cell leukemia/lymphoma (ATLL) successfully treated by autologous CD34+ peripheral blood stem cell transplantation after fractionated total body irradiation and high-dose cytarabine and cyclophosphamide.	Cyclophosphamide	241-257	CD34 molecule	Homo sapiens	121-125
10536484-2	1999	We described here a 15-year-old boy with positive anti-neutrophil cytoplasmic antibody (MPO-ANCA) and severe mPAN, who was effectively treated with intravenous methylprednisolone pulse therapy followed by monthly cyclophosphamide pulses for 1 year.	Cyclophosphamide	213-229	myeloperoxidase	Homo sapiens	88-91
10629646-0	1999	Effects on blood coagulation of adjuvant CNF (cyclophosphamide, novantrone, 5-fluorouracil) chemotherapy in stage II breast cancer patients.	Cyclophosphamide	46-62	NPHS1 adhesion molecule, nephrin	Homo sapiens	41-44
10444162-2	1999	Combination chemotherapy such as CHOP (cyclophosphamide, doxorubicin, vincristine, prednisolone) or purine analogues including fludarabine are frequently used and the anti-CD20 monoclonal antibody rituximab has recently been licensed for use.	Cyclophosphamide	39-55	keratin 20	Homo sapiens	172-176
10339466-5	1999	Cyclophosphamide exposure cooperated strongly with heterozygous inactivation of Nf1 in myeloid leukemogenesis, while etoposide did not.	Cyclophosphamide	0-16	neurofibromin 1	Mus musculus	80-83
10397267-5	1999	A significant association between expression of c-erbB-2 mRNA and survival was obtained for the subgroup of patients who received a standard chemotherapy with carboplatin or cisplatin and cyclophosphamide (P = 0.0003), whereas only a nonsignificant trend was observed for patients who did not receive a standard chemotherapy (P = 0.124).	Cyclophosphamide	188-204	erb-b2 receptor tyrosine kinase 2	Homo sapiens	48-56
10390196-7	1999	The outcome of cyclophosphamide/G-CSF mobilization was correlated with the response to the test dose of G-CSF.	Cyclophosphamide	15-31	colony stimulating factor 3	Homo sapiens	104-109
10385089-4	1999	RESULTS: Three weeks after a single dose of cyclophosphamide, bone marrow and splenic cellularity was reduced by 50% and the production of TNF-alpha to LPS stimulation by macrophages was also markedly impaired (both before and after total body irradiation).	Cyclophosphamide	44-60	tumor necrosis factor	Homo sapiens	139-148
10385089-7	1999	This reduction occurred despite equivalent serum levels of lipopolysaccharide, consistent with the reductions in TNF-alpha and interleukin-1beta production by host macrophages after cyclophosphamide pretreatment.	Cyclophosphamide	182-198	tumor necrosis factor	Homo sapiens	113-122
10385089-7	1999	This reduction occurred despite equivalent serum levels of lipopolysaccharide, consistent with the reductions in TNF-alpha and interleukin-1beta production by host macrophages after cyclophosphamide pretreatment.	Cyclophosphamide	182-198	interleukin 1 beta	Homo sapiens	127-144
10397244-4	1999	We report here the contribution of AGT in protecting against the toxic and mutagenic effects of cyclophosphamide.	Cyclophosphamide	96-112	angiotensinogen	Cricetulus griseus	35-38
10397244-11	1999	The present study demonstrates that AGT plays an important role in protecting against the toxic and mutagenic effect of cyclophosphamide and suggests that acrolein, not PM, is responsible for generating the toxic and mutagenic lesion(s) protected by the AGT protein.	Cyclophosphamide	120-136	angiotensinogen	Cricetulus griseus	36-39
10445392-4	1999	The present study was undertaken to investigate the influence of immunosuppressants cyclophosphamide and dexamethasone on the CYP2D 1-dependent metabolism of dextromethorphan (DEM) in the isolated perfused liver from male rat donors (Wistar albino, 250-310 g).	Cyclophosphamide	84-100	cytochrome P450, family 2, subfamily d, polypeptide 1	Rattus norvegicus	126-133
10393266-0	1999	Relatively low-dose cyclophosphamide is likely to induce apoptotic cell death in rat thymus through Fas/Fas ligand pathway.	Cyclophosphamide	20-36	Fas ligand	Rattus norvegicus	104-114
10414907-0	1999	Successful peripheral blood stem cell mobilization with etoposide (VP-16) in patients with relapsed or resistant lymphoma who failed cyclophosphamide mobilization.	Cyclophosphamide	133-149	host cell factor C1	Homo sapiens	67-72
10464704-0	1999	Enhanced antitumor immune responses of IL-2 gene-modified tumor vaccine by combination with IL-1 and low dose cyclophosphamide.	Cyclophosphamide	110-126	interleukin 2	Mus musculus	39-43
10414907-9	1999	These results indicate that etoposide + G-CSF is a highly effective mobilization regimen in patients who have failed cyclophosphamide mobilization.	Cyclophosphamide	117-133	colony stimulating factor 3	Homo sapiens	40-45
10348794-1	1999	The contributions of specific human liver cytochrome P-450 (CYP) enzymes to the activation, via 4-hydroxylation, of the oxazaphosphorine anticancer prodrugs cyclophosphamide (CPA) and ifosfamide (IFA) were investigated.	Cyclophosphamide	157-173	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	42-58
10348794-1	1999	The contributions of specific human liver cytochrome P-450 (CYP) enzymes to the activation, via 4-hydroxylation, of the oxazaphosphorine anticancer prodrugs cyclophosphamide (CPA) and ifosfamide (IFA) were investigated.	Cyclophosphamide	157-173	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	60-63
10348794-1	1999	The contributions of specific human liver cytochrome P-450 (CYP) enzymes to the activation, via 4-hydroxylation, of the oxazaphosphorine anticancer prodrugs cyclophosphamide (CPA) and ifosfamide (IFA) were investigated.	Cyclophosphamide	175-178	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	42-58
10348794-1	1999	The contributions of specific human liver cytochrome P-450 (CYP) enzymes to the activation, via 4-hydroxylation, of the oxazaphosphorine anticancer prodrugs cyclophosphamide (CPA) and ifosfamide (IFA) were investigated.	Cyclophosphamide	175-178	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	60-63
10348794-2	1999	Analysis of a panel of 15 human P-450 cDNAs expressed in human lymphoblasts and/or baculovirus-infected insect cells (Supersomes) demonstrated that CYPs 2A6, 2B6, 3A4, 3A5, and three CYP2C enzymes (2C9, 2C18, 2C19) exhibited significant oxazaphosphorine 4-hydroxylase activity, with 2B6 and 3A4 displaying the highest activity toward CPA and IFA, respectively.	Cyclophosphamide	334-337	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	148-161
10348794-3	1999	CYP2B6 metabolized CPA at a approximately 16-fold higher in vitro intrinsic clearance (apparent Vmax/Km) than IFA, whereas 3A4 demonstrated approximately 2-fold higher Vmax/Km toward IFA.	Cyclophosphamide	19-22	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	0-6
10348794-10	1999	These data further establish the significance of human liver CYP2B6 for the activation of the clinically important cancer chemotherapeutic prodrug CPA.	Cyclophosphamide	147-150	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	61-67
10414919-2	1999	Aliquots of PBPC were obtained after 4 days of G-CSF and/or GM-CSF and again during G-CSF-stimulated recovery from myelosuppressive doses of cyclophosphamide.	Cyclophosphamide	141-157	colony stimulating factor 3	Homo sapiens	84-89
10471061-2	1999	Its expression in Saccharomyces cerevisiae enabled us to obtain, at a high level, an active yeast-expressed CYP2B6 protein, so as to assess its role in the metabolism of ethoxyresorufin, pentoxyresorufin, benzyloxyresorufin, ethoxycoumarin, testosterone and cyclophosphamide.	Cyclophosphamide	258-274	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	108-114
10414919-6	1999	There was a greater frequency of tumor cell contamination in aphereses performed during G-CSF-stimulated recovery from cyclophosphamide than in collections primed by cytokine alone (13% vs 23%; P = 0.08), although this did not reach statistical significance.	Cyclophosphamide	119-135	colony stimulating factor 3	Homo sapiens	88-93
10418556-3	1999	METHODS: A multicenter dose-finding study of glycosylated G-CSF (lenograstim) for the mobilization of PBSCs following adjuvant CAF chemotherapy (cyclophosphamide, doxorubicin and 5-fluorouracil) was performed in 38 patients with postoperative breast cancer.	Cyclophosphamide	145-161	colony stimulating factor 3	Homo sapiens	58-63
10422440-16	1999	Although 2 cycles of CAV/PE therapy with cyclophosphamide, doxorubicin, vincristine, CDDP, and VP-16 were performed following resection of the retroperitoneal tumor, he showed no response and decreased 24 months after surgery.	Cyclophosphamide	41-57	caveolin 2	Homo sapiens	21-27
10472362-1	1999	Expression of mutant p53 in 19 patients with stage III moderately differentiated serous cystadenocarcinoma of the ovary, who all had optimal primary cytoreductive surgery and six cycles of cisplatin and cyclophosphamide was analyzed to determine its prognostic significance.	Cyclophosphamide	203-219	tumor protein p53	Homo sapiens	21-24
10470143-14	1999	Therefore, it can be concluded, that in the xenografted breast cancer cell lines a regulation of CD44 isoforms by farmorubicine, cyclophosphamide, estradiol, progesterone or tamoxifen could not be found, while serum levels were influenced in some cases probably due to tumour cell kill and shedding of surface proteins into blood stream.	Cyclophosphamide	129-145	CD44 molecule (Indian blood group)	Homo sapiens	97-101
10233433-8	1999	For patient 2, the severity of the cutaneous lesions also led to the use of cyclophosphamide, and this therapy resulted in total correction of VWF levels.	Cyclophosphamide	76-92	von Willebrand factor	Homo sapiens	143-146
10335450-3	1999	This strategy has been exemplified for the alkylating agents cyclophosphamide and ifosfamide, which are bioactivated by select P450 enzymes whose expression is generally high in liver and deficient in tumor cells.	Cyclophosphamide	61-77	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	127-131
10481938-4	1999	In this study we investigated regulation of BAX and BCL-2 expression by VP-16 and cyclophosphamide as a potential mechanism for the induction of breast cancer cell death induced by this regimen.	Cyclophosphamide	82-98	BCL2 associated X, apoptosis regulator	Homo sapiens	44-47
10481938-4	1999	In this study we investigated regulation of BAX and BCL-2 expression by VP-16 and cyclophosphamide as a potential mechanism for the induction of breast cancer cell death induced by this regimen.	Cyclophosphamide	82-98	BCL2 apoptosis regulator	Homo sapiens	52-57
10505100-8	1999	These levels are sufficient to neutralize IFN gamma in vivo, and to prevent either MDSD or cyclophosphamide (CYP)-accelerated diabetes in NOD mice, which are both characterized by systemic release of IFN gamma.	Cyclophosphamide	91-107	interferon gamma	Mus musculus	200-209
10467104-7	1999	Hsf1(+) drastically enhances expression of major Hsps in the absence of stress and induces tolerance against heat, simulated ischemia and toxicity by cyclophosphamide.	Cyclophosphamide	150-166	heat shock transcription factor 1	Homo sapiens	0-4
10461865-16	1999	The present results show that cyclophosphamide administration to female NOD mice results in a rapid influx of CD4 and CD8 cells and macrophages.	Cyclophosphamide	30-46	CD4 antigen	Mus musculus	110-113
10471061-11	1999	We also found that CYP2B6 is induced at protein and mRNA levels by phenobarbital (2 mM) and cyclophosphamide (1 mM), an anticancer drug known to be metabolized by CYP2B6.	Cyclophosphamide	92-108	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	19-25
10471061-11	1999	We also found that CYP2B6 is induced at protein and mRNA levels by phenobarbital (2 mM) and cyclophosphamide (1 mM), an anticancer drug known to be metabolized by CYP2B6.	Cyclophosphamide	92-108	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	163-169
10204687-2	1999	In the group treated with cyclophosphamide the amplitude of the contraction induced by the selective bradykinin B1 receptor agonist des-Arg9-bradykinin was larger than that in controls and dexamethasone prevented the up-regulation of this response induced by inflammation.	Cyclophosphamide	26-42	bradykinin receptor B1	Rattus norvegicus	101-123
10204687-4	1999	The bladder contraction induced by des-Arg9-bradykinin in cyclophosphamide-treated rats was antagonized by the bradykinin B1 receptor antagonist des-Arg9-D-Arg-[Hyp3,Thi5,D-Tic7,Oic8]bradykinin (des-Arg10-Hoe 140).	Cyclophosphamide	58-74	bradykinin receptor B1	Rattus norvegicus	111-133
9950898-3	1999	Intravenous PAF caused dose-dependent increases in the area density of Monastral blue-labeled vessels and neutrophil influx, and the former effect was inhibited by depletion of circulating neutrophils by cyclophosphamide or treatment with the neutrophil elastase inhibitor ONO-5046.	Cyclophosphamide	204-220	PCNA clamp associated factor	Rattus norvegicus	12-15
10089919-10	1999	After 24 hours of in vitro IL-2 activation, the cytotoxic effector cell function of the Cy-mobilized PBSC population was lower than that of paclitaxel-mobilized cells when tested against three tumor cell lines (B16, melanoma; C1498, AML; and Yak-1, lymphoma).	Cyclophosphamide	88-90	interleukin 2	Mus musculus	27-31
10489747-0	1999	Effect of pinacidil on the contractile response of cyclophosphamide-treated rat vas deferens.	Cyclophosphamide	51-67	arginine vasopressin	Rattus norvegicus	80-83
10489747-1	1999	Effect of pinacidil, a K+ channel opener, was studied on contractility of cyclophosphamide-treated rat vas deferens.	Cyclophosphamide	74-90	arginine vasopressin	Rattus norvegicus	103-106
10489747-4	1999	These findings indicate that the responsiveness of rat vas deferens smooth muscle to pinacidil is reduced following cyclophosphamide treatment.	Cyclophosphamide	116-132	arginine vasopressin	Rattus norvegicus	55-58
12205906-4	1999	The results also showed that PLGC could restore the capacity of macrophage for secreting IL-1 that had been inhibited by cyclophosphamide and PLGC could enhance the release of IL-2 from spleen cell in the experiment group (P < 0.05-0.01).	Cyclophosphamide	121-137	interleukin 1 complex	Mus musculus	89-93
9973423-3	1999	Intratracheal challenge with Aspergillus fumigatus conidia in both neutropenic (cyclophosphamide-treated) and nonneutropenic BALB/c mice resulted in the time-dependent increase in lung TNF-alpha levels, which correlated with the histologic development of a patchy, peribronchial infiltration of mononuclear and polymorphonuclear cells.	Cyclophosphamide	80-96	tumor necrosis factor	Mus musculus	185-194
9973423-4	1999	Ab-mediated neutralization of TNF-alpha resulted in an increase in mortality in both normal and cyclophosphamide-treated animals, which was associated with increased lung fungal burden as determined by histology and as quantified by chitin content.	Cyclophosphamide	96-112	tumor necrosis factor	Mus musculus	30-39
9973423-5	1999	Depletion of TNF-alpha resulted in a reduced lung neutrophil influx in both normal and cyclophosphamide-treated animals, which occurred in association with a decrease in lung levels of the C-X-C chemokine, macrophage inflammatory protein-2 and the C-C chemokines macrophage inflammatory protein-1alpha and JE.	Cyclophosphamide	87-103	tumor necrosis factor	Mus musculus	13-22
9973423-6	1999	In cyclophosphamide-treated animals, intratracheal administration of a TNF-alpha agonist peptide (TNF70-80) 3 days before, but not concomitant with, the administration of Aspergillus conidia resulted in improved survival from 9% in control mice to 55% in TNF70-80-treated animals.	Cyclophosphamide	3-19	tumor necrosis factor	Mus musculus	71-80
10595815-14	1999	The cost of chemotherapy administration, more doses of G-CSF, transfusions, and hospitalizations caused cyclophosphamide, etoposide, and G-CSF to be more expensive than G-CSF alone.	Cyclophosphamide	104-120	colony stimulating factor 3	Homo sapiens	55-60
11741210-8	1999	The calculated %inhibition of ALDH1 activity by acrolein and BCNU in patients receiving BCNU in 4 split doses with CY was 81%, and it increased to 92% in single dose BCNU regimen.	Cyclophosphamide	115-117	aldehyde dehydrogenase 1 family member A1	Homo sapiens	30-35
10052129-5	1999	The mice administered Cy and SPG or SPG-OH expressed and produced higher levels of IL-6 mRNA and protein than the mice administered only Cy.	Cyclophosphamide	22-24	interleukin 6	Mus musculus	83-87
10052129-6	1999	Gene expression of NK1.1 was also induced by Cy/SPG (or SPG-OH) treatment.	Cyclophosphamide	45-47	killer cell lectin-like receptor subfamily B member 1C	Mus musculus	19-24
10550566-12	1999	CONCLUSION: Oral etoposide and oral cyclophosphamide given days 1-14 every 28 days is well tolerated and results in an acceptable response rate and median survival in poor-prognosis (poor performance status or low serum albumin) extensive disease small-cell lung cancer.	Cyclophosphamide	36-52	albumin	Homo sapiens	220-227
9884322-3	1999	Here, the mechanism for the decrease in ALDH1 activity after CY administration was investigated.	Cyclophosphamide	61-63	aldehyde dehydrogenase 1 family member A1	Homo sapiens	40-45
9884322-8	1999	The percentage of inhibition of ALDH1 activity in vivo by acrolein in patients receiving CY was calculated based on the in vitro Ki of acrolein, the in vitro Km of HCY, and the in vivo peak blood concentrations of HCY and acrolein.	Cyclophosphamide	89-91	aldehyde dehydrogenase 1 family member A1	Homo sapiens	32-37
10529740-0	1999	Tissue-specific mutant frequencies and mutational spectra in cyclophosphamide-treated lacI transgenic mice.	Cyclophosphamide	61-77	tissue factor pathway inhibitor	Mus musculus	86-90
10529741-0	1999	Detection of cyclophosphamide-induced mutations at the Hprt but not the lacI locus in splenic lymphocytes of exposed mice.	Cyclophosphamide	13-29	hypoxanthine guanine phosphoribosyl transferase	Mus musculus	55-59
11399572-4	1999	An 8-year-old boy with a rare type X-linked cytochrome b positive chronic granulomatous disease underwent allogeneic bone marrow transplantation after conditioning with busulfan and cyclophosphamide.	Cyclophosphamide	182-198	mitochondrially encoded cytochrome b	Homo sapiens	44-56
9884322-9	1999	The calculations indicated that the activity of ALDH1 was inhibited by 85, 88, and 91% on days 1, 2, and 3 (24 h after the dose on day 2) of CY administration, respectively.	Cyclophosphamide	141-143	aldehyde dehydrogenase 1 family member A1	Homo sapiens	48-53
27420550-2	1999	The progenitor cells were mobilized by treatment with cyclophosphamide + granulocyte-colony stimulating factor (G-CSF) in patients with multiple myeloma.	Cyclophosphamide	54-70	colony stimulating factor 3	Homo sapiens	112-117
10218130-2	1999	with cyclophosphamide (CTX) pretreatment.	Cyclophosphamide	5-21	V-set and immunoglobulin domain containing 2	Mus musculus	23-26
9885374-0	1999	Optimal timing (Preemptive versus supportive) of granulocyte colony-stimulating factor administration following high-dose cyclophosphamide.	Cyclophosphamide	122-138	colony stimulating factor 3	Homo sapiens	49-86
27093737-0	1999	CYCLOPHOSPHAMIDE TREATMENT ALTERS THE CONTRACTILITY OF ISOLATED RAT VAS DEFERENS.	Cyclophosphamide	0-16	arginine vasopressin	Rattus norvegicus	68-71
27093737-1	1999	Influence of cyclophosphamide treatment (40. mg/kg, ip on alternate days for 5 times) was assessed on 1 m mol BaCl2-induced in vitro rhythmic contractions in isolated rat vas deferens.	Cyclophosphamide	13-29	arginine vasopressin	Rattus norvegicus	171-174
27093737-3	1999	These findings indicate a decrease in the contractility and, therefore, functioning of rat vas deferens under cyclophosphamide therapy.	Cyclophosphamide	110-126	arginine vasopressin	Rattus norvegicus	91-94
11399566-2	1999	The progenitor cells were mobilized by treatment with cyclophosphamide + granulocyte - colony stimulating factor (G-CSF) in patients with multiple myeloma.	Cyclophosphamide	54-70	colony stimulating factor 3	Homo sapiens	114-119
10463009-13	1999	CHOP (cyclophosphamide 650 mg/m2 day 1, vincristine 1.4 mg/m2 day 1, doxorubicin--45 mg/m2 day 1 and prednisone 100 mg/m2 day 1-5) was the most common chemotherapy regimen used.	Cyclophosphamide	6-22	DNA damage inducible transcript 3	Homo sapiens	0-4
10037025-2	1999	CD34 positive selection using the CellPro Ceprate CD34 column was performed on PB mononuclear cells obtained after cyclophosphamide/G-CSF mobilization.	Cyclophosphamide	115-131	CD34 molecule	Homo sapiens	0-4
10495452-0	1999	Cellular events and the pattern of p53 protein expression following cyclophosphamide-initiated cell death in various organs of developing embryo.	Cyclophosphamide	68-84	transformation related protein 53, pseudogene	Mus musculus	35-38
10495452-1	1999	This study was aimed at characterizing the temporal patterns of cell responses and p53 protein expression in the limbs, head, and liver of embryos responding to cyclophosphamide (CP)-induced teratogenic insult.	Cyclophosphamide	161-177	transformation related protein 53, pseudogene	Mus musculus	83-86
9989882-3	1998	As mobilising chemotherapy, cyclophosphamide, etoposide, doxorubicin and cytosine arabinoside were the drugs most frequently used in association with G-CSF for a total of 47 courses.	Cyclophosphamide	28-44	colony stimulating factor 3	Homo sapiens	150-155
9862733-1	1998	Previous studies have demonstrated that IL-15 administration after cyclophosphamide (CY) injection of C57BL/6J mice bearing the i.m.	Cyclophosphamide	67-83	interleukin 15	Mus musculus	40-45
9862733-1	1998	Previous studies have demonstrated that IL-15 administration after cyclophosphamide (CY) injection of C57BL/6J mice bearing the i.m.	Cyclophosphamide	85-87	interleukin 15	Mus musculus	40-45
9894718-5	1998	Our results showed that after CY a median of 3.6 x 10(6)/kg (0.5-12.8) CD34+ cells were collected with a median of two aphereses in 14 out of 17 patients; three failed to mobilize a number of CD34+ cells adequate for subsequent manipulation.	Cyclophosphamide	30-32	CD34 molecule	Homo sapiens	71-75
9951689-4	1998	Chemosensitivity data, according to a short-term assay (FMCA), indicated that tumours with p53 mutation were more resistant to cisplatin and cyclophosphamide.	Cyclophosphamide	141-157	tumor protein p53	Homo sapiens	91-94
9797215-3	1998	Treating mice with recombinant human IL-10 (rhIL-10) at 1.0 or 5.0 microg/mouse twice a day following the second cyclophosphamide administration significantly increased the survival rate compared to that of control mice treated with saline; however, treatment with rhIL-10 at 0.1 microg/mouse did not result in significant protection.	Cyclophosphamide	113-129	interleukin 10	Homo sapiens	37-42
9797215-11	1998	Furthermore, acceleration of leukocyte recovery by IL-10 after cyclophosphamide-induced depression may also play an important role in this protection.	Cyclophosphamide	63-79	interleukin 10	Mus musculus	51-56
9829841-6	1998	Preliminary in vitro studies indicated that IL-2 or IFN antagonized the severe inhibition of NKA induced by hydroxy-peroxy-cyclophosphamide (in vitro active derivative of cyclophosphamide), alone or associated with methotrexate + 5-fluorouracil.	Cyclophosphamide	123-139	interleukin 2	Homo sapiens	44-55
9972318-2	1998	Rats injected with a single dose of cyclophosphamide (200 mg kg-1 body weight) showed an increase in the levels of serum glutamate-oxaloacetate transaminase, serum glutamate-pyruvate transaminase, glucose-6-phosphate dehydrogenase and creatine phosphokinase isoenzyme by 53, 24, 55 and 135%, respectively.	Cyclophosphamide	36-52	glucose-6-phosphate dehydrogenase	Rattus norvegicus	197-230
9792146-0	1998	Diuretic response to cyclophosphamide in rats bearing a matrix metalloproteinase-9-producing tumour.	Cyclophosphamide	21-37	matrix metallopeptidase 9	Rattus norvegicus	56-82
9833936-8	1998	A selective downregulation of Th1-type cytokine expression was observed in a second set of experiments in which diabetes development was synchronised by cyclophosphamide.	Cyclophosphamide	153-169	negative elongation factor complex member C/D, Th1l	Mus musculus	30-33
9783811-0	1998	Further characterization of cyclophosphamide resistance: expression of CD95 and of bcl-2 in a CML cell line.	Cyclophosphamide	28-44	Fas cell surface death receptor	Homo sapiens	71-75
9783811-0	1998	Further characterization of cyclophosphamide resistance: expression of CD95 and of bcl-2 in a CML cell line.	Cyclophosphamide	28-44	BCL2 apoptosis regulator	Homo sapiens	83-88
9862192-0	1998	Mutation studies in lacI transgenic mice after exposure to radiation or cyclophosphamide.	Cyclophosphamide	72-88	tissue factor pathway inhibitor	Mus musculus	20-24
9792146-3	1998	Conversely, in rats bearing matrix metalloproteinase-9 (MMP-9) producing 13762NF mammary adenocarcinoma (MTLn3 clone), polyuria occurred chiefly during the first 24 h after CY treatment.	Cyclophosphamide	173-175	matrix metallopeptidase 9	Rattus norvegicus	28-54
9792146-3	1998	Conversely, in rats bearing matrix metalloproteinase-9 (MMP-9) producing 13762NF mammary adenocarcinoma (MTLn3 clone), polyuria occurred chiefly during the first 24 h after CY treatment.	Cyclophosphamide	173-175	matrix metallopeptidase 9	Rattus norvegicus	56-61
9792146-4	1998	In parallel with urine volume, a decrease in the urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG) was observed during the first 5 days after CY treatment in normal rats, but it increased in MTLn3-bearing rats.	Cyclophosphamide	151-153	O-GlcNAcase	Rattus norvegicus	70-101
9792146-4	1998	In parallel with urine volume, a decrease in the urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG) was observed during the first 5 days after CY treatment in normal rats, but it increased in MTLn3-bearing rats.	Cyclophosphamide	151-153	O-GlcNAcase	Rattus norvegicus	103-106
9792146-6	1998	Both urine volume and urinary excretion of NAG after CY treatment were lower in rats bearing the MTC clone (lower production of MMP-9) than for those bearing the MTLn3 clone.	Cyclophosphamide	53-55	O-GlcNAcase	Rattus norvegicus	43-46
9792146-6	1998	Both urine volume and urinary excretion of NAG after CY treatment were lower in rats bearing the MTC clone (lower production of MMP-9) than for those bearing the MTLn3 clone.	Cyclophosphamide	53-55	matrix metallopeptidase 9	Rattus norvegicus	128-133
9766669-4	1998	Intratumoral cytochrome P450 expression conferred substantial sensitivity to CPA cytotoxicity, with the most dramatic effects seen with CYP2B6.	Cyclophosphamide	77-80	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	136-142
9766669-5	1998	Strong CPA chemosensitivity was also seen following transduction of CYP2C18-Met, despite a very low level of CYP protein expression (>60-fold lower than that of 2B6).	Cyclophosphamide	7-10	cytochrome P450 family 2 subfamily C member 18	Homo sapiens	68-75
9766669-10	1998	CYP2B6 plus P450 reductase and CYP2C18-Met plus P450 reductase thus appear to be excellent gene combinations for use with CPA in P450/prodrug activation-based cancer gene therapy.	Cyclophosphamide	122-125	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	0-6
9766669-10	1998	CYP2B6 plus P450 reductase and CYP2C18-Met plus P450 reductase thus appear to be excellent gene combinations for use with CPA in P450/prodrug activation-based cancer gene therapy.	Cyclophosphamide	122-125	cytochrome P450 family 2 subfamily C member 18	Homo sapiens	31-38
9714064-0	1998	O6-methylguanine-DNA methyltransferase activity and sensitivity to cyclophosphamide and cisplatin in human lung tumor xenografts.	Cyclophosphamide	67-83	O-6-methylguanine-DNA methyltransferase	Homo sapiens	0-38
10379842-3	1999	Thus, the percentage of cyclophosphamide (CP)-treated embryos exhibiting limb malformations was shown to decrease significantly following GM-CSF administration.	Cyclophosphamide	24-40	colony stimulating factor 2	Homo sapiens	138-144
9747866-1	1998	BACKGROUND: We have previously reported that high expression of the erbB-2 gene (also known as HER-2/neu and ERBB2) in breast cancer is associated with patient response to dose-intensive treatment with cyclophosphamide, doxorubicin (Adriamycin), and 5-flurouracil (CAF) on the basis of short-term follow-up of 397 patients (set A) with axillary lymph node-positive tumors who were enrolled in Cancer and Leukemia Group B (CALGB) protocol 8541.	Cyclophosphamide	202-218	erb-b2 receptor tyrosine kinase 2	Homo sapiens	68-74
9714064-2	1998	The purpose of our study was to assay MGMT activity in cells of lung cancers and to correlate MGMT levels with chemotherapy response to cyclophosphamide (CTX) and cisplatin (DDP).	Cyclophosphamide	136-152	O-6-methylguanine-DNA methyltransferase	Homo sapiens	94-98
9776515-1	1998	This article is the fifth of a series aimed at mapping brain activities as they result from the development of cyclophosphamide (CP) cystitis in behaving rats using c-fos and Krox-24 expression.	Cyclophosphamide	111-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	165-170
9854510-4	1998	Alkylating agents such as cyclophosphamide altered the antitumor effect qualitatively, leading to complete regression which TNF alone could not achieve.	Cyclophosphamide	26-42	tumor necrosis factor	Mus musculus	124-127
9854510-8	1998	The amount of endogenous TNF induced by LPSp or ONO-4007 around a tumor lesion with CY was 4-5 fold higher than that without CY.	Cyclophosphamide	84-86	tumor necrosis factor	Mus musculus	25-28
9854510-8	1998	The amount of endogenous TNF induced by LPSp or ONO-4007 around a tumor lesion with CY was 4-5 fold higher than that without CY.	Cyclophosphamide	125-127	tumor necrosis factor	Mus musculus	25-28
9728932-9	1998	We conclude that mobilization by cyclophosphamide plus G-CSF leads to a lower number of malignant cells per CD34+ cell in LPs compared with G-CSF alone.	Cyclophosphamide	33-49	CD34 molecule	Homo sapiens	108-112
9776515-1	1998	This article is the fifth of a series aimed at mapping brain activities as they result from the development of cyclophosphamide (CP) cystitis in behaving rats using c-fos and Krox-24 expression.	Cyclophosphamide	111-127	early growth response 1	Rattus norvegicus	175-182
10322772-6	1998	CONCLUSION: The CHL-3A4 cell line established did express human cytochrome P450 3A4 and could lead metabolic activation for three genotoxic chemicals AFB1, STC and CPA.	Cyclophosphamide	164-167	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	64-83
9827356-4	1998	CHOP protocol is containing both proved carcinogenic cyclophosphamide and highly mutagenic doxorubicyn.	Cyclophosphamide	53-69	DNA damage inducible transcript 3	Homo sapiens	0-4
9785606-3	1998	Development of EAU induced by the interphotoreceptor retinoid binding protein (IRBP) was abolished almost completely by either TBI or Cy treatment, followed by SBMT, instituted one week after priming.	Cyclophosphamide	134-136	retinol binding protein 3, interstitial	Mus musculus	34-77
9785606-3	1998	Development of EAU induced by the interphotoreceptor retinoid binding protein (IRBP) was abolished almost completely by either TBI or Cy treatment, followed by SBMT, instituted one week after priming.	Cyclophosphamide	134-136	retinol binding protein 3, interstitial	Mus musculus	79-83
9722065-7	1998	Upon hematologic recovery, a second G-CSF mobilized non-T cell-depleted peripheral stem cell transplant from the same donor was given after pretransplant conditioning with busulphan and cyclophosphamide.	Cyclophosphamide	186-202	colony stimulating factor 3	Homo sapiens	36-41
9703286-0	1998	Therapy effect of either paclitaxel or cyclophosphamide combination treatment in patients with epithelial ovarian cancer and relation to TP53 gene status.	Cyclophosphamide	39-55	tumor protein p53	Homo sapiens	137-141
9671594-2	1998	The purpose of this study was to investigate the role of the tumor suppressor/cell cycle checkpoint gene, p53, and of cell cycle arrest in the response of the limbs to cyclophosphamide.	Cyclophosphamide	168-184	transformation related protein 53, pseudogene	Mus musculus	106-109
9702422-0	1998	Successful treatment with plasmapheresis, cyclophosphamide, and cyclosporin A in type B syndrome of insulin resistance.	Cyclophosphamide	42-58	insulin	Homo sapiens	100-107
9702422-14	1998	DISCUSSION: Severe type B insulin resistance may respond favorably to treatment with plasmapheresis and cyclophosphamide followed by cyclosporin A in combination with azathioprin.	Cyclophosphamide	104-120	insulin	Homo sapiens	26-33
9725052-0	1998	[The in vitro combination-effect of toremifene with CAF (cyclophosphamide, adriamycin, 5-fluorouracil) on growth of various human mammary carcinomas].	Cyclophosphamide	57-73	lysine acetyltransferase 2B	Homo sapiens	52-55
9711921-0	1998	A phase I trial of standard and cyclophosphamide dose-escalated CHOP with granulocyte colony stimulating factor in elderly patients with non-Hodgkin"s lymphoma.	Cyclophosphamide	32-48	DNA damage inducible transcript 3	Homo sapiens	64-68
9747866-1	1998	BACKGROUND: We have previously reported that high expression of the erbB-2 gene (also known as HER-2/neu and ERBB2) in breast cancer is associated with patient response to dose-intensive treatment with cyclophosphamide, doxorubicin (Adriamycin), and 5-flurouracil (CAF) on the basis of short-term follow-up of 397 patients (set A) with axillary lymph node-positive tumors who were enrolled in Cancer and Leukemia Group B (CALGB) protocol 8541.	Cyclophosphamide	202-218	erb-b2 receptor tyrosine kinase 2	Homo sapiens	95-104
9711921-0	1998	A phase I trial of standard and cyclophosphamide dose-escalated CHOP with granulocyte colony stimulating factor in elderly patients with non-Hodgkin"s lymphoma.	Cyclophosphamide	32-48	colony stimulating factor 3	Homo sapiens	74-111
9747866-1	1998	BACKGROUND: We have previously reported that high expression of the erbB-2 gene (also known as HER-2/neu and ERBB2) in breast cancer is associated with patient response to dose-intensive treatment with cyclophosphamide, doxorubicin (Adriamycin), and 5-flurouracil (CAF) on the basis of short-term follow-up of 397 patients (set A) with axillary lymph node-positive tumors who were enrolled in Cancer and Leukemia Group B (CALGB) protocol 8541.	Cyclophosphamide	202-218	erb-b2 receptor tyrosine kinase 2	Homo sapiens	109-114
9711921-1	1998	The purpose of this study was to assess the safety and feasibility of using standard and escalated doses of cyclophosphamide with doxorubicin, vincristine and prednisone (CHOP) plus granulocyte colony stimulating factor (G-CSF) to treat elderly patients who have advanced stage intermediate grade lymphoma.	Cyclophosphamide	108-124	DNA damage inducible transcript 3	Homo sapiens	171-175
9711921-1	1998	The purpose of this study was to assess the safety and feasibility of using standard and escalated doses of cyclophosphamide with doxorubicin, vincristine and prednisone (CHOP) plus granulocyte colony stimulating factor (G-CSF) to treat elderly patients who have advanced stage intermediate grade lymphoma.	Cyclophosphamide	108-124	colony stimulating factor 3	Homo sapiens	221-226
9683547-0	1998	Pulse cyclophosphamide plus methylprednisolone induces myelin-antigen-specific IL-4-secreting T cells in multiple sclerosis patients.	Cyclophosphamide	6-22	interleukin 4	Homo sapiens	79-83
9683547-2	1998	Thus therapies which decrease T cells secreting IFN-gamma production or increase IL-4 production would be expected to have an ameliorating effect on MS. We have previously reported increased anti-CD3-induced IL-4 secretion by T cells in progressive MS patients treated with cyclophosphamide plus methylprednisolone (CY/MP) which was associated with eosinophilia.	Cyclophosphamide	274-290	interleukin 4	Homo sapiens	208-212
9616158-11	1998	In contrast, recipients that had received CD4-depleted BMCs with CY plus fractionated irradiation (5Gy x 2) survived for more than 40 weeks without showing graft-versus-host reaction (GVHR).	Cyclophosphamide	65-67	CD4 antigen	Mus musculus	42-45
10200514-3	1998	We show that three teratogens, hyperthermia, cyclophosphamide and sodium arsenite induce an increase in cell death in day 9.0 mouse embryos with concurrent induction of DNA fragmentation, activation of caspase-3 and the cleavage of poly (ADP-ribose) polymerase (PARP).	Cyclophosphamide	45-61	caspase 3	Mus musculus	202-211
10200514-3	1998	We show that three teratogens, hyperthermia, cyclophosphamide and sodium arsenite induce an increase in cell death in day 9.0 mouse embryos with concurrent induction of DNA fragmentation, activation of caspase-3 and the cleavage of poly (ADP-ribose) polymerase (PARP).	Cyclophosphamide	45-61	poly (ADP-ribose) polymerase family, member 1	Mus musculus	232-260
10200514-3	1998	We show that three teratogens, hyperthermia, cyclophosphamide and sodium arsenite induce an increase in cell death in day 9.0 mouse embryos with concurrent induction of DNA fragmentation, activation of caspase-3 and the cleavage of poly (ADP-ribose) polymerase (PARP).	Cyclophosphamide	45-61	poly (ADP-ribose) polymerase family, member 1	Mus musculus	262-266
9667250-1	1998	PURPOSE: Standard cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy repeated at 3-week intervals is difficult to deliver in elderly patients with non-Hodgkin"s lymphoma (NHL).	Cyclophosphamide	18-34	DNA damage inducible transcript 3	Homo sapiens	78-82
9667258-2	1998	METHODS: We determined plasma levels of c-erbB-2 in 79 stages II and III breast cancer patients who received cyclophosphamide, methotrexate, and flourouracil (CMF)/cyclophosphamide, methotrexate, fluorouracil, vincristine, and prednisone (CMFVP) chemotherapy.	Cyclophosphamide	109-125	erb-b2 receptor tyrosine kinase 2	Homo sapiens	40-48
9714700-0	1998	Enhanced expressions of glucose-6-phosphate dehydrogenase and cytosolic aldehyde dehydrogenase and elevation of reduced glutathione level in cyclophosphamide-resistant human leukemia cells.	Cyclophosphamide	141-157	glucose-6-phosphate dehydrogenase	Homo sapiens	24-57
9609744-8	1998	Because the number of BAL neutrophils was strongly correlated with BALF and BAL cell-associated uPA activity, their involvement in uPA upregulation was addressed by inducing neutropenia with cyclophosphamide (200 mg/kg ip) before administration of the silica.	Cyclophosphamide	191-207	plasminogen activator, urokinase	Mus musculus	131-134
9714700-1	1998	Elevation of activity and mRNA level of a cytosolic aldehyde dehydrogenase-1 (ALDH1), which oxidizes aldophosphamide, was previously observed in a cyclophosphamide-resistant murine leukemia cell line.	Cyclophosphamide	147-163	aldehyde dehydrogenase family 1, subfamily A1	Mus musculus	78-83
9590137-1	1998	As reported previously, cyclophosphamide plus tumor necrosis factor-alpha treatment of C57BL/6 mice bearing advanced EL4 lymphoma induced approx.	Cyclophosphamide	24-40	epilepsy 4	Mus musculus	117-120
9649147-3	1998	CHOP therapy (cyclophosphamide, doxorubicin, vincristine and prednisolone) only slightly induces pulmonary toxicity.	Cyclophosphamide	14-30	DNA damage inducible transcript 3	Homo sapiens	0-4
9626212-6	1998	CAV/PE consisted of cyclophosphamide 800 mg/m2; doxorubicin 50 mg/m2; and vincristine 1.4 mg/m2 on day 1, which alternated every 3 weeks with cisplatin 80 mg/m2 on day 1 and etoposide 100 mg/m2 on days 1 to 3.	Cyclophosphamide	20-36	caveolin 2	Homo sapiens	0-6
9600968-5	1998	In vivo localization of technetium 99m hydrazinonicotinamide-annexin V was tested in three models: fuminant hepatic apoptosis induced by anti-Fas antibody injection in BALB/c mice; acute rejection in ACI rats with transplanted heterotopic PVG cardiac allografts; and cyclophosphamide treatment of transplanted 38C13 murine B cell lymphomas.	Cyclophosphamide	267-283	annexin A5	Mus musculus	61-70
9673408-2	1998	Similarly, IL-1 is reported to accelerate recovery following myelosuppressive treatment with doxorubicin (AdR), cis-platinum (DDP) and cyclophosphamide (CTx).	Cyclophosphamide	135-151	interleukin 1 complex	Mus musculus	11-15
9673353-0	1998	Augmentation of IL-2 activated natural killer cell adoptive immunotherapy with cyclophosphamide.	Cyclophosphamide	79-95	interleukin 2	Homo sapiens	16-20
9673408-2	1998	Similarly, IL-1 is reported to accelerate recovery following myelosuppressive treatment with doxorubicin (AdR), cis-platinum (DDP) and cyclophosphamide (CTx).	Cyclophosphamide	135-151	V-set and immunoglobulin domain containing 2	Mus musculus	153-156
9586906-7	1998	One patient, previously treated with mitoxantrone and cyclophosphamide for breast cancer, presented a new and, to our knowledge not previously reported, type of fusion transcript, with breakpoint at nt 399 of the CBFB gene and at nt 2134 of the MYH11 gene.	Cyclophosphamide	54-70	core-binding factor subunit beta	Homo sapiens	213-217
9610789-0	1998	p53 mutations in cyclophosphamide-associated bladder cancer.	Cyclophosphamide	17-33	tumor protein p53	Homo sapiens	0-3
9610789-3	1998	We examined 19 cyclophosphamide-related bladder tumors to test the hypothesis that they might contain somatic mutations in the p53 tumor suppressor gene that could link a specific metabolite to the etiology of these cancers.	Cyclophosphamide	15-31	tumor protein p53	Homo sapiens	127-130
9610789-5	1998	The p53 mutation spectrum of these cyclophosphamide-associated bladder cancers differed significantly from patterns reported for sporadic (P = 0.020), smoking-related (0.043), and schistosomiasis-linked (P = 0.002) tumors but not arylamine-associated neoplasms (P = 0.860).	Cyclophosphamide	35-51	tumor protein p53	Homo sapiens	4-7
9586906-7	1998	One patient, previously treated with mitoxantrone and cyclophosphamide for breast cancer, presented a new and, to our knowledge not previously reported, type of fusion transcript, with breakpoint at nt 399 of the CBFB gene and at nt 2134 of the MYH11 gene.	Cyclophosphamide	54-70	myosin heavy chain 11	Homo sapiens	245-250
9597676-3	1998	Either PE (platinum plus etoposide) or CAV (cyclophosphamide, Adriamycin, and vincristine) is a reasonable first-line therapy.	Cyclophosphamide	44-60	caveolin 2	Homo sapiens	39-42
9574530-10	1998	Finally, we found that immunization of mice with cyclophosphamide-induced pregnancy loss while decreasing the resorption rate in these females resulted in a decline in TNF-alpha expression at the fetomaternal interface.	Cyclophosphamide	49-65	tumor necrosis factor	Mus musculus	168-177
9592392-0	1998	An oncolytic viral mutant that delivers the CYP2B1 transgene and augments cyclophosphamide chemotherapy.	Cyclophosphamide	74-90	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	44-50
9592392-2	1998	A recombinant HSV-1 was generated by knock-out of Hsrr and insertion of the rat CYP2B1 transgene responsible for the bioactivation of the prodrugs, cyclophosphamide and ifosfamide.	Cyclophosphamide	148-164	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	80-86
9563896-4	1998	Clinical studies support an association between HER2 overexpression and resistance to alkylating agents (cisplatinum and cyclophosphamide).	Cyclophosphamide	121-137	erb-b2 receptor tyrosine kinase 2	Homo sapiens	48-52
9655358-4	1998	Both had primary steroid- and cyclophosphamide-resistant focal segmental glomerulo sclerosis (FSGS).	Cyclophosphamide	30-46	actinin alpha 4	Homo sapiens	94-98
11477927-4	1998	RESULTS: Fr1, the ethanol-soluble fraction, and Fr2, the ethanol insoluble fraction of LWDHD, both significantly improved the antibody production response in Cy-treated mice, in which Fr2 showed stronger activity than that of Fr1.	Cyclophosphamide	158-160	aldo-keto reductase family 1, member B8	Mus musculus	9-12
11477927-4	1998	RESULTS: Fr1, the ethanol-soluble fraction, and Fr2, the ethanol insoluble fraction of LWDHD, both significantly improved the antibody production response in Cy-treated mice, in which Fr2 showed stronger activity than that of Fr1.	Cyclophosphamide	158-160	aldo-keto reductase family 1, member B8	Mus musculus	226-229
9551609-1	1998	Previously, we have reported the successful expression of human aldehyde dehydrogenase class-1 (ALDH-1) in K562 leukemia cells using a retroviral vector and demonstrated low expression that resulted in up to three-fold increase in resistance to 4-hydroperoxycyclophosphamide (4-HC), an active derivative to cyclophosphamide.	Cyclophosphamide	258-274	aldehyde dehydrogenase 1 family member A1	Homo sapiens	64-94
9711921-9	1998	Six of 11 patients (55%) given CHOP with cyclophosphamide 900 mg/m2 (CHOP-900) completed treatment.	Cyclophosphamide	41-57	DNA damage inducible transcript 3	Homo sapiens	31-35
9711921-9	1998	Six of 11 patients (55%) given CHOP with cyclophosphamide 900 mg/m2 (CHOP-900) completed treatment.	Cyclophosphamide	41-57	DNA damage inducible transcript 3	Homo sapiens	69-73
9711921-12	1998	The received dose intensities of cyclophosphamide relative to standard CHOP measured over the actual time on therapy were 96% with standard CHOP and 115% with CHOP-900.	Cyclophosphamide	33-49	DNA damage inducible transcript 3	Homo sapiens	140-144
9711921-12	1998	The received dose intensities of cyclophosphamide relative to standard CHOP measured over the actual time on therapy were 96% with standard CHOP and 115% with CHOP-900.	Cyclophosphamide	33-49	DNA damage inducible transcript 3	Homo sapiens	140-144
9592981-5	1998	RESULTS: G-CSF support significantly reduced the frequency of day-1 drug dose reductions (p < 0.001) and of chemotherapy delays (p < 0.001), and improved the actual delivered doses of adriamycin, cyclophosphamide and etoposide (p < 0.02).	Cyclophosphamide	202-218	colony stimulating factor 3	Homo sapiens	9-14
9579368-0	1998	Cyclophosphamide given after active specific immunization augments antitumor immunity by modulation of Th1 commitment of CD4+ T cells.	Cyclophosphamide	0-16	negative elongation factor complex member C/D, Th1l	Mus musculus	103-106
9579368-0	1998	Cyclophosphamide given after active specific immunization augments antitumor immunity by modulation of Th1 commitment of CD4+ T cells.	Cyclophosphamide	0-16	CD4 antigen	Mus musculus	121-124
9579368-5	1998	In early stage (day 0) after ASI-CPA treatment, the CD4+ T cells were determined to play an important role in the protective immunity for the following reasons: 1) the CD4+/CD8+ ratio of spleen cells from immunized mice was higher than that of the control or CPA alone treated group; and 2) the tumor neutralizing activity of fresh spleen cells was abrogated by CD4+ T-cell depletion in vitro.	Cyclophosphamide	33-36	CD4 antigen	Mus musculus	52-55
9579368-7	1998	CONCLUSIONS: These results suggest that the protective immunity induced by ASI was augmented through the modification of the Th1 and Th2 balance by CPA injection after ASI.	Cyclophosphamide	148-151	negative elongation factor complex member C/D, Th1l	Mus musculus	125-128
9579368-7	1998	CONCLUSIONS: These results suggest that the protective immunity induced by ASI was augmented through the modification of the Th1 and Th2 balance by CPA injection after ASI.	Cyclophosphamide	148-151	heart and neural crest derivatives expressed 2	Mus musculus	133-136
9551609-1	1998	Previously, we have reported the successful expression of human aldehyde dehydrogenase class-1 (ALDH-1) in K562 leukemia cells using a retroviral vector and demonstrated low expression that resulted in up to three-fold increase in resistance to 4-hydroperoxycyclophosphamide (4-HC), an active derivative to cyclophosphamide.	Cyclophosphamide	258-274	aldehyde dehydrogenase 1 family member A1	Homo sapiens	96-102
9570859-4	1998	Flow cytometry of splenic T-lymphocyte subsets in normal mice indicates a significant decrease in the number of CD3+, CD4+, and CD8+ subsets after treatment with cyclophosphamide and after application of restraint stress; the interaction of the two treatments is significant for CD3+ and marginally significant for CD4+ subsets.	Cyclophosphamide	162-178	CD3 antigen, epsilon polypeptide	Mus musculus	112-115
9519935-7	1998	We describe a patient with non-Hodgkin"s lymphoma treated with conventional cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy and high-dose steroids who developed a rapidly progressive fatal leukoencephalopathy.	Cyclophosphamide	76-92	DNA damage inducible transcript 3	Homo sapiens	136-140
9528829-0	1998	Timing of recombinant human granulocyte colony-stimulating factor administration on neutropenia induced by cyclophosphamide in normal mice.	Cyclophosphamide	107-123	colony stimulating factor 3	Homo sapiens	28-65
9535035-9	1998	Cyclophosphamide + G-CSF significantly increased the yield of CD34+ cells but did not increase apoptosis.	Cyclophosphamide	0-16	CD34 molecule	Homo sapiens	62-66
9543059-0	1998	CD34+ cells mobilized by cyclophosphamide and granulocyte colony-stimulating factor (G-CSF) are functionally different from CD34+ cells mobilized by G-CSF.	Cyclophosphamide	25-41	CD34 molecule	Homo sapiens	0-4
9570859-4	1998	Flow cytometry of splenic T-lymphocyte subsets in normal mice indicates a significant decrease in the number of CD3+, CD4+, and CD8+ subsets after treatment with cyclophosphamide and after application of restraint stress; the interaction of the two treatments is significant for CD3+ and marginally significant for CD4+ subsets.	Cyclophosphamide	162-178	CD4 antigen	Mus musculus	118-121
9570859-4	1998	Flow cytometry of splenic T-lymphocyte subsets in normal mice indicates a significant decrease in the number of CD3+, CD4+, and CD8+ subsets after treatment with cyclophosphamide and after application of restraint stress; the interaction of the two treatments is significant for CD3+ and marginally significant for CD4+ subsets.	Cyclophosphamide	162-178	CD3 antigen, epsilon polypeptide	Mus musculus	279-282
9570859-4	1998	Flow cytometry of splenic T-lymphocyte subsets in normal mice indicates a significant decrease in the number of CD3+, CD4+, and CD8+ subsets after treatment with cyclophosphamide and after application of restraint stress; the interaction of the two treatments is significant for CD3+ and marginally significant for CD4+ subsets.	Cyclophosphamide	162-178	CD4 antigen	Mus musculus	315-318
9551361-0	1998	Cyclophosphamide enhances the CTL precursor frequency in mice immunized with MUC1-mannan fusion protein (M-FP).	Cyclophosphamide	0-16	mucin 1, transmembrane	Mus musculus	77-81
9752311-1	1998	The CHOP regimen (cyclophosphamide vincristine, adriamycin, prednisone) is considered since twenty years as the standard treatment of disseminated aggressive non-Hodgkin"s lymphomas and cures approximately 30% of patients.	Cyclophosphamide	18-34	DNA damage inducible transcript 3	Homo sapiens	4-8
9611965-11	1998	DISCUSSION: The activity of enzyme acetylcholinesterase depends on functional state of the liver, as well as the therapy with some drugs (cyclophosphamide, ecothiopate etc.).	Cyclophosphamide	138-154	acetylcholinesterase (Cartwright blood group)	Homo sapiens	35-55
9492821-7	1998	Patients with rapidly progressing and/or endocrine-resistant tumor should be treated with anthracycline containing regimen such as CAF (cyclophosphamide, adriamycin, 5-fluorouracil).	Cyclophosphamide	136-152	lysine acetyltransferase 2B	Homo sapiens	131-134
9486479-0	1998	Increase of growth-associated protein-43 immunoreactivity following cyclophosphamide-induced cystitis in rats.	Cyclophosphamide	68-84	growth associated protein 43	Rattus norvegicus	12-40
9480725-5	1998	Acceleration of male IDDM by cyclophosphamide led to a marked increase in IFN-gamma secreting islet T cells.	Cyclophosphamide	29-45	interferon gamma	Mus musculus	74-83
9613979-7	1998	When compared to G-CSF only, mobilization with high dose cyclophosphamide appeared to result in superior hematopoietic stem cell collections.	Cyclophosphamide	57-73	colony stimulating factor 3	Homo sapiens	17-22
9551941-7	1998	Cyclophosphamide (CTX)-treated neutropenic mice expressed significantly less IL-1beta in IPNMC after hemorrhage or endotoxemia compared with CTX-untreated controls.	Cyclophosphamide	0-16	interleukin 1 beta	Mus musculus	77-85
9486479-1	1998	We examined the effect of inflammation on immunoreactivity of growth-associated protein (GAP-43) in the rat urinary bladder in which acute cystitis was induced with cyclophosphamide (CPA).	Cyclophosphamide	165-181	growth associated protein 43	Rattus norvegicus	89-95
9427742-4	1998	Spontaneous progression to diabetes, which can be accelerated by cyclophosphamide injection, is accompanied by a 10-fold increase in IFN-gamma and a 3-fold decrease in IL-10 and IL-4 production by the locally residing antigen-specific T cells.	Cyclophosphamide	65-81	interferon gamma	Mus musculus	133-142
9486479-1	1998	We examined the effect of inflammation on immunoreactivity of growth-associated protein (GAP-43) in the rat urinary bladder in which acute cystitis was induced with cyclophosphamide (CPA).	Cyclophosphamide	183-186	growth associated protein 43	Rattus norvegicus	89-95
9427742-4	1998	Spontaneous progression to diabetes, which can be accelerated by cyclophosphamide injection, is accompanied by a 10-fold increase in IFN-gamma and a 3-fold decrease in IL-10 and IL-4 production by the locally residing antigen-specific T cells.	Cyclophosphamide	65-81	interleukin 10	Mus musculus	168-173
9427742-4	1998	Spontaneous progression to diabetes, which can be accelerated by cyclophosphamide injection, is accompanied by a 10-fold increase in IFN-gamma and a 3-fold decrease in IL-10 and IL-4 production by the locally residing antigen-specific T cells.	Cyclophosphamide	65-81	interleukin 4	Mus musculus	178-182
9486479-2	1998	Following CPA injection, the number of GAP-43 labeled nerves was significantly increased in the muscle layer.	Cyclophosphamide	10-13	growth associated protein 43	Rattus norvegicus	39-45
9950097-10	1998	These results suggest that antitumor activity by ASI and CY is transduced by sequential population shift from CD4 alone to both of CD4 and CD8.	Cyclophosphamide	57-59	CD4 antigen	Mus musculus	110-113
9950097-10	1998	These results suggest that antitumor activity by ASI and CY is transduced by sequential population shift from CD4 alone to both of CD4 and CD8.	Cyclophosphamide	57-59	CD4 antigen	Mus musculus	131-134
9474247-3	1998	The effector cells induced in the mice treated with CY and allogeneic lymphocytes expressed the Lyt 1.2, Lyt 2.2, IL-2R antigens on their membrane surface and did not express the H2KbDb (donor H-2) antigen, and they showed a specific cytostatic activity against S180 cells.	Cyclophosphamide	52-54	interleukin 2 receptor, alpha chain	Mus musculus	114-119
9389719-0	1997	Cyclophosphamide, doxorubicin, vincristine, prednisone dose intensification with granulocyte colony-stimulating factor markedly depletes stem cell reserve for autologous bone marrow transplantation.	Cyclophosphamide	0-16	colony stimulating factor 3	Homo sapiens	81-118
9434797-4	1998	In contrast, the content of c-myb and p53 mRNA is greater (P < 0.05) in submandibular tissues of female relative to those of male mice; and (3) testosterone or cyclophosphamide treatment led to a significant (P < 0.05) decline in the mRNA levels of c-myb, bcl-2, and/or AR, but an increase (P < 0.05) in the mRNA amount of Bax, in lacrimal, but not in salivary, glands of female mice.	Cyclophosphamide	163-179	myeloblastosis oncogene	Mus musculus	28-33
9434797-4	1998	In contrast, the content of c-myb and p53 mRNA is greater (P < 0.05) in submandibular tissues of female relative to those of male mice; and (3) testosterone or cyclophosphamide treatment led to a significant (P < 0.05) decline in the mRNA levels of c-myb, bcl-2, and/or AR, but an increase (P < 0.05) in the mRNA amount of Bax, in lacrimal, but not in salivary, glands of female mice.	Cyclophosphamide	163-179	transformation related protein 53, pseudogene	Mus musculus	38-41
9434797-4	1998	In contrast, the content of c-myb and p53 mRNA is greater (P < 0.05) in submandibular tissues of female relative to those of male mice; and (3) testosterone or cyclophosphamide treatment led to a significant (P < 0.05) decline in the mRNA levels of c-myb, bcl-2, and/or AR, but an increase (P < 0.05) in the mRNA amount of Bax, in lacrimal, but not in salivary, glands of female mice.	Cyclophosphamide	163-179	myeloblastosis oncogene	Mus musculus	255-260
9434797-4	1998	In contrast, the content of c-myb and p53 mRNA is greater (P < 0.05) in submandibular tissues of female relative to those of male mice; and (3) testosterone or cyclophosphamide treatment led to a significant (P < 0.05) decline in the mRNA levels of c-myb, bcl-2, and/or AR, but an increase (P < 0.05) in the mRNA amount of Bax, in lacrimal, but not in salivary, glands of female mice.	Cyclophosphamide	163-179	B cell leukemia/lymphoma 2	Mus musculus	262-267
9434797-4	1998	In contrast, the content of c-myb and p53 mRNA is greater (P < 0.05) in submandibular tissues of female relative to those of male mice; and (3) testosterone or cyclophosphamide treatment led to a significant (P < 0.05) decline in the mRNA levels of c-myb, bcl-2, and/or AR, but an increase (P < 0.05) in the mRNA amount of Bax, in lacrimal, but not in salivary, glands of female mice.	Cyclophosphamide	163-179	androgen receptor	Mus musculus	276-278
9434797-4	1998	In contrast, the content of c-myb and p53 mRNA is greater (P < 0.05) in submandibular tissues of female relative to those of male mice; and (3) testosterone or cyclophosphamide treatment led to a significant (P < 0.05) decline in the mRNA levels of c-myb, bcl-2, and/or AR, but an increase (P < 0.05) in the mRNA amount of Bax, in lacrimal, but not in salivary, glands of female mice.	Cyclophosphamide	163-179	BCL2-associated X protein	Mus musculus	332-335
9536121-4	1998	In naive mice, irradiated and cyclophosphamide-treated mice, GM-CSF did not affect the course of L. monocytogenes infection in thigh muscle, spleen and liver.	Cyclophosphamide	30-46	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	61-67
9928576-7	1998	For women with 4-9 involved nodes, sequential treatment A(doxorubicin)-T(paclitaxel)-C(cyclophosphamide) with G-CSF is being compared to AC x 4 followed by high-dose chemotherapy with stem cell support.	Cyclophosphamide	87-103	colony stimulating factor 3	Homo sapiens	110-115
9409065-1	1997	Cyclophosphamide, doxorubicin, vincristine (Oncovin), and prednisolone (CHOP) has for many years been the standard chemotherapeutic regimen for patients with aggressive non-Hodgkin"s lymphoma.	Cyclophosphamide	0-16	DNA damage inducible transcript 3	Homo sapiens	72-76
9537818-0	1997	Effects of a 5-HT1A receptor agonist on acute and delayed cyclophosphamide-induced vomiting.	Cyclophosphamide	58-74	5-hydroxytryptamine receptor 1A	Homo sapiens	13-28
9403711-5	1997	During cyclophosphamide-induced follicle dystrophy and alopecia, massive keratinocyte apoptosis occurred in the entire proximal hair bulb, except in the dermal papilla, despite a strong up-regulation of Bax and p75NTR immunoreactivity.	Cyclophosphamide	7-23	BCL2-associated X protein	Mus musculus	203-206
9403711-5	1997	During cyclophosphamide-induced follicle dystrophy and alopecia, massive keratinocyte apoptosis occurred in the entire proximal hair bulb, except in the dermal papilla, despite a strong up-regulation of Bax and p75NTR immunoreactivity.	Cyclophosphamide	7-23	nerve growth factor receptor (TNFR superfamily, member 16)	Mus musculus	211-217
9432038-0	1997	A randomized phase II study of BB-10010: a variant of human macrophage inflammatory protein-1alpha for patients receiving high-dose etoposide and cyclophosphamide for malignant lymphoma and breast cancer.	Cyclophosphamide	146-162	C-C motif chemokine ligand 3	Homo sapiens	60-98
9815632-18	1997	We conclude that two courses of high-dose cyclophosphamide and doxorubicin using granulocyte colony-stimulating factor are feasible and safe with tolerable myocardial toxicity as evidenced by serial endomyocardial biopsies.	Cyclophosphamide	42-58	colony stimulating factor 3	Homo sapiens	81-118
9396566-3	1997	The model was prepared by feeding ovalbumin to BALB/c mice after intraperitoneal injection of cyclophosphamide.	Cyclophosphamide	94-110	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	34-43
9394035-1	1997	Detoxification of cyclophosphamide is effected, in part, by hepatic class 1 aldehyde dehydrogenase (ALDH-1)-catalyzed oxidation of aldophosphamide, a pivotal aldehyde intermediate, to the nontoxic metabolite, carboxyphosphamide.	Cyclophosphamide	18-34	aldehyde dehydrogenase 1 family member A1	Homo sapiens	100-106
9491847-0	1997	Results of treatment with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) for non-Hodgkin"s aggressive lymphoma analyzed according to the International Prognostic Index.	Cyclophosphamide	26-42	DNA damage inducible transcript 3	Homo sapiens	85-89
9416813-1	1997	OBJECTIVES: To report the long term effect of the combined treatment with high dose intravenous immunoglobulins (i.v.Ig) and oral cyclophosphamide (CTX) in patients with multifocal motor neuropathy, and to determine whether the association of oral CTX in these patients may help to delay and, possibly, suspend i.v.Ig infusions.	Cyclophosphamide	130-146	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	148-151
9416813-1	1997	OBJECTIVES: To report the long term effect of the combined treatment with high dose intravenous immunoglobulins (i.v.Ig) and oral cyclophosphamide (CTX) in patients with multifocal motor neuropathy, and to determine whether the association of oral CTX in these patients may help to delay and, possibly, suspend i.v.Ig infusions.	Cyclophosphamide	130-146	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	248-251
9382956-3	1997	In the present study, an attempt was made to endow human stem cell (CD34+ cells) with resistance to cyclophosphamide, a well-known AA, and adriamycin (ADM) by transducing the glutathione-S-transferase pi (GST-pi) gene whose product is thought to detoxify AA by conjugating them with glutathione and to remove a toxic peroxide formed by ADM.	Cyclophosphamide	100-116	CD34 molecule	Homo sapiens	68-72
9467301-3	1997	Moreover, the effect of lysozyme dimer on the humoral response in cyclophosphamide-treated mice was studied depending on the dose applied and time of exposure to the drug in relation to SRBC.	Cyclophosphamide	66-82	lysozyme C, kidney isozyme	Ovis aries	24-32
9467301-10	1997	It has also been found that lysozyme dimer significantly reduces the suppressive effect of a high cyclophosphamide dose (200 mg/kg) on the humoral response of SRBC-immunized mice.	Cyclophosphamide	98-114	lysozyme C, kidney isozyme	Ovis aries	28-36
9467301-14	1997	We have also found that the protective action of three doses of lysozyme dimer (2 or 20 micrograms/kg each) administered between cyclophosphamide injection and the antigen, or after antigen administration is weaker than such a treatment prior to cyclophosphamide immunosuppression.	Cyclophosphamide	129-145	lysozyme C, kidney isozyme	Ovis aries	64-72
9467301-14	1997	We have also found that the protective action of three doses of lysozyme dimer (2 or 20 micrograms/kg each) administered between cyclophosphamide injection and the antigen, or after antigen administration is weaker than such a treatment prior to cyclophosphamide immunosuppression.	Cyclophosphamide	246-262	lysozyme C, kidney isozyme	Ovis aries	64-72
9354446-1	1997	Intratumoral expression of cytochrome P450 2B1 sensitizes tumor cells to the cytotoxic action of the alkylating agent prodrug cyclophosphamide (CPA) and provides a novel strategy for cancer gene therapy that may enhance the selectivity and the effectiveness of this class of antitumor drugs [L. Chen and D. J. Waxman, Cancer Res., 55: 581-589, 1995].	Cyclophosphamide	126-142	cytochrome P450 2B1	Rattus norvegicus	27-46
9354446-1	1997	Intratumoral expression of cytochrome P450 2B1 sensitizes tumor cells to the cytotoxic action of the alkylating agent prodrug cyclophosphamide (CPA) and provides a novel strategy for cancer gene therapy that may enhance the selectivity and the effectiveness of this class of antitumor drugs [L. Chen and D. J. Waxman, Cancer Res., 55: 581-589, 1995].	Cyclophosphamide	144-147	cytochrome P450 2B1	Rattus norvegicus	27-46
9815579-1	1997	Molecular determinants of cellular sensitivity to cyclophosphamide, long the mainstay of chemotherapeutic regimens used to treat metastatic breast cancer, include class 1 and class 3 aldehyde dehydrogenases (ALDH-1 and ALDH-3, respectively), which catalyze the detoxification of this agent.	Cyclophosphamide	50-66	aldehyde dehydrogenase 1 family member A1	Homo sapiens	208-214
9815579-1	1997	Molecular determinants of cellular sensitivity to cyclophosphamide, long the mainstay of chemotherapeutic regimens used to treat metastatic breast cancer, include class 1 and class 3 aldehyde dehydrogenases (ALDH-1 and ALDH-3, respectively), which catalyze the detoxification of this agent.	Cyclophosphamide	50-66	aldehyde dehydrogenase 3 family member A1	Homo sapiens	219-225
9382956-7	1997	The GST-pi gene-transduced CD34+ cells formed almost 3- and 2.5-fold more CFU-GM than neo gene-transduced CD34+ cells in the presence of 2.5 microg/ml of 4-hydroperoxycyclophosphamide (4-HC), an active form of cyclophosphamide, and 30 ng/ml ADM, respectively.	Cyclophosphamide	167-183	CD34 molecule	Homo sapiens	27-31
9402167-0	1997	Multiple cycles of high-dose doxorubicin and cyclophosphamide with G-CSF mobilized peripheral blood progenitor cell support in patients with metastatic breast cancer.	Cyclophosphamide	45-61	colony stimulating factor 3	Homo sapiens	67-72
9363868-0	1997	Randomized placebo-controlled study of recombinant human interleukin-11 to prevent chemotherapy-induced thrombocytopenia in patients with breast cancer receiving dose-intensive cyclophosphamide and doxorubicin.	Cyclophosphamide	177-193	interleukin 11	Homo sapiens	57-71
9373186-7	1997	Reg II mRNA was particularly increased in overtly diabetic female mice and in cyclophosphamide-treated male mice.	Cyclophosphamide	78-94	regenerating family member 1 alpha	Homo sapiens	0-3
9402167-1	1997	BACKGROUND: In a previous study we applied doxorubicin and cyclophosphamide in a dose-intensive regimen with GM-CSF to patients with metastatic breast cancer (MBC).	Cyclophosphamide	59-75	colony stimulating factor 2	Homo sapiens	109-115
9326216-0	1997	The granulocyte colony-stimulating factor receptor is required for the mobilization of murine hematopoietic progenitors into peripheral blood by cyclophosphamide or interleukin-8 but not flt-3 ligand.	Cyclophosphamide	145-161	colony stimulating factor 3 receptor (granulocyte)	Mus musculus	4-50
9352076-0	1997	Dual temperature model for the estimation of energetics parameters for acetylcholinesterase inhibition by cyclophosphamide.	Cyclophosphamide	106-122	acetylcholinesterase (Cartwright blood group)	Gallus gallus	71-91
9326216-8	1997	These results show that the G-CSFR is required for mobilization in response to cyclophosphamide or IL-8 but not flt-3 ligand and suggest that the G-CSFR may play an important and previously unexpected role in HPC migration.	Cyclophosphamide	79-95	colony stimulating factor 3 receptor (granulocyte)	Mus musculus	28-34
9331082-6	1997	On the basis of cytochrome P450 (CYP) isoform-specific chemical inhibitor and cDNA-expressed human P450 isozyme studies, CYP2C9 and CYP3A4/5 seemed to be the major P450 isoforms responsible for HCY formation at low (0.1 mM) and high (0.7 and 5 mM) concentrations of CY, respectively.	Cyclophosphamide	33-35	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	121-127
9383226-10	1997	We suggest that "patient-dependent" criteria for starting G-CSF are reasonable especially in patients conditioned with protocols only slowly inducing neutropenia: eg NHL and HD patients after BEAM, MM after L-PAM or patients after busulphan and cyclophosphamide (BUCY2).	Cyclophosphamide	245-261	colony stimulating factor 3	Homo sapiens	58-63
9331082-6	1997	On the basis of cytochrome P450 (CYP) isoform-specific chemical inhibitor and cDNA-expressed human P450 isozyme studies, CYP2C9 and CYP3A4/5 seemed to be the major P450 isoforms responsible for HCY formation at low (0.1 mM) and high (0.7 and 5 mM) concentrations of CY, respectively.	Cyclophosphamide	33-35	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	132-138
9344509-0	1997	Adverse effects of tumour necrosis factor in cyclophosphamide-treated mice subjected to gut-derived Pseudomonas aeruginosa sepsis.	Cyclophosphamide	45-61	tumor necrosis factor	Mus musculus	19-41
9344509-3	1997	In this model, TNF-alpha was detected in serum from the next day after the second cyclophosphamide administration, increasing to level of 3 ng/ml in lethal conditions.	Cyclophosphamide	82-98	tumor necrosis factor	Mus musculus	15-24
9390210-0	1997	A phase II study of high-dose epirubicin (EPI) plus cyclophosphamide (CPA) with G-CSF for breast cancer patients with visceral metastases or hormone-independent tumors: a trial of the Japan Clinical Oncology Group.	Cyclophosphamide	70-73	colony stimulating factor 3	Homo sapiens	80-85
9336363-1	1997	PURPOSE: To determine the maximum-tolerated dose (MTD) of cyclophosphamide (CTX) when administered over 2 consecutive days followed by hematopoetic stem-cell rescue given as two sequential courses to children with glioblastoma multiforme, poor-prognosis pontine gliomas, and other recurrent CNS tumors.	Cyclophosphamide	58-74	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	76-79
9402332-0	1997	Viability and quantification of progenitor cells in venesected blood from patients receiving escalated-dose epirubicin and cyclophosphamide with G-CSF for lymphoma: potential role in further increasing dose-intensity.	Cyclophosphamide	123-139	colony stimulating factor 3	Homo sapiens	145-150
9374100-15	1997	At these doses, four cycles of doxorubicin, paclitaxel, and cyclophosphamide with PBPC and granulocyte colony-stimulating factor support every 21 days was well tolerated and showed evidence of activity.	Cyclophosphamide	60-76	colony stimulating factor 3	Homo sapiens	91-128
9815838-13	1997	Sequential IL-3/G-CSF given prior to and following high-dose etoposide and cyclophosphamide is safe and is a feasible strategy to compare in prospective randomized trials to patients treated with only postchemotherapy IL-3 and G-CSF and to patients treated with peripheral blood stem cell support.	Cyclophosphamide	75-91	interleukin 3	Homo sapiens	11-15
9307252-0	1997	Immune deviation following pulse cyclophosphamide/methylprednisolone treatment of multiple sclerosis: increased interleukin-4 production and associated eosinophilia.	Cyclophosphamide	33-49	interleukin 4	Homo sapiens	112-125
9815838-13	1997	Sequential IL-3/G-CSF given prior to and following high-dose etoposide and cyclophosphamide is safe and is a feasible strategy to compare in prospective randomized trials to patients treated with only postchemotherapy IL-3 and G-CSF and to patients treated with peripheral blood stem cell support.	Cyclophosphamide	75-91	colony stimulating factor 3	Homo sapiens	16-21
9446257-5	1997	In a randomized study by Ardizzoni et al., the administration of GM-CSF at the dose of 10 micrograms/kg following CEF program (cyclophosphamide, epirubicin and fluorouracil) was effective in reducing from 20 to 16 days the time interval among cycles.	Cyclophosphamide	127-143	colony stimulating factor 2	Homo sapiens	65-71
9322086-1	1997	Class 1 aldehyde dehydrogenases (ALDH-1) function as drug resistance gene products by catalyzing the irreversible conversion of aldophosphamide, an active metabolite of cyclophosphamide, to an inert compound.	Cyclophosphamide	169-185	aldehyde dehydrogenase 1 family member A1	Homo sapiens	33-39
9322086-2	1997	Because the dose-limiting toxicity of cyclophosphamide is myelosuppression, retrovirus-mediated transfer of ALDH-1 to bone marrow cells has been proposed as a protective strategy.	Cyclophosphamide	38-54	aldehyde dehydrogenase 1 family member A1	Homo sapiens	108-114
9308634-10	1997	CONCLUSION: A regimen of cyclophosphamide, etoposide, and granulocyte-colony-stimulating factor led to the successful collection of adequate numbers of CD34+ cells in most patients without excessive toxicity.	Cyclophosphamide	25-41	CD34 molecule	Homo sapiens	152-156
9446257-10	1997	achieved acceleration of cyclophosphamide-cisplatin combination by GM-CSF at the dose of 3 micrograms/kg.	Cyclophosphamide	25-41	colony stimulating factor 2	Homo sapiens	67-73
9291435-2	1997	mdm-2 mRNA expression was an independent prognostic factor for patients with primary ovarian cancer, FIGO (International Federation of Gynecology and Obstetrics) stages III and IV (n = 57), who all received chemotherapy with carboplatin or cisplatin and cyclophosphamide.	Cyclophosphamide	254-270	MDM2 proto-oncogene	Homo sapiens	0-5
9291435-6	1997	Our results suggest that mdm-2, which is known to disrupt p53 function, sensitizes ovarian-cancer cells to cisplatin/cyclophosphamide, possibly by inhibition of p53-mediated G1 cell-cycle arrest and p53-stimulated nucleotide-excision repair.	Cyclophosphamide	117-133	MDM2 proto-oncogene	Homo sapiens	25-30
9291435-6	1997	Our results suggest that mdm-2, which is known to disrupt p53 function, sensitizes ovarian-cancer cells to cisplatin/cyclophosphamide, possibly by inhibition of p53-mediated G1 cell-cycle arrest and p53-stimulated nucleotide-excision repair.	Cyclophosphamide	117-133	tumor protein p53	Homo sapiens	58-61
9291435-6	1997	Our results suggest that mdm-2, which is known to disrupt p53 function, sensitizes ovarian-cancer cells to cisplatin/cyclophosphamide, possibly by inhibition of p53-mediated G1 cell-cycle arrest and p53-stimulated nucleotide-excision repair.	Cyclophosphamide	117-133	tumor protein p53	Homo sapiens	161-164
9291435-6	1997	Our results suggest that mdm-2, which is known to disrupt p53 function, sensitizes ovarian-cancer cells to cisplatin/cyclophosphamide, possibly by inhibition of p53-mediated G1 cell-cycle arrest and p53-stimulated nucleotide-excision repair.	Cyclophosphamide	117-133	tumor protein p53	Homo sapiens	161-164
9280407-7	1997	CYP2B6-expressing cells were found to be more sensitive than control cells to the cytotoxicity and mutagenicity of cyclophosphamide, aflatoxin B1, and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone.	Cyclophosphamide	115-131	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	0-6
9257887-2	1997	The aim of this study was to evaluate the feasibility of a high-dose intensity doxorubicin-cyclophosphamide regimen with supporting G-CSF and blood stem cells.	Cyclophosphamide	91-107	colony stimulating factor 3	Homo sapiens	132-137
9257887-11	1997	We have established a safe, outpatient, high-dose intensity doxorubicin-cyclophosphamide regimen with supporting G-CSF and blood stem cells which can be submitted for comparison with the current standards.	Cyclophosphamide	72-88	colony stimulating factor 3	Homo sapiens	113-118
9298933-0	1997	Interleukin-1alpha synergistic in vivo enhancement of cyclophosphamide- and carboplatin-mediated antitumor activity.	Cyclophosphamide	54-70	interleukin 1 alpha	Homo sapiens	0-18
9298933-2	1997	Studies were undertaken to examine the ability of IL-1alpha to enhance the activity of cyclophosphamide (CTX) administered in combination with carboplatin.	Cyclophosphamide	87-103	interleukin 1 alpha	Homo sapiens	50-59
9279349-0	1997	[Efficacy of combination chemotherapy of cyclophosphamide and 5"-deoxy-5-fluorouridine in a mammary tumor xenograft model, MX-1].	Cyclophosphamide	41-57	MX dynamin like GTPase 1	Homo sapiens	123-127
9237796-4	1997	Bone marrow cells obtained from IL-3-treated NOD mice protected NOD mice from cyclophosphamide-induced diabetes but failed to prevent adoptively transferred diabetes.	Cyclophosphamide	78-94	interleukin 3	Mus musculus	32-36
9237796-5	1997	In vitro culture of bone marrow cells in medium containing IL-3 produced a Thy-1+CD3epsilonloCD4-CD8-CD25- immature T cell clone which prevented cyclophosphamide-induced diabetes.	Cyclophosphamide	145-161	interleukin 3	Mus musculus	59-63
9233591-6	1997	The median yield of CD34+ cells per leukapheresis was almost twice as high in patients receiving IVE (1.94 x 10(6)/kg) compared to cyclophosphamide (1.03 x 10(6)/kg) (P = 0.035).	Cyclophosphamide	131-147	CD34 molecule	Homo sapiens	20-24
9180915-3	1997	A case of AML-2 with t(8;21) and t(3;15) occurring 4 years after treatment for an Ewing"s sarcoma with cyclophosphamide, doxorubicin, vincristine, dactinomycin, and radiotherapy, is reported.	Cyclophosphamide	103-119	RUNX family transcription factor 3	Homo sapiens	10-15
9288115-9	1997	Expression of IL-2 and IFN-gamma was near undetectable in CTLA4Ig and cyclophosphamide rats but was only moderately reduced by cyclosporine and antilymphocyte serum.	Cyclophosphamide	70-86	interleukin 2	Rattus norvegicus	14-18
9288115-9	1997	Expression of IL-2 and IFN-gamma was near undetectable in CTLA4Ig and cyclophosphamide rats but was only moderately reduced by cyclosporine and antilymphocyte serum.	Cyclophosphamide	70-86	interferon gamma	Rattus norvegicus	23-32
9259773-0	1997	IL-15 mediates anti-tumor effects after cyclophosphamide injection of tumor-bearing mice and enhances adoptive immunotherapy: the potential role of NK cell subpopulations.	Cyclophosphamide	40-56	interleukin 15	Mus musculus	0-5
9259773-1	1997	The daily administration of IL-15 to cyclophosphamide (CY)-injected mice bearing the 76-9 rhabdomyosarcoma was shown to prolong the period of remission induced by CY.	Cyclophosphamide	37-53	interleukin 15	Mus musculus	28-33
9259773-1	1997	The daily administration of IL-15 to cyclophosphamide (CY)-injected mice bearing the 76-9 rhabdomyosarcoma was shown to prolong the period of remission induced by CY.	Cyclophosphamide	55-57	interleukin 15	Mus musculus	28-33
9259773-1	1997	The daily administration of IL-15 to cyclophosphamide (CY)-injected mice bearing the 76-9 rhabdomyosarcoma was shown to prolong the period of remission induced by CY.	Cyclophosphamide	163-165	interleukin 15	Mus musculus	28-33
9377092-3	1997	In this paper we summarize our efforts to exploit this metabolic pathway to develop latent nitrogen mustard derivatives related to the oxazaphosphorine antitumor agent cyclophosphamide which may target MAO-A and/or MAO-B rich cells.	Cyclophosphamide	168-184	monoamine oxidase A	Homo sapiens	202-207
9377092-3	1997	In this paper we summarize our efforts to exploit this metabolic pathway to develop latent nitrogen mustard derivatives related to the oxazaphosphorine antitumor agent cyclophosphamide which may target MAO-A and/or MAO-B rich cells.	Cyclophosphamide	168-184	monoamine oxidase B	Homo sapiens	215-220
9266107-7	1997	Hepatic toxicity was induced in breast cancer patients by adjuvant CMF/CNF therapy (cyclophosphamide, methotrexate, 5-fluorouracil, mitoxantrone).	Cyclophosphamide	84-100	NPHS1 adhesion molecule, nephrin	Homo sapiens	71-74
9179527-4	1997	Conventional chemotherapy with CHOP (a chemotherapeutic regimen consisting of a combination of cyclophosphamide, doxorubicin, vincristine and prednisone) or other equivalent third-generation regimens may be considered the standard treatment for the good prognosis group.	Cyclophosphamide	95-111	DNA damage inducible transcript 3	Homo sapiens	31-35
9218827-5	1997	Interestingly, the mortality rate increased significantly when anti-TNF-alpha antibody was combined with G-CSF, although it was intermediate between CPA alone and CPA-G-CSF-treated mice.	Cyclophosphamide	163-166	colony stimulating factor 3 (granulocyte)	Mus musculus	167-172
9225039-6	1997	However, when mice were pretreated with cyclophosphamide, p65 primed for a strong DTH response to a level similar to that induced by p59 in mice either pretreated or not treated with cyclophosphamide.	Cyclophosphamide	40-56	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	58-61
9167751-0	1997	Standard-dose recombinant human granulocyte colony-stimulating factor (rhG-CSF) allows safe and repeated administration of high-dose cyclophosphamide, etoposide, and cisplatin (CEP).	Cyclophosphamide	133-149	colony stimulating factor 3	Homo sapiens	32-69
9240625-9	1997	The GnRH-a and chemotherapy cotreatment may be also suggested for young women treated by cyclophosphamide pulse therapy or other gonadotoxic treatments for systemic lupus erythematosus, organ transplantation and other autoimmune diseases.	Cyclophosphamide	89-105	gonadotropin releasing hormone 1	Rattus norvegicus	4-10
9267668-6	1997	The mean daily collection of CD34+ cells was 5.46 x 10(6)/kg for patients receiving 200 mg/m2 of paclitaxel and 3 gm/m2 of Cy as compared to 2.77 for patients receiving the lower doses (p = 0.0005).	Cyclophosphamide	123-125	CD34 molecule	Homo sapiens	29-33
9222281-11	1997	IL-2 administered on days 6-10 was therapeutically effective in this model when mice were treated with cyclophosphamide on day 6.	Cyclophosphamide	103-119	interleukin 2	Mus musculus	0-4
9166662-0	1997	Treatment with neutralizing antibodies specific for IL-1beta prevents cyclophosphamide-induced diabetes in nonobese diabetic mice.	Cyclophosphamide	70-86	interleukin 1 beta	Mus musculus	52-60
9222642-0	1997	Suppression of cyclophosphamide induced diabetes development and pancreatic Th1 reactivity in NOD mice treated with the interleukin (IL)-12 antagonist IL-12(p40)2.	Cyclophosphamide	15-31	negative elongation factor complex member C/D, Th1l	Mus musculus	76-79
9222642-0	1997	Suppression of cyclophosphamide induced diabetes development and pancreatic Th1 reactivity in NOD mice treated with the interleukin (IL)-12 antagonist IL-12(p40)2.	Cyclophosphamide	15-31	interleukin 12b	Mus musculus	157-160
9222642-2	1997	Here we report that treatment with the homodimeric IL-12p40 subunit, an antagonist of the bioactive IL-12p35/p40 heterodimer, suppresses diabetes development in cyclophosphamide-injected NOD mice.	Cyclophosphamide	161-177	interleukin 12b	Mus musculus	51-67
9222642-2	1997	Here we report that treatment with the homodimeric IL-12p40 subunit, an antagonist of the bioactive IL-12p35/p40 heterodimer, suppresses diabetes development in cyclophosphamide-injected NOD mice.	Cyclophosphamide	161-177	interleukin 12a	Mus musculus	100-108
9222642-2	1997	Here we report that treatment with the homodimeric IL-12p40 subunit, an antagonist of the bioactive IL-12p35/p40 heterodimer, suppresses diabetes development in cyclophosphamide-injected NOD mice.	Cyclophosphamide	161-177	interleukin 12b	Mus musculus	56-59
9218751-3	1997	Cyclophosphamide-induced IGIF expression was also observed in MHC congenic NOR mice, but not in MHC class II-incompatible NON mice.	Cyclophosphamide	0-16	interleukin 18	Mus musculus	25-29
9197327-2	1997	Single doses of cyclophosphamide (CTX) from 80 to 200 mg/kg were administered to C57B16/J mice.	Cyclophosphamide	16-32	V-set and immunoglobulin domain containing 2	Mus musculus	34-37
9218751-6	1997	We conclude that cyclophosphamide induces a systemic shift in antigen presenting cells towards favouring Th1 responses, in an MHC dependent manner.	Cyclophosphamide	17-33	negative elongation factor complex member C/D, Th1l	Mus musculus	105-108
9241661-0	1997	Identification of the polymorphically expressed CYP2C19 and the wild-type CYP2C9-ILE359 allele as low-Km catalysts of cyclophosphamide and ifosfamide activation.	Cyclophosphamide	118-134	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	48-55
9241661-0	1997	Identification of the polymorphically expressed CYP2C19 and the wild-type CYP2C9-ILE359 allele as low-Km catalysts of cyclophosphamide and ifosfamide activation.	Cyclophosphamide	118-134	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	74-80
10173030-3	1997	One such treatment that is considered to have a low potential for inducing fever and neutropenia is the CHOP regimen (cyclophosphamide, doxorubicin, vincristine and prednisone) for non-Hodgkin"s lymphoma.	Cyclophosphamide	118-134	DNA damage inducible transcript 3	Homo sapiens	104-108
9241661-1	1997	Cyclophosphamide and ifosfamide are alkylating agent prodrugs that require activation by cytochrome P450 (CYP) to manifest their cancer chemotherapeutic activity.	Cyclophosphamide	0-16	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	89-104
9241661-1	1997	Cyclophosphamide and ifosfamide are alkylating agent prodrugs that require activation by cytochrome P450 (CYP) to manifest their cancer chemotherapeutic activity.	Cyclophosphamide	0-16	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	106-109
9241661-2	1997	The present study investigates the activity of four individual human CYP2C enzymes and their allelic variants in cyclophosphamide and ifosfamide activation as an initial attempt to gain insight into the underlying basis for the large interpatient differences in the clinical pharmacokinetics and metabolism of these anticancer drugs.	Cyclophosphamide	113-129	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	69-74
9241661-4	1997	With cyclophosphamide as substrate, CYP2C19 had the lowest apparent Km, followed by CYP2C9, CYP2C18 and CYP2C8, whereas in the case of ifosfamide, the rank order was: Km CYP2C19 < CYP2C18 < CYP2C9 < CYP2C8.	Cyclophosphamide	5-21	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	36-43
9241661-4	1997	With cyclophosphamide as substrate, CYP2C19 had the lowest apparent Km, followed by CYP2C9, CYP2C18 and CYP2C8, whereas in the case of ifosfamide, the rank order was: Km CYP2C19 < CYP2C18 < CYP2C9 < CYP2C8.	Cyclophosphamide	5-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
9241661-4	1997	With cyclophosphamide as substrate, CYP2C19 had the lowest apparent Km, followed by CYP2C9, CYP2C18 and CYP2C8, whereas in the case of ifosfamide, the rank order was: Km CYP2C19 < CYP2C18 < CYP2C9 < CYP2C8.	Cyclophosphamide	5-21	cytochrome P450 family 2 subfamily C member 18	Homo sapiens	92-99
9241661-4	1997	With cyclophosphamide as substrate, CYP2C19 had the lowest apparent Km, followed by CYP2C9, CYP2C18 and CYP2C8, whereas in the case of ifosfamide, the rank order was: Km CYP2C19 < CYP2C18 < CYP2C9 < CYP2C8.	Cyclophosphamide	5-21	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	104-110
9241661-4	1997	With cyclophosphamide as substrate, CYP2C19 had the lowest apparent Km, followed by CYP2C9, CYP2C18 and CYP2C8, whereas in the case of ifosfamide, the rank order was: Km CYP2C19 < CYP2C18 < CYP2C9 < CYP2C8.	Cyclophosphamide	5-21	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	170-177
9241661-4	1997	With cyclophosphamide as substrate, CYP2C19 had the lowest apparent Km, followed by CYP2C9, CYP2C18 and CYP2C8, whereas in the case of ifosfamide, the rank order was: Km CYP2C19 < CYP2C18 < CYP2C9 < CYP2C8.	Cyclophosphamide	5-21	cytochrome P450 family 2 subfamily C member 18	Homo sapiens	183-190
9241661-4	1997	With cyclophosphamide as substrate, CYP2C19 had the lowest apparent Km, followed by CYP2C9, CYP2C18 and CYP2C8, whereas in the case of ifosfamide, the rank order was: Km CYP2C19 < CYP2C18 < CYP2C9 < CYP2C8.	Cyclophosphamide	5-21	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	196-202
9241661-4	1997	With cyclophosphamide as substrate, CYP2C19 had the lowest apparent Km, followed by CYP2C9, CYP2C18 and CYP2C8, whereas in the case of ifosfamide, the rank order was: Km CYP2C19 < CYP2C18 < CYP2C9 < CYP2C8.	Cyclophosphamide	5-21	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	208-214
9241661-5	1997	CYP2C18 had the highest in vitro intrinsic clearance/catalytic efficiency (apparent Vmax/Km) in cyclophosphamide and ifosfamide activation, followed by 2C19 > 2C9 approximately 2C8.	Cyclophosphamide	96-112	cytochrome P450 family 2 subfamily C member 18	Homo sapiens	0-7
9241661-6	1997	Examination of a panel of CYP2C allelic variants revealed that CYP2C18-Thr385 had both a higher Vmax and a higher apparent Km toward cyclophosphamide than CYP2C18-Met385 with no difference in catalytic efficiency, whereas with ifosfamide the Thr385 allele exhibited a strikingly lower apparent Km resulting in a six-fold higher catalytic efficiency.	Cyclophosphamide	133-149	cytochrome P450 family 2 subfamily C member 18	Homo sapiens	63-70
9241661-7	1997	In the case of CYP2C9, a Ile359 to Leu mutation associated with poor metabolism of the hypoglycemic drug tolbutamide decreased catalytic efficiency toward cyclophosphamide by increasing the apparent Km, whereas the same mutation reduced the efficiency of this P450 toward ifosfamide by decreasing the Vmax.	Cyclophosphamide	155-171	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	15-21
9241661-8	1997	Substitution of CYP2C9-Gly417 by Asp resulted in a two-fold lower catalytic efficiency for cyclophosphamide metabolism but a three-fold higher efficiency for ifosfamide metabolism.	Cyclophosphamide	91-107	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	16-22
9241661-11	1997	Thus (a) wild type CYP2C19 and CYP2C9 are relatively low Km catalysts of cyclophosphamide and ifosfamide activation, and (b) all four human CYP2C enzymes activate these two anticancer prodrugs with varying efficiencies and with striking differences among naturally occurring allelic variants in the case of CYP2C9 and CYP2C18.	Cyclophosphamide	73-89	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	19-26
9241661-11	1997	Thus (a) wild type CYP2C19 and CYP2C9 are relatively low Km catalysts of cyclophosphamide and ifosfamide activation, and (b) all four human CYP2C enzymes activate these two anticancer prodrugs with varying efficiencies and with striking differences among naturally occurring allelic variants in the case of CYP2C9 and CYP2C18.	Cyclophosphamide	73-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	31-37
9241661-11	1997	Thus (a) wild type CYP2C19 and CYP2C9 are relatively low Km catalysts of cyclophosphamide and ifosfamide activation, and (b) all four human CYP2C enzymes activate these two anticancer prodrugs with varying efficiencies and with striking differences among naturally occurring allelic variants in the case of CYP2C9 and CYP2C18.	Cyclophosphamide	73-89	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	19-24
9241661-11	1997	Thus (a) wild type CYP2C19 and CYP2C9 are relatively low Km catalysts of cyclophosphamide and ifosfamide activation, and (b) all four human CYP2C enzymes activate these two anticancer prodrugs with varying efficiencies and with striking differences among naturally occurring allelic variants in the case of CYP2C9 and CYP2C18.	Cyclophosphamide	73-89	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	307-313
9241661-11	1997	Thus (a) wild type CYP2C19 and CYP2C9 are relatively low Km catalysts of cyclophosphamide and ifosfamide activation, and (b) all four human CYP2C enzymes activate these two anticancer prodrugs with varying efficiencies and with striking differences among naturally occurring allelic variants in the case of CYP2C9 and CYP2C18.	Cyclophosphamide	73-89	cytochrome P450 family 2 subfamily C member 18	Homo sapiens	318-325
9157990-8	1997	These studies: (a) demonstrate an underlying metabolic basis for the clinically important oxazaphosphorine autoinduction pharmacokinetics seen with these drugs in cancer patients; and (b) identify rifampin and other CYP inducers as potentially useful for increasing the rates of cyclophosphamide 4-hydroxylation and ifosfamide 4-hydroxylation in human liver in a manner that could favorably impact the clinical pharmacokinetics of these anticancer prodrugs.	Cyclophosphamide	279-295	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	216-219
9163618-3	1997	Most CD34-positive PBPC are quiescent (<1% in S phase) when they are collected from the bloodstream of patients treated with cyclophosphamide and granulocyte colony-stimulating factor (G-CSF), but we have shown that they are able to resume proliferation rapidly in vitro by measuring the kinetics of CFU-GM production by primitive plastic-adherent (Pdelta) cells.	Cyclophosphamide	128-144	CD34 molecule	Homo sapiens	5-9
9216680-4	1997	In combination with cyclophosphamide given once prior to the administration of LPS, however, the antitumor effects by intradermal administration of LPS were significantly augmented and there was complete regression in all types of tumors.	Cyclophosphamide	20-36	toll-like receptor 4	Mus musculus	148-151
9216680-7	1997	Thus clinical application of LPS administered intradermally in combination with chemotherapeutics such as cyclophosphamide appears promising in terms of its antitumor effect as well as toxicity.	Cyclophosphamide	106-122	toll-like receptor 4	Mus musculus	29-32
9115450-3	1997	Cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy is well tolerated in patients who have a good performance status and who have aggressive histology lymphoma, but briefer 8-week regimens appear to offer similar benefits more quickly.	Cyclophosphamide	0-16	DNA damage inducible transcript 3	Homo sapiens	60-64
9377855-1	1997	BACKGROUND: Carboplatin (CBDCA), cyclophosphamide (CTX) and etoposide (VP-16) combination chemotherapy is active in many tumors.	Cyclophosphamide	33-49	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	51-54
9174132-0	1997	Interleukin-2 increases intracellular glutathione levels and reverses the growth inhibiting effects of cyclophosphamide on B16 melanoma cells.	Cyclophosphamide	103-119	interleukin 2	Mus musculus	0-13
9155150-8	1997	Cancer cell lines indicated resistant to anti-cancer drugs, such as mitomycin C, doxorubicin, tamoxifen, cyclophosphamide and their derivatives, by a high activity of GST and a low activity of P450 in general.	Cyclophosphamide	105-121	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	193-197
9176841-9	1997	When NZB/W mice were treated with cyclophosphamide up to 12 months of age, expression of MCP-1 in the renal tissue remained low, the influx of inflammatory cells did not appear, and glomerular and tubular structures remained well preserved.	Cyclophosphamide	34-50	chemokine (C-C motif) ligand 2	Mus musculus	89-94
9116299-2	1997	This study compares the therapeutic efficacy of anti-CD3-activated CD4+ or CD8+ T-cell subsets, when given with cyclophosphamide (Cy) and liposome-encapsulated IL-2 (L-IL2) in a murine model.	Cyclophosphamide	130-132	CD3 antigen, epsilon polypeptide	Mus musculus	53-56
9180391-1	1997	In this study 194 women with breast cancer received adjuvant CNF combination therapy (cyclophosphamide, mitoxantrone and 5-fluorouracil).	Cyclophosphamide	86-102	NPHS1 adhesion molecule, nephrin	Homo sapiens	61-64
9116299-2	1997	This study compares the therapeutic efficacy of anti-CD3-activated CD4+ or CD8+ T-cell subsets, when given with cyclophosphamide (Cy) and liposome-encapsulated IL-2 (L-IL2) in a murine model.	Cyclophosphamide	130-132	CD4 antigen	Mus musculus	67-70
9116299-9	1997	The timing of Cy doses in relation to adoptive transfer was critical in obtaining the optimal antitumor effect by CD4+ cells.	Cyclophosphamide	14-16	CD4 antigen	Mus musculus	114-117
9116299-10	1997	Injecting Cy 4 days before the infusion of CD4+ cells greatly enhanced the antitumor effect of the CD4+ cells and improved survival of the mice compared with other Cy regimens.	Cyclophosphamide	10-12	CD4 antigen	Mus musculus	43-46
9116299-10	1997	Injecting Cy 4 days before the infusion of CD4+ cells greatly enhanced the antitumor effect of the CD4+ cells and improved survival of the mice compared with other Cy regimens.	Cyclophosphamide	10-12	CD4 antigen	Mus musculus	99-102
9145296-3	1997	A human T-cell lymphoma cell line, LM-2-JCK, implanted in nude mice, was resistant to treatment with 65 mg/kg of cyclophosphamide, but this tumor showed sensitivity to the same treatment when implanted in either SCID mice or mice with a recombination activating gene 2 defect [BALB/cA-TgH (Rag2)], suggesting that the genetic immune background of the host mouse should not be overlooked as a factor affecting tumors.	Cyclophosphamide	113-129	NIMA related kinase 8	Homo sapiens	40-43
9042403-0	1997	Induction of DNA crosslinks and DNA strand lesions by cyclophosphamide after activation by cytochrome P450 2B1.	Cyclophosphamide	54-70	LOW QUALITY PROTEIN: cytochrome P450 2B1	Cricetulus griseus	91-110
9193328-0	1997	Comparative study of dose escalation versus interval reduction to obtain dose-intensification of epirubicin and cyclophosphamide with granulocyte colony-stimulating factor in advanced breast cancer.	Cyclophosphamide	112-128	colony stimulating factor 3	Homo sapiens	134-171
9084504-0	1997	Impaired secretion of heart lipoprotein lipase in cyclophosphamide-treated rabbit.	Cyclophosphamide	50-66	lipoprotein lipase	Oryctolagus cuniculus	28-46
9084504-1	1997	Cyclophosphamide administration into fasted rabbits induces a hypertriglyceridaemia and a defect in vascular lipoprotein lipase.	Cyclophosphamide	0-16	lipoprotein lipase	Oryctolagus cuniculus	109-127
9084504-4	1997	Cyclophosphamide administration resulted in a profound decline in the heparin-releasable lipoprotein lipase activity, concordant with a higher recovery in the residual heart tissue.	Cyclophosphamide	0-16	lipoprotein lipase	Oryctolagus cuniculus	89-107
9084504-8	1997	These results suggest that a defective secretion of lipoprotein lipase may contribute to the poor expression of lipolytic activity in the vascular bed and to the occurrence of hypertriglyceridaemia during cyclophosphamide treatment.	Cyclophosphamide	205-221	lipoprotein lipase	Oryctolagus cuniculus	52-70
9594342-1	1997	OBJECTIVE: To investigate the effects of pulse methylprednisolone (MP) and monthly intravenous cyclophosphamide (CTX) therapy (MP + CTX) on renal infiltrating cells in patients with rapid progressive glomerular nephritis (RPGN).	Cyclophosphamide	95-111	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	113-116
9149745-3	1997	Transplantation of CD34+ cells from haploidentical parents was performed after the children were conditioned with fractionated total body irradiation, cyclophosphamide, and antithymocyte globulin (ATG).	Cyclophosphamide	151-167	CD34 molecule	Homo sapiens	19-23
9110342-2	1997	HER2 overexpression has been linked to sensitivity and/or resistance to hormone therapy and chemotherapeutic regimens, including CMF (cyclophosphamide, methotrexate, and fluoruracil) and anthracyclines.	Cyclophosphamide	134-150	erb-b2 receptor tyrosine kinase 2	Homo sapiens	0-4
9012476-0	1997	Keratinocyte growth factor ameliorates cyclophosphamide-induced ulcerative hemorrhagic cystitis.	Cyclophosphamide	39-55	fibroblast growth factor 7	Rattus norvegicus	0-26
9208370-0	1997	Thermodynamic investigation of camel retina acetylcholinesterase inhibition by cyclophosphamide.	Cyclophosphamide	79-95	acetylcholinesterase	Camelus bactrianus	44-64
9022080-5	1997	Levels of IGIF mRNA increased rapidly after cyclophosphamide treatment and preceded a rise in IFN-gamma mRNA, and subsequently diabetes.	Cyclophosphamide	44-60	interleukin 18	Mus musculus	10-14
9022080-8	1997	When extending our study to macrophages of the spleen we observed that NOD mouse macrophages responded to cyclophosphamide with IGIF gene expression while macrophages from Balb/c mice treated in parallel did not.	Cyclophosphamide	106-122	interleukin 18	Mus musculus	128-132
9208370-1	1997	The present work addresses the estimation of energy parameters such as Gibb"s free energy change (delta G), enthalpy change (delta H); entropy change (delta S) and activation energy (E a) of acetylcholinesterase (AChE, EC 3.1.1.7) from camel retina in the absence and presence of the antineoplastic drug cyclophosphamide (CP).	Cyclophosphamide	304-320	acetylcholinesterase	Camelus bactrianus	191-211
9208370-1	1997	The present work addresses the estimation of energy parameters such as Gibb"s free energy change (delta G), enthalpy change (delta H); entropy change (delta S) and activation energy (E a) of acetylcholinesterase (AChE, EC 3.1.1.7) from camel retina in the absence and presence of the antineoplastic drug cyclophosphamide (CP).	Cyclophosphamide	304-320	acetylcholinesterase	Camelus bactrianus	213-217
9066630-1	1997	The antitumor effect of endogenous tumor necrosis factor (en-TNF) with cyclophosphamide (CY) was analyzed using the murine Meth A tumor model.	Cyclophosphamide	71-87	tumor necrosis factor	Mus musculus	61-64
9066630-5	1997	A combination therapy of en-TNF with CY showed the strongest antitumor effect among several combinations and caused complete tumor regression (40-70%), while none of the combinations with the other chemotherapeutics did so.	Cyclophosphamide	37-39	tumor necrosis factor	Mus musculus	28-31
9066630-7	1997	The amount of en-TNF induced around a tumor lesion with CY was two fold higher than that without CY.	Cyclophosphamide	56-58	tumor necrosis factor	Mus musculus	17-20
9066630-7	1997	The amount of en-TNF induced around a tumor lesion with CY was two fold higher than that without CY.	Cyclophosphamide	97-99	tumor necrosis factor	Mus musculus	17-20
9066630-8	1997	En-TNF was observed to be induced in tumor lesion solely by CY injection.	Cyclophosphamide	60-62	tumor necrosis factor	Mus musculus	3-6
9523002-0	1997	Does cyclophosphamide combined with methylprednisolone affect the expression of leukocyte function associated antigen 1 in refractory rheumatoid arthritis.	Cyclophosphamide	5-21	integrin subunit alpha L	Homo sapiens	80-119
9066630-9	1997	All these results suggest that the antitumor effect of en-TNF can be augmented by addition of a chemotherapeutic agent such as CY.	Cyclophosphamide	127-129	tumor necrosis factor	Mus musculus	58-61
9523002-1	1997	In the present study, in order to get a better insight into the mechanism of action of cyclophosphamide (CY) in rheumatoid arthritis (RA), we monitored the changes in lymphocytes" expression of leukocyte function associated antigen 1 (LFA-1).	Cyclophosphamide	87-103	integrin subunit alpha L	Homo sapiens	194-240
9523002-1	1997	In the present study, in order to get a better insight into the mechanism of action of cyclophosphamide (CY) in rheumatoid arthritis (RA), we monitored the changes in lymphocytes" expression of leukocyte function associated antigen 1 (LFA-1).	Cyclophosphamide	105-107	integrin subunit alpha L	Homo sapiens	194-240
9192972-0	1997	Continuous infusion of macrophage inflammatory protein MIP-1alpha enhances leucocyte recovery and haemopoietic progenitor cell mobilization after cyclophosphamide.	Cyclophosphamide	146-162	chemokine (C-C motif) ligand 3	Mus musculus	55-65
9192972-3	1997	We have now shown that BB-10010, a stable mutant of MIP-1alpha, (a) is more effective when administered as a continuous infusion than when bolus injected and (b), when administered via a 7-day infusion during and after cyclophosphamide treatment, results in an earlier recovery of leucocyte numbers.	Cyclophosphamide	219-235	chemokine (C-C motif) ligand 3	Mus musculus	52-62
9096241-4	1997	Supernatants collected from P388D1 cells treated with CA, VS, CS, MMC, HU or LPS demonstrated enhanced production of tumor necrosis factor (TNF) confirmed by bioassay on L929 tumor target cells and increased interleukin-1 (IL-1) production by standard thymocyte proliferation bioassay.	Cyclophosphamide	62-64	tumor necrosis factor	Mus musculus	117-138
9116319-2	1997	The de novo p-gp expression rate was 26% and increased up to 58% (p = 0.03) with the FAC (5-fluorouracil, adriamycin, cyclophosphamide) regimen.	Cyclophosphamide	118-134	ATP binding cassette subfamily B member 1	Homo sapiens	12-16
9157990-1	1997	The anticancer oxazaphosphorine prodrugs cyclophosphamide and ifosfamide are activated in human liver by a 4-hydroxylation reaction catalyzed by multiple cytochrome P450 (CYP) enzymes.	Cyclophosphamide	41-57	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	154-169
9157990-1	1997	The anticancer oxazaphosphorine prodrugs cyclophosphamide and ifosfamide are activated in human liver by a 4-hydroxylation reaction catalyzed by multiple cytochrome P450 (CYP) enzymes.	Cyclophosphamide	41-57	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	171-174
9157990-6	1997	CYP3A4, CYP2C8, and CYP2C9 protein levels were also increased by exposure of the hepatocytes to cyclophosphamide or ifosfamide (50 microM), which thereby enhanced their own rates of 4-hydroxylation in the cultured hepatocytes.	Cyclophosphamide	96-112	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	0-6
9157990-6	1997	CYP3A4, CYP2C8, and CYP2C9 protein levels were also increased by exposure of the hepatocytes to cyclophosphamide or ifosfamide (50 microM), which thereby enhanced their own rates of 4-hydroxylation in the cultured hepatocytes.	Cyclophosphamide	96-112	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	8-14
9157990-6	1997	CYP3A4, CYP2C8, and CYP2C9 protein levels were also increased by exposure of the hepatocytes to cyclophosphamide or ifosfamide (50 microM), which thereby enhanced their own rates of 4-hydroxylation in the cultured hepatocytes.	Cyclophosphamide	96-112	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	20-26
9157990-7	1997	In one human hepatocyte culture that contained the polymorphically expressed CYP3A5 in addition to the more widely expressed CYP3A4, only CYP3A4 was induced by cyclophosphamide, ifosfamide, and rifampin.	Cyclophosphamide	160-176	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	77-83
9157990-7	1997	In one human hepatocyte culture that contained the polymorphically expressed CYP3A5 in addition to the more widely expressed CYP3A4, only CYP3A4 was induced by cyclophosphamide, ifosfamide, and rifampin.	Cyclophosphamide	160-176	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	125-131
9157990-7	1997	In one human hepatocyte culture that contained the polymorphically expressed CYP3A5 in addition to the more widely expressed CYP3A4, only CYP3A4 was induced by cyclophosphamide, ifosfamide, and rifampin.	Cyclophosphamide	160-176	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	138-144
9201247-9	1997	administration of cyclophosphamide (CP, 15 mg/kg) in mice simultaneously in bone marrow and in PAM.	Cyclophosphamide	18-34	peptidylglycine alpha-amidating monooxygenase	Mus musculus	95-98
9104735-9	1997	These findings suggest that CY treatment has a differential effect on the infiltration of leukocyte subtypes and strengthen the hypothesis that some abnormal behaviour in MRL/lpr mice may be related to the presence of immunocompetent cells in the brain.	Cyclophosphamide	28-30	Fas (TNF receptor superfamily member 6)	Mus musculus	175-178
9096241-4	1997	Supernatants collected from P388D1 cells treated with CA, VS, CS, MMC, HU or LPS demonstrated enhanced production of tumor necrosis factor (TNF) confirmed by bioassay on L929 tumor target cells and increased interleukin-1 (IL-1) production by standard thymocyte proliferation bioassay.	Cyclophosphamide	62-64	tumor necrosis factor	Mus musculus	140-143
9096241-4	1997	Supernatants collected from P388D1 cells treated with CA, VS, CS, MMC, HU or LPS demonstrated enhanced production of tumor necrosis factor (TNF) confirmed by bioassay on L929 tumor target cells and increased interleukin-1 (IL-1) production by standard thymocyte proliferation bioassay.	Cyclophosphamide	62-64	interleukin 1 complex	Mus musculus	208-227
9090787-6	1997	Cyclophosphamide (CY) increased the frequency of CD34+ cells and the corresponding MK/MNC yield for both cytokines, but had no effect on the MK/CD34+ yield.	Cyclophosphamide	0-16	CD34 molecule	Homo sapiens	49-53
9646687-0	1997	Cyclophosphamide-induced changes of serum angiotensin converting enzyme activity and pulmonary microvessels ultrastructure.	Cyclophosphamide	0-16	angiotensin I converting enzyme	Rattus norvegicus	42-71
9090787-6	1997	Cyclophosphamide (CY) increased the frequency of CD34+ cells and the corresponding MK/MNC yield for both cytokines, but had no effect on the MK/CD34+ yield.	Cyclophosphamide	18-20	CD34 molecule	Homo sapiens	49-53
9037362-1	1996	PURPOSE: To identify the highest possible dose of cyclophosphamide (C) and etoposide (E) to be given with high-dose doxorubicin (D) and filgrastim (G-CSF) but without stem cell support in high-risk non-Hodgkin"s lymphoma.	Cyclophosphamide	50-66	colony stimulating factor 3	Homo sapiens	148-153
8978792-3	1996	The efficacy of dose intensification of CPA in CHOP regimen for patients with aggressive lymphoma is being investigated in some clinical trials.	Cyclophosphamide	40-43	DNA damage inducible transcript 3	Homo sapiens	47-51
8940385-8	1996	Unexpectedly, in the cyclophosphamide-induced model, sIFNgammaR turned out to be less effective than either of the two anti-IFNgamma mAbs.	Cyclophosphamide	21-37	interferon gamma	Mus musculus	54-62
9052873-2	1996	Induction of TNF-beta mRNA in lymphoid cells is greatly enhanced by gamma-irradiation, cyclophosphamide and cimetidine, agents that each inhibit activation of suppressive cells.	Cyclophosphamide	87-103	lymphotoxin alpha	Homo sapiens	13-21
8917683-2	1996	Exposure of HepG2 cells to cytotoxic concentrations of bromobenzene, cadmium, cyclophosphamide, or diethylnitrosamine increased the level of hsp 70I protein and mRNA, while carbon tetrachloride and cocaine had no effect on hsp 70I or mRNA levels.	Cyclophosphamide	78-94	heat shock protein family A (Hsp70) member 1A	Homo sapiens	141-148
8917683-2	1996	Exposure of HepG2 cells to cytotoxic concentrations of bromobenzene, cadmium, cyclophosphamide, or diethylnitrosamine increased the level of hsp 70I protein and mRNA, while carbon tetrachloride and cocaine had no effect on hsp 70I or mRNA levels.	Cyclophosphamide	78-94	heat shock protein family A (Hsp70) member 1A	Homo sapiens	223-230
8906215-5	1996	Cyclosporin A, FK-506, and cyclophosphamide clearly inhibited the antigen-induced increase of IL-5 and eosinophils in BALF.	Cyclophosphamide	27-43	interleukin 5	Mus musculus	94-98
8855989-0	1996	Phase I study of simultaneous dose escalation and schedule acceleration of cyclophosphamide-doxorubicin-etoposide using granulocyte colony-stimulating factor with or without antimicrobial prophylaxis in patients with small-cell lung cancer.	Cyclophosphamide	75-91	colony stimulating factor 3	Homo sapiens	120-157
8878389-5	1996	The analyses showed that an increase in IFN-gamma and neopterin serum levels was a specific feature of cyclophosphamide administration and was not observed after other cytostatic drugs or total body irradiation, and that an increase in IFN-gamma, neopterin, beta2-microglobulin, and IFN-alpha release depends on the presence of T cells in the graft.	Cyclophosphamide	103-119	interferon gamma	Homo sapiens	40-49
8913281-0	1996	Granulocyte-macrophage colony-stimulating factor (GM-CSF) priming of high-dose etoposide and cyclophosphamide: a pilot trial.	Cyclophosphamide	93-109	colony stimulating factor 2	Homo sapiens	0-48
8913281-0	1996	Granulocyte-macrophage colony-stimulating factor (GM-CSF) priming of high-dose etoposide and cyclophosphamide: a pilot trial.	Cyclophosphamide	93-109	colony stimulating factor 2	Homo sapiens	50-56
8933279-9	1996	Substantial numbers of Th1 cells (positive for IFN-gamma, TNF-alpha, IL-2 and/or IL-2 receptor) were observed only after acceleration of diabetes development by a single injection of cyclophosphamide (250 mg/kg i.p.).	Cyclophosphamide	183-199	negative elongation factor complex member C/D, Th1l	Mus musculus	23-26
8933279-9	1996	Substantial numbers of Th1 cells (positive for IFN-gamma, TNF-alpha, IL-2 and/or IL-2 receptor) were observed only after acceleration of diabetes development by a single injection of cyclophosphamide (250 mg/kg i.p.).	Cyclophosphamide	183-199	tumor necrosis factor	Mus musculus	58-67
8933279-9	1996	Substantial numbers of Th1 cells (positive for IFN-gamma, TNF-alpha, IL-2 and/or IL-2 receptor) were observed only after acceleration of diabetes development by a single injection of cyclophosphamide (250 mg/kg i.p.).	Cyclophosphamide	183-199	interleukin 2	Mus musculus	69-73
8933279-9	1996	Substantial numbers of Th1 cells (positive for IFN-gamma, TNF-alpha, IL-2 and/or IL-2 receptor) were observed only after acceleration of diabetes development by a single injection of cyclophosphamide (250 mg/kg i.p.).	Cyclophosphamide	183-199	interleukin 2	Mus musculus	81-85
8897562-9	1996	Cyclophosphamide therapy for children with steroid-resistant FSGS is not recommended.	Cyclophosphamide	0-16	actinin alpha 4	Homo sapiens	61-65
8903460-6	1996	Phenotypic analysis of cellular subset of spleen by flow cytometry revealed that low-dose CY, when given to both naive and tumor-bearing mice, causes significant reduction of both absolute number and percentage of cells with CD4-CD8- subset in the spleens of TBM.	Cyclophosphamide	90-92	CD4 antigen	Mus musculus	225-228
8903460-9	1996	Evidence from in vitro cytotoxicity assays on panel tumor cells and phenotypic analysis revealed that this enhancement of host antitumor immunity, following low-dose CY pretreatment, may be due to augmenting the activity of NK, LAK, and CD11b+ myeloid/macrophages in addition to cytotoxic T lymphocytes.	Cyclophosphamide	166-168	ADP-ribosylation factor-like 4C	Mus musculus	228-231
8903460-9	1996	Evidence from in vitro cytotoxicity assays on panel tumor cells and phenotypic analysis revealed that this enhancement of host antitumor immunity, following low-dose CY pretreatment, may be due to augmenting the activity of NK, LAK, and CD11b+ myeloid/macrophages in addition to cytotoxic T lymphocytes.	Cyclophosphamide	166-168	integrin alpha M	Mus musculus	237-242
8940829-8	1996	Under the diagnosis of MPO-ANCA-associated CreGN, cocktail therapy consisting of prednisolone, cyclophosphamide, dilazep hydrochloride and warfarin was started.	Cyclophosphamide	95-111	myeloperoxidase	Homo sapiens	23-26
8914613-0	1996	The inhibitory effect of cyclophosphamide on camel retina acetylcholinesterase activity.	Cyclophosphamide	25-41	acetylcholinesterase	Camelus bactrianus	58-78
8914613-1	1996	Kinetic parameters for the effect of cyclophosphamide (CP) on the camel retina acetylcholinesterase (AChE) activity were investigated for the first time in the present study.	Cyclophosphamide	37-53	acetylcholinesterase	Camelus bactrianus	79-99
8914613-1	1996	Kinetic parameters for the effect of cyclophosphamide (CP) on the camel retina acetylcholinesterase (AChE) activity were investigated for the first time in the present study.	Cyclophosphamide	37-53	acetylcholinesterase	Camelus bactrianus	101-105
8932983-7	1996	As positive controls, a group of patients treated with cyclophosphamide/G-CSF showed significant increases in GM-CFU (P = 0.018), E-BFU (P = 0.018) and P delta progenitors (P = 0.028).	Cyclophosphamide	55-71	colony stimulating factor 3	Homo sapiens	72-77
8830831-9	1996	Concomitantly, analysis of animals treated for 8 days after injection of cyclophosphamide, with IL-4 and IL-10, revealed a reduction of IL-12 mRNA in the pancreas.	Cyclophosphamide	73-89	interleukin 4	Mus musculus	96-100
8830831-9	1996	Concomitantly, analysis of animals treated for 8 days after injection of cyclophosphamide, with IL-4 and IL-10, revealed a reduction of IL-12 mRNA in the pancreas.	Cyclophosphamide	73-89	interleukin 10	Mus musculus	105-110
8886850-1	1996	Alkylating agents, cyclophosphamide (CY) and the related compound mechlorethamine (NM), significantly increase in vivo the blood level of IL-6 but not of IL-1.	Cyclophosphamide	19-35	interleukin 6	Mus musculus	138-142
8886850-1	1996	Alkylating agents, cyclophosphamide (CY) and the related compound mechlorethamine (NM), significantly increase in vivo the blood level of IL-6 but not of IL-1.	Cyclophosphamide	19-35	interleukin 1 complex	Mus musculus	154-158
8886850-1	1996	Alkylating agents, cyclophosphamide (CY) and the related compound mechlorethamine (NM), significantly increase in vivo the blood level of IL-6 but not of IL-1.	Cyclophosphamide	37-39	interleukin 6	Mus musculus	138-142
8886850-1	1996	Alkylating agents, cyclophosphamide (CY) and the related compound mechlorethamine (NM), significantly increase in vivo the blood level of IL-6 but not of IL-1.	Cyclophosphamide	37-39	interleukin 1 complex	Mus musculus	154-158
8877715-7	1996	A significantly higher yield of CD34+ cells and a better correlation between CD34+ cells in the peripheral blood and the leukapheresis product were found after priming with high-dose cyclophosphamide plus rhG-CSF, compared with priming with rhG-CSF alone.	Cyclophosphamide	183-199	CD34 molecule	Homo sapiens	32-36
8757341-8	1996	Cyclophosphamide-induced granulocytopenia led to a reduction of sTNFR-p75 release, whereas levels of bioactive TNF in response to fungal infection were increased.	Cyclophosphamide	0-16	tumor necrosis factor receptor superfamily, member 1b	Mus musculus	70-73
8940753-1	1996	PURPOSE: Cyclophosphamide (CTX) combined with fractionated total body irradiation (TBI) is frequently used in the conditioning of patients prior to bone marrow transplantation (BMT).	Cyclophosphamide	9-25	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	27-30
8706342-9	1996	After peptide challenge of splenocytes in vitro, protection against CY-accelerated diabetes was associated with higher peptide-specific production of T helper type 2 (Th2)-associated interleukins 4 and 10, whereas Th1-associated interferon-gamma and IL-2 were proportionally less represented.	Cyclophosphamide	68-70	negative elongation factor complex member C/D, Th1l	Mus musculus	214-217
8706342-9	1996	After peptide challenge of splenocytes in vitro, protection against CY-accelerated diabetes was associated with higher peptide-specific production of T helper type 2 (Th2)-associated interleukins 4 and 10, whereas Th1-associated interferon-gamma and IL-2 were proportionally less represented.	Cyclophosphamide	68-70	interleukin 2	Mus musculus	250-254
8864824-5	1996	We found that CY-treated EA chimeras displayed an increase in the NOD:B6 lymphocyte ratio and 32% of them developed diabetes that could be adoptively transferred to irradiated NOD or NOD-rag-2-/- mice.	Cyclophosphamide	14-16	recombination activating gene 2	Mus musculus	187-192
8751797-2	1996	Combination chemotherapy with cisplatin/etoposide (PE) or CAV (cyclophosphamide, adriamycin and vincristine) alternating with PE was established as standard regimens.	Cyclophosphamide	63-79	caveolin 2	Homo sapiens	58-61
8699079-1	1996	This study assesses the effect of granulocyte colony-stimulating factor (G-CSF) on the outcome of infection with Listeria monocytogenes or Staphylococcus aureus in mice during leukocytopenia induced by sublethal total body irradiation or cyclophosphamide treatment.	Cyclophosphamide	238-254	colony stimulating factor 3 (granulocyte)	Mus musculus	73-78
8877715-7	1996	A significantly higher yield of CD34+ cells and a better correlation between CD34+ cells in the peripheral blood and the leukapheresis product were found after priming with high-dose cyclophosphamide plus rhG-CSF, compared with priming with rhG-CSF alone.	Cyclophosphamide	183-199	CD34 molecule	Homo sapiens	77-81
8679463-2	1996	Expression of Bcl-2 was determined using immunohistochemistry on paraffin-embedded sections in a series of 441 premenopausal, lymph node-negative breast cancers of patients randomised to receive perioperative chemotherapy (5-fluorouracil, doxorubicin, cyclophosphamide) or no perioperative chemotherapy.	Cyclophosphamide	252-268	BCL2 apoptosis regulator	Homo sapiens	14-19
8783668-2	1996	Mutations at the HPRT locus increase in frequency as a function of the dose of cyclophosphamide used.	Cyclophosphamide	79-95	hypoxanthine guanine phosphoribosyl transferase	Mus musculus	17-21
8783668-8	1996	However, amifostine 100 mg/kg was effective in reducing cyclophosphamide-induced HPRT mutation frequency in mice from 160 to 35 per 10(5) viable cells regardless of whether it was administered 30 minutes before or 2 hours after the cyclophosphamide.	Cyclophosphamide	56-72	hypoxanthine guanine phosphoribosyl transferase	Mus musculus	81-85
8688335-5	1996	mRNA expression of TGF-beta 1 was not detected in untreated tumour tissues by reverse transcription-polymerase chain reaction (RT-PCR), but was detected in tumour tissues treated with cyclophosphamide.	Cyclophosphamide	184-200	transforming growth factor, beta 1	Mus musculus	19-29
8688335-7	1996	Anti-TGF-beta 1 antibody inhibited LAK-attractant activity in the conditioned medium of tumour tissues treated with cyclophosphamide to approximately 35% that of control at 100 micrograms ml-1.	Cyclophosphamide	116-132	transforming growth factor, beta 1	Mus musculus	5-15
8688344-1	1996	A combination of cyclophosphamide, doxorubicin, vincristine and prednisolone (CHOP) has been a standard therapy for histologically aggressive non-Hodgkin"s lymphomas for over 20 years, but several newer regimens, referred to as second or third generation, have been reported to give improved results in single-centre studies.	Cyclophosphamide	17-33	DNA damage inducible transcript 3	Homo sapiens	78-82
8807097-15	1996	Twenty-two of 24 (92%) patients receiving CE with G-CSF achieved a target level of 5 x 10(6) CD34+ cells/kg or more as compared to 11 of 19 (58%) patients receiving G-CSF alone (P = 0.01) and six of 14 (43%) patients receiving CY with G or GM-CSF (P = 0.001).	Cyclophosphamide	227-229	colony stimulating factor 3	Homo sapiens	50-55
9024937-0	1996	Kinetics of serum granulocyte-colony stimulating factor (G-CSF) concentration and G-CSF receptor expression during G-CSF treatment of cyclophosphamide-treated mice.	Cyclophosphamide	134-150	colony stimulating factor 3 (granulocyte)	Mus musculus	18-55
9024937-0	1996	Kinetics of serum granulocyte-colony stimulating factor (G-CSF) concentration and G-CSF receptor expression during G-CSF treatment of cyclophosphamide-treated mice.	Cyclophosphamide	134-150	colony stimulating factor 3 receptor (granulocyte)	Mus musculus	82-96
9024937-0	1996	Kinetics of serum granulocyte-colony stimulating factor (G-CSF) concentration and G-CSF receptor expression during G-CSF treatment of cyclophosphamide-treated mice.	Cyclophosphamide	134-150	colony stimulating factor 3 (granulocyte)	Mus musculus	82-87
8662658-2	1996	Human class 1 aldehyde dehydrogenase (hALDH-1) can oxidize aldophosphamide, a key aldehyde intermediate in the activation pathway of cyclophosphamide and other oxazaphosphorine (OAP) anti-cancer alkylating agents.	Cyclophosphamide	133-149	aldehyde dehydrogenase 1 family member A1	Homo sapiens	38-45
8799456-1	1996	The present work addresses the effects of three antineoplastic drugs [cyclophosphamide (CP), cisplatin (CDDP) and methotrexate (MTX) which are in current use for the treatment of various tumors] on turnover kinetics of human erythrocyte membrane-bound acetylcholinesterase (AcChoEase, EC 3.1.1.7).	Cyclophosphamide	70-86	acetylcholinesterase (Cartwright blood group)	Homo sapiens	252-272
8799456-1	1996	The present work addresses the effects of three antineoplastic drugs [cyclophosphamide (CP), cisplatin (CDDP) and methotrexate (MTX) which are in current use for the treatment of various tumors] on turnover kinetics of human erythrocyte membrane-bound acetylcholinesterase (AcChoEase, EC 3.1.1.7).	Cyclophosphamide	70-86	acetylcholinesterase (Cartwright blood group)	Homo sapiens	274-283
8611717-7	1996	The drug combination CCE (cyclophosphamide, cisplatin, and etoposide) alone could increase the lifespan of the Namalwa/mdr-1 tumor-burdened mice by 129% compared with untreated controls.	Cyclophosphamide	26-42	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	119-124
8699079-5	1996	However, during infection in cyclophosphamide-treated mice, G-CSF increased the number of granulocytes in the circulation and at the site of infection and decreased the number of bacteria in the tissues.	Cyclophosphamide	29-45	colony stimulating factor 3 (granulocyte)	Mus musculus	60-65
8708567-1	1996	Monoclonal antibodies (mAbs) specific for the LH receptor (LHR) were generated through a modified auto-anti-idiotypic approach in which human chorionic gonadotropin (hCG) was used as the immunogen followed by cyclophosphamide to induce anti-idiotypic antibodies.	Cyclophosphamide	209-225	luteinizing hormone/choriogonadotropin receptor	Homo sapiens	59-62
8844499-10	1996	We observed a decrease in the percentage of CD3+CD8+ in patients treated with methylprednisolone/cyclophosphamide.	Cyclophosphamide	97-113	CD8a molecule	Homo sapiens	48-51
8877724-0	1996	Enhancing the effect of THERATOPE STn-KLH cancer vaccine in patients with metastatic breast cancer by pretreatment with low-dose intravenous cyclophosphamide.	Cyclophosphamide	141-157	eukaryotic translation elongation factor 1 alpha 2	Homo sapiens	34-37
8877724-4	1996	The anti-STn and anti-OSM antibody titers were higher in the patients who received cyclo intravenously before THERATOPE.	Cyclophosphamide	83-88	eukaryotic translation elongation factor 1 alpha 2	Homo sapiens	9-12
8877724-6	1996	Although it is not clear how the anti-STn antibody response modifies tumor biology, we noted that patients in the intravenously administered cyclo group had a lower percentage of patients showing progressive disease at 9 weeks, and that there was an inverse correlation between serum anti-STN antibody titer and growth of measurable tumors.	Cyclophosphamide	141-146	eukaryotic translation elongation factor 1 alpha 2	Homo sapiens	38-41
8877724-6	1996	Although it is not clear how the anti-STn antibody response modifies tumor biology, we noted that patients in the intravenously administered cyclo group had a lower percentage of patients showing progressive disease at 9 weeks, and that there was an inverse correlation between serum anti-STN antibody titer and growth of measurable tumors.	Cyclophosphamide	141-146	eukaryotic translation elongation factor 1 alpha 2	Homo sapiens	289-292
8774842-0	1996	Effects of streptolysin O, polyriboinosinic-polyribocytidylic acid and combinations with cyclophosphamide on the hepatic arylamine N-acetyltransferase and cytochrome P450-dependent monooxygenases in rats.	Cyclophosphamide	89-105	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	155-170
8611717-4	1996	In vivo cyclophosphamide, cisplatin, vincristine, doxorubicin, and etoposide as single agents, were effective in prolonging the survival of SCID mice burdened with the Namalwa tumor, whereas only cyclophosphamide and cisplatin were effective on Namalwa/mdr-1 tumors.	Cyclophosphamide	8-24	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	253-258
8665574-14	1996	Intradermally administered, LPS was less toxic and elicited a tumor response in combination with cyclophosphamide; it can thus can be applied to cancer treatment even in humans.	Cyclophosphamide	97-113	interferon regulatory factor 6	Homo sapiens	28-31
8622080-1	1996	PURPOSE: The goals of this study were to define the efficacy and toxicity of doxorubicin and dose-escalated cyclophosphamide (Cy) along with granulocyte colony-stimulating factor (G-CSF) in the treatment of hormone-refractory prostate cancer (HRPC), to determine the maximal-tolerated dose (MTD) of Cy in this regimen, and to evaluate the impact of prior pelvic irradiation (XRT) on MTD and toxicity.	Cyclophosphamide	299-301	colony stimulating factor 3	Homo sapiens	180-185
8797041-0	1996	Granulocyte colony-stimulating factor shortens the optimal interval of repetition of chemotherapy with cyclophosphamide in mice.	Cyclophosphamide	103-119	colony stimulating factor 3 (granulocyte)	Mus musculus	0-37
8797041-1	1996	To examine the effect of human granulocyte colony-stimulating factor (G-CSF) on the hemopoietic response to repeated treatment with the anticancer drug cyclophosphamide (CPA) in mice, we determined the optimal time interval between CPA doses which was required to equalize the recovery of neutrophils in the first and second cycle.	Cyclophosphamide	170-173	colony stimulating factor 3	Homo sapiens	70-75
8797041-2	1996	G-CSF-treatment significantly shortened the optimal time interval of CPA doses when compared with treatment with the control vehicle.	Cyclophosphamide	69-72	colony stimulating factor 3 (granulocyte)	Mus musculus	0-5
8797041-3	1996	The studies on resistance to a second CPA cycle and hemopoietic parameters indicated that the resistance correlated positively with the granulocyte colony-forming cel (G-CFC) population in marrow, in both control and G-CSF-treated mice.	Cyclophosphamide	38-41	PAX3 and PAX7 binding protein 1	Mus musculus	136-173
8797041-3	1996	The studies on resistance to a second CPA cycle and hemopoietic parameters indicated that the resistance correlated positively with the granulocyte colony-forming cel (G-CFC) population in marrow, in both control and G-CSF-treated mice.	Cyclophosphamide	38-41	colony stimulating factor 3 (granulocyte)	Mus musculus	217-222
8797041-5	1996	These results suggest that G-CSF shortens the optimal time interval between CPA doses not only by accelerating the recovery of G-CFC but also by affecting the hemopoietic environment.	Cyclophosphamide	76-79	colony stimulating factor 3 (granulocyte)	Mus musculus	27-32
8622073-11	1996	CONCLUSION: A dose of CY at 2,000 mg/m2 can be administered every 2 weeks with DOX and G-CSF for eight cycles in the outpatient setting with manageable toxicity.	Cyclophosphamide	22-24	colony stimulating factor 3	Homo sapiens	87-92
8622080-0	1996	Doxorubicin and dose-escalated cyclophosphamide with granulocyte colony-stimulating factor for the treatment of hormone-resistant prostate cancer.	Cyclophosphamide	31-47	colony stimulating factor 3	Homo sapiens	53-90
8622093-9	1996	The average CRA rate reported in regimens based on cyclophosphamide, methotrexate, and fluorouracil (CMF) is 68% (95% confidence interval [CI], 66% to 70%), with a range of 20% to 100%.	Cyclophosphamide	51-67	myotubularin related protein 11	Homo sapiens	12-15
8817519-2	1996	Here, we examined the effect of inflammation on expression of the low affinity neurotrophin receptor p75, using the model of cyclophosphamide-induced cystitis in rats.	Cyclophosphamide	125-141	nerve growth factor receptor	Rattus norvegicus	101-104
8817519-4	1996	At 2 and 3 days after injection of cyclophosphamide, numbers of p75-positive fine fibres in the muscle layer were dramatically increased.	Cyclophosphamide	35-51	nerve growth factor receptor	Rattus norvegicus	64-67
8602629-0	1996	Randomized placebo-controlled trial of granulocyte-macrophage colony-stimulating-factor support for dose-intensive cyclophosphamide, etoposide, and cisplatin.	Cyclophosphamide	115-131	colony stimulating factor 2	Homo sapiens	39-87
8602629-1	1996	This is a double-blind randomized placebo-controlled trial to evaluate the efficacy and safety of granulocyte-macrophage colony-stimulating-factor (GM-CSF) after dose-intensive cyclophosphamide, etoposide, and cisplatin (DICEP).	Cyclophosphamide	177-193	colony stimulating factor 2	Homo sapiens	98-146
8630380-1	1996	We conducted a prospective randomized trial to evaluate the ability of the interleukin-3/granulocyte-macrophage colony-stimulating factor (GM-CSF) fusion protein, PIXY321, to ameliorate cumulative thrombocytopenia after multiple cycles of 5-fluorouracil, leucovorin, doxorubicin, cyclophosphamide (FLAC) chemotherapy compared with GM-CSF in patients with advanced breast cancer.	Cyclophosphamide	280-296	colony stimulating factor 2	Homo sapiens	75-137
8738973-4	1996	We now report that cyclophosphamide constitutes an apoptosis signal to peripheral lymphocytes and we provide evidence that NOD B cells as well as both CD4 and CD8 T cells display resistance to cyclophosphamide-induced apoptosis.	Cyclophosphamide	193-209	CD4 antigen	Mus musculus	151-154
8630380-1	1996	We conducted a prospective randomized trial to evaluate the ability of the interleukin-3/granulocyte-macrophage colony-stimulating factor (GM-CSF) fusion protein, PIXY321, to ameliorate cumulative thrombocytopenia after multiple cycles of 5-fluorouracil, leucovorin, doxorubicin, cyclophosphamide (FLAC) chemotherapy compared with GM-CSF in patients with advanced breast cancer.	Cyclophosphamide	280-296	colony stimulating factor 2	Homo sapiens	139-145
8613443-10	1996	Dose survival studies with use of a tetrazolium colorimetric assay showed that the MOS/ADR1 cells were cross-resistant to vincristine, vinblastine, etoposide, bleomycin, mitomycin C, and actinomycin D but not to dacarbazine, cisplatin, carboplatin, cytosine arabinoside, carmustine, cyclophosphamide, ifosfamide, methotrexate, and 5-fluorouracil.	Cyclophosphamide	283-299	Moloney sarcoma oncogene	Mus musculus	83-86
8640822-0	1996	Sensitization of human breast cancer cells to cyclophosphamide and ifosfamide by transfer of a liver cytochrome P450 gene.	Cyclophosphamide	46-62	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	112-116
8640822-1	1996	The cancer chemotherapeutic agent cyclophosphamide (CPA) and its isomer ifosfamide (IFA) are alkylating agent prodrugs that require metabolism by liver cytochrome P450 (P450) enzymes for antitumor activity.	Cyclophosphamide	34-50	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	163-167
8640822-1	1996	The cancer chemotherapeutic agent cyclophosphamide (CPA) and its isomer ifosfamide (IFA) are alkylating agent prodrugs that require metabolism by liver cytochrome P450 (P450) enzymes for antitumor activity.	Cyclophosphamide	34-50	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	169-173
8731685-6	1996	Treatment with prednisone and cyclophosphamide was started with a good clinical response, stabilization of renal insufficiency and disappearance of P-ANCA (MPO).	Cyclophosphamide	30-46	myeloperoxidase	Homo sapiens	156-159
8562935-4	1996	Overexpression of the ALDH1 gene resulted in a significant increases in cyclophosphamide resistance in transduced L1210 and U937 cells (50% inhibition concentration [IC50], approximately 13 mumol/L).	Cyclophosphamide	72-88	aldehyde dehydrogenase family 1, subfamily A1	Mus musculus	22-27
8640822-1	1996	The cancer chemotherapeutic agent cyclophosphamide (CPA) and its isomer ifosfamide (IFA) are alkylating agent prodrugs that require metabolism by liver cytochrome P450 (P450) enzymes for antitumor activity.	Cyclophosphamide	52-55	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	163-167
8640822-1	1996	The cancer chemotherapeutic agent cyclophosphamide (CPA) and its isomer ifosfamide (IFA) are alkylating agent prodrugs that require metabolism by liver cytochrome P450 (P450) enzymes for antitumor activity.	Cyclophosphamide	52-55	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	169-173
8640822-3	1996	Transfer of a liver cytochrome P450 gene, CYP2B1, into human breast MCF-7 cancer cells is presently shown to greatly sensitize these cells to oxazaphosphorine toxicity as a consequence of the acquired capacity for intratumoral CPA and IFA activation.	Cyclophosphamide	227-230	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	31-35
8562935-6	1996	ALDH1 transduction into peripheral blood human hematopoietic progenitor cells also led to significant increases (4- to 10-fold; IC50, approximately 3 to 4 mumol/L) in cyclophosphamide resistance in an in vitro colony-forming assay.	Cyclophosphamide	167-183	aldehyde dehydrogenase 1 family member A1	Homo sapiens	0-5
8629263-5	1996	The CHOP-regime, consisting of doxorubicin, cyclophosphamide, oncovin and prednisolon, is the standard therapy that should be given outside of clinical trials.	Cyclophosphamide	44-60	DNA damage inducible transcript 3	Homo sapiens	4-8
8636747-1	1996	PURPOSE: To determine the maximum-tolerated dose of cyclophosphamide (CTX) when administered sequentially with melphalan 60 mg/m2/d for 3 days, followed by autologous bone marrow rescue (ABMR), in children with recurrent or progressive malignant brain tumors, and to make preliminary observations on efficacy.	Cyclophosphamide	52-68	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	70-73
8562935-7	1996	These findings indicate that ALDH1 overexpression is sufficient to induce cyclophosphamide resistance in vitro and provide a basis for testing the efficacy of ALDH1 gene transduction to protect bone marrow cells from high-dose cyclophosphamide in vivo.	Cyclophosphamide	74-90	aldehyde dehydrogenase 1 family member A1	Homo sapiens	29-34
8562935-7	1996	These findings indicate that ALDH1 overexpression is sufficient to induce cyclophosphamide resistance in vitro and provide a basis for testing the efficacy of ALDH1 gene transduction to protect bone marrow cells from high-dose cyclophosphamide in vivo.	Cyclophosphamide	227-243	aldehyde dehydrogenase 1 family member A1	Homo sapiens	29-34
8612316-2	1996	Treatment of tumor bearing animals with anti-TGF-beta antibodies by intraperitoneal injection daily on days 0-8 post-tumor cell implantation increased the sensitivity of the EMT-6/Parent tumor to cyclophosphamide (CTX) and cisplatin (CDDP) and markedly increased the sensitivity of the EMT-6/CTX tumor to CTX and the EMT6/CDDP tumor to CDDP, as determined by tumor cell survival assay.	Cyclophosphamide	196-212	transforming growth factor beta 1	Homo sapiens	45-53
8629035-12	1996	However, granulocyte colony-stimulating factor has ameliorated myelosuppression and allowed considerable dose escalation of cyclophosphamide.	Cyclophosphamide	124-140	colony stimulating factor 3	Homo sapiens	9-46
8823488-0	1996	Erythropoietin and granulocyte-macrophage colony-stimulating factor allow acceleration and dose escalation of cyclophosphamide/epidoxorubicin/5-fluorouracil chemotherapy: a dose-finding study in patients with advanced breast cancer.	Cyclophosphamide	110-126	erythropoietin	Homo sapiens	0-14
8636770-9	1996	Treatment with cyclophosphamide, doxorubicin vincristine, and prednisone (CHOP) or cyclophosphomide, vincristine, and prednisone (COP) resulted in a complete remission in 14 of 15 cases.	Cyclophosphamide	15-31	DNA damage inducible transcript 3	Homo sapiens	74-78
8823488-0	1996	Erythropoietin and granulocyte-macrophage colony-stimulating factor allow acceleration and dose escalation of cyclophosphamide/epidoxorubicin/5-fluorouracil chemotherapy: a dose-finding study in patients with advanced breast cancer.	Cyclophosphamide	110-126	colony stimulating factor 2	Homo sapiens	19-67
8636780-1	1996	PURPOSE: We compared hematologic and clinical effects of granulocyte-macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF) after treatment with high-dose cyclophosphamide (HD-CTX, 7 g/m2), given as the first phase of a high-dose sequential chemotherapy program that includes a myeloablative therapy with mobilized progenitor cell autografting.	Cyclophosphamide	196-212	colony stimulating factor 3	Homo sapiens	119-156
8823488-1	1996	To verify whether the association of granulocyte-macrophage colony-stimulating factor (GM-CSF) and erythropoietin (EPO) would allow both the acceleration and the dose escalation of the cyclophosphamide/epidoxorubicin/5-fluorouracil (CEF) regimen as first-line therapy in advanced breast cancer patients, we conducted a dose-finding study.	Cyclophosphamide	185-201	colony stimulating factor 2	Homo sapiens	37-85
8823488-1	1996	To verify whether the association of granulocyte-macrophage colony-stimulating factor (GM-CSF) and erythropoietin (EPO) would allow both the acceleration and the dose escalation of the cyclophosphamide/epidoxorubicin/5-fluorouracil (CEF) regimen as first-line therapy in advanced breast cancer patients, we conducted a dose-finding study.	Cyclophosphamide	185-201	colony stimulating factor 2	Homo sapiens	87-93
8823488-1	1996	To verify whether the association of granulocyte-macrophage colony-stimulating factor (GM-CSF) and erythropoietin (EPO) would allow both the acceleration and the dose escalation of the cyclophosphamide/epidoxorubicin/5-fluorouracil (CEF) regimen as first-line therapy in advanced breast cancer patients, we conducted a dose-finding study.	Cyclophosphamide	185-201	erythropoietin	Homo sapiens	99-113
8823488-1	1996	To verify whether the association of granulocyte-macrophage colony-stimulating factor (GM-CSF) and erythropoietin (EPO) would allow both the acceleration and the dose escalation of the cyclophosphamide/epidoxorubicin/5-fluorouracil (CEF) regimen as first-line therapy in advanced breast cancer patients, we conducted a dose-finding study.	Cyclophosphamide	185-201	erythropoietin	Homo sapiens	115-118
8522062-3	1996	In this study, we have examined the level of reg gene expression at various degrees of diabetogenesis in the pancreas of the NOD mouse (male, female, and cyclophosphamide-treated male) using both human reg cDNA as the probe and dot blot analysis.	Cyclophosphamide	154-170	regenerating family member 1 alpha	Homo sapiens	45-48
8522062-6	1996	In addition, overexpression of the reg gene was found in male mice treated by cyclophosphamide, an agent known to be a potent inducer of diabetes in male NOD mice.	Cyclophosphamide	78-94	regenerating family member 1 alpha	Homo sapiens	35-38
8625076-6	1995	In the early group, cyclophosphamide/methotrexate/5-fluorouracil (CMF) was administered to 32 patients, doxorubicin, cyclophosphamide or cyclophosphamide, doxorubicin, 5-fluorouracil (AC or CAF) to 6 patients, and other regimens to 4 patients; in the delayed group, CMF was given to 29 patients, CAF to 12 patients, and L-PAM/5-fluorouracil to 1 patient.	Cyclophosphamide	20-36	lysine acetyltransferase 2B	Homo sapiens	190-193
8720612-7	1996	mRNA expression of the p40 chain of interleukin-12 in response to cyclophosphamide was not seen in macrophages of Balb/c mice and thus represents an immune abnormality of non-obese diabetic mice favouring T-helper type 1 reactions.	Cyclophosphamide	66-82	interleukin 12b	Mus musculus	23-26
27406619-2	1996	The present study was thus designed to investigate EPO production during acute hypoxemia in a mouse model in which the oxygen-carrying capacity of blood, the plasma EPO level, and the plasma EPO half-life were within normal values in spite of a marked depression of the red cell production rate (RCPR) induced by cyclophosphamide (CP) administration.	Cyclophosphamide	313-329	erythropoietin	Mus musculus	51-54
8852598-0	1996	Anti-CD4 monoclonal antibody reduces the dose of cyclophosphamide required to induce tolerance to H-2 haplotype identical skin allografts in mice.	Cyclophosphamide	49-65	CD4 antigen	Mus musculus	5-8
8852598-0	1996	Anti-CD4 monoclonal antibody reduces the dose of cyclophosphamide required to induce tolerance to H-2 haplotype identical skin allografts in mice.	Cyclophosphamide	49-65	histocompatibility-2, MHC	Mus musculus	98-101
8717162-13	1996	These findings have potential clinical significance, since it has been recently shown that CYP3A5 catalyzes the activation of the anticancer pro-drugs cyclophosphamide and ifosfamide.	Cyclophosphamide	151-167	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	91-97
8856281-0	1996	Treatment of severe leukopenia with RHG-CSF in systemic lupus erythematosus treated with cyclophosphamide.	Cyclophosphamide	89-105	colony stimulating factor 2	Homo sapiens	40-43
8625076-6	1995	In the early group, cyclophosphamide/methotrexate/5-fluorouracil (CMF) was administered to 32 patients, doxorubicin, cyclophosphamide or cyclophosphamide, doxorubicin, 5-fluorouracil (AC or CAF) to 6 patients, and other regimens to 4 patients; in the delayed group, CMF was given to 29 patients, CAF to 12 patients, and L-PAM/5-fluorouracil to 1 patient.	Cyclophosphamide	20-36	lysine acetyltransferase 2B	Homo sapiens	296-299
8520789-4	1995	With 10(4) CFU, the CPA group showed an increased T/P ratio of 0.22 +/- 0.03 versus 0.14 +/- 0.01 in the control and 0.11 +/- 0.01 (mean +/- SEM) in the rG-CSF groups (p < 0.01).	Cyclophosphamide	20-23	colony stimulating factor 3	Rattus norvegicus	153-159
8520789-7	1995	With 10(8) CFU, the mortality rate was increased in the rG-CSF group (7 of 10) as compared with the control (0 of 9) and CPA groups (1 of 9) (p < 0.05), which reflected an increased LW/BW (g/kg) ratio (16 +/- 2 versus 12 +/- 1) in the CPA group (p < 0.05).	Cyclophosphamide	238-241	colony stimulating factor 3	Rattus norvegicus	56-62
8652232-5	1995	In high-grade lymphomas combination chemotherapy with cyclophosphamide, hydroxydaunorubin, vincristine and prednisone (CHOP) represents the treatment of first choice, and may be restricted to 3-4 cycles in patients with limited stages of the disease when followed by involved field radiotherapy.	Cyclophosphamide	54-70	DNA damage inducible transcript 3	Homo sapiens	119-123
9815949-3	1995	Because both P-glycoprotein- and platinum-induced resistance appear to be clinically important and can be reversed in vitro with a short exposure of cyclosporin A (CSA) at 2000 and 5000 ng/ml, respectively, we undertook a trial of high-dose chemotherapy with carboplatin (1500mg/m2), mitoxantrone (75 mg/m2), and cyclophosphamide (120 mg/kg) over a 5-day period combined with escalating doses of CSA.	Cyclophosphamide	313-329	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	164-167
8746558-5	1995	Both B7-1 and B7-2 were, however, highly expressed on the majority of islet-infiltrating inflammatory cells in NOD mice between days 7 and 12 after the administration of cyclophosphamide which results in accelerated beta cell destruction.	Cyclophosphamide	170-186	CD80 antigen	Mus musculus	5-18
8523055-3	1995	The study was designed to determine the maximum-tolerated dosages (MTD) of cyclophosphamide and doxorubicin that could be used in a high-dose cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) regimen with granulocyte colony-stimulating factor (G-CSF) support and to assess preliminarily the efficacy of the regimen.	Cyclophosphamide	75-91	DNA damage inducible transcript 3	Homo sapiens	202-206
8523055-3	1995	The study was designed to determine the maximum-tolerated dosages (MTD) of cyclophosphamide and doxorubicin that could be used in a high-dose cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) regimen with granulocyte colony-stimulating factor (G-CSF) support and to assess preliminarily the efficacy of the regimen.	Cyclophosphamide	75-91	colony stimulating factor 3	Homo sapiens	221-258
8523055-3	1995	The study was designed to determine the maximum-tolerated dosages (MTD) of cyclophosphamide and doxorubicin that could be used in a high-dose cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) regimen with granulocyte colony-stimulating factor (G-CSF) support and to assess preliminarily the efficacy of the regimen.	Cyclophosphamide	75-91	colony stimulating factor 3	Homo sapiens	260-265
7591249-6	1995	The specific anti-EL4 effector cell from the cyclophosphamide-induced immune-LTS was CD4- CD8+; however, approximately 50% of those from combination-treated immune-LTS appeared to be CD4+CD8+.	Cyclophosphamide	45-61	epilepsy 4	Mus musculus	18-21
7579367-13	1995	Patients receiving high-dose cyclophosphamide, thiotepa, and carboplatin had more rapid platelet recovery than patients receiving other regimens (P = .006), and patients requiring 2 mobilization procedures versus 1 mobilization procedure to achieve > or = 2.5 x 10(6) CD34+ cells/kg experienced slower platelet recovery (P = .005).	Cyclophosphamide	29-45	CD34 molecule	Homo sapiens	271-275
7591249-6	1995	The specific anti-EL4 effector cell from the cyclophosphamide-induced immune-LTS was CD4- CD8+; however, approximately 50% of those from combination-treated immune-LTS appeared to be CD4+CD8+.	Cyclophosphamide	45-61	CD4 antigen	Mus musculus	85-88
8749950-0	1995	Shorter interval between cycles of cyclophosphamide, doxorubicin, cisplatin using recombinant human granulocyte colony-stimulating factor for urothelial cancer--phase I/II study.	Cyclophosphamide	35-51	colony stimulating factor 3	Homo sapiens	100-137
8597884-0	1995	Effect of cyclophosphamide on lymphokine production in MRL/lpr.Yaa mice.	Cyclophosphamide	10-26	accelerated autoimmunity and lymphoproliferation transposition	Mus musculus	63-66
8749950-3	1995	METHODS: A phase I/II study was conducted to assess whether the interval between cycles of CISCA (cyclophosphamide, doxorubicin, cisplatin) chemotherapy could be shortened under support of recombinant human granulocyte colony-stimulating factor (rhG-CSF) for urothelial cancer.	Cyclophosphamide	98-114	colony stimulating factor 3	Homo sapiens	207-244
8578886-6	1995	Intractable cases (under daily cyclophosphamide + prednisolone) may profit from additional high dose IVIG therapy or from monoclonal antibodies against CD4 and CDw52 molecules.	Cyclophosphamide	31-47	CD4 molecule	Homo sapiens	152-155
8578759-14	1995	Cytochrome b5 content was significantly reduced (p < 0.0001) 7 and 10 days following cyclophosphamide administration (control, 0.46 +/- 0.13; 7-day, 0.28 +/- 0.07 and 10-day group, 0.20 +/- 0.03 nmol/mg).	Cyclophosphamide	88-104	cytochrome b5 type A	Rattus norvegicus	0-13
8578759-16	1995	The significant reductions in the activity of rat hepatic microsomal 2D1 following cyclophosphamide administration, as seen by the alterations in mean Vmax for dextrorphan formation, do not appear to be due to a single factor, but may result from a combination of several events, including reductions in relative 2D1 content, reduced nicotinamide adenine dinucleotide phosphate P450-reductase activity and cytochrome b5 content.	Cyclophosphamide	83-99	cytochrome b5 type A	Rattus norvegicus	406-419
8563240-3	1995	Because cyclophosphamide enhanced lesion growth within the skull, we administered an intravenous infusion of interleukin-2 with remarkable efficacy.	Cyclophosphamide	8-24	interleukin 2	Homo sapiens	109-122
7547218-4	1995	Therefore, in this study we evaluated, in cancer patients, the temporal relationships between the increases in plasma CgA and urinary 5-hydroxyindoleacetic acid (5-HIAA) and the development of vomiting following dacarbazine, nitrogen mustard and cyclophosphamide treatments.	Cyclophosphamide	246-262	chromogranin A	Homo sapiens	118-121
8634684-0	1995	Participation of TNF-alpha and IL-1 in the pathogenesis of cyclophosphamide-induced hemorrhagic cystitis.	Cyclophosphamide	59-75	tumor necrosis factor	Mus musculus	17-26
8634684-0	1995	Participation of TNF-alpha and IL-1 in the pathogenesis of cyclophosphamide-induced hemorrhagic cystitis.	Cyclophosphamide	59-75	interleukin 1 complex	Mus musculus	31-35
8529761-5	1995	Pregestimil protected female NOD mice against spontaneous diabetes and male NOD mice against acute Cy-induced diabetes.	Cyclophosphamide	99-101	atrophin 1	Homo sapiens	76-79
7549508-6	1995	Moreover, FK-506, mizoribine and cyclophosphamide clearly inhibited the antigen-induced IL-5 production and cyclosporin A showed the tendency to inhibit IL-5 production.	Cyclophosphamide	33-49	interleukin 5	Mus musculus	88-92
8697977-1	1995	Twenty seven Patients with advanced breast cancer were treated with CAC (carboplatin, adriamycin, cyclophosphamide) regimen.	Cyclophosphamide	98-114	carbonic anhydrase 2	Homo sapiens	68-71
8785707-2	1996	To investigate the direct role of the human aldehyde dehydrogenase class 1 (ALDH-1) in the resistance to one of these agents, 4-hydroperoxycyclophosphamide (4-HC), an active metabolite of cyclophosphamide, neomycin-selectable plasmid or retroviral constructs harboring the wild-type ALDH-1 complementary DNA in the sense orientation were transfected into K562 leukemic cell lines.	Cyclophosphamide	139-155	aldehyde dehydrogenase 1 family member A1	Homo sapiens	44-74
8785707-2	1996	To investigate the direct role of the human aldehyde dehydrogenase class 1 (ALDH-1) in the resistance to one of these agents, 4-hydroperoxycyclophosphamide (4-HC), an active metabolite of cyclophosphamide, neomycin-selectable plasmid or retroviral constructs harboring the wild-type ALDH-1 complementary DNA in the sense orientation were transfected into K562 leukemic cell lines.	Cyclophosphamide	139-155	aldehyde dehydrogenase 1 family member A1	Homo sapiens	76-82
8654195-1	1995	The cytosolic class aldehyde dehydrogenase (ALDH-3) present in human normal tissues/secretions is apparently much less able to catalyze the oxidation aldophosphamide to carboxyphosphamide than is the ALDH-3 present in human tumor cells/tissues, suggesting that the former may be less able to protect cells from the cytotoxic action of cyclophosphamide, mafosfamide, and other oxazaphosphorines.	Cyclophosphamide	335-351	aldehyde dehydrogenase 3 family member A1	Homo sapiens	44-50
8654195-1	1995	The cytosolic class aldehyde dehydrogenase (ALDH-3) present in human normal tissues/secretions is apparently much less able to catalyze the oxidation aldophosphamide to carboxyphosphamide than is the ALDH-3 present in human tumor cells/tissues, suggesting that the former may be less able to protect cells from the cytotoxic action of cyclophosphamide, mafosfamide, and other oxazaphosphorines.	Cyclophosphamide	335-351	aldehyde dehydrogenase 3 family member A1	Homo sapiens	200-206
7561698-7	1995	In contrast, nonobese diabetic (NOD) TCR alpha hemizygotes are significantly protected from cyclophosphamide-accelerated insulitis and diabetes.	Cyclophosphamide	92-108	T cell receptor alpha chain	Mus musculus	37-46
8578886-6	1995	Intractable cases (under daily cyclophosphamide + prednisolone) may profit from additional high dose IVIG therapy or from monoclonal antibodies against CD4 and CDw52 molecules.	Cyclophosphamide	31-47	CD52 molecule	Homo sapiens	160-165
7620183-3	1995	Absence of significant release of TNF alpha in the period of busulphan (BUS) treatment, but significant induction of TNF alpha by total body irradiation (TBI) and cyclophosphamide (CY) conditioning were correlated with significantly earlier onset of acute GVHD in patients receiving TBI/CY regimens as compared with BUS/CY-treated patients.	Cyclophosphamide	181-183	tumor necrosis factor	Homo sapiens	117-126
7563172-0	1995	Accumulation of p53 protein as a possible predictor of response to adjuvant combination chemotherapy with cyclophosphamide, methotrexate, fluorouracil, and prednisone for breast cancer.	Cyclophosphamide	106-122	tumor protein p53	Homo sapiens	16-19
7543988-0	1995	Anti-MAG antibody-associated polyneuropathies: improvement following immunotherapy with monthly plasma exchange and IV cyclophosphamide.	Cyclophosphamide	119-135	myelin associated glycoprotein	Homo sapiens	5-8
8522358-5	1995	In the recipient C3H mice treated with anti-CD4 mAb, F344 s.c. plus BMC and CY, mixed chimerism in the periphery was detected for a few days after CY administration, although intrathymic chimerism was not detected throughout this study.	Cyclophosphamide	147-149	CD4 antigen	Mus musculus	44-47
8535401-0	1995	Increase in total blood leukocyte count following intranasal administration of recombinant human granulocyte colony-stimulating factor (rhG-CSF) in rabbits with cyclophosphamide-induced leukopenia.	Cyclophosphamide	161-177	colony stimulating factor 3	Homo sapiens	97-134
7543988-2	1995	We used plasma exchange and cyclophosphamide to treat four patients with anti-MAG antibody-associated polyneuropathies whose symptoms had progressed in the preceding year.	Cyclophosphamide	28-44	myelin associated glycoprotein	Homo sapiens	78-81
9816036-2	1995	The purpose of this study was to evaluate the effect of conjugation to a carrier and administration with an adjuvant and cyclophosphamide (CTX) on the immunogenicity of anti-id mAb MK2-23 in patients with malignant melanoma and to analyze the relationship between development of humoral immunity and survival time of patients.	Cyclophosphamide	121-137	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	139-142
7622294-0	1995	Correlation between the sensitivity or resistance to IL-2 and the response to cyclophosphamide of 4 tumors transplantable in the same murine host.	Cyclophosphamide	78-94	interleukin 2	Mus musculus	53-57
8537251-8	1995	Because GnRH antagonist-antiandrogen treatment can protect stem spermatogonial survival and/or function in the rat from cyclophosphamide-induced damage, if the same principles are applicable in human, hormonal pretreatment should be useful for preventing the prolonged azoospermia caused by chemotherapy with cyclophosphamide-containing protocols.	Cyclophosphamide	120-136	gonadotropin releasing hormone 1	Rattus norvegicus	8-12
8537251-8	1995	Because GnRH antagonist-antiandrogen treatment can protect stem spermatogonial survival and/or function in the rat from cyclophosphamide-induced damage, if the same principles are applicable in human, hormonal pretreatment should be useful for preventing the prolonged azoospermia caused by chemotherapy with cyclophosphamide-containing protocols.	Cyclophosphamide	309-325	gonadotropin releasing hormone 1	Rattus norvegicus	8-12
7539582-0	1995	Etoposide, dexamethasone, and continuous-infusion cyclophosphamide with G-CSF for VAD-resistant multiple myeloma.	Cyclophosphamide	50-66	colony stimulating factor 3	Homo sapiens	72-77
7541450-1	1995	PURPOSE: Here we evaluate Taxol (paclitaxel; Bristol-Myers Squibb, Princeton, NJ) and cyclophosphamide (CY) with recombinant human granulocyte colony-stimulating factor (rhG-CSF) for mobilization of peripheral-blood stem cells (PBSCs) for autologous stem-cell transplantation in patients with breast and ovarian cancer.	Cyclophosphamide	104-106	colony stimulating factor 3	Homo sapiens	131-168
7541450-7	1995	The mean daily yield of CD34+ cells/kg/collection was 3.5 (range, 0.8 to 28.9) after Taxol and CY, as compared with 1.3 (range, 0.1 to 7.0) for patients who received CY alone (P = .01).	Cyclophosphamide	95-97	CD34 molecule	Homo sapiens	24-28
7541450-8	1995	All patients who received CY and Taxol reached a target level of 5 x 10(6) CD34+ cells/kg, as compared with five of nine patients (55.5%) who received CY alone (P = .03).	Cyclophosphamide	26-28	CD34 molecule	Homo sapiens	75-79
8533110-0	1995	Induction of apoptosis and cathepsin D in limbs exposed in vitro to an activated analog of cyclophosphamide.	Cyclophosphamide	91-107	cathepsin D	Mus musculus	27-38
7627991-6	1995	In each case the effect seen with the combination of a moderate CY dose (150 mg/kg) with TNF alpha was better than that seen with either dose of CY alone and equal to or better than that seen with the higher dose of CY combined with TNF alpha.	Cyclophosphamide	64-66	tumor necrosis factor	Mus musculus	89-98
7751644-6	1995	A single, low dose (20 mg/kg) of the DNA-targeted drug cyclophosphamide (Cy) caused a massive decrease in frequency for the responding CD8+ CTLp, though the mice survived infection with the HKx31 virus and there was no long-term exhaustion of the CTLp pool in the MLN, spleen, or lung.	Cyclophosphamide	55-71	CD8a molecule	Homo sapiens	135-138
7751644-6	1995	A single, low dose (20 mg/kg) of the DNA-targeted drug cyclophosphamide (Cy) caused a massive decrease in frequency for the responding CD8+ CTLp, though the mice survived infection with the HKx31 virus and there was no long-term exhaustion of the CTLp pool in the MLN, spleen, or lung.	Cyclophosphamide	73-75	CD8a molecule	Homo sapiens	135-138
8535664-0	1995	Increased LAK and T cell activation in responding renal cell carcinoma patients after low dose cyclophosphamide, IL-2 and alpha-IFN.	Cyclophosphamide	95-111	alpha kinase 1	Homo sapiens	10-13
7629651-4	1995	When conventional immunosuppressive therapy with prednisolone and cyclophosphamide was applied, the patients" symptoms subsided as the cANCA titer decreased, and thus it also seemed useful for the follow-up of Wegener"s granulomatosis patients.	Cyclophosphamide	66-82	proteinase 3	Homo sapiens	135-140
7671131-6	1995	Immunological analysis on admission showed a high level of soluble ICAM-1 and ANCA negative, but that of soluble ICAM-1 was reduced after surgical operation and remained within normal range during an administration of prednisolone and cyclophosphamide.	Cyclophosphamide	235-251	intercellular adhesion molecule 1	Homo sapiens	113-119
7786310-2	1995	The role of other drug-metabolizing enzymes such as glutathione S-transferase (GST) in CPA resistance is, however, less certain.	Cyclophosphamide	87-90	glutathione S-transferase kappa 1	Homo sapiens	52-77
7786310-2	1995	The role of other drug-metabolizing enzymes such as glutathione S-transferase (GST) in CPA resistance is, however, less certain.	Cyclophosphamide	87-90	glutathione S-transferase kappa 1	Homo sapiens	79-82
7786310-9	1995	These studies establish that in addition to ALDH, GST overexpression can contribute to acquired resistance of tumor cells to 4HC and, furthermore, suggest that modulators that target the GSH/GST system could be useful in overcoming CPA resistance in the clinic.	Cyclophosphamide	232-235	glutathione S-transferase kappa 1	Homo sapiens	50-53
7786310-9	1995	These studies establish that in addition to ALDH, GST overexpression can contribute to acquired resistance of tumor cells to 4HC and, furthermore, suggest that modulators that target the GSH/GST system could be useful in overcoming CPA resistance in the clinic.	Cyclophosphamide	232-235	glutathione S-transferase kappa 1	Homo sapiens	191-194
7538976-5	1995	In the surviving breast cancer patients there was a significant decrease in the percentage of non-B lymphocyte HLA-DR+ (CD20-HLA-DR+) cells following cyclophosphamide treatment.	Cyclophosphamide	150-166	keratin 20	Homo sapiens	120-124
7538976-7	1995	Breast cancer patients who showed a greater than median decrease in CD20-HLA-DR+ lymphocytes following cyclophosphamide treatment had a survival advantage over patients who had less than the median decrease in the percent CD20-HLA-DR+ lymphocytes.	Cyclophosphamide	103-119	keratin 20	Homo sapiens	68-72
7538976-7	1995	Breast cancer patients who showed a greater than median decrease in CD20-HLA-DR+ lymphocytes following cyclophosphamide treatment had a survival advantage over patients who had less than the median decrease in the percent CD20-HLA-DR+ lymphocytes.	Cyclophosphamide	103-119	keratin 20	Homo sapiens	222-226
7759164-9	1995	Interleukin (IL)-2 added to pre-T3CS CD4-depleted ALT cells cultured with T3CS restored anti-tumor activity when combined with CY.	Cyclophosphamide	127-129	interleukin 2	Mus musculus	0-18
7749762-2	1995	The purpose of this study was to develop a multicycle, high-dose intensity cyclophosphamide regimen with granulocyte-macrophage colony-stimulating factor (GM-CSF) and to assess its activity against malignant glioma and primitive neuroectodermal tumor (PNET).	Cyclophosphamide	75-91	colony stimulating factor 2	Homo sapiens	105-153
7727773-5	1995	CPA and IL-1ra increased absolute neutrophil counts (ANCs) at days 2 (P = .001) and 14 (P = .0025) after CPA.	Cyclophosphamide	105-108	interleukin 1 receptor antagonist	Mus musculus	8-14
7727773-2	1995	In the present study, the ability of recombinant human IL-1 receptor antagonist (IL-1ra) to protect hematopoietic progenitors was studied in a murine model of cyclophosphamide (CPA)-induced myelotoxicity.	Cyclophosphamide	159-175	interleukin 1 receptor antagonist	Homo sapiens	55-79
7727773-2	1995	In the present study, the ability of recombinant human IL-1 receptor antagonist (IL-1ra) to protect hematopoietic progenitors was studied in a murine model of cyclophosphamide (CPA)-induced myelotoxicity.	Cyclophosphamide	159-175	interleukin 1 receptor antagonist	Homo sapiens	81-87
7727773-2	1995	In the present study, the ability of recombinant human IL-1 receptor antagonist (IL-1ra) to protect hematopoietic progenitors was studied in a murine model of cyclophosphamide (CPA)-induced myelotoxicity.	Cyclophosphamide	177-180	interleukin 1 receptor antagonist	Homo sapiens	55-79
7727773-6	1995	In IL-1ra-treated mice, colony-forming units granulocyte-macrophage (CFU-GM)/tibia were increased twofold and threefold at days 2 (P = .0047) and 7 (P = .023), respectively, whereas high proliferative potential colony-forming cells (HPP-CFC)/tibia were decreased twofold to threefold at 8 hours (P = .039) and 24 hours (P = .0033), but were approximately threefold higher than HSA-treated mice at day 7 after CPA.	Cyclophosphamide	409-412	interleukin 1 receptor antagonist	Mus musculus	3-9
7727773-8	1995	In vivo, IL-1ra protected HPP-CFC, but not CFU-GM, from hydroxyurea suicide after a single dose of CPA, suggesting that IL-1ra inhibited cycling of HPP-CFC.	Cyclophosphamide	99-102	interleukin 1 receptor antagonist	Mus musculus	9-15
7727773-10	1995	These data suggest that IL-1ra acts as an indirect negative regulator of hematopoiesis and protects HPP-CFC from CPA, possibly by inhibiting IL-1-enhanced proliferation of early myeloid progenitors.	Cyclophosphamide	113-116	interleukin 1 receptor antagonist	Mus musculus	24-30
7600560-7	1995	Thus, the addition of low-dose IL-2 (25 x 10(3) IU daily, from day 4 to day 7) to high-dose CY (300 mg/kg, days 3 and 8) significantly increased tumor growth in both the early and later periods, compared to the effect of CY alone.	Cyclophosphamide	221-223	interleukin 2	Mus musculus	31-35
7749762-2	1995	The purpose of this study was to develop a multicycle, high-dose intensity cyclophosphamide regimen with granulocyte-macrophage colony-stimulating factor (GM-CSF) and to assess its activity against malignant glioma and primitive neuroectodermal tumor (PNET).	Cyclophosphamide	75-91	colony stimulating factor 2	Homo sapiens	155-161
7640348-2	1995	This effect was induced rapidly (within 1 h) and persisted for 4 h. Mice made leukopenic with cyclophosphamide retained the ability to respond to GM-CSF.	Cyclophosphamide	94-110	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	146-152
7538247-4	1995	PSA returned to normal during lymphoma-specific chemotherapy with a cyclophosphamide, mechlorethamine, vincristine, procarbazine, prednisone regimen.	Cyclophosphamide	68-84	kallikrein related peptidase 3	Homo sapiens	0-3
7897201-4	1995	Mice with the anti-GM-CSF activity reconstituted their peripheral white blood cells with identical kinetics as control mice after high dose cyclophosphamide treatment, sublethal irradiation, or lethal irradiation followed by syngeneic bone marrow transplantation.	Cyclophosphamide	140-156	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	19-25
7672880-19	1995	administration of low SEA concentration alone or in combination with CY IP, was associated with a decrease in the granuloma intralesional L3T4+/Lyt2+ ratio.	Cyclophosphamide	69-71	sepia	Mus musculus	22-25
7630433-1	1995	Effects of indomethacin, N omega-nitro-L-arginine (NNA) and naloxone, and of pretreatment with cyclophosphamide (CY), on the interleukin (IL)-1 beta induced inhibition of exocytotic noradrenaline release were investigated in the isolated, vascularly perfused spleen of the rat.	Cyclophosphamide	95-111	interleukin 1 beta	Rattus norvegicus	125-148
7630433-1	1995	Effects of indomethacin, N omega-nitro-L-arginine (NNA) and naloxone, and of pretreatment with cyclophosphamide (CY), on the interleukin (IL)-1 beta induced inhibition of exocytotic noradrenaline release were investigated in the isolated, vascularly perfused spleen of the rat.	Cyclophosphamide	113-115	interleukin 1 beta	Rattus norvegicus	125-148
7705673-11	1995	rhu IL-3 may reduced the thrombocytopenia associated with aggressive treatment with cyclophosphamide and carboplatin, although this remains to be confirmed in a randomized, placebo-controlled trial.	Cyclophosphamide	84-100	interleukin 3	Homo sapiens	4-8
7730156-6	1995	Moreover, the antitumor effect of CY against EL-4 was enhanced by CNG in increasing the number of cured mice, in CY treatment on days 1 and 2, and on days 1, 5 and 9.	Cyclophosphamide	34-36	epilepsy 4	Mus musculus	45-49
7730156-6	1995	Moreover, the antitumor effect of CY against EL-4 was enhanced by CNG in increasing the number of cured mice, in CY treatment on days 1 and 2, and on days 1, 5 and 9.	Cyclophosphamide	113-115	epilepsy 4	Mus musculus	45-49
7533827-2	1995	PATIENTS AND METHODS: Twenty-three patients with breast cancer received cyclophosphamide (4 g/m2) and granulocyte-macrophage colony-stimulating factor ([GM-CSF] 5 micrograms/kg/d x 15 days) for PBPC mobilization.	Cyclophosphamide	72-88	colony stimulating factor 2	Homo sapiens	90-150
7884433-0	1995	Recombinant human interleukin-3 to dose-intensify carboplatin and cyclophosphamide chemotherapy in epithelial ovarian cancer: a phase I trial.	Cyclophosphamide	66-82	interleukin 3	Homo sapiens	18-31
7536433-0	1995	The feasibility of using glycosylated recombinant human granulocyte colony-stimulating factor (G-CSF) to increase the planned dose intensity of doxorubicin, cyclophosphamide and etoposide (ACE) in the treatment of small cell lung cancer.	Cyclophosphamide	157-173	colony stimulating factor 3	Homo sapiens	56-93
7711205-0	1995	Luteinizing hormone-releasing hormone agonist inhibits cyclophosphamide-induced ovarian follicular depletion in rhesus monkeys.	Cyclophosphamide	55-71	gonadotropin releasing hormone 1	Macaca mulatta	0-37
7834628-1	1995	Cyclophosphamide and its isomer ifosfamide are cell cycle-nonspecific alkylating agents that undergo bioactivation catalyzed by liver cytochrome P-450 enzymes.	Cyclophosphamide	0-16	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	134-150
7834628-4	1995	Here we show that 9L gliosarcoma cells stably transfected with a cDNA encoding rat CYP2B1 are highly sensitive to cyclophosphamide and ifosfamide cytotoxicity as compared to parental 9L cells or 9L cells transfected with an Escherichia coli beta-galactosidase gene.	Cyclophosphamide	114-130	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	83-89
7834628-6	1995	Moreover, CYP2B1-expressing 9L cells potentiate the cytotoxic effects of cyclophosphamide and ifosfamide toward cocultured CYP2B1-negative 9L tumor cells.	Cyclophosphamide	73-89	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	10-16
7834628-6	1995	Moreover, CYP2B1-expressing 9L cells potentiate the cytotoxic effects of cyclophosphamide and ifosfamide toward cocultured CYP2B1-negative 9L tumor cells.	Cyclophosphamide	73-89	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	123-129
7834628-8	1995	In vivo experiments using Fischer 344 rats implanted s.c. with CYP2B1-expressing 9L tumor cells demonstrated that intratumoral expression of the CYP2B1 gene provides a substantial therapeutic advantage over that provided by liver cytochrome P-450-dependent drug activation alone; cyclophosphamide treatment resulted in complete growth inhibition of CYP2B1-positive tumors, whereas only a modest growth delay effect was obtained with CYP2B1-negative tumors.	Cyclophosphamide	280-296	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	63-69
7834628-8	1995	In vivo experiments using Fischer 344 rats implanted s.c. with CYP2B1-expressing 9L tumor cells demonstrated that intratumoral expression of the CYP2B1 gene provides a substantial therapeutic advantage over that provided by liver cytochrome P-450-dependent drug activation alone; cyclophosphamide treatment resulted in complete growth inhibition of CYP2B1-positive tumors, whereas only a modest growth delay effect was obtained with CYP2B1-negative tumors.	Cyclophosphamide	280-296	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	145-151
7834628-8	1995	In vivo experiments using Fischer 344 rats implanted s.c. with CYP2B1-expressing 9L tumor cells demonstrated that intratumoral expression of the CYP2B1 gene provides a substantial therapeutic advantage over that provided by liver cytochrome P-450-dependent drug activation alone; cyclophosphamide treatment resulted in complete growth inhibition of CYP2B1-positive tumors, whereas only a modest growth delay effect was obtained with CYP2B1-negative tumors.	Cyclophosphamide	280-296	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	145-151
7834628-8	1995	In vivo experiments using Fischer 344 rats implanted s.c. with CYP2B1-expressing 9L tumor cells demonstrated that intratumoral expression of the CYP2B1 gene provides a substantial therapeutic advantage over that provided by liver cytochrome P-450-dependent drug activation alone; cyclophosphamide treatment resulted in complete growth inhibition of CYP2B1-positive tumors, whereas only a modest growth delay effect was obtained with CYP2B1-negative tumors.	Cyclophosphamide	280-296	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	145-151
9815973-11	1995	In the cyclophosphamide-methotrexate-fluorouracil-treated group, bcl-2 absence was significant for poor overall survival (P = 0.02) as well as a number of nodes above 3 (P = 0.04) and a tumor size above 2 cm (P = 0.05).	Cyclophosphamide	7-23	BCL2 apoptosis regulator	Homo sapiens	65-70
7863507-0	1995	Inhibition of human acetylcholinesterase by cyclophosphamide.	Cyclophosphamide	44-60	acetylcholinesterase (Cartwright blood group)	Homo sapiens	20-40
7863507-1	1995	The inhibitory effect of cyclophosphamide (CP) on human erythrocyte membrane bound acetylcholinesterase (AChE) was investigated in the present study.	Cyclophosphamide	25-41	acetylcholinesterase (Cartwright blood group)	Homo sapiens	83-103
7863507-1	1995	The inhibitory effect of cyclophosphamide (CP) on human erythrocyte membrane bound acetylcholinesterase (AChE) was investigated in the present study.	Cyclophosphamide	25-41	acetylcholinesterase (Cartwright blood group)	Homo sapiens	105-109
7742742-0	1995	Survival after ABO-incompatible allogeneic bone marrow transplant after a preparative regimen of busulfan and cyclophosphamide.	Cyclophosphamide	110-126	ABO, alpha 1-3-N-acetylgalactosaminyltransferase and alpha 1-3-galactosyltransferase	Homo sapiens	15-18
7749066-2	1995	Significantly higher levels of bioactive TNF were observed in mice rendered granulocytopenic (< 0.05 x 10(9) granulocytes/litre) with cyclophosphamide than in normal mice.	Cyclophosphamide	137-153	tumor necrosis factor	Mus musculus	41-44
7536433-0	1995	The feasibility of using glycosylated recombinant human granulocyte colony-stimulating factor (G-CSF) to increase the planned dose intensity of doxorubicin, cyclophosphamide and etoposide (ACE) in the treatment of small cell lung cancer.	Cyclophosphamide	157-173	colony stimulating factor 3	Homo sapiens	95-100
7860617-0	1995	Interleukin-2 gene therapy of residual EL-4 leukaemia potentiates the effect of cyclophosphamide pretreatment.	Cyclophosphamide	80-96	interleukin 2	Mus musculus	0-13
7481481-12	1995	The addition of low doses of cytotoxic drugs (oral cyclophosphamide or azathioprine) resulted in an improvement in the capacity to absorb IL-2 and a reduction in spontaneous IL-1 production.	Cyclophosphamide	51-67	interleukin 2	Homo sapiens	138-142
7481481-12	1995	The addition of low doses of cytotoxic drugs (oral cyclophosphamide or azathioprine) resulted in an improvement in the capacity to absorb IL-2 and a reduction in spontaneous IL-1 production.	Cyclophosphamide	51-67	interleukin 1 alpha	Homo sapiens	174-178
7987845-0	1994	Combined interleukin-1 beta/interleukin-6 treatment in mice: synergistic myelostimulatory activity and myelorestorative effect after cyclophosphamide-induced myelosuppression.	Cyclophosphamide	133-149	interleukin 1 beta	Mus musculus	9-27
7987845-0	1994	Combined interleukin-1 beta/interleukin-6 treatment in mice: synergistic myelostimulatory activity and myelorestorative effect after cyclophosphamide-induced myelosuppression.	Cyclophosphamide	133-149	interleukin 6	Mus musculus	28-41
7987845-7	1994	Furthermore, combined treatment with IL-1 beta/IL-6 accelerated and potentiated the recovery of myeloid cells after cyclophosphamide injection, whereas the single regimen treatment was not effective.	Cyclophosphamide	116-132	interleukin 1 beta	Mus musculus	37-46
7987845-7	1994	Furthermore, combined treatment with IL-1 beta/IL-6 accelerated and potentiated the recovery of myeloid cells after cyclophosphamide injection, whereas the single regimen treatment was not effective.	Cyclophosphamide	116-132	interleukin 6	Mus musculus	47-51
7954469-0	1994	Involvement of human glutathione S-transferase isoenzymes in the conjugation of cyclophosphamide metabolites with glutathione.	Cyclophosphamide	80-96	glutathione S-transferase kappa 1	Homo sapiens	21-46
7954469-3	1994	However, little is known about the GSH-/GST-dependent biotransformation of alkylating agents, including cyclophosphamide.	Cyclophosphamide	104-120	glutathione S-transferase kappa 1	Homo sapiens	40-43
7954469-6	1994	In this paper we describe the involvement of purified human glutathione S-transferases isoenzymes GST A1-1, A2-2, M1a-1a, and P1-1 in the formation of two types of glutathionyl conjugates of cyclophosphamide, i.e., 4-glutathionylcyclophosphamide (4-GSCP) and monochloromonoglutathionylphosphoramide mustard.	Cyclophosphamide	191-207	glutathione S-transferase alpha 1	Homo sapiens	98-106
7954469-6	1994	In this paper we describe the involvement of purified human glutathione S-transferases isoenzymes GST A1-1, A2-2, M1a-1a, and P1-1 in the formation of two types of glutathionyl conjugates of cyclophosphamide, i.e., 4-glutathionylcyclophosphamide (4-GSCP) and monochloromonoglutathionylphosphoramide mustard.	Cyclophosphamide	191-207	S100 calcium binding protein A10	Homo sapiens	126-130
7954469-13	1994	Since all of the human GSTs tested did catalyze the formation of 4-GSCP, the role of 4-GSCP either as a transport form of activated cyclophosphamide or as a detoxification product is discussed.	Cyclophosphamide	132-148	glutathione S-transferase kappa 1	Homo sapiens	23-27
7989942-1	1994	PURPOSE: This randomized, multicenter, dose-finding study was undertaken to determine the dose of recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF) that can safely reduce neutropenia after cyclophosphamide, doxorubicin, and etoposide (CAVP-16) chemotherapy in patients with small-cell lung cancer (SCLC).	Cyclophosphamide	217-233	colony stimulating factor 2	Homo sapiens	116-164
7884433-1	1995	PURPOSE: To define the optimal dose of recombinant human interleukin-3 (rhIL-3) required to intensify the dose of carboplatin and cyclophosphamide for advanced epithelial ovarian cancer.	Cyclophosphamide	130-146	interleukin 3	Homo sapiens	57-70
7860617-0	1995	Interleukin-2 gene therapy of residual EL-4 leukaemia potentiates the effect of cyclophosphamide pretreatment.	Cyclophosphamide	80-96	epilepsy 4	Mus musculus	39-43
7860617-1	1995	Experiments were designed to investigate a possible therapeutic role of interleukin-2 (IL-2) gene transfer in the model of murine (EL-4) leukaemia pretreated with cyclophosphamide.	Cyclophosphamide	163-179	interleukin 2	Mus musculus	87-91
7525710-9	1994	CD34+ cells mobilized with granulocyte colony stimulating factor (G-CSF) or cyclophosphamide also bind VCAM-1 via VLA-4.	Cyclophosphamide	76-92	CD34 molecule	Homo sapiens	0-4
7528861-8	1994	We conclude that the first progenitors appearing in the peripheral blood after priming with high-dose cyclophosphamide and GM- or G-CSF have a more primitive immunophenotype, CD34+/33-.	Cyclophosphamide	102-118	CD34 molecule	Homo sapiens	175-179
7974716-0	1994	The inhibitory effect of cyclophosphamide-induced MAC-1+ natural suppressor cells on IL-2 and IL-4 utilization in MLR.	Cyclophosphamide	25-41	integrin alpha M	Mus musculus	50-55
7974716-0	1994	The inhibitory effect of cyclophosphamide-induced MAC-1+ natural suppressor cells on IL-2 and IL-4 utilization in MLR.	Cyclophosphamide	25-41	interleukin 2	Mus musculus	85-89
7974716-0	1994	The inhibitory effect of cyclophosphamide-induced MAC-1+ natural suppressor cells on IL-2 and IL-4 utilization in MLR.	Cyclophosphamide	25-41	interleukin 4	Mus musculus	94-98
7974716-1	1994	Treatment of adult mice with high doses of the immunosuppressive drug cyclophosphamide (CY) induces transient splenic natural suppressor (NS) cell activity mediated largely by cells bearing the MAC-1+ cell-surface marker.	Cyclophosphamide	70-86	integrin alpha M	Mus musculus	194-199
7974716-1	1994	Treatment of adult mice with high doses of the immunosuppressive drug cyclophosphamide (CY) induces transient splenic natural suppressor (NS) cell activity mediated largely by cells bearing the MAC-1+ cell-surface marker.	Cyclophosphamide	88-90	integrin alpha M	Mus musculus	194-199
7525710-9	1994	CD34+ cells mobilized with granulocyte colony stimulating factor (G-CSF) or cyclophosphamide also bind VCAM-1 via VLA-4.	Cyclophosphamide	76-92	vascular cell adhesion molecule 1	Homo sapiens	103-109
7525710-11	1994	VLA-4 function in CD34+ cells mobilized with G-CSF or cyclophosphamide is equivalent to steady state CD34+ cells.	Cyclophosphamide	54-70	CD34 molecule	Homo sapiens	18-22
7872701-7	1994	A human trial of oral cyclophosphamide using prostate specific antigen as an intermediate endpoint may be warranted.	Cyclophosphamide	22-38	kallikrein related peptidase 3	Homo sapiens	45-70
7949168-8	1994	Injection of N2/CMVGM-CSF/CMS5 # 6 cells in cyclophosphamide-treated mice was as effective in accelerating neutrophil recovery as twice daily subcutaneous injections of rmGM-CSF.	Cyclophosphamide	44-60	notch 2	Mus musculus	13-25
7530630-4	1994	Two comparative studies have demonstrated that prophylactic administration of filgrastim 230 micrograms/m2/day significantly reduces the incidence, duration and severity of neutropenia in patients with previously untreated small-cell lung cancer receiving standard-dose chemotherapy with CDE (cyclophosphamide, doxorubicin plus etoposide).	Cyclophosphamide	293-309	colony stimulating factor 3	Homo sapiens	78-88
7532600-0	1994	Cyclophosphamide treatment of female non-obese diabetic mice causes enhanced expression of inducible nitric oxide synthase and interferon-gamma, but not of interleukin-4.	Cyclophosphamide	0-16	nitric oxide synthase 2, inducible	Mus musculus	91-122
7532600-0	1994	Cyclophosphamide treatment of female non-obese diabetic mice causes enhanced expression of inducible nitric oxide synthase and interferon-gamma, but not of interleukin-4.	Cyclophosphamide	0-16	interferon gamma	Mus musculus	127-143
7532600-2	1994	Strong iNOS expression as determined at the level of transcription, translation and of enzyme activity was associated with destructive insulitis as seen 8-10 days after cyclophosphamide treatment of 70- to 80-day-old female NOD mice.	Cyclophosphamide	169-185	nitric oxide synthase 2, inducible	Mus musculus	7-11
7532600-4	1994	The enhancement of iNOS after cyclophosphamide correlated with an increase of T-helper type 1 (Th1) associated interferon-gamma expression while T-helper type 2 (Th2) associated interleukin-4 was the dominant cytokine prior to cyclophosphamide and after diabetes onset.	Cyclophosphamide	30-46	nitric oxide synthase 2, inducible	Mus musculus	19-23
7532600-4	1994	The enhancement of iNOS after cyclophosphamide correlated with an increase of T-helper type 1 (Th1) associated interferon-gamma expression while T-helper type 2 (Th2) associated interleukin-4 was the dominant cytokine prior to cyclophosphamide and after diabetes onset.	Cyclophosphamide	30-46	interferon gamma	Mus musculus	111-127
7532600-4	1994	The enhancement of iNOS after cyclophosphamide correlated with an increase of T-helper type 1 (Th1) associated interferon-gamma expression while T-helper type 2 (Th2) associated interleukin-4 was the dominant cytokine prior to cyclophosphamide and after diabetes onset.	Cyclophosphamide	227-243	nitric oxide synthase 2, inducible	Mus musculus	19-23
7867692-2	1994	A single intraperitoneal injection of cyclophosphamide markedly altered the levels of several biomarkers in bronchoalveolar lavage fluid: total protein, albumin, angiotensin converting enzyme, lactate dehydrogenase, lactate, N-acetyl-beta-D-glucosaminidase, alkaline phosphatase, acid phosphatase and lipid peroxidation product were significantly elevated.	Cyclophosphamide	38-54	O-GlcNAcase	Rattus norvegicus	225-256
7925782-6	1994	In vivo administration of 0.1 microgram hIL-10 per day to mice treated with a single sublethal dose of cyclophosphamide (CY) resulted in a dramatic and accelerated recovery of CFU-pre-B numbers as compared to vehicle-administered mice.	Cyclophosphamide	103-119	interleukin 10	Homo sapiens	40-46
7925782-6	1994	In vivo administration of 0.1 microgram hIL-10 per day to mice treated with a single sublethal dose of cyclophosphamide (CY) resulted in a dramatic and accelerated recovery of CFU-pre-B numbers as compared to vehicle-administered mice.	Cyclophosphamide	121-123	interleukin 10	Homo sapiens	40-46
7957569-6	1994	DC propagated from the blood of cyclophosphamide-treated mice in granulocyte/macrophage-colony stimulating factor-supplemented media also expressed E-cadherin.	Cyclophosphamide	32-48	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	65-113
7957569-6	1994	DC propagated from the blood of cyclophosphamide-treated mice in granulocyte/macrophage-colony stimulating factor-supplemented media also expressed E-cadherin.	Cyclophosphamide	32-48	cadherin 1	Mus musculus	148-158
7534745-0	1994	Cyclophosphamide (3.6 g/m2) therapy with G-CSF support for resistant myeloma.	Cyclophosphamide	0-16	colony stimulating factor 3	Homo sapiens	41-46
7522393-0	1994	The efficacy of recombinant human granulocyte colony-stimulating factor and recombinant human granulocyte macrophage colony-stimulating factor in permitting the administration of higher doses of cyclophosphamide in a doxorubicin-cyclophosphamide combination.	Cyclophosphamide	195-211	colony stimulating factor 3	Homo sapiens	34-71
7522393-0	1994	The efficacy of recombinant human granulocyte colony-stimulating factor and recombinant human granulocyte macrophage colony-stimulating factor in permitting the administration of higher doses of cyclophosphamide in a doxorubicin-cyclophosphamide combination.	Cyclophosphamide	195-211	colony stimulating factor 2	Homo sapiens	94-142
7522393-4	1994	This study evaluates the efficacy of granulocyte macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF) in allowing administration of high-dose cyclophosphamide in combination with doxorubicin.	Cyclophosphamide	185-201	colony stimulating factor 2	Homo sapiens	37-85
7522393-4	1994	This study evaluates the efficacy of granulocyte macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF) in allowing administration of high-dose cyclophosphamide in combination with doxorubicin.	Cyclophosphamide	185-201	colony stimulating factor 2	Homo sapiens	87-93
7522393-4	1994	This study evaluates the efficacy of granulocyte macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF) in allowing administration of high-dose cyclophosphamide in combination with doxorubicin.	Cyclophosphamide	185-201	colony stimulating factor 3	Homo sapiens	99-136
7522393-4	1994	This study evaluates the efficacy of granulocyte macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF) in allowing administration of high-dose cyclophosphamide in combination with doxorubicin.	Cyclophosphamide	185-201	colony stimulating factor 3	Homo sapiens	138-143
7945481-0	1994	Characteristics of HPRT-mutant T cell lines in a lupus patient treated with cyclophosphamide.	Cyclophosphamide	76-92	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	19-23
7945481-3	1994	When HPRT- cell lines were derived 6 days after pulse cyclophosphamide (CYC) treatment, they were predominantly CD8+ and T cell receptor (TCR) gamma/delta+, producing interferon-gamma (IFN gamma).	Cyclophosphamide	54-70	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	5-9
7945481-3	1994	When HPRT- cell lines were derived 6 days after pulse cyclophosphamide (CYC) treatment, they were predominantly CD8+ and T cell receptor (TCR) gamma/delta+, producing interferon-gamma (IFN gamma).	Cyclophosphamide	72-75	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	5-9
7521788-8	1994	The safety of increasing the dose of cyclophosphamide during biweekly CHOP then was tested.	Cyclophosphamide	37-53	DNA damage inducible transcript 3	Homo sapiens	70-74
7521788-18	1994	CONCLUSIONS: The dose of cyclophosphamide in biweekly CHOP can be increased up to 1500 mg/m2 with no increase in the incidence of treatment-related early mortalities without any organ damage in younger patients.	Cyclophosphamide	25-41	DNA damage inducible transcript 3	Homo sapiens	54-58
7521788-19	1994	The efficacy of this dose intensification of CHOP currently is being investigated in a multicenter prospective randomized trial using three different dose levels of cyclophosphamide.	Cyclophosphamide	165-181	DNA damage inducible transcript 3	Homo sapiens	45-49
7728738-3	1994	Acrolein and phosphoramide mustard are the metabolites of cyclophosphamide which are among the causative agents which reduce the activity of superoxide dismultase, catalase, glutathione peroxidase, glutathione reductase, glutathione-S-transferase and glucose-6-phosphate dehydrogenase in erythrocytes of CMF treated breast cancer patients.	Cyclophosphamide	58-74	catalase	Homo sapiens	164-172
7728738-3	1994	Acrolein and phosphoramide mustard are the metabolites of cyclophosphamide which are among the causative agents which reduce the activity of superoxide dismultase, catalase, glutathione peroxidase, glutathione reductase, glutathione-S-transferase and glucose-6-phosphate dehydrogenase in erythrocytes of CMF treated breast cancer patients.	Cyclophosphamide	58-74	glutathione-disulfide reductase	Homo sapiens	198-219
7728738-3	1994	Acrolein and phosphoramide mustard are the metabolites of cyclophosphamide which are among the causative agents which reduce the activity of superoxide dismultase, catalase, glutathione peroxidase, glutathione reductase, glutathione-S-transferase and glucose-6-phosphate dehydrogenase in erythrocytes of CMF treated breast cancer patients.	Cyclophosphamide	58-74	glutathione S-transferase kappa 1	Homo sapiens	221-246
7728738-3	1994	Acrolein and phosphoramide mustard are the metabolites of cyclophosphamide which are among the causative agents which reduce the activity of superoxide dismultase, catalase, glutathione peroxidase, glutathione reductase, glutathione-S-transferase and glucose-6-phosphate dehydrogenase in erythrocytes of CMF treated breast cancer patients.	Cyclophosphamide	58-74	glucose-6-phosphate dehydrogenase	Homo sapiens	251-284
8087867-2	1994	NSF binds selectively to Ia-positive, cyclophosphamide-sensitive, and plastic-adherent non-T cells (named intermediate cells) present in the spleen.	Cyclophosphamide	38-54	N-ethylmaleimide sensitive fusion protein	Mus musculus	0-3
8087867-9	1994	NSF still blocks the ability of FITC-LNC to induce CS after treatment with cyclophosphamide.	Cyclophosphamide	75-91	N-ethylmaleimide sensitive fusion protein	Mus musculus	0-3
7930875-12	1994	Treatment with methylprednisolone and cyclophosphamide dramatically reduced TNF-alpha but not IL-6.	Cyclophosphamide	38-54	tumor necrosis factor	Mus musculus	76-85
7930875-12	1994	Treatment with methylprednisolone and cyclophosphamide dramatically reduced TNF-alpha but not IL-6.	Cyclophosphamide	38-54	interleukin 6	Mus musculus	94-98
8085859-0	1994	[Feasibility of adjuvant high-dose CAF (cyclophosphamide, adriamycin, 5-FU) therapy for primary breast cancer patients].	Cyclophosphamide	40-56	lysine acetyltransferase 2B	Homo sapiens	35-38
8083225-1	1994	Overexpression of either class 1 or class 3 aldehyde dehydrogenase (ALDH) has been found in cell lines selected for resistance to the oxazaphosphorine (OAP) alkylating anticancer agent cyclophosphamide (CPA).	Cyclophosphamide	185-201	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	68-72
8083225-1	1994	Overexpression of either class 1 or class 3 aldehyde dehydrogenase (ALDH) has been found in cell lines selected for resistance to the oxazaphosphorine (OAP) alkylating anticancer agent cyclophosphamide (CPA).	Cyclophosphamide	203-206	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	68-72
8083225-2	1994	Direct oxidation of the CPA metabolic intermediate aldophosphamide (ALDO) is catalyzed efficiently in vitro by the class 1 ALDH isozyme, but the involvement of the class 3 isozyme in OAP resistance is problematic since in vitro studies do not show efficient oxidation of ALDO.	Cyclophosphamide	24-27	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	123-127
8083225-4	1994	Clonogenic survival assay data indicated that even modest expression of rat class 3 ALDH was associated with resistance (2-4-fold) to the CPA analog mafosfamide and that the fold resistance was directly proportional to the class 3 ALDH activity expressed in clonal transfectants.	Cyclophosphamide	138-141	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	84-88
8042652-4	1994	A kidney biopsy was consistent with Wegener"s granulomatosis, and treatment with prednisone and cyclophosphamide was associated with normalization of serum calcium levels, improved renal function, a marked decrease in serum 1,25(OH)2D levels, and increased serum intact parathyroid hormone levels.	Cyclophosphamide	96-112	parathyroid hormone	Homo sapiens	270-289
7833624-0	1994	Changes in tumor-associated NK 1.1+ large granular lymphocyte precursors after cyclophosphamide injection: in vitro characterization and potential therapeutic application.	Cyclophosphamide	79-95	killer cell lectin-like receptor subfamily B member 1C	Mus musculus	28-34
7955579-0	1994	A single dose of cyclophosphamide (Cph) does increase erythropoietin concentration in patients with hypertension due to vasculitis.	Cyclophosphamide	17-33	erythropoietin	Homo sapiens	54-68
8044973-4	1994	Neutropenia was achieved by treatment with cyclophosphamide (50 mg/kg, 4 days before the experiment), which decreased circulating leukocyte count by 92% and almost abolished neutrophil aggregation to N-formyl-methionyl-leucyl-phenylalanine without affecting blood platelet count, hematocrit, hemoglobin concentration, or whole blood platelet aggregation to ADP.	Cyclophosphamide	43-59	HGB	Sus scrofa	292-302
7955579-0	1994	A single dose of cyclophosphamide (Cph) does increase erythropoietin concentration in patients with hypertension due to vasculitis.	Cyclophosphamide	35-38	erythropoietin	Homo sapiens	54-68
7959938-4	1994	Pretreatment with either MPG or WR-77913 individually, or in combination could prevent the depletion of GSH and induction of lipid peroxidation after cyclophosphamide treatment.	Cyclophosphamide	150-166	N-methylpurine DNA glycosylase	Homo sapiens	25-28
7812215-5	1994	Combination chemotherapy with vincristine, adriamycin, cyclophosphamide and prednisolone was given to the patient with disappearance of the lymphadenopathy and subsequent normalization of PTHrP levels.	Cyclophosphamide	55-71	parathyroid hormone like hormone	Homo sapiens	188-193
8063245-2	1994	The intent was to determine whether the addition of a gonadotropin-releasing hormone analogue would alter the response rates and toxicity profile of cyclophosphamide and cisplatin in patients with advanced ovarian cancer.	Cyclophosphamide	149-165	gonadotropin releasing hormone 1	Homo sapiens	54-84
7518861-4	1994	RESULTS: When G-CSF (10 micrograms/kg/d) was administered from the day after the cyclophosphamide, neutropenia developed on day 8 followed by an abrupt increase in the WBC count.	Cyclophosphamide	81-97	colony stimulating factor 3	Homo sapiens	14-19
7804526-6	1994	(b) In mice with advanced metastatic carcinoma previously treated with chemotherapy (cyclophosphamide), the survival was two to six times greater following administration of SSL-IL-2 as compared with IL-2 (p < 0.05; log-rank test).	Cyclophosphamide	85-101	interleukin 2	Mus musculus	178-182
8033053-12	1994	In patients treated with cyclophosphamide plus GM-CSF and cyclophosphamide alone, a median of 5.52 x 10(6) CD34+ cells/kg (range, 0.26-30.49) and 5.72 x 10(6) (range, 1.25-15.66) were collected, respectively.	Cyclophosphamide	25-41	CD34 molecule	Homo sapiens	107-111
8033053-12	1994	In patients treated with cyclophosphamide plus GM-CSF and cyclophosphamide alone, a median of 5.52 x 10(6) CD34+ cells/kg (range, 0.26-30.49) and 5.72 x 10(6) (range, 1.25-15.66) were collected, respectively.	Cyclophosphamide	58-74	CD34 molecule	Homo sapiens	107-111
8033092-5	1994	Interestingly, experiments with blood from patients undergoing chemotherapy show a gradual formation of R-MGMT in 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea and an induced MGMT deficiency in cyclophosphamide-treated patients.	Cyclophosphamide	193-209	O-6-methylguanine-DNA methyltransferase	Homo sapiens	106-110
8033054-9	1994	CONCLUSIONS: Intensive chemotherapy using cyclophosphamide, platinum compounds, epipodophyllotoxins, doxorubicin, and vincristine was effective in orbital involvement of retinoblastoma even with associated extra-CNS metastases.	Cyclophosphamide	42-58	RB transcriptional corepressor 1	Homo sapiens	170-184
8016086-10	1994	Mice homozygous for Nhe-1 developed diabetes after cyclophosphamide treatment, but heterozygotes were largely protected from disease.	Cyclophosphamide	51-67	solute carrier family 9 (sodium/hydrogen exchanger), member 1	Mus musculus	20-25
8167175-4	1994	Three of these four patients had been treated with combined modality therapy followed by maintenance COP chemotherapy, resulting in high cumulative doses of cyclophosphamide (range: 12-43 g).	Cyclophosphamide	157-173	caspase recruitment domain family member 16	Homo sapiens	101-104
8189597-3	1994	Phenotypic analysis of cells from spleen showed that cyclophosphamide pretreatment and postoperative vaccine, either singly or in combination, induced a significant increase of both CD44+ memory T cells and CD11b+ myeloid/macrophage cells.	Cyclophosphamide	53-69	CD44 molecule (Indian blood group)	Homo sapiens	182-186
8189597-3	1994	Phenotypic analysis of cells from spleen showed that cyclophosphamide pretreatment and postoperative vaccine, either singly or in combination, induced a significant increase of both CD44+ memory T cells and CD11b+ myeloid/macrophage cells.	Cyclophosphamide	53-69	integrin subunit alpha M	Homo sapiens	207-212
8010605-2	1994	The enhancement of antibody response was associated with increased induction of T helper cell activity and IL-2 production as evidenced in mice immunodepressed by aging or by cyclophosphamide treatment.	Cyclophosphamide	175-191	interleukin 2	Mus musculus	107-111
7908410-9	1994	CONCLUSIONS: There is a significant dose-response effect of adjuvant chemotherapy with cyclophosphamide, doxorubicin, and fluorouracil in patients with overexpression of c-erbB-2 but not in patients with no c-erbB-2 expression or minimal c-erbB-2 expression.	Cyclophosphamide	87-103	erb-b2 receptor tyrosine kinase 2	Homo sapiens	170-178
7908410-9	1994	CONCLUSIONS: There is a significant dose-response effect of adjuvant chemotherapy with cyclophosphamide, doxorubicin, and fluorouracil in patients with overexpression of c-erbB-2 but not in patients with no c-erbB-2 expression or minimal c-erbB-2 expression.	Cyclophosphamide	87-103	erb-b2 receptor tyrosine kinase 2	Homo sapiens	207-215
7908410-9	1994	CONCLUSIONS: There is a significant dose-response effect of adjuvant chemotherapy with cyclophosphamide, doxorubicin, and fluorouracil in patients with overexpression of c-erbB-2 but not in patients with no c-erbB-2 expression or minimal c-erbB-2 expression.	Cyclophosphamide	87-103	erb-b2 receptor tyrosine kinase 2	Homo sapiens	207-215
7513596-4	1994	rG-CSF at a dose of 100 micrograms/kg was administered subcutaneously twice a day for 5 consecutive d beginning 2 d after the CPA pretreatment.	Cyclophosphamide	126-129	colony stimulating factor 3	Rattus norvegicus	0-6
7513596-11	1994	In conclusion, pretreatment with rG-CSF increased sequestration of neutrophils into the lung and exacerbated the lung injury induced by intratracheal endotoxin in CPA-treated guinea pigs.	Cyclophosphamide	163-166	colony stimulating factor 3	Rattus norvegicus	33-39
8176939-3	1994	This antitumor effect was abolished when administration of CPA preceded that of IL-1.	Cyclophosphamide	59-62	interleukin 1 complex	Mus musculus	80-84
8160773-2	1994	We introduce cyclophosphamide-induced alopecia (CYP-IA) in C57BL-6 mice as a clinically relevant model for studying the biology of chemotherapy-induced alopecia and for developing anti-alopecia drugs.	Cyclophosphamide	13-29	peptidyl-prolyl isomerase G (cyclophilin G)	Mus musculus	48-51
7517260-3	1994	CY-VP-G products had a threefold higher median number of mononuclear cells collected, a fivefold higher median concentration of CD34 and LTC-IC and a threefold higher concentration of initial-CFC when compared with CY products.	Cyclophosphamide	0-2	CD34 molecule	Homo sapiens	128-132
7517260-6	1994	Analysis of the regression lines indicated that slopes of these regression lines were significantly different with a ratio of CD34 to initial CFC of 15:1 in the CY-VP-G products versus 5.2:1 with the CY products.	Cyclophosphamide	161-163	CD34 molecule	Homo sapiens	126-130
7517260-8	1994	Significant correlations of r = 0.9 (CY) and r = 0.53 (CY-VP-G) were observed when the initial CD34 concentration and the LTC-IC were compared.	Cyclophosphamide	37-39	CD34 molecule	Homo sapiens	95-99
7517260-8	1994	Significant correlations of r = 0.9 (CY) and r = 0.53 (CY-VP-G) were observed when the initial CD34 concentration and the LTC-IC were compared.	Cyclophosphamide	55-57	CD34 molecule	Homo sapiens	95-99
8019466-1	1994	VP-16 was administered in high doses (30-45 mg/kg) in combination with busulfan (BU) and cyclophosphamide (CY).	Cyclophosphamide	89-105	host cell factor C1	Homo sapiens	0-5
8168119-6	1994	In euthymic mice injected with IL-2 (5 x 10(4) Cetus units twice daily for 4-5 days), 5-FU augmented (up to 37-fold, days 1-9) and CY reduced (up to day 6) LAK activity, as compared with that in the IL-2 control.	Cyclophosphamide	131-133	interleukin 2	Mus musculus	31-35
8168119-7	1994	In bulk cultures containing IL-2 (1000 CU/ml, 3-4 days), both 5-FU and CY reduced LAK activity of euthymic mice splenocytes for up to 6 days after chemotherapy, which was followed on day 9 by full recovery.	Cyclophosphamide	71-73	interleukin 2	Mus musculus	28-32
8168119-7	1994	In bulk cultures containing IL-2 (1000 CU/ml, 3-4 days), both 5-FU and CY reduced LAK activity of euthymic mice splenocytes for up to 6 days after chemotherapy, which was followed on day 9 by full recovery.	Cyclophosphamide	71-73	alpha-kinase 1	Mus musculus	82-85
8168119-8	1994	In splenocytes of nude mice, 5-FU increased and CY diminished LAK activation in bulk cultures, starting 3 days after chemotherapy.	Cyclophosphamide	48-50	alpha-kinase 1	Mus musculus	62-65
8005733-2	1994	In reviewing a group of patients treated with cisplatin, doxorubicin, and cyclophosphamide, we were surprised to find that 90% of specimens tested by biochemical analysis were positive for estrogen receptor (ER), progesterone receptor (PR), or both.	Cyclophosphamide	74-90	progesterone receptor	Homo sapiens	213-234
8183257-0	1994	Aldose reductase-catalyzed reduction of acrolein: implications in cyclophosphamide toxicity.	Cyclophosphamide	66-82	aldo-keto reductase family 1 member B	Homo sapiens	0-16
8090696-10	1994	Disulfiram slightly potentiated the antitumour activity of cyclophosphamide against Sarcoma 180 or EL-4 leukaemia in vivo when administered simultaneously with cyclophosphamide.	Cyclophosphamide	59-75	epilepsy 4	Mus musculus	99-103
8057794-0	1994	31P NMR spectroscopic studies of the effects of cyclophosphamide on perfused RIF-1 tumor cells.	Cyclophosphamide	48-64	replication timing regulatory factor 1	Homo sapiens	77-82
8123484-0	1994	A phase I/II trial of recombinant human granulocyte-macrophage colony-stimulating factor in the intensification of cisplatin and cyclophosphamide chemotherapy for advanced ovarian cancer.	Cyclophosphamide	129-145	colony stimulating factor 2	Homo sapiens	40-88
8112893-3	1994	Sequential analyses of FcR, MAC-I and Class-II MHC antigen expressed by tumor-associated cells (TAC) showed that CY injection or CY/AIT induced marked increases in the proportions of all 3 parameters as compared with the relatively stable levels in progressing tumors.	Cyclophosphamide	113-115	Fc receptor	Mus musculus	23-26
7513783-3	1994	In the rats given G-CSF with CY, the neutrophil counts significantly increased over that of the CY-treated rats (p < 0.01).	Cyclophosphamide	29-31	colony stimulating factor 3	Rattus norvegicus	18-23
7513783-3	1994	In the rats given G-CSF with CY, the neutrophil counts significantly increased over that of the CY-treated rats (p < 0.01).	Cyclophosphamide	96-98	colony stimulating factor 3	Rattus norvegicus	18-23
8311500-2	1994	Eight course of CTF (cyclophosphamide, THP-adriamycin, 5-fluorouracil) and subsequent 4"-epi-adriamycin were performed for locally advanced breast cancer and multiple bone metastases, but the ulcerated breast cancer enlarged.	Cyclophosphamide	21-37	nuclear factor I C	Homo sapiens	16-19
8157285-4	1994	T cells from CY/OVA treated mice and cells from mice injected subcutaneously with OVA in CFA responded well to both OVA and the H2d restricted peptide epitope pOVA323-339 releasing GM-CSF.	Cyclophosphamide	13-15	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	181-187
8300198-5	1994	Mice with cyclophosphamide-induced leukopenia exhibiting increased susceptibility to P. aeruginosa were also endowed with resistance by the same dose of MCAF.	Cyclophosphamide	10-26	chemokine (C-C motif) ligand 2	Mus musculus	153-157
7976117-2	1994	Treatment with rEPO increased enzyme activities and cell number of erythroid series in bone marrow cells; it also increased organ weight and S-phase cells in the spleen, followed by an augmentation of the number of erythrocytes and a rise in the hemoglobin and hematocrit levels in peripheral blood with or without Cy treatment.	Cyclophosphamide	315-317	erythropoietin	Rattus norvegicus	15-19
8166473-1	1994	In the late sixties the first randomized placebo controlled study with cyclophosphamide demonstrated improved survival in patients with extensive small cell lung cancer (SCLC).	Cyclophosphamide	71-87	SCLC1	Homo sapiens	170-174
7985935-3	1994	Possibly, therapeutic results can be improved by means of a "synchronized" combination of plasmaphereses followed by pulse cyclophosphamide (Ctx).	Cyclophosphamide	123-139	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	141-144
7719383-0	1994	Antitumor effect of exogenous/endogenous TNF (EET) therapy with cyclophosphamide on C6 glioma in rat.	Cyclophosphamide	64-80	tumor necrosis factor	Rattus norvegicus	41-44
8135883-1	1994	31P nuclear magnetic resonance (NMR) spectroscopy was used in conjunction with cell perfusion techniques to monitor the intracellular chemistry of the cyclophosphamide (CP, CAS 6055-19-2) metabolites 4-hydroxy-cyclophosphamide (4-HO-CP) and aldophosphamide (AP) in U937 human histiocytic (CP-sensitive) and K562 human erythroleukemia (CP-resistant) cells.	Cyclophosphamide	151-167	BCAR1 scaffold protein, Cas family member	Homo sapiens	173-176
7946592-1	1994	The usefulness of CAF [cyclophosphamide (CPA)/doxorubicin (ADR)/5-fluorouracil (5-FU)] + medroxyprogesterone acetate (MPA) therapy for advanced/recurrent breast cancer was studied in a randomised trial at 56 institutions.	Cyclophosphamide	23-39	lysine acetyltransferase 2B	Homo sapiens	18-21
7923563-5	1994	CAI increased the cytotoxicity of cyclophosphamide toward FSaIIC tumor cells when animals were treated with single doses of both drugs.	Cyclophosphamide	34-50	protein disulfide isomerase associated 4	Mus musculus	0-3
7923563-6	1994	The effect of CAI on tumor cell killing by cyclophosphamide was greatest at high doses of the antitumor alkylating agent.	Cyclophosphamide	43-59	protein disulfide isomerase associated 4	Mus musculus	14-17
7923563-8	1994	Administration of CAI on days 4-18 did not alter the growth of the Lewis lung carcinoma but did result in an increase in the tumor-growth delay produced by treatment with CDDP, cyclophosphamide, melphalan, BCNU, and fractionated radiation.	Cyclophosphamide	177-193	protein disulfide isomerase associated 4	Mus musculus	18-21
7505211-4	1994	Comparative studies of CD34 cells showed that the percentage of CD34+ mononuclear cells was greatest in blood samples from patients following mobilization treatment with cyclophosphamide/etoposide/G-CSF averaging 2%.	Cyclophosphamide	170-186	CD34 molecule	Homo sapiens	64-68
7857714-0	1994	Aldehyde dehydrogenase involvement in a variant of the brown Norway rat acute myelocytic leukaemia (BNML) that acquired cyclophosphamide resistance in vivo.	Cyclophosphamide	120-136	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	0-22
8119654-1	1994	The author examined effects of BRMs such as Lentinan (LTN) and Krestin (PSK) on antitumor effector activities of spleen cells suppressed by cyclophosphamide (CY: 150 mg/kg, i.v.)	Cyclophosphamide	140-156	TAO kinase 2	Mus musculus	72-75
7590413-4	1994	Based on these and previous results showing that a low dose of cyclophosphamide readily abrogates the resistance to EAE and enhances the IL 2 production.	Cyclophosphamide	63-79	interleukin 2	Rattus norvegicus	137-141
7960506-5	1994	It was also demonstrated that this Cy-induced permanent or complete regression of L5178Y tumour is mediated by releasing memory antineoplasm effector cells from the inhibitory influence of suppressor Ly 1+ T cells.	Cyclophosphamide	35-37	CD5 antigen	Mus musculus	200-204
8054512-0	1994	Recombinant human interleukin-1 alpha: a potent bio-immunomodifier in vivo in immunosuppressed mice induced by cyclophosphamide, retroviral infection and surgical stress.	Cyclophosphamide	111-127	interleukin 1 alpha	Homo sapiens	18-37
8054512-1	1994	Recombinant human Interleukin-1 Alpha (rhu IL-1 alpha) was assessed for its efficacy in modifying the immunosuppression of mice compromised by Cyclophosphamide (CY), retrovirus infection or surgical stress.	Cyclophosphamide	143-159	interleukin 1 alpha	Homo sapiens	18-37
8054512-1	1994	Recombinant human Interleukin-1 Alpha (rhu IL-1 alpha) was assessed for its efficacy in modifying the immunosuppression of mice compromised by Cyclophosphamide (CY), retrovirus infection or surgical stress.	Cyclophosphamide	143-159	interleukin 1 alpha	Homo sapiens	43-53
8054512-1	1994	Recombinant human Interleukin-1 Alpha (rhu IL-1 alpha) was assessed for its efficacy in modifying the immunosuppression of mice compromised by Cyclophosphamide (CY), retrovirus infection or surgical stress.	Cyclophosphamide	161-163	interleukin 1 alpha	Homo sapiens	18-37
7960506-6	1994	Tumour regression induced by Cy administration may be associated with elimination of Ly 1+ suppressor T lymphocytes, since the therapeutic effect of Cy was reversed by passive transfer of Ly 1+ T cells obtained from donor mice bearing a 14-days L5178Y lymphoma; thus, these results suggest that the therapeutic effect of Cy in this model is through its capability to preferentially eliminate Ly 1+ suppressor T lymphocytes, thereby permitting memory antitumour immune cells to generate a strong secondary immune response against this immunogenic lymphoma.	Cyclophosphamide	29-31	CD5 antigen	Mus musculus	85-89
7960506-6	1994	Tumour regression induced by Cy administration may be associated with elimination of Ly 1+ suppressor T lymphocytes, since the therapeutic effect of Cy was reversed by passive transfer of Ly 1+ T cells obtained from donor mice bearing a 14-days L5178Y lymphoma; thus, these results suggest that the therapeutic effect of Cy in this model is through its capability to preferentially eliminate Ly 1+ suppressor T lymphocytes, thereby permitting memory antitumour immune cells to generate a strong secondary immune response against this immunogenic lymphoma.	Cyclophosphamide	149-151	CD5 antigen	Mus musculus	188-192
7960506-6	1994	Tumour regression induced by Cy administration may be associated with elimination of Ly 1+ suppressor T lymphocytes, since the therapeutic effect of Cy was reversed by passive transfer of Ly 1+ T cells obtained from donor mice bearing a 14-days L5178Y lymphoma; thus, these results suggest that the therapeutic effect of Cy in this model is through its capability to preferentially eliminate Ly 1+ suppressor T lymphocytes, thereby permitting memory antitumour immune cells to generate a strong secondary immune response against this immunogenic lymphoma.	Cyclophosphamide	149-151	CD5 antigen	Mus musculus	188-192
7960506-6	1994	Tumour regression induced by Cy administration may be associated with elimination of Ly 1+ suppressor T lymphocytes, since the therapeutic effect of Cy was reversed by passive transfer of Ly 1+ T cells obtained from donor mice bearing a 14-days L5178Y lymphoma; thus, these results suggest that the therapeutic effect of Cy in this model is through its capability to preferentially eliminate Ly 1+ suppressor T lymphocytes, thereby permitting memory antitumour immune cells to generate a strong secondary immune response against this immunogenic lymphoma.	Cyclophosphamide	149-151	CD5 antigen	Mus musculus	188-192
7960506-6	1994	Tumour regression induced by Cy administration may be associated with elimination of Ly 1+ suppressor T lymphocytes, since the therapeutic effect of Cy was reversed by passive transfer of Ly 1+ T cells obtained from donor mice bearing a 14-days L5178Y lymphoma; thus, these results suggest that the therapeutic effect of Cy in this model is through its capability to preferentially eliminate Ly 1+ suppressor T lymphocytes, thereby permitting memory antitumour immune cells to generate a strong secondary immune response against this immunogenic lymphoma.	Cyclophosphamide	149-151	CD5 antigen	Mus musculus	188-192
7505047-4	1994	The patient subsequently received radiotherapy and adjuvant chemotherapy consisting of cisplatin rotating monthly with vincristine and cyclophosphamide, with dramatic tumor regression and return of AFP to normal.	Cyclophosphamide	135-151	alpha fetoprotein	Homo sapiens	198-201
7873514-1	1994	Porous material of the CuX zeolite type has been synthesized and used as support for a classic antitumoral drug--cyclophosphamide (CP).	Cyclophosphamide	111-129	cut like homeobox 1	Homo sapiens	23-26
8203059-6	1994	In one of our cases of multicentric origin, the synergistic effect of pelvic irradiation and cyclophosphamide chemotherapy in a patient with a previous squamous cell carcinoma of the cervix, may be responsible for the pathogenesis of the ARP.	Cyclophosphamide	93-109	mesencephalic astrocyte derived neurotrophic factor	Homo sapiens	238-241
7816283-0	1994	Inverse relationship between serum cholinesterase activity and the administration of cyclophosphamide: an index of cyclophosphamide therapy.	Cyclophosphamide	85-101	butyrylcholinesterase	Homo sapiens	35-49
7816283-0	1994	Inverse relationship between serum cholinesterase activity and the administration of cyclophosphamide: an index of cyclophosphamide therapy.	Cyclophosphamide	115-131	butyrylcholinesterase	Homo sapiens	35-49
7535498-6	1994	Our data suggest that the number of MNCs and CD34+ cells obtained after combined mobilization with cyclophosphamide and G-CSF can be used as predictor of the number of granulomonocytic progenitors.	Cyclophosphamide	99-115	CD34 molecule	Homo sapiens	45-49
8405701-0	1993	Tolerance to IDDM induced by CD4 antibodies in nonobese diabetic mice is reversed by cyclophosphamide.	Cyclophosphamide	85-101	CD4 antigen	Mus musculus	29-32
8116835-1	1993	The compound 4-(diethylamino)benzaldehyde (DEAB) is a potent inhibitor of cytosolic (class 1) aldehyde dehydrogenase (ALDH) in vitro and can overcome cyclophosphamide resistance in murine leukemia cells characterized by their high content of ALDH.	Cyclophosphamide	150-166	aldehyde dehydrogenase family 3, subfamily A1	Mus musculus	118-122
8116835-1	1993	The compound 4-(diethylamino)benzaldehyde (DEAB) is a potent inhibitor of cytosolic (class 1) aldehyde dehydrogenase (ALDH) in vitro and can overcome cyclophosphamide resistance in murine leukemia cells characterized by their high content of ALDH.	Cyclophosphamide	150-166	aldehyde dehydrogenase family 3, subfamily A1	Mus musculus	242-246
8038494-13	1993	In a previous randomized trial, the French Co-operative Group on CLL showed a beneficial role for low-dose adriamycin given with cyclophosphamide, vincristine and prednisone (mini-CHOP) in patients with stage C disease.	Cyclophosphamide	129-145	DNA damage inducible transcript 3	Homo sapiens	180-184
8242617-1	1993	The present study identifies the specific human cytochrome P-450 (CYP) enzymes involved in hydroxylation leading to activation of the anticancer drug cyclophosphamide and its isomeric analogue, ifosphamide.	Cyclophosphamide	150-166	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	48-64
8242617-1	1993	The present study identifies the specific human cytochrome P-450 (CYP) enzymes involved in hydroxylation leading to activation of the anticancer drug cyclophosphamide and its isomeric analogue, ifosphamide.	Cyclophosphamide	150-166	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	66-69
8242617-5	1993	Expressed CYP2A6, -2B6, -2C8, -2C9, and -3A4 were catalytically competent in hydroxylating cyclophosphamide and ifosphamide.	Cyclophosphamide	91-107	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	10-16
8242617-8	1993	Furthermore, growth of cultured CYP2A6- and CYP2B6-expressing B-lymphoblastoid cells, but not of CYP-negative control cells, was inhibited by cyclophosphamide and ifosphamide as a consequence of prodrug activation to cytotoxic metabolites.	Cyclophosphamide	142-158	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	32-38
8242617-8	1993	Furthermore, growth of cultured CYP2A6- and CYP2B6-expressing B-lymphoblastoid cells, but not of CYP-negative control cells, was inhibited by cyclophosphamide and ifosphamide as a consequence of prodrug activation to cytotoxic metabolites.	Cyclophosphamide	142-158	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	44-50
8242617-8	1993	Furthermore, growth of cultured CYP2A6- and CYP2B6-expressing B-lymphoblastoid cells, but not of CYP-negative control cells, was inhibited by cyclophosphamide and ifosphamide as a consequence of prodrug activation to cytotoxic metabolites.	Cyclophosphamide	142-158	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	32-35
8242617-10	1993	Orphenadrine (a CYP2B6 inhibitor) and anti-CYP2B IgG inhibited microsomal cyclophosphamide hydroxylation to a greater extent than ifosphamide hydroxylation, consistent with the 8-fold higher activity of complementary DNA-expressed CYP2B6 with cyclophosphamide.	Cyclophosphamide	74-90	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	16-22
8242617-13	1993	Overall, the present study establishes that liver microsomal CYP2B and CYP3A preferentially catalyze cyclophosphamide and ifosphamide 4-hydroxylation, respectively, suggesting that liver P-450-inducing agents targeted at these enzymes might be used in cancer patients to enhance drug activation and therapeutic efficacy.	Cyclophosphamide	101-117	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	61-66
8242617-13	1993	Overall, the present study establishes that liver microsomal CYP2B and CYP3A preferentially catalyze cyclophosphamide and ifosphamide 4-hydroxylation, respectively, suggesting that liver P-450-inducing agents targeted at these enzymes might be used in cancer patients to enhance drug activation and therapeutic efficacy.	Cyclophosphamide	101-117	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	71-76
8285167-9	1993	After systemic chemotherapy of cyclophosphamide, adriamycin, vincristine, prednisone (CHOP) regimen, renal function improved and the tumor of stomach reduced, but his respiratory condition rapidly worsened, and he died about 1 month after chemotherapy.	Cyclophosphamide	31-47	DNA damage inducible transcript 3	Homo sapiens	86-90
8246030-0	1993	Phase I trial of recombinant human granulocyte-macrophage colony-stimulating factor derived from yeast in patients with breast cancer receiving cyclophosphamide, doxorubicin, and fluorouracil.	Cyclophosphamide	144-160	colony stimulating factor 2	Homo sapiens	35-83
7504035-2	1993	In mice rendered granulocytopenic with 200 mg/kg cyclophosphamide, daily coinjection of SCF (100 micrograms/kg) and G-CSF (10 micrograms/kg) for 5 days synergistically stimulated granulocyte recovery compared with either factor alone.	Cyclophosphamide	49-65	kit ligand	Mus musculus	88-91
7504035-2	1993	In mice rendered granulocytopenic with 200 mg/kg cyclophosphamide, daily coinjection of SCF (100 micrograms/kg) and G-CSF (10 micrograms/kg) for 5 days synergistically stimulated granulocyte recovery compared with either factor alone.	Cyclophosphamide	49-65	peripheral blood stem cell response to granulocyte colony stimulating factor 1	Mus musculus	116-121
8238533-6	1993	The effects of TNF on lung MPO and effluent O2- were prevented using cyclophosphamide intraperitoneally (100 mg/kg 5 days before, and 50 mg/kg 1 day before, treatment with TNF or control).	Cyclophosphamide	69-85	tumor necrosis factor	Cavia porcellus	15-18
8238533-6	1993	The effects of TNF on lung MPO and effluent O2- were prevented using cyclophosphamide intraperitoneally (100 mg/kg 5 days before, and 50 mg/kg 1 day before, treatment with TNF or control).	Cyclophosphamide	69-85	myeloperoxidase	Cavia porcellus	27-30
8238533-6	1993	The effects of TNF on lung MPO and effluent O2- were prevented using cyclophosphamide intraperitoneally (100 mg/kg 5 days before, and 50 mg/kg 1 day before, treatment with TNF or control).	Cyclophosphamide	69-85	tumor necrosis factor	Cavia porcellus	172-175
8280657-0	1993	Recombinant human interleukin-3 hastens trilineage hematopoietic recovery following high-dose (7 g/m2) cyclophosphamide cancer therapy.	Cyclophosphamide	103-119	interleukin 3	Homo sapiens	18-31
8280657-1	1993	BACKGROUND: Interleukin-3, a recombinant cytokine with multilineage stimulatory effect on hematopoietic cells, was administered to 22 previously untreated breast cancer patients following high-dose therapy with cyclophosphamide (7 g/m2).	Cyclophosphamide	211-227	interleukin 3	Homo sapiens	12-25
8280657-7	1993	CONCLUSIONS: Interleukin-3 represents a well-tolerated cytokine, clinically useful for accelerating trilineage hematopoietic recovery following severely myelotoxic treatments such as high-dose cyclophosphamide.	Cyclophosphamide	193-209	interleukin 3	Homo sapiens	13-26
8405701-2	1993	It has previously been established that transferred diabetes can be prevented by treatment with a nondepleting CD4 monoclonal antibody; however, we report herein that cyclophosphamide-induced diabetes also can be prevented using this antibody.	Cyclophosphamide	167-183	CD4 antigen	Mus musculus	111-114
20732286-3	1993	In this study, a human liver S-9 fraction was used as an enzyme source for the bioactivation of cyclophosphamide (CP) in vitro, to assess whether this model mimics more nearly the human situation.	Cyclophosphamide	96-112	ribosomal protein S9	Homo sapiens	29-32
8231237-0	1993	Cyclophosphamide treatment of an SJL murine B-cell lymphoma increases the proportion of suppressive CD8+ over tumor-stimulatory CD4+ T-lymphocytes.	Cyclophosphamide	0-16	CD8a molecule	Homo sapiens	100-103
8231237-0	1993	Cyclophosphamide treatment of an SJL murine B-cell lymphoma increases the proportion of suppressive CD8+ over tumor-stimulatory CD4+ T-lymphocytes.	Cyclophosphamide	0-16	CD4 antigen	Mus musculus	128-131
8231237-3	1993	Cyclophosphamide treatment of tumor-bearing mice (RCS/Cy) decreases in vitro tumor-stimulated CD4+ T-cell proliferation and, in turn, tumor growth, in part, through the suppressive action of CD8+ T-lymphocytes.	Cyclophosphamide	0-16	CD4 antigen	Mus musculus	94-97
8231237-3	1993	Cyclophosphamide treatment of tumor-bearing mice (RCS/Cy) decreases in vitro tumor-stimulated CD4+ T-cell proliferation and, in turn, tumor growth, in part, through the suppressive action of CD8+ T-lymphocytes.	Cyclophosphamide	0-16	CD8a molecule	Homo sapiens	191-194
8169326-7	1994	Depending on the time of exposure to cyclophosphamide, DTC either increased the percentage of CD4 thymocytes or decreased the percentage of CD8, which subsequently led increased CD4/CD8 coefficient.	Cyclophosphamide	37-53	CD4 antigen	Mus musculus	94-97
8169326-7	1994	Depending on the time of exposure to cyclophosphamide, DTC either increased the percentage of CD4 thymocytes or decreased the percentage of CD8, which subsequently led increased CD4/CD8 coefficient.	Cyclophosphamide	37-53	CD4 antigen	Mus musculus	178-181
8216347-0	1993	NADPH-dependent enzyme-catalyzed reduction of aldophosphamide, the pivotal metabolite of cyclophosphamide.	Cyclophosphamide	89-105	2,4-dienoyl-CoA reductase 1	Homo sapiens	0-5
8103811-5	1993	Among the 19 patients harvested after chemotherapy plus GM-CSF, more progenitor cells were obtained in the cyclophosphamide group than in the MIV group.	Cyclophosphamide	107-123	colony stimulating factor 2	Homo sapiens	56-62
8340944-4	1993	PURPOSE: The purpose of this study was to determine the maximum tolerated dose and the toxic effects of cyclophosphamide administered every 2 weeks with GM-CSF support.	Cyclophosphamide	104-120	colony stimulating factor 2	Homo sapiens	153-159
8340944-17	1993	Our results suggest that, with GM-CSF support, high cumulative doses of cyclophosphamide can be given to achieve optimal dose intensity, with reproducible blood cell count recovery and without the need for autologous bone marrow transplantation.	Cyclophosphamide	72-88	colony stimulating factor 2	Homo sapiens	31-37
8514386-6	1993	Significantly larger amounts of IL-4 protein and mRNA were produced in vitro by cells from mice given PT at the time of immunization than by cells from mice given antigen alone, PT alone, or the combination of antigen with cyclophosphamide.	Cyclophosphamide	223-239	interleukin 4	Mus musculus	32-36
7690534-3	1993	To induce endogenous LAK, intra-arterial immunochemotherapy with cyclophosphamide (CPM) and OK-432 was performed.	Cyclophosphamide	65-81	ADP ribosylation factor like GTPase 4C	Homo sapiens	21-24
8365149-5	1993	The newly developed method was as follows; cyclophosphamide 200 mg/kg intraperitoneal administration 3 days before the 1st sensitization of the AP2 test (cyclophosphamide, adjuvant and 24-h occlusive patch 2x test: CAP2 test).	Cyclophosphamide	43-59	adenylyl cyclase-associated protein 2	Cavia porcellus	215-219
8406572-0	1993	Interleukin-5 is necessary for eosinophilia induced by cyclophosphamide in immunized mice.	Cyclophosphamide	55-71	interleukin 5	Mus musculus	0-13
8406572-10	1993	These experiments indicate that IL-5 is required for the eosinophilia induced by CY in immunized mice.	Cyclophosphamide	81-83	interleukin 5	Mus musculus	32-36
8401354-1	1993	I. Optimal synergism between cyclophosphamide and total body irradiation for eradication of murine B cell leukemia (BCL1).	Cyclophosphamide	29-45	cyclin D1	Mus musculus	116-120
8229153-2	1993	The rationale for the addition of ifosfamide and VP-16 to the four drugs of the standard chemotherapy of this tumor was that this drug combination was previously very effective in the treatment of metastases from Ewing"s sarcoma even in patients who did not respond to cyclophosphamide.	Cyclophosphamide	269-285	host cell factor C1	Homo sapiens	49-54
8399071-0	1993	Immunomodulation of interleukin-2 by cyclophosphamide: a phase IB trial.	Cyclophosphamide	37-53	interleukin 2	Homo sapiens	20-33
8399071-1	1993	The objective of this phase IB trial was to determine if cyclophosphamide (CY) could enhance the immune effects of interleukin-2 (IL-2), and if it could, was there an optimal immunomodulatory dosage.	Cyclophosphamide	57-73	interleukin 2	Homo sapiens	115-128
8399071-1	1993	The objective of this phase IB trial was to determine if cyclophosphamide (CY) could enhance the immune effects of interleukin-2 (IL-2), and if it could, was there an optimal immunomodulatory dosage.	Cyclophosphamide	57-73	interleukin 2	Homo sapiens	130-134
8399071-1	1993	The objective of this phase IB trial was to determine if cyclophosphamide (CY) could enhance the immune effects of interleukin-2 (IL-2), and if it could, was there an optimal immunomodulatory dosage.	Cyclophosphamide	75-77	interleukin 2	Homo sapiens	115-128
8399071-1	1993	The objective of this phase IB trial was to determine if cyclophosphamide (CY) could enhance the immune effects of interleukin-2 (IL-2), and if it could, was there an optimal immunomodulatory dosage.	Cyclophosphamide	75-77	interleukin 2	Homo sapiens	130-134
8399071-5	1993	The group of patients that received low-dosage CY (300 mg/m2) and IL-2 produced the highest and most sustained levels of LAK and NK activity (p < 0.05) when compared with the cohorts receiving IL-2 alone or to those receiving the higher dosages of CY.	Cyclophosphamide	251-253	interleukin 2	Homo sapiens	66-70
8399071-7	1993	Although low-dosage CY does increase the LAK activity seen with IL-2, only randomized clinical trials can determine if this enhancement will improve tumor responses.	Cyclophosphamide	20-22	interleukin 2	Homo sapiens	64-68
8098666-11	1993	Consideration of our results together with earlier findings led to the conclusion that CD4+ T cells are primarily responsible for insulitis and that CD8+ T cells migrate into islets and are differentiated into mature killer cells against beta-cells with the aid of CD4+ T cells in both spontaneous and cyclophosphamide-induced diabetes.	Cyclophosphamide	302-318	CD4 antigen	Mus musculus	265-268
8495410-0	1993	Cyclophosphamide modulates rat hepatic cytochrome P450 2C11 and steroid 5 alpha-reductase activity and messenger RNA levels through the combined action of acrolein and phosphoramide mustard.	Cyclophosphamide	0-16	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	39-59
8495410-1	1993	Cyclophosphamide treatment of adult male rats leads to sustained decreases in several liver microsomal cytochrome P450 (CYP) activities, including CYP 2C11-catalyzed cyclophosphamide activation, via a process that is associated with a feminization of the overall pattern of liver enzyme expression (G. A. LeBlanc and D. J. Waxman, Cancer Res., 50:5720-5726, 1990).	Cyclophosphamide	0-16	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	103-118
8495410-1	1993	Cyclophosphamide treatment of adult male rats leads to sustained decreases in several liver microsomal cytochrome P450 (CYP) activities, including CYP 2C11-catalyzed cyclophosphamide activation, via a process that is associated with a feminization of the overall pattern of liver enzyme expression (G. A. LeBlanc and D. J. Waxman, Cancer Res., 50:5720-5726, 1990).	Cyclophosphamide	0-16	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	120-123
8495410-1	1993	Cyclophosphamide treatment of adult male rats leads to sustained decreases in several liver microsomal cytochrome P450 (CYP) activities, including CYP 2C11-catalyzed cyclophosphamide activation, via a process that is associated with a feminization of the overall pattern of liver enzyme expression (G. A. LeBlanc and D. J. Waxman, Cancer Res., 50:5720-5726, 1990).	Cyclophosphamide	0-16	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	147-155
8495410-1	1993	Cyclophosphamide treatment of adult male rats leads to sustained decreases in several liver microsomal cytochrome P450 (CYP) activities, including CYP 2C11-catalyzed cyclophosphamide activation, via a process that is associated with a feminization of the overall pattern of liver enzyme expression (G. A. LeBlanc and D. J. Waxman, Cancer Res., 50:5720-5726, 1990).	Cyclophosphamide	166-182	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	103-118
8495410-1	1993	Cyclophosphamide treatment of adult male rats leads to sustained decreases in several liver microsomal cytochrome P450 (CYP) activities, including CYP 2C11-catalyzed cyclophosphamide activation, via a process that is associated with a feminization of the overall pattern of liver enzyme expression (G. A. LeBlanc and D. J. Waxman, Cancer Res., 50:5720-5726, 1990).	Cyclophosphamide	166-182	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	120-123
8495410-1	1993	Cyclophosphamide treatment of adult male rats leads to sustained decreases in several liver microsomal cytochrome P450 (CYP) activities, including CYP 2C11-catalyzed cyclophosphamide activation, via a process that is associated with a feminization of the overall pattern of liver enzyme expression (G. A. LeBlanc and D. J. Waxman, Cancer Res., 50:5720-5726, 1990).	Cyclophosphamide	166-182	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	147-155
8495410-2	1993	The present study compares the effects of cyclophosphamide and its isomeric analogue ifosphamide on the gender-dependent expression of hepatic CYP 2C11 and steroid 5 alpha-reductase in adult male rats and also examines the role of the cyclophosphamide metabolites acrolein and phosphoramide mustard in feminizing the expression of these liver enzymes.	Cyclophosphamide	42-58	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	143-151
8495410-3	1993	Ifosphamide (a) suppressed the male-specific CYP 2C11 mRNA and CYP 2C11-catalyzed liver microsomal testosterone 2 alpha-hydroxylation and cyclophosphamide and ifosphamide 4-hydroxylation and (b) elevated the female-dominant liver enzyme steroid 5 alpha-reductase and its mRNA 7-9 days after drug treatment, both occurring in a manner similar to that of cyclophosphamide, but requiring a 50% higher dose (180 mg/kg, single i.p.	Cyclophosphamide	138-154	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	45-53
8495410-3	1993	Ifosphamide (a) suppressed the male-specific CYP 2C11 mRNA and CYP 2C11-catalyzed liver microsomal testosterone 2 alpha-hydroxylation and cyclophosphamide and ifosphamide 4-hydroxylation and (b) elevated the female-dominant liver enzyme steroid 5 alpha-reductase and its mRNA 7-9 days after drug treatment, both occurring in a manner similar to that of cyclophosphamide, but requiring a 50% higher dose (180 mg/kg, single i.p.	Cyclophosphamide	138-154	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	63-71
8495410-3	1993	Ifosphamide (a) suppressed the male-specific CYP 2C11 mRNA and CYP 2C11-catalyzed liver microsomal testosterone 2 alpha-hydroxylation and cyclophosphamide and ifosphamide 4-hydroxylation and (b) elevated the female-dominant liver enzyme steroid 5 alpha-reductase and its mRNA 7-9 days after drug treatment, both occurring in a manner similar to that of cyclophosphamide, but requiring a 50% higher dose (180 mg/kg, single i.p.	Cyclophosphamide	353-369	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	45-53
8495410-3	1993	Ifosphamide (a) suppressed the male-specific CYP 2C11 mRNA and CYP 2C11-catalyzed liver microsomal testosterone 2 alpha-hydroxylation and cyclophosphamide and ifosphamide 4-hydroxylation and (b) elevated the female-dominant liver enzyme steroid 5 alpha-reductase and its mRNA 7-9 days after drug treatment, both occurring in a manner similar to that of cyclophosphamide, but requiring a 50% higher dose (180 mg/kg, single i.p.	Cyclophosphamide	353-369	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	63-71
8495410-8	1993	These studies establish that ifosphamide is less potent than cyclophosphamide in modulating the pattern of cytochrome P450 and steroid 5 alpha-reductase expression and that phosphoramide mustard is responsible for the modulation of liver enzyme expression by cyclophosphamide, with acrolein potentiating the modulating activity of the mustard.	Cyclophosphamide	61-77	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	107-122
7683585-0	1993	Therapeutic effect of granulocyte colony-stimulating factor and cephem antibiotics against experimental infections in neutropenic mice induced by cyclophosphamide.	Cyclophosphamide	146-162	colony stimulating factor 3 (granulocyte)	Mus musculus	22-59
8369658-11	1993	Our successful treatment is radiation therapy combined with six courses of CHOP chemotherapy (cyclophosphamide, adriamycin, vincristine, prednisolone).	Cyclophosphamide	94-110	DNA damage inducible transcript 3	Homo sapiens	75-79
8398836-5	1993	Actinomycin D and cyclophosphamide also inhibited GM-CSF stimulated protein biosynthesis.	Cyclophosphamide	18-34	colony stimulating factor 2	Homo sapiens	50-56
7684770-16	1993	PBPs, harvested during the G-CSF-augmented rebound from CPA-induced cytopenia, produce rapid hematologic recovery in patients undergoing high-dose chemotherapy (HDC).	Cyclophosphamide	56-59	colony stimulating factor 3	Homo sapiens	27-32
8501906-9	1993	FAC regimen (5-fluorouracil, Adriamycin, and cyclophosphamide) was given to 6 patients (40%).	Cyclophosphamide	45-61	FA complementation group C	Homo sapiens	0-3
7680764-1	1993	BACKGROUND: CHOP is a first-generation, combination-chemotherapy regimen consisting of cyclophosphamide, doxorubicin, vincristine, and prednisone that has cured approximately 30 percent of patients with advanced stages of intermediate-grade or high-grade non-Hodgkin"s lymphoma in national cooperative-group trials.	Cyclophosphamide	87-103	DNA damage inducible transcript 3	Homo sapiens	12-16
8482321-3	1993	Significant clastogenic effects were observed after an 18 h exposure to aflatoxin B1 and cyclophosphamide in CYP2B1 expressing cells, to benzo[a]pyrene in CYP1A1 and CYP1A2 expressing cells, to 7,12-dimethylbenz[a]anthracene and dimethylnitrosamine in cells, expressing CYP1A2 with or without acetyltransferase, and to cyclophosphamide in cells expressing both CYP1A2 and acetyltransferase.	Cyclophosphamide	89-105	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	109-115
8475071-1	1993	EMT-6 murine mammary tumor sublines highly resistant to cyclophosphamide, cis-diamminedichloro-platinum(II), or N,N",N"-triethylenethiophosphoramide were generated in vivo by sequential treatment of tumor-bearing mice with the respective drugs.	Cyclophosphamide	56-72	IL2 inducible T cell kinase	Mus musculus	0-3
8469201-6	1993	TREATMENT AND OUTCOME: After initial response to CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine, prednisolone), she relapsed and died with central nervous system involvement eight months after the initial diagnosis.	Cyclophosphamide	68-84	DNA damage inducible transcript 3	Homo sapiens	49-53
8400772-0	1993	[Enhancing effect of jian pi jin dan on immune functions of normal and cyclophosphamide induced immunosuppressed mice].	Cyclophosphamide	71-87	NBL1, DAN family BMP antagonist	Mus musculus	33-36
8400772-1	1993	UNLABELLED: By means of normal and cyclophosphamide (CY) injected NIH mice, the effect of Jian Pi Jin Dan on immuno-modulation was studied which could treat the "Gan" disease effectively in TCM.	Cyclophosphamide	35-51	NBL1, DAN family BMP antagonist	Mus musculus	102-105
8400772-1	1993	UNLABELLED: By means of normal and cyclophosphamide (CY) injected NIH mice, the effect of Jian Pi Jin Dan on immuno-modulation was studied which could treat the "Gan" disease effectively in TCM.	Cyclophosphamide	53-55	NBL1, DAN family BMP antagonist	Mus musculus	102-105
8349185-0	1993	Reduction of plasma fibrinolytic activity following high-dose cyclophosphamide is neutralized in vivo by GM-CSF administration.	Cyclophosphamide	62-78	colony stimulating factor 2	Homo sapiens	105-111
8426200-8	1993	CONCLUSION: Pelvic XRT and cumulative cyclophosphamide dosages greater than 9.5 g/m2 are associated with a high risk of permanent sterility in lymphoma patients treated with the CHOP-Bleo regimen.	Cyclophosphamide	38-54	DNA damage inducible transcript 3	Homo sapiens	178-182
8428003-4	1993	Administration of IL-11 to mice pretreated with cyclophosphamide decreased the time required to regain normal levels of neutrophil and platelet counts in peripheral blood.	Cyclophosphamide	48-64	interleukin 11	Mus musculus	18-23
8425189-0	1993	Combined interleukin 1 beta/interleukin 2 treatment in mice: synergistic myelostimulatory activity and protection against cyclophosphamide-induced myelosuppression.	Cyclophosphamide	122-138	interleukin 1 beta	Mus musculus	9-41
8425189-6	1993	Combined IL-1 beta/IL-2 treatment dampened the decrease and accelerated the recovery of myeloid cells after cyclophosphamide injection, whereas the single cytokine regimen was not effective.	Cyclophosphamide	108-124	interleukin 1 beta	Mus musculus	9-18
8425189-6	1993	Combined IL-1 beta/IL-2 treatment dampened the decrease and accelerated the recovery of myeloid cells after cyclophosphamide injection, whereas the single cytokine regimen was not effective.	Cyclophosphamide	108-124	interleukin 2	Mus musculus	19-23
8507933-2	1993	The IL-6 and CRP levels, which were extremely high before treatment, declined rapidly with corticosteroid and cyclophosphamide.	Cyclophosphamide	110-126	interleukin 6	Homo sapiens	4-8
8507933-2	1993	The IL-6 and CRP levels, which were extremely high before treatment, declined rapidly with corticosteroid and cyclophosphamide.	Cyclophosphamide	110-126	C-reactive protein	Homo sapiens	13-16
8509824-3	1993	Survival of chemo-adoptive immunotherapy treated groups given intraperitoneal cyclophosphamide and intracranial lymphokine activated killer cells and recombinant Interleukin-2 was significantly extended when compared to sham treated control groups, to groups given chemotherapy with intraperitoneal cyclophosphamide, and to groups treated by local adoptive immunotherapy with intracranial lymphokine activated killer cells and Interleukin-2.	Cyclophosphamide	299-315	interleukin 2	Rattus norvegicus	162-175
8424816-1	1993	Several murine aldehyde dehydrogenases, most notably AHD-2, are known to catalyze the detoxification of cyclophosphamide, mafosfamide, and other oxazaphosphorines.	Cyclophosphamide	104-120	aldehyde dehydrogenase family 1, subfamily A1	Mus musculus	53-58
7678881-2	1993	Whereas an immunotoxin constructed from the murine anti-CD19(B43) monoclonal antibody and the plant toxin pokeweed antiviral protein (B43-PAP) has a potent in vitro anti-leukemic effect against clonogenic RS4;11 cells, its activity is further potentiated by the active cyclophosphamide congener mafosfamid.	Cyclophosphamide	269-285	CD19 molecule	Homo sapiens	56-60
8430432-0	1993	The toxicological effect of cyclophosphamide on acetylcholinesterase activity.	Cyclophosphamide	28-44	acetylcholinesterase (Cartwright blood group)	Gallus gallus	48-68
8430432-1	1993	Cyclophosphamide (CP; 2.5-10.0 mM) reversibly inhibits acetylcholinesterase (AChE) activity of chicken brain (58-84%) in a concentration-dependent manner, the IC50 (the concentration causing 50% inhibition) being about 2.0 mM.	Cyclophosphamide	0-16	acetylcholinesterase (Cartwright blood group)	Gallus gallus	55-75
8430432-1	1993	Cyclophosphamide (CP; 2.5-10.0 mM) reversibly inhibits acetylcholinesterase (AChE) activity of chicken brain (58-84%) in a concentration-dependent manner, the IC50 (the concentration causing 50% inhibition) being about 2.0 mM.	Cyclophosphamide	0-16	acetylcholinesterase (Cartwright blood group)	Gallus gallus	77-81
8431519-3	1993	The RNA synthesis-inhibiting drugs daunorubicin, cyclophosphamide, ifosfamide, and cis-diamine-dichloroplatinum produced a dose-dependent decrease of the production of erythropoietin.	Cyclophosphamide	49-65	erythropoietin	Homo sapiens	168-182
7685182-0	1993	Restoration of the acute phase response after infection in cyclophosphamide-treated mice by granulocyte colony-stimulating factor.	Cyclophosphamide	59-75	colony stimulating factor 3 (granulocyte)	Mus musculus	92-129
7685182-4	1993	The capacity to produce interleukin 1-beta and TNF-alpha of peritoneal macrophages and also that to produce IL-6 of spleen cells were significantly enhanced by the in vivo administration of rhG-CSF in CY-treated mice.	Cyclophosphamide	201-203	interleukin 1 beta	Mus musculus	24-42
7685182-4	1993	The capacity to produce interleukin 1-beta and TNF-alpha of peritoneal macrophages and also that to produce IL-6 of spleen cells were significantly enhanced by the in vivo administration of rhG-CSF in CY-treated mice.	Cyclophosphamide	201-203	tumor necrosis factor	Mus musculus	47-56
7685182-4	1993	The capacity to produce interleukin 1-beta and TNF-alpha of peritoneal macrophages and also that to produce IL-6 of spleen cells were significantly enhanced by the in vivo administration of rhG-CSF in CY-treated mice.	Cyclophosphamide	201-203	interleukin 6	Mus musculus	108-112
7685182-1	1993	The therapeutic effect of granulocyte colony-stimulating factor (G-CSF) against intramuscular infection with Pseudomonas aeruginosa in cyclophosphamide (CY)-treated mice was analyzed by measuring plasma levels of amyloid P-component (APC) and proinflammatory cytokine levels.	Cyclophosphamide	135-151	colony stimulating factor 3 (granulocyte)	Mus musculus	26-63
7685182-1	1993	The therapeutic effect of granulocyte colony-stimulating factor (G-CSF) against intramuscular infection with Pseudomonas aeruginosa in cyclophosphamide (CY)-treated mice was analyzed by measuring plasma levels of amyloid P-component (APC) and proinflammatory cytokine levels.	Cyclophosphamide	135-151	colony stimulating factor 3 (granulocyte)	Mus musculus	65-70
7685182-1	1993	The therapeutic effect of granulocyte colony-stimulating factor (G-CSF) against intramuscular infection with Pseudomonas aeruginosa in cyclophosphamide (CY)-treated mice was analyzed by measuring plasma levels of amyloid P-component (APC) and proinflammatory cytokine levels.	Cyclophosphamide	153-155	colony stimulating factor 3 (granulocyte)	Mus musculus	26-63
7685182-1	1993	The therapeutic effect of granulocyte colony-stimulating factor (G-CSF) against intramuscular infection with Pseudomonas aeruginosa in cyclophosphamide (CY)-treated mice was analyzed by measuring plasma levels of amyloid P-component (APC) and proinflammatory cytokine levels.	Cyclophosphamide	153-155	colony stimulating factor 3 (granulocyte)	Mus musculus	65-70
7685182-2	1993	CY (100 mg/kg) treatment of mice significantly suppressed plasma concentrations of APC and tumor-necrosis factor-alpha (TNF-alpha) following infection with P. aeruginosa, in associated with enhanced susceptibility of the treated mice to this bacterium.	Cyclophosphamide	0-2	tumor necrosis factor	Mus musculus	91-118
7685182-2	1993	CY (100 mg/kg) treatment of mice significantly suppressed plasma concentrations of APC and tumor-necrosis factor-alpha (TNF-alpha) following infection with P. aeruginosa, in associated with enhanced susceptibility of the treated mice to this bacterium.	Cyclophosphamide	0-2	tumor necrosis factor	Mus musculus	120-129
7685182-3	1993	A 4-day treatment of CY-treated mice with recombinant human G-CSF (rhG-CSF) increased resistance of CY-treated mice, together with the marked restoration of APC and TNF-alpha productions.	Cyclophosphamide	21-23	colony stimulating factor 3	Homo sapiens	60-65
7685182-3	1993	A 4-day treatment of CY-treated mice with recombinant human G-CSF (rhG-CSF) increased resistance of CY-treated mice, together with the marked restoration of APC and TNF-alpha productions.	Cyclophosphamide	21-23	tumor necrosis factor	Mus musculus	165-174
7685182-3	1993	A 4-day treatment of CY-treated mice with recombinant human G-CSF (rhG-CSF) increased resistance of CY-treated mice, together with the marked restoration of APC and TNF-alpha productions.	Cyclophosphamide	100-102	colony stimulating factor 3	Homo sapiens	60-65
8439986-2	1993	However, most BALB/c mice bearing a late-stage RPC-5 tumor were cured by cyclophosphamide therapy (100 mg/kg) in conjunction with adoptive immunotherapy using tumor-infiltrated spleen cells (TISpC) that had been cultured with inactivated RPC-5 tumor cells plus polyethylene glycol 6000, even though this protocol was not effective for the therapy of mice bearing a barely palpable, early-stage RPC-5 tumor.	Cyclophosphamide	73-89	polymerase (RNA) III (DNA directed) polypeptide E	Mus musculus	47-52
8251651-3	1993	mdr1-RNA was never detected in 29 primary breast tumors including 5 samples from patients previously treated by 6 courses of 5-fluorouracil, epirubicin, cyclophosphamide (FEC).	Cyclophosphamide	153-169	ATP binding cassette subfamily B member 1	Homo sapiens	0-4
8269595-8	1993	The severely reduced activity of GST in the L1210/BCNU strain was markedly increased when these cells were made resistant to CPA; the GSSG-R activity, however, remained low, suggesting an irreversible injury of this enzyme by BCNU.	Cyclophosphamide	125-128	hematopoietic prostaglandin D synthase	Mus musculus	33-36
8441736-0	1993	Inhibition of the vitamin B12 binding capacity of proteins by the hydrolysis product of cyclophosphamide.	Cyclophosphamide	88-104	NADH:ubiquinone oxidoreductase subunit B3	Homo sapiens	26-29
7903668-16	1993	MDR1-related resistance appeared to play a role in the failure of SCLC-6 chemotherapy; frequent recurrences after treatment with cisplatin and Cpa, two drugs that are not recognized by the P-glycoprotein, indicated that other modes of resistance were simultaneously active.	Cyclophosphamide	143-146	ATP binding cassette subfamily B member 1	Homo sapiens	0-4
7903668-16	1993	MDR1-related resistance appeared to play a role in the failure of SCLC-6 chemotherapy; frequent recurrences after treatment with cisplatin and Cpa, two drugs that are not recognized by the P-glycoprotein, indicated that other modes of resistance were simultaneously active.	Cyclophosphamide	143-146	ATP binding cassette subfamily B member 1	Homo sapiens	189-203
8507545-1	1993	In patients with Stage II or III breast cancer and in patients with liver metastases from breast cancer, we examined cellular interaction in the cytotoxicity against autologous tumor cells by interleukin-2(IL-2)-cultured lymphocytes (CL) and fresh peripheral blood lymphocytes (FPBL) treated with immunochemotherapy including OK-432 and cyclophosphamide.	Cyclophosphamide	337-353	interleukin 2	Homo sapiens	206-210
8441736-1	1993	The inhibitory effect of cyclophosphamide hydrolysis product (CPHP) on vitamin B12 binding ability to proteins has been established.	Cyclophosphamide	25-41	NADH:ubiquinone oxidoreductase subunit B3	Homo sapiens	79-82
1423178-2	1992	BACKGROUND: Between August 1984 and November 1989, the Hoosier Oncology Group conducted a Phase III study comparing cyclophosphamide (CTX) with cyclophosphamide, doxorubicin, and methotrexate (CAM) in patients with hormone-refractory metastatic prostatic cancer to determine whether the addition of doxorubicin and methotrexate to the cyclophosphamide regimen conferred any survival advantage.	Cyclophosphamide	116-132	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	134-137
7505076-6	1993	In both cases, however, mobilization of haematopoietic progenitor cells by G-CSF following cyclophosphamide (50 and 70 mg/kg body weight, respectively) led to much higher CFU-GM peak values (5324 in patient 3 and 2245 in patient 4), thus allowing an adequate harvest of mononuclear cells and CD 34+ cell numbers to achieve, in all probability, the prompt and complete reconstitution of haematopoiesis in case of transplantation.	Cyclophosphamide	91-107	colony stimulating factor 3	Homo sapiens	75-80
1419639-0	1992	Glutathione S-transferase activity and isoenzyme composition in benign ovarian tumours, untreated malignant ovarian tumours, and malignant ovarian tumours after platinum/cyclophosphamide chemotherapy.	Cyclophosphamide	170-186	glutathione S-transferase kappa 1	Homo sapiens	0-25
1438311-7	1992	Normally compatible A strain skin grafts, but not Skn-compatible B6 skin grafts, were rejected by cyclophosphamide-treated (B6 x A)F1 recipients of (B6 x A)/B6 spleen cells from Skn-primed chimera donors.	Cyclophosphamide	98-114	hedgehog acyltransferase	Mus musculus	178-181
1383819-8	1992	The median normalized dose intensity for both cyclophosphamide and doxorubicin was found to be greater in the patients treated with CHOP than in those treated with m-BACOD.	Cyclophosphamide	46-62	DNA damage inducible transcript 3	Homo sapiens	132-136
1419639-4	1992	GST isoenzyme patterns were identical in benign tumours and malignant tumours before and after platinum/cyclophosphamide chemotherapy, while GST pi was the predominant transferase.	Cyclophosphamide	104-120	glutathione S-transferase kappa 1	Homo sapiens	0-3
1419639-5	1992	Mean GST activity and GST pi amount were decreased (P < 0.05) in malignant ovarian tumours after platinum/cyclophosphamide chemotherapy compared to untreated ovarian malignant tumours.	Cyclophosphamide	109-125	glutathione S-transferase kappa 1	Homo sapiens	22-25
1290956-7	1992	While IL-1 and TNF-alpha stimulate both of these enzymes, other mechanisms are probably also operative for other forms of chemotherapy, i.e. IL-1 and TNF-alpha were shown to protect hematopoietic progenitors from phenylketophosphamide, a cyclophosphamide derivative that is not metabolized by the enzyme aldehyde dehydrogenase.	Cyclophosphamide	238-254	interleukin 1 complex	Mus musculus	6-10
1290956-7	1992	While IL-1 and TNF-alpha stimulate both of these enzymes, other mechanisms are probably also operative for other forms of chemotherapy, i.e. IL-1 and TNF-alpha were shown to protect hematopoietic progenitors from phenylketophosphamide, a cyclophosphamide derivative that is not metabolized by the enzyme aldehyde dehydrogenase.	Cyclophosphamide	238-254	tumor necrosis factor	Mus musculus	15-24
1290956-7	1992	While IL-1 and TNF-alpha stimulate both of these enzymes, other mechanisms are probably also operative for other forms of chemotherapy, i.e. IL-1 and TNF-alpha were shown to protect hematopoietic progenitors from phenylketophosphamide, a cyclophosphamide derivative that is not metabolized by the enzyme aldehyde dehydrogenase.	Cyclophosphamide	238-254	interleukin 1 complex	Mus musculus	141-145
1290956-7	1992	While IL-1 and TNF-alpha stimulate both of these enzymes, other mechanisms are probably also operative for other forms of chemotherapy, i.e. IL-1 and TNF-alpha were shown to protect hematopoietic progenitors from phenylketophosphamide, a cyclophosphamide derivative that is not metabolized by the enzyme aldehyde dehydrogenase.	Cyclophosphamide	238-254	tumor necrosis factor	Mus musculus	150-159
1521924-4	1992	The effects of the anti-rheumatic drugs indometacin, dexamethasone, cyclophosphamide and cyclosporin A (CsA) on IL-6 levels during FAA were determined.	Cyclophosphamide	68-84	interleukin 6	Rattus norvegicus	112-116
1380297-2	1992	In CY- or CBDCA-pretreated rats, significantly higher peripheral white blood cell (WBC) count was observed in animals treated with G-CSF and IL-1 alpha, while the platelet (PLT) count was elevated by IL-6 treatment.	Cyclophosphamide	3-5	colony stimulating factor 3	Rattus norvegicus	131-136
1380297-2	1992	In CY- or CBDCA-pretreated rats, significantly higher peripheral white blood cell (WBC) count was observed in animals treated with G-CSF and IL-1 alpha, while the platelet (PLT) count was elevated by IL-6 treatment.	Cyclophosphamide	3-5	interleukin 1 alpha	Rattus norvegicus	141-151
1380297-2	1992	In CY- or CBDCA-pretreated rats, significantly higher peripheral white blood cell (WBC) count was observed in animals treated with G-CSF and IL-1 alpha, while the platelet (PLT) count was elevated by IL-6 treatment.	Cyclophosphamide	3-5	interleukin 6	Rattus norvegicus	200-204
1326212-3	1992	Significant improvement has been noted in patients with advanced ovarian cancer following the administration of modified PAC 1 (adriamycin, cytoxan and cyclophosphamide) immediately following primary debulking surgery (within 24 hours) and repeated for 11 monthly cycles.	Cyclophosphamide	140-147	dual specificity phosphatase 2	Homo sapiens	121-126
1326212-3	1992	Significant improvement has been noted in patients with advanced ovarian cancer following the administration of modified PAC 1 (adriamycin, cytoxan and cyclophosphamide) immediately following primary debulking surgery (within 24 hours) and repeated for 11 monthly cycles.	Cyclophosphamide	152-168	dual specificity phosphatase 2	Homo sapiens	121-126
1351538-12	1992	CONCLUSION: We conclude that tumors with overexpression of the c-erbB-2 oncogene are less responsive to cyclophosphamide, methotrexate, and fluorouracil (CMF)-containing adjuvant therapy regimens than those with a normal amount of gene product.	Cyclophosphamide	104-120	erb-b2 receptor tyrosine kinase 2	Homo sapiens	63-71
1629914-1	1992	BACKGROUND: Experiments in animal tumor models suggest that the antitumor effects of interleukin-2 (IL-2) or IL-2 in combination with lymphokine-activated killer (LAK) cells can be enhanced by chemotherapy agents such as cyclophosphamide or doxorubicin or by the biologic agent interferon alpha.	Cyclophosphamide	221-237	interleukin 2	Homo sapiens	85-98
1629914-1	1992	BACKGROUND: Experiments in animal tumor models suggest that the antitumor effects of interleukin-2 (IL-2) or IL-2 in combination with lymphokine-activated killer (LAK) cells can be enhanced by chemotherapy agents such as cyclophosphamide or doxorubicin or by the biologic agent interferon alpha.	Cyclophosphamide	221-237	interleukin 2	Homo sapiens	100-104
1629914-1	1992	BACKGROUND: Experiments in animal tumor models suggest that the antitumor effects of interleukin-2 (IL-2) or IL-2 in combination with lymphokine-activated killer (LAK) cells can be enhanced by chemotherapy agents such as cyclophosphamide or doxorubicin or by the biologic agent interferon alpha.	Cyclophosphamide	221-237	interleukin 2	Homo sapiens	109-113
1629914-1	1992	BACKGROUND: Experiments in animal tumor models suggest that the antitumor effects of interleukin-2 (IL-2) or IL-2 in combination with lymphokine-activated killer (LAK) cells can be enhanced by chemotherapy agents such as cyclophosphamide or doxorubicin or by the biologic agent interferon alpha.	Cyclophosphamide	221-237	interleukin 2	Homo sapiens	134-144
1374589-3	1992	The authors have produced a novel anti-CK 18 monoclonal antibody (ACK-156) using a modified immunization procedure that included sequential injections of human epidermal keratin, cyclophosphamide, and enriched cytoskeletal extracts from a human lung carcinoma cell line.	Cyclophosphamide	179-195	keratin 18	Homo sapiens	39-44
8445340-0	1993	Lipoprotein lipase regulation in the cyclophosphamide-treated rabbit: dependence on nutritional status.	Cyclophosphamide	37-53	lipoprotein lipase	Oryctolagus cuniculus	0-18
8445340-1	1993	Cyclophosphamide injection into the fasted rabbit induces a hypertriglyceridemia (4.6 mM vs. 0.8 mM in controls) and a defect of lipoprotein lipase (LPL), as measured in post-heparin plasma (PHP).	Cyclophosphamide	0-16	lipoprotein lipase	Oryctolagus cuniculus	129-147
8445340-1	1993	Cyclophosphamide injection into the fasted rabbit induces a hypertriglyceridemia (4.6 mM vs. 0.8 mM in controls) and a defect of lipoprotein lipase (LPL), as measured in post-heparin plasma (PHP).	Cyclophosphamide	0-16	lipoprotein lipase	Oryctolagus cuniculus	149-152
8445340-3	1993	The effects of cyclophosphamide on LPL activity and synthesis, depending on the nutritional state, were thus studied in two sites: periepididymal adipose tissue and heart.	Cyclophosphamide	15-31	lipoprotein lipase	Oryctolagus cuniculus	35-38
8445340-8	1993	Cyclophosphamide administration to the fed rabbit led to decreases of LPL activity and synthesis in the adipose tissue, similar to those observed upon starvation.	Cyclophosphamide	0-16	lipoprotein lipase	Oryctolagus cuniculus	70-73
8445340-11	1993	However, cyclophosphamide induced opposite effects, depending on the nutritional state: after injection into fed animals, heart LPL activity increased up to 477.2 mIU/g (P < 0.01) with a concomitant increase in the LPL synthesis rate.	Cyclophosphamide	9-25	lipoprotein lipase	Oryctolagus cuniculus	128-131
8445340-11	1993	However, cyclophosphamide induced opposite effects, depending on the nutritional state: after injection into fed animals, heart LPL activity increased up to 477.2 mIU/g (P < 0.01) with a concomitant increase in the LPL synthesis rate.	Cyclophosphamide	9-25	lipoprotein lipase	Oryctolagus cuniculus	218-221
8445340-14	1993	Hence, although insensitive to nutritional modulations, heart LPL responded differently to cyclophosphamide, depending on the nutritional state.	Cyclophosphamide	91-107	lipoprotein lipase	Oryctolagus cuniculus	62-65
8445340-18	1993	Hence, a defect of heart and postheparin plasma LPL appears as a major determinant of hypertriglyceridemia in cyclophosphamide-treated fasted rabbits.	Cyclophosphamide	110-126	lipoprotein lipase	Oryctolagus cuniculus	48-51
1398912-6	1992	TNF was detectable between 6 and 60 h, with peak levels at 24 h. Both TNF and IL-6 levels were significantly higher in cyclophosphamide-treated mice than in normal mice.	Cyclophosphamide	119-135	tumor necrosis factor	Mus musculus	0-3
1398912-6	1992	TNF was detectable between 6 and 60 h, with peak levels at 24 h. Both TNF and IL-6 levels were significantly higher in cyclophosphamide-treated mice than in normal mice.	Cyclophosphamide	119-135	tumor necrosis factor	Mus musculus	70-73
1398912-6	1992	TNF was detectable between 6 and 60 h, with peak levels at 24 h. Both TNF and IL-6 levels were significantly higher in cyclophosphamide-treated mice than in normal mice.	Cyclophosphamide	119-135	interleukin 6	Mus musculus	78-82
1520868-4	1992	Neo-resistance gene transfer was documented also in a CD34+/cyclophosphamide-resistant precursor to granulocyte-macrophage colonies, an undifferentiated progenitor close to the hematopoietic stem cell.	Cyclophosphamide	60-76	CD34 molecule	Homo sapiens	54-58
1387348-2	1992	NSF binds selectively to Ia-positive, cyclophosphamide (CY)-sensitive, and plastic-adherent cells (named intermediate cells) present in the normal spleen.	Cyclophosphamide	38-54	N-ethylmaleimide sensitive factor, vesicle fusing ATPase	Homo sapiens	0-3
1387348-2	1992	NSF binds selectively to Ia-positive, cyclophosphamide (CY)-sensitive, and plastic-adherent cells (named intermediate cells) present in the normal spleen.	Cyclophosphamide	56-58	N-ethylmaleimide sensitive factor, vesicle fusing ATPase	Homo sapiens	0-3
1339197-4	1992	When mice were given cyclophosphamide after PSK-treatment, virus titers from the early to late phases of infection were lower than those in untreated mice.	Cyclophosphamide	21-37	TAO kinase 2	Mus musculus	44-47
1433946-7	1992	Treatment with F-COP (epirubicine, cyclophosphamide, vincristine, prednisolone) therapy, resulted in a dramatic improvement of her condition.	Cyclophosphamide	35-51	caspase recruitment domain family member 16	Homo sapiens	17-20
1421440-5	1992	It was concluded that CY-treated spleen cells, which exhibited high EPM and histamine receptors, comprise the natural suppressor cells which are Ig-, Thy-1- and aGM-1.	Cyclophosphamide	22-24	thymus cell antigen 1, theta	Mus musculus	150-155
1421440-5	1992	It was concluded that CY-treated spleen cells, which exhibited high EPM and histamine receptors, comprise the natural suppressor cells which are Ig-, Thy-1- and aGM-1.	Cyclophosphamide	22-24	phosphoglucomutase 3	Mus musculus	161-166
1638519-2	1992	The results presented herein demonstrate that the pretreatment of mice with recombinant human interleukin 1 alpha (rhIL-1 alpha) protects mice from the lethal effects of several myelotoxic chemotherapeutic drugs, including 5-fluorouracil (5FUra), cyclophosphamide, cis-diammine(1,1-cyclobutanedicarboxylato)platinum(II), and 1,3-bis-(2-chloroethyl)-1-nitrosourea.	Cyclophosphamide	247-263	interleukin 1 alpha	Homo sapiens	94-113
1644896-6	1992	Lymphocytes from mice treated with CY and SBMT showed reduced in vitro proliferative responses to myelin basic protein (GMBP) and PPD, even after the rechallenge with MSCH.	Cyclophosphamide	35-37	myelin basic protein	Mus musculus	98-118
1644239-3	1992	Islets of non-obese diabetic mice which were treated with cyclophosphamide, known to accelerate the development of insulitis and diabetes mellitus, have shown both a significantly increased number of retrovirus-like particles (type C) and enhanced expression of gag protein p30, compared to those of mice not treated with cyclophosphamide.	Cyclophosphamide	58-74	melanoma antigen	Mus musculus	262-265
1644239-3	1992	Islets of non-obese diabetic mice which were treated with cyclophosphamide, known to accelerate the development of insulitis and diabetes mellitus, have shown both a significantly increased number of retrovirus-like particles (type C) and enhanced expression of gag protein p30, compared to those of mice not treated with cyclophosphamide.	Cyclophosphamide	58-74	high mobility group box 1	Mus musculus	274-277
1517151-6	1992	The enhancement of concomitant immunity by PSK treatment was completely impaired by previous intravenous administration of an alkylating agent, cyclophosphamide (CY).	Cyclophosphamide	144-160	TAO kinase 2	Mus musculus	43-46
1517151-6	1992	The enhancement of concomitant immunity by PSK treatment was completely impaired by previous intravenous administration of an alkylating agent, cyclophosphamide (CY).	Cyclophosphamide	162-164	TAO kinase 2	Mus musculus	43-46
1632821-0	1992	Investigation of the mechanism by which cyclophosphamide alters cytochrome P450 in male rats.	Cyclophosphamide	40-56	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	64-79
1632821-1	1992	The effects of administration of the cytotoxic agent cyclophosphamide on cytochrome P450 have been examined in the liver microsomes of male rats.	Cyclophosphamide	53-69	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	73-88
1632821-11	1992	The results of these investigations suggest that cyclophosphamide inactivates hepatic cytochrome P450 in vitro and in vivo via different mechanisms.	Cyclophosphamide	49-65	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	86-101
1357834-1	1992	We have studied the patterns of P-glycoprotein expression before and after 3 cycles of induction chemotherapy (5-fluorouracil, adriamycin and cyclophosphamide) using immunohistochemically stained paraffin-embedded specimen of 28 patients with locally advanced breast cancer.	Cyclophosphamide	142-158	ATP binding cassette subfamily B member 1	Homo sapiens	32-46
1586713-0	1992	Recombinant human interleukin-3 and recombinant human granulocyte-macrophage colony-stimulating factor administered in vivo after high-dose cyclophosphamide cancer chemotherapy: effect on hematopoiesis and microenvironment in human bone marrow.	Cyclophosphamide	140-156	colony stimulating factor 2	Homo sapiens	54-102
1521924-5	1992	Complete normalization of serum IL-6 levels was observed with dexamethasone, cyclophosphamide and CsA whereas indometacin only partly reduced serum IL-6 levels.	Cyclophosphamide	77-93	interleukin 6	Rattus norvegicus	32-36
1630019-6	1992	The patient was treated with the CHOP regimen (doxorubicin, cyclophosphamide, vincristine and prednisolone), which achieved complete remission.	Cyclophosphamide	60-76	DNA damage inducible transcript 3	Homo sapiens	33-37
1375670-0	1992	[In-vivo enhancement of neutrophil function by administration of recombinant human granulocyte colony-stimulating factor (rhG-CSF) in cyclophosphamide (CPA) treated mice].	Cyclophosphamide	134-150	colony stimulating factor 3	Homo sapiens	83-120
1375670-0	1992	[In-vivo enhancement of neutrophil function by administration of recombinant human granulocyte colony-stimulating factor (rhG-CSF) in cyclophosphamide (CPA) treated mice].	Cyclophosphamide	152-155	colony stimulating factor 3	Homo sapiens	83-120
1536940-6	1992	Further studies showed that the administration of IL-7 to mice that had been rendered leukopenic by the injection of cyclophosphamide (Cy) or 5-fluorouracil (5FU) exhibited a more rapid recovery and/or overshoot in their peripheral blood lymphocytes when compared with mice treated with Cy or 5FU alone.	Cyclophosphamide	117-133	interleukin 7	Mus musculus	50-54
1536940-6	1992	Further studies showed that the administration of IL-7 to mice that had been rendered leukopenic by the injection of cyclophosphamide (Cy) or 5-fluorouracil (5FU) exhibited a more rapid recovery and/or overshoot in their peripheral blood lymphocytes when compared with mice treated with Cy or 5FU alone.	Cyclophosphamide	135-137	interleukin 7	Mus musculus	50-54
1536940-6	1992	Further studies showed that the administration of IL-7 to mice that had been rendered leukopenic by the injection of cyclophosphamide (Cy) or 5-fluorouracil (5FU) exhibited a more rapid recovery and/or overshoot in their peripheral blood lymphocytes when compared with mice treated with Cy or 5FU alone.	Cyclophosphamide	287-289	interleukin 7	Mus musculus	50-54
1534792-2	1992	The enhancement of the antibody response is associated with increased induction of T helper cell activity and IL-2 production, as evidenced in mice immunodepressed by aging or by cyclophosphamide treatment.	Cyclophosphamide	179-195	interleukin 2	Mus musculus	110-114
1936625-5	1991	Immunohistochemical studies showed that islet-infiltrating cells in CY-treated control mice were composed mainly of both L3T4+ and Lyt-2+ T lymphocytes, whereas many L3T4+ and very few Lyt-2+ lymphocytes infiltrated within the islets in anti-Kd MoAb-injected mice.	Cyclophosphamide	68-70	CD8 antigen, alpha chain	Mus musculus	131-136
1371964-6	1992	The daily administration of IL-1 alpha after CPA treatment markedly increased splenic CFU-C or neutrophils over the normal level following the increase of bone marrow CFU-C.	Cyclophosphamide	45-48	interleukin 1 alpha	Mus musculus	28-38
1371964-7	1992	Thus, in both 5-FU- and CPA-treated mice, the increase of bone marrow CFU-C after the administration of IL-1 alpha was observed several days earlier than the increase of splenic CFU-C and neutrophils in blood.	Cyclophosphamide	24-27	interleukin 1 alpha	Mus musculus	104-114
1728412-1	1992	The present study was designed to examine the effect of epidermal growth factor (EGF) and fibroblast growth factor (FGF) on 1-beta-D-arabinofuranosylcytosine (ARA-C)- and cyclophosphamide-induced alopecia in the young rat model.	Cyclophosphamide	171-187	epidermal growth factor like 1	Rattus norvegicus	56-79
1728412-1	1992	The present study was designed to examine the effect of epidermal growth factor (EGF) and fibroblast growth factor (FGF) on 1-beta-D-arabinofuranosylcytosine (ARA-C)- and cyclophosphamide-induced alopecia in the young rat model.	Cyclophosphamide	171-187	epidermal growth factor like 1	Rattus norvegicus	81-84
1615753-0	1992	Antileukemic effects of recombinant human tumor necrosis factor alpha (rh-TNF alpha) with cyclophosphamide or methotrexate on leukemia L1210 and leukemia P388 in mice.	Cyclophosphamide	90-106	tumor necrosis factor	Homo sapiens	42-69
12285731-0	1992	Cyclophosphamide, doxorubicin, dexamethasone and procarbazine: effect on seminal plasma sialyltransferase activity.	Cyclophosphamide	0-16	ST6 beta-galactoside alpha-2,6-sialyltransferase 2	Homo sapiens	88-105
12285731-1	1992	The influence of chemotherapy agents, doxorubicin (adriamycin), cyclophosphamide, procarbazine, and dexamethasone on the activity of sialyltransferase in human semen has been examined.	Cyclophosphamide	64-80	ST6 beta-galactoside alpha-2,6-sialyltransferase 2	Homo sapiens	133-150
12285731-4	1992	Doxorubicin and cyclophosphamide, at the maximal concentration of 800 mcg/incubation mixture exhibited an inhibiting effect on sialyltransferase activity which accounted for 15.7 +or- 16% and 12.2 +or- 16%, respectively.	Cyclophosphamide	16-32	ST6 beta-galactoside alpha-2,6-sialyltransferase 2	Homo sapiens	127-144
1417088-1	1992	Erythropoietin levels have been determined in 24 patients with different gynecologic malignancies, who were treated with cisplatinum and endoxan.	Cyclophosphamide	137-144	erythropoietin	Homo sapiens	0-14
1361881-5	1992	The immune effectors generated by TSTA plus CY bear the Thy 1, L3T4, Lyt 2 phenotype.	Cyclophosphamide	44-46	thymus cell antigen 1, theta	Mus musculus	56-61
1361881-5	1992	The immune effectors generated by TSTA plus CY bear the Thy 1, L3T4, Lyt 2 phenotype.	Cyclophosphamide	44-46	CD4 antigen	Mus musculus	63-67
1361881-7	1992	Thus, a triple regimen using TSTA, CY, and IS-IL-2 appears to augment CTL induction in tumor-bearing hosts undergoing stimulation of helper elements by TSTA and inhibition of suppressor cells by CY.	Cyclophosphamide	195-197	interleukin 2	Mus musculus	46-50
1373636-1	1992	This study reports the outcome of POMB/ACE (cisplatin, vincristine, methotrexate, bleomycin, actinomycin D, cyclophosphamide, etoposide) chemotherapy in 53 male patients with metastatic non-seminomatous germ cell tumour (NSGCT) treated between 1983 and 1989 in one centre.	Cyclophosphamide	108-124	angiotensin I converting enzyme	Homo sapiens	39-42
1526289-0	1992	Chemoimmunotherapy of cancer: cyclophosphamide-resistant tumour cells are equally sensitive as the original tumour cell population to local IL-2 immunotherapy.	Cyclophosphamide	30-46	interleukin 2	Homo sapiens	140-144
1530960-7	1992	In mice immunosuppressed by cyclophosphamide treatment, rhuIL-11 administration significantly augmented the number of spleen SRBC-specific PFC as well as serum SRBC-specific antibody titer when compared with the cyclophosphamide-treated mice without IL-11 treatment.	Cyclophosphamide	28-44	interleukin 11	Mus musculus	59-64
1530960-7	1992	In mice immunosuppressed by cyclophosphamide treatment, rhuIL-11 administration significantly augmented the number of spleen SRBC-specific PFC as well as serum SRBC-specific antibody titer when compared with the cyclophosphamide-treated mice without IL-11 treatment.	Cyclophosphamide	212-228	interleukin 11	Mus musculus	59-64
1354896-1	1992	The modulatory effect of vitamin C (Vit C) on the mutagenic effect of the antineoplastic drug cyclophosphamide (CP) was assessed in the in vivo micronucleus test in Swiss mice.	Cyclophosphamide	94-110	vitrin	Mus musculus	36-39
1329443-3	1992	Both MDP-Lys(L18) and GM-CSF were effective for the protection against HSV infection in cyclophosphamide (CY)-treated mice.	Cyclophosphamide	88-104	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	22-28
1329443-3	1992	Both MDP-Lys(L18) and GM-CSF were effective for the protection against HSV infection in cyclophosphamide (CY)-treated mice.	Cyclophosphamide	106-108	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	22-28
1537055-2	1992	The addition of non-cytotoxic concentrations of Adriamycin (doxorubicin), vincristine and 4-OOH-cyclophosphamide (the in vitro active analogue of cyclophosphamide) resulted in suppression of IL-6 release.	Cyclophosphamide	96-112	interleukin 6	Homo sapiens	191-195
1382047-1	1992	The proportion of hypoxic cells in the RIF-1 tumor was observed for 24 hr after treatments with bleomycin, cisplatin, cyclophosphamide, and mitomycin C.	Cyclophosphamide	118-134	replication timing regulatory factor 1	Homo sapiens	39-44
1535119-7	1992	Suppression of S-antigen-induced EAU was abrogated by pretreatment of donor animals with cyclophosphamide.	Cyclophosphamide	89-105	S-antigen visual arrestin	Rattus norvegicus	15-24
1279727-0	1992	Characterization of CD34+ cells mobilized to the peripheral blood during the recovery from cyclophosphamide chemotherapy.	Cyclophosphamide	91-107	CD34 molecule	Homo sapiens	20-24
1585385-4	1992	In contrast, the activation of cyclophosphamide (cytoxan, CTX), which was used in these studies as a comparative control, was not affected by the absence of the hormone supplement.	Cyclophosphamide	31-47	V-set and immunoglobulin domain containing 2	Mus musculus	58-61
1585424-2	1992	In this study we tested ST 789 in vivo for protective effects in Cyclophosphamide-immunosuppressed CD1 mice experimentally infected with several bacterial and fungal pathogens.	Cyclophosphamide	65-81	CD1 antigen complex	Mus musculus	99-102
1835471-6	1991	IL-2 prevented neutropenia and exacerbated lymphopenia caused by cyclophosphamide.	Cyclophosphamide	65-81	interleukin 2	Mus musculus	0-4
1835471-9	1991	Thus, IL-2 unexpectedly enhanced the translocation of E. coli C25 from the gastrointestinal tracts of both cyclophosphamide-pretreated and normal mice.	Cyclophosphamide	107-123	interleukin 2	Mus musculus	6-10
1783802-2	1991	CPA-treated BALB/c mice allowed an increase of TK-1 strain up to 1.7 x 10(6) coxiellar particles/mg spleen.	Cyclophosphamide	0-3	thymidine kinase 1	Mus musculus	47-51
1682037-5	1991	P-gp expression (range, 5-100% positive staining cells) was found in 3 of 6 cystadenomas, 0 of 2 borderline tumors, 15 of 21 untreated ovarian cancers, and 8 of 13 platinum/cyclophosphamide treated ovarian cancers.	Cyclophosphamide	173-189	ATP binding cassette subfamily B member 1	Homo sapiens	0-4
1800893-3	1991	In the genetically engineered cell lines, benzo[a]pyrene was metabolized specifically by the 3-methylcholanthrene inducible rat liver CYP1A1 (cell line XEM2) whereas cyclophosphamide increased the micronucleus frequency only in cultures expressing the phenobarbital inducible CYP2B1 (SD1).	Cyclophosphamide	166-182	CUP2Q35	Homo sapiens	284-287
1741771-1	1991	These investigations were performed to clarify the molecular basis for the enhanced expression of cytosolic aldehyde dehydrogenase (ALDH-1) enzymatic activity in the cyclophosphamide-resistant L1210/CPA murine leukemia cell line, as compared to the parental L1210/O strain.	Cyclophosphamide	166-182	aldehyde dehydrogenase family 1, subfamily A1	Mus musculus	132-138
1959241-5	1991	Cy induced in mice a transient decrease in the T and B cell populations of the PPs with a drastic fall of B cell counts and a profound decrease of intestinal IgA secretion due to a reduction of lamina propria plasma cells.	Cyclophosphamide	0-2	immunoglobulin heavy constant alpha	Mus musculus	158-161
1656891-2	1991	He was treated three times with CAV (cyclophosphamide, doxorubicin, vincristine) therapy and a partial response was achieved.	Cyclophosphamide	37-53	caveolin 2	Homo sapiens	32-35
1919629-1	1991	Cyclophosphamide (CTX) 600 mg/m2, carboplatin 280 mg/m2, and cisplatin 50 mg/m2 were administered on day 1 every 4 weeks to 41 previously untreated ovarian cancer patients with residual disease greater than 2.0 cm after primary laparotomy.	Cyclophosphamide	0-16	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	18-21
1684994-3	1991	This is the third reported case of systemic necrotizing vasculitis in association with alpha-1 antitrypsin deficiency of the PI ZZ type, and the first to show significant response to cyclophosphamide and steroids.	Cyclophosphamide	183-199	serpin family A member 1	Homo sapiens	87-106
1936625-5	1991	Immunohistochemical studies showed that islet-infiltrating cells in CY-treated control mice were composed mainly of both L3T4+ and Lyt-2+ T lymphocytes, whereas many L3T4+ and very few Lyt-2+ lymphocytes infiltrated within the islets in anti-Kd MoAb-injected mice.	Cyclophosphamide	68-70	CD8 antigen, alpha chain	Mus musculus	185-190
1720432-3	1991	Administration of appropriate antibiotics afforded a dose-related inhibition of death from infection in normal mice and mice treated with rG-CSF after cyclophosphamide injection.	Cyclophosphamide	151-167	colony stimulating factor 3	Rattus norvegicus	138-144
1944193-2	1991	LAK/NK activities in PBL from the patients receiving IL-2 plus cyclophosphamide (CY) splenic infusion were much potent than those of the patients receiving IL-2 alone.	Cyclophosphamide	63-79	alpha kinase 1	Homo sapiens	0-3
1944193-2	1991	LAK/NK activities in PBL from the patients receiving IL-2 plus cyclophosphamide (CY) splenic infusion were much potent than those of the patients receiving IL-2 alone.	Cyclophosphamide	81-83	alpha kinase 1	Homo sapiens	0-3
1944193-2	1991	LAK/NK activities in PBL from the patients receiving IL-2 plus cyclophosphamide (CY) splenic infusion were much potent than those of the patients receiving IL-2 alone.	Cyclophosphamide	81-83	interleukin 2	Homo sapiens	156-160
1942535-13	1991	M-protein was decreased and the size of the tumor was reduced after treatment with VCAP (vincristine, cyclophosphamide, adriamycin, prednisolone) regimen and interferon-alpha for multiple myeloma.	Cyclophosphamide	102-118	myomesin 2	Homo sapiens	0-9
1657333-0	1991	In vivo stimulation of myelopoiesis in cyclophosphamide-treated mice by purified human GM-CSF.	Cyclophosphamide	39-55	colony stimulating factor 2	Homo sapiens	87-93
1657333-4	1991	The cytoxan-treated mice were then injected intraperitoneally with 10,000 units of purified hGM-CSF/mouse daily for three days.	Cyclophosphamide	4-11	colony stimulating factor 2	Homo sapiens	92-99
1657333-9	1991	In addition, the loss in body weight caused by cytoxan was less in the mice with subsequent hGM-CSF than those without CSF.	Cyclophosphamide	47-54	colony stimulating factor 2	Homo sapiens	92-99
1749117-1	1991	We evaluated short term clinical effects of intravenous cyclophosphamide (iv CyP) therapy performed by every three month in 7 patients with steroid-resistant lupus nephritis.	Cyclophosphamide	56-72	peptidylprolyl isomerase G	Homo sapiens	77-80
1835471-5	1991	The median numbers of translocated E. coli C25/g of mesenteric lymph node were significantly (P less than .005) higher after both 3 days (659 vs. 117) and 5 days (550 vs. 50) of treatment with IL-2 with cyclophosphamide and after 5 days (1784 vs. 225) of IL-2 without cyclophosphamide.	Cyclophosphamide	203-219	interleukin 2	Mus musculus	193-197
1835471-5	1991	The median numbers of translocated E. coli C25/g of mesenteric lymph node were significantly (P less than .005) higher after both 3 days (659 vs. 117) and 5 days (550 vs. 50) of treatment with IL-2 with cyclophosphamide and after 5 days (1784 vs. 225) of IL-2 without cyclophosphamide.	Cyclophosphamide	268-284	interleukin 2	Mus musculus	193-197
1911464-0	1991	Response to high dose cyclophosphamide with GM-CSF in Merkel cell tumor.	Cyclophosphamide	22-38	colony stimulating factor 2	Homo sapiens	44-50
1924852-1	1991	The interaction between fractionated heat treatment and fractionated drug treatment with cyclophosphamide (CTX) was investigated in a transplantable C3H mouse mammary carcinoma inoculated into the hind leg of C3D2F1/Bom mice.	Cyclophosphamide	89-105	V-set and immunoglobulin domain containing 2	Mus musculus	107-110
1672870-3	1991	Cyclophosphamide/ACTH infusions significantly decreased the proportion of peripheral blood CD4+ T cells at 2, 6 and 12 months following treatment while there was a tendency for increased CD8 expression.	Cyclophosphamide	0-16	proopiomelanocortin	Homo sapiens	17-21
2053788-1	1991	Growth hormone was given to 13 children (nine boys, four girls) with acute leukaemia who had undergone treatment with cyclophosphamide and total body irradiation before bone marrow transplantation.	Cyclophosphamide	118-134	growth hormone 1	Homo sapiens	0-14
1910623-1	1991	We have evaluated the effect of Interleukin-2 [IL-2] after Cyclophosphamide (C) chemotherapy in 41 patients with metastatic cancer.	Cyclophosphamide	59-75	interleukin 2	Homo sapiens	32-45
1672870-3	1991	Cyclophosphamide/ACTH infusions significantly decreased the proportion of peripheral blood CD4+ T cells at 2, 6 and 12 months following treatment while there was a tendency for increased CD8 expression.	Cyclophosphamide	0-16	CD4 molecule	Homo sapiens	91-94
1672870-3	1991	Cyclophosphamide/ACTH infusions significantly decreased the proportion of peripheral blood CD4+ T cells at 2, 6 and 12 months following treatment while there was a tendency for increased CD8 expression.	Cyclophosphamide	0-16	CD8a molecule	Homo sapiens	187-190
1672870-6	1991	The only T cell populations predictive of improvement were percentages of either CD3+ or CD4+ cells where increased percentages of either these populations at 2 months following cyclophosphamide/ACTH infusions were associated with improvement at both 6 and 12 months.	Cyclophosphamide	178-194	CD4 molecule	Homo sapiens	89-92
1672870-7	1991	In terms of functional immune measures, we found that cyclophosphamide/ACTH treatment decreased the level of proliferation in the allogeneic mixed lymphocyte reaction (MLR) at 2 months and of spontaneous proliferation of mononuclear cells at 12 months following therapy.	Cyclophosphamide	54-70	proopiomelanocortin	Homo sapiens	71-75
1724550-1	1991	Prophylactic treatment with human granulocyte colony-stimulating factor (hG-CSF) affords significant protection against systemic aspergillosis or pulmonary aspergillosis in neutropenic (cyclophosphamide-treated) mice but not in cortisone-treated animals.	Cyclophosphamide	186-202	colony stimulating factor 3	Homo sapiens	34-71
1724550-1	1991	Prophylactic treatment with human granulocyte colony-stimulating factor (hG-CSF) affords significant protection against systemic aspergillosis or pulmonary aspergillosis in neutropenic (cyclophosphamide-treated) mice but not in cortisone-treated animals.	Cyclophosphamide	186-202	colony stimulating factor 3	Homo sapiens	73-79
1826279-7	1991	Administration of cyclophosphamide (CY), which accelerates the appearance of diabetes in NOD mice, caused similar depletions of CD4+CD8+ and V beta 8lo thymic T lymphocytes.	Cyclophosphamide	18-34	CD4 antigen	Mus musculus	128-131
1826279-7	1991	Administration of cyclophosphamide (CY), which accelerates the appearance of diabetes in NOD mice, caused similar depletions of CD4+CD8+ and V beta 8lo thymic T lymphocytes.	Cyclophosphamide	36-38	CD4 antigen	Mus musculus	128-131
1679332-4	1991	After cyclophosphamide, the CD4:CD8 ratio of pancreatic lymphocytes increased to 2.30 +/- 0.24 at day 7.	Cyclophosphamide	6-22	CD4 antigen	Mus musculus	28-31
2066940-3	1991	We compared 3 drugs with different mechanisms, i.e., tenidap, dexamethasone and cyclophosphamide, on both CRP levels and soft tissue swelling in the rat adjuvant arthritis model.	Cyclophosphamide	80-96	C-reactive protein	Rattus norvegicus	106-109
1909135-3	1991	Treatment of mice with anti-IFN gamma mAb prevented the induction of early IDDM by cyclophosphamide as well as the adoptive transfer of diabetes by spleen cells from diabetic NOD mice.	Cyclophosphamide	83-99	interferon gamma	Mus musculus	28-37
1909135-4	1991	The protection against induction of diabetes by cyclophosphamide was observed in animals treated with the anti-IFN gamma mAb within 24 h following the first cyclophosphamide injection but not in animals in which mAb treatment was started 7 days later.	Cyclophosphamide	48-64	interferon gamma	Mus musculus	111-120
1909135-4	1991	The protection against induction of diabetes by cyclophosphamide was observed in animals treated with the anti-IFN gamma mAb within 24 h following the first cyclophosphamide injection but not in animals in which mAb treatment was started 7 days later.	Cyclophosphamide	157-173	interferon gamma	Mus musculus	111-120
2066940-6	1991	Cyclophosphamide was without effect in the primary response, but inhibited both swelling and CRP in the secondary response.	Cyclophosphamide	0-16	C-reactive protein	Rattus norvegicus	93-96
2020314-12	1991	CONCLUSION: A dose of 3 and 6 micrograms/kg/day GM-CSF reduces the severity of neutropenia and thrombocytopenia after carboplatin-cyclophosphamide chemotherapy, which may lead to more effective chemotherapy for ovarian cancer in the future.	Cyclophosphamide	130-146	colony stimulating factor 2	Homo sapiens	48-54
1991327-2	1991	The results of this study indicate that pretreatment in vitro (100 ng/ml for 1 hr) or in vivo (200 micrograms/kg/day for 4 days) with thymosin alpha 1 (TA1), significantly increased the IL-2 (from 100 to 500 U/ml) in vitro induced cytotoxic activity of spleen lymphocytes, collected from both normal and cyclophosphamide and tumor-suppressed animals, against both YAC-1 (NK sensitive) and MBL-2 (NK resistant) cell lines.	Cyclophosphamide	304-320	interleukin 2	Mus musculus	186-190
1648333-1	1991	Both CAV (Cyclophosphamide, Doxorubicin, Vincristine) and PE (Cisplatin, Etoposide) are effective and non cross-resistant regimens in the treatment of SCLC.	Cyclophosphamide	10-26	caveolin 2	Homo sapiens	5-8
1993845-0	1991	Administration of IL-7 to mice with cyclophosphamide-induced lymphopenia accelerates lymphocyte repopulation.	Cyclophosphamide	36-52	interleukin 7	Mus musculus	18-22
1993845-3	1991	In comparison to the control cyclophosphamide-treated mice, animals receiving cyclophosphamide and IL-7 had an accelerated regeneration of splenic and lymph node cellularity.	Cyclophosphamide	29-45	interleukin 7	Mus musculus	99-103
1993845-7	1991	IL-7 administration to cyclophosphamide-treated mice also resulted in an accelerated recovery of peripheral CD4+ and CD8+ cell numbers in the spleen and lymph node.	Cyclophosphamide	23-39	interleukin 7	Mus musculus	0-4
1993845-7	1991	IL-7 administration to cyclophosphamide-treated mice also resulted in an accelerated recovery of peripheral CD4+ and CD8+ cell numbers in the spleen and lymph node.	Cyclophosphamide	23-39	CD4 antigen	Mus musculus	108-111
1993845-8	1991	The numbers of CD8+ cells were increased by twofold over normal levels in cyclophosphamide-treated mice receiving IL-7.	Cyclophosphamide	74-90	interleukin 7	Mus musculus	114-118
1993845-9	1991	Myeloid recovery was determined in cyclophosphamide treated mice by assessing the numbers of CFU-granulocyte-macrophage and Mac 1+ cells.	Cyclophosphamide	35-51	integrin alpha M	Mus musculus	124-129
1995731-2	1991	In mice myelosuppressed by cyclophosphamide, subcutaneously administered rmGM-CSF was a potent stimulus of granulopoiesis by increasing the number of GM-CSF-responsive precursor cells in bone marrow followed by a profound neutrophilia.	Cyclophosphamide	27-43	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	75-81
1829436-2	1991	Longitudinal studies showed reduced numbers of CD45R+CD4+ lymphocytes in patients treated with cyclophosphamide or azathioprine.	Cyclophosphamide	95-111	protein tyrosine phosphatase receptor type C	Homo sapiens	47-52
1721105-1	1991	Prophylactic treatment with human granulocyte colony stimulating factor (hG-CSF) affords significant protection against systemic infections caused by C. albicans in cyclophosphamide-treated but not in cortisone-treated mice.	Cyclophosphamide	165-181	colony stimulating factor 3	Homo sapiens	34-71
1721105-1	1991	Prophylactic treatment with human granulocyte colony stimulating factor (hG-CSF) affords significant protection against systemic infections caused by C. albicans in cyclophosphamide-treated but not in cortisone-treated mice.	Cyclophosphamide	165-181	colony stimulating factor 3	Homo sapiens	73-79
1825477-5	1991	injection of cyclophosphamide prior to immunizations; (d) Epi-induced specific immunosuppression can be adoptively transferred by nylon wool-nonadherent cells 6 days following i.v.	Cyclophosphamide	13-29	mucin 21	Mus musculus	58-61
1903312-4	1991	Whereas the PRCA repeatedly responded to immunosuppression with high-dose cyclosporin A (CSA) and CSA plus plasmapheresis, IFN antibody production continued during treatment with cyclophosphamide and CSA.	Cyclophosphamide	179-195	interferon alpha 1	Homo sapiens	123-126
1847877-7	1991	BP-3+ reticular cells were observed in the collapsed periarterial lymphatic sheaths of adult mice depleted of T and B cells by cyclophosphamide treatment and in mice with severe combined immunodeficiency (scid), indicating that development of this reticular network is lymphocyte independent.	Cyclophosphamide	127-143	bone marrow stromal cell antigen 1	Mus musculus	0-4
1899431-5	1991	IFN-gamma activity at low levels (2.7 +/- 0.3 U/ml) could be detected only in culture supernatants from islets isolated at day 7 post-cyclophosphamide.	Cyclophosphamide	134-150	interferon gamma	Mus musculus	0-9
1991694-0	1991	Interleukin-1 modification of the effects of cyclophosphamide and fractionated irradiation.	Cyclophosphamide	45-61	interleukin 1 alpha	Homo sapiens	0-13
1991694-1	1991	Studies were performed to determine whether recombinant human interleukin-1 (IL-1) modifies the tumor cytotoxicity of cyclophosphamide (CY) combined with fractionated X-irradiation.	Cyclophosphamide	118-134	interleukin 1 alpha	Homo sapiens	62-75
1991694-1	1991	Studies were performed to determine whether recombinant human interleukin-1 (IL-1) modifies the tumor cytotoxicity of cyclophosphamide (CY) combined with fractionated X-irradiation.	Cyclophosphamide	118-134	interleukin 1 alpha	Homo sapiens	77-81
1991694-1	1991	Studies were performed to determine whether recombinant human interleukin-1 (IL-1) modifies the tumor cytotoxicity of cyclophosphamide (CY) combined with fractionated X-irradiation.	Cyclophosphamide	136-138	interleukin 1 alpha	Homo sapiens	62-75
1991694-1	1991	Studies were performed to determine whether recombinant human interleukin-1 (IL-1) modifies the tumor cytotoxicity of cyclophosphamide (CY) combined with fractionated X-irradiation.	Cyclophosphamide	136-138	interleukin 1 alpha	Homo sapiens	77-81
1991694-6	1991	From these findings, it appears that IL-1 enhances the cytotoxic effects of CY and X ray against tumors, an effect that would have considerable practical significance in the light of the protective effects shown elsewhere for the same lymphokine on normal tissues.	Cyclophosphamide	76-78	interleukin 1 alpha	Homo sapiens	37-41
2018856-9	1991	These findings indicated that the administration of rGM-CSF to cyclophosphamide-treated animals causes an absolute increase in circulating myeloid cells and that these increases are derived from the spleen.	Cyclophosphamide	63-79	colony stimulating factor 2	Rattus norvegicus	52-59
2053494-0	1991	Role of aldehyde dehydrogenase (ALDH) in the detoxication of cyclophosphamide (CP) in rat embryos.	Cyclophosphamide	61-77	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	8-30
2053494-0	1991	Role of aldehyde dehydrogenase (ALDH) in the detoxication of cyclophosphamide (CP) in rat embryos.	Cyclophosphamide	61-77	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	32-36
1760819-0	1991	Importance in timing of cyclophosphamide on the enhancement of interleukin-2-induced cytolysis.	Cyclophosphamide	24-40	interleukin 2	Mus musculus	63-76
1760819-1	1991	We investigated the in vivo effects of cyclophosphamide (CY) on interleukin-2(IL-2)-induced cytolytic function and spleen cell immunophenotype.	Cyclophosphamide	57-59	interleukin 2	Mus musculus	64-77
1760819-5	1991	In contrast, when CY was given on day -5, the cytotoxicity against YAC-1 was not enhanced.	Cyclophosphamide	18-20	ADP-ribosyltransferase 1	Mus musculus	67-72
1760819-6	1991	Phenotypic analysis of splenocytes obtained from mice treated with CY on day -10 or -15 revealed a relative decrease in L3T4- and Lyt2-positive T cells.	Cyclophosphamide	67-69	CD8 antigen, alpha chain	Mus musculus	130-134
1760819-8	1991	These findings provide evidence that CY may be used more effectively in IL-2-based immunotherapy protocols, if consideration is given to timing of CY and IL-2 administration.	Cyclophosphamide	37-39	interleukin 2	Mus musculus	72-76
1826435-1	1991	In 20 patients with non-Hodgkin lymphoma or breast cancer, high-dose cyclophosphamide induced, during the post-nadir period of rapid leucocyte recovery, on median day 19 about a 30-fold increase in the peak concentration of granulocyte-macrophage (CFU-GM) and erythroid (BFU-E) colony-forming cells, and an even higher increase in the more immature pluripotent progenitors (CFU-Mix, 72-fold).	Cyclophosphamide	69-85	Mix paired-like homeobox	Homo sapiens	378-381
1761361-2	1991	Intact or cyclophosphamide-treated mice received human rIL-1 beta according to different regimens, and their sera were assayed for CSA at 4, 24 or 48 h. The results indicated that (1) cyclophosphamide alone significantly increased the level of circulating CSA, (2) administration of IL-1 to intact or neutropenic mice resulted in a biphasic pattern of CSA response, an early burst at 4 h being followed at 24-48 h by a significant decrease.	Cyclophosphamide	10-26	interleukin 1 beta	Rattus norvegicus	55-65
1761361-2	1991	Intact or cyclophosphamide-treated mice received human rIL-1 beta according to different regimens, and their sera were assayed for CSA at 4, 24 or 48 h. The results indicated that (1) cyclophosphamide alone significantly increased the level of circulating CSA, (2) administration of IL-1 to intact or neutropenic mice resulted in a biphasic pattern of CSA response, an early burst at 4 h being followed at 24-48 h by a significant decrease.	Cyclophosphamide	10-26	interleukin 1 complex	Mus musculus	56-60
1766265-9	1991	This is the first report of regression of proven monoclonal CD8+ T gamma-cell expansion and the associated anemia following cyclophosphamide therapy.	Cyclophosphamide	124-140	CD8a molecule	Homo sapiens	60-63
1717812-1	1991	Decrease in resistance to systemic Pseudomonas infection in cyclophosphamide (CPA)-induced neutropenic mice was prevented by injections of recombinant human granulocyte colony-stimulating factor (rG-CSF).	Cyclophosphamide	60-76	colony stimulating factor 3	Homo sapiens	157-194
1717812-1	1991	Decrease in resistance to systemic Pseudomonas infection in cyclophosphamide (CPA)-induced neutropenic mice was prevented by injections of recombinant human granulocyte colony-stimulating factor (rG-CSF).	Cyclophosphamide	60-76	colony stimulating factor 3	Rattus norvegicus	196-202
1717812-1	1991	Decrease in resistance to systemic Pseudomonas infection in cyclophosphamide (CPA)-induced neutropenic mice was prevented by injections of recombinant human granulocyte colony-stimulating factor (rG-CSF).	Cyclophosphamide	78-81	colony stimulating factor 3	Homo sapiens	157-194
1717812-1	1991	Decrease in resistance to systemic Pseudomonas infection in cyclophosphamide (CPA)-induced neutropenic mice was prevented by injections of recombinant human granulocyte colony-stimulating factor (rG-CSF).	Cyclophosphamide	78-81	colony stimulating factor 3	Rattus norvegicus	196-202
1717812-2	1991	In order to explore mechanism of the prevention of CPA-induced decrease in the anti-infectious resistance by rG-CSF, CPA-treated and then rG-CSF-injected mice were inoculated i.p.	Cyclophosphamide	51-54	colony stimulating factor 3	Rattus norvegicus	109-115
1717812-2	1991	In order to explore mechanism of the prevention of CPA-induced decrease in the anti-infectious resistance by rG-CSF, CPA-treated and then rG-CSF-injected mice were inoculated i.p.	Cyclophosphamide	51-54	colony stimulating factor 3	Rattus norvegicus	138-144
1717812-4	1991	In the mice who had received 4 daily s.c. injections of rG-CSF from the day after CPA-injection, a large number of neutrophils were mobilized into the peritoneal cavity in response to the bacterial inoculation and growth of the infecting Pseudomonas in the cavity was markedly inhibited, whereas in CPA-induced neutropenic mice few neutrophils were mobilized and the infecting bacteria proliferated vigorously in the peritoneal cavity.	Cyclophosphamide	82-85	colony stimulating factor 3	Rattus norvegicus	56-62
1717812-4	1991	In the mice who had received 4 daily s.c. injections of rG-CSF from the day after CPA-injection, a large number of neutrophils were mobilized into the peritoneal cavity in response to the bacterial inoculation and growth of the infecting Pseudomonas in the cavity was markedly inhibited, whereas in CPA-induced neutropenic mice few neutrophils were mobilized and the infecting bacteria proliferated vigorously in the peritoneal cavity.	Cyclophosphamide	299-302	colony stimulating factor 3	Rattus norvegicus	56-62
1717812-5	1991	These results suggest that administration of rG-CSF prevents CPA-induced neutropenia and neutrophils circulating at normal level in the number are normally mobilized into the peritoneal cavity in response to Pseudomonas inoculation, and that the mobilized neutrophils inhibit proliferation of the infecting Pseudomonas.	Cyclophosphamide	61-64	colony stimulating factor 3	Rattus norvegicus	45-51
2014029-6	1991	Our clinical data indicate that intratumoral injection of large dose OK-432 and continuous administration of rIL-2 via hepatic artery, pretreated with cyclophosphamide, were clinically effective immunotherapy for reduction of metastatic liver tumor.	Cyclophosphamide	151-167	interleukin 2	Rattus norvegicus	109-114
1665662-4	1991	Marked lowering of the BCP due to the use of cyclophosphamide is accompanied by the minimum size of the FSS and the minimum FSS/AAC ratio (spine hypoplasia).	Cyclophosphamide	45-61	glycine-N-acyltransferase	Rattus norvegicus	128-131
1964750-5	1990	By contrast, platelet counts in patients with SCCL were negatively correlated with the absolute amount of cyclophosphamide and adriamycin given, and declined most dramatically with disease progression and death.	Cyclophosphamide	106-122	SCLC1	Homo sapiens	46-50
2258610-2	1990	In this study, recombinant human IL-1 alpha (rhIL-1 alpha) was used to protect normal and tumor-bearing BALB/c mice from the acute toxicity caused by lethal doses of cyclophosphamide (Cy) and 5-fluorouracil.	Cyclophosphamide	166-182	interleukin 1 alpha	Homo sapiens	33-43
2258610-2	1990	In this study, recombinant human IL-1 alpha (rhIL-1 alpha) was used to protect normal and tumor-bearing BALB/c mice from the acute toxicity caused by lethal doses of cyclophosphamide (Cy) and 5-fluorouracil.	Cyclophosphamide	184-186	interleukin 1 alpha	Homo sapiens	33-43
1830248-1	1991	In an effort to improve the therapeutic efficacy and selectivity of cyclophosphamide (CTX), cis-diamminedichloroplatinum(II) (CDDP), and carboplatin (Carbo), these antitumor alkylating agents were combined with the 2-nitroimidazole drug etanidazole (ETA).	Cyclophosphamide	68-84	V-set and immunoglobulin domain containing 2	Mus musculus	86-89
1988077-13	1991	We conclude that a dose of 3 and 6 micrograms/kg/day GM-CSF reduces the severity of neutropenia and thrombocytopenia after carboplatin-cyclophosphamide.	Cyclophosphamide	135-151	colony stimulating factor 2	Homo sapiens	53-59
1829927-0	1991	Sequential proleukin(rIL-2) by continuous infusion with cisplatin and cyclophosphamide in patients with unresectable ovarian cancer.	Cyclophosphamide	70-86	interleukin 2	Rattus norvegicus	21-26
1680689-14	1991	Cyclophosphamide (CP) resistance has been attributed to an increased activity of two different enzymes, glutathione S-transferase, also involved in MDR phenotype, and aldehyde dehydrogenase, which catalyzes inactivation of CP in non cytotoxic metabolites.	Cyclophosphamide	0-16	glutathione S-transferase kappa 1	Homo sapiens	104-129
27463490-4	1991	Chlorambucil (chl) given intermittently was compared with the combination COP in CLL 1: no differences in survival or response were observed although the response rate (CR + PR) of COP rose from 53% to 73% when the dose of cyclophosphamide was doubled; CR + PR with chl was 62%.	Cyclophosphamide	223-239	caspase recruitment domain family member 16	Homo sapiens	181-184
2028560-3	1991	Sequential determination of AAC levels at different stages of tumor growth, i.e. from the primary to the metastatic stage, performed with the original purpose of demonstrating that any disturbance in the immunoregulatory mechanism of the host was due to cyclophosphamide rather than to changes in tumor load, revealed that levels of AACs parallel disease progression in the initial stages of primary tumor growth but rapidly decrease to near-normal levels in the presence of heavy tumor burden.	Cyclophosphamide	254-270	glycine-N-acyltransferase	Rattus norvegicus	28-31
2087493-0	1990	Voluntary consumption of cyclophosphamide by nondeprived Mrl-lpr/lpr and Mrl +/+ mice.	Cyclophosphamide	25-41	Fas (TNF receptor superfamily member 6)	Mus musculus	61-64
1705961-5	1990	In mice treated with cyclophosphamide (150 mg/kg), G-CSF treatment caused an elevation of WBC and an enhancement of antibacterial resistance.	Cyclophosphamide	21-37	colony stimulating factor 3 (granulocyte)	Mus musculus	51-56
1700831-11	1990	In 3-week-old cyclophosphamide-treated chicks, the presence of CIa+ CT-3- tumors bearing hematopoietic lineage markers, such as CLA-3 and 5M19, are most likely to have been derived from cells within the myeloid lineage.	Cyclophosphamide	14-30	nuclear receptor coactivator 5	Homo sapiens	63-66
1700831-11	1990	In 3-week-old cyclophosphamide-treated chicks, the presence of CIa+ CT-3- tumors bearing hematopoietic lineage markers, such as CLA-3 and 5M19, are most likely to have been derived from cells within the myeloid lineage.	Cyclophosphamide	14-30	cancer antigen 1	Homo sapiens	68-72
1700831-11	1990	In 3-week-old cyclophosphamide-treated chicks, the presence of CIa+ CT-3- tumors bearing hematopoietic lineage markers, such as CLA-3 and 5M19, are most likely to have been derived from cells within the myeloid lineage.	Cyclophosphamide	14-30	cerebellar ataxia, infantile nonprogressive, autosomal recessive	Homo sapiens	128-133
2087493-0	1990	Voluntary consumption of cyclophosphamide by nondeprived Mrl-lpr/lpr and Mrl +/+ mice.	Cyclophosphamide	25-41	Fas (TNF receptor superfamily member 6)	Mus musculus	65-68
2087493-1	1990	Cyclophosphamide dissolved in several dilutions of chocolate milk was presented for 20 hr daily to nondeprived, symptomatic, autoimmune Mrl-lpr/lpr and asymptomatic Mrl +/+ mice.	Cyclophosphamide	0-16	Fas (TNF receptor superfamily member 6)	Mus musculus	140-143
2087493-1	1990	Cyclophosphamide dissolved in several dilutions of chocolate milk was presented for 20 hr daily to nondeprived, symptomatic, autoimmune Mrl-lpr/lpr and asymptomatic Mrl +/+ mice.	Cyclophosphamide	0-16	Fas (TNF receptor superfamily member 6)	Mus musculus	144-147
2087493-8	1990	Autoimmune lpr/lpr mice consumed more cyclophosphamide than +/+ mice.	Cyclophosphamide	38-54	Fas (TNF receptor superfamily member 6)	Mus musculus	11-14
2087493-8	1990	Autoimmune lpr/lpr mice consumed more cyclophosphamide than +/+ mice.	Cyclophosphamide	38-54	Fas (TNF receptor superfamily member 6)	Mus musculus	15-18
2087493-11	1990	It is hypothesized that autoimmune lpr/lpr mice voluntarily consume more cyclophosphamide than asymptomatic +/+ mice in an effort to "correct" their immune system dysregulation.	Cyclophosphamide	73-89	Fas (TNF receptor superfamily member 6)	Mus musculus	35-38
2087493-11	1990	It is hypothesized that autoimmune lpr/lpr mice voluntarily consume more cyclophosphamide than asymptomatic +/+ mice in an effort to "correct" their immune system dysregulation.	Cyclophosphamide	73-89	Fas (TNF receptor superfamily member 6)	Mus musculus	39-42
2400994-13	1990	Our results show that low dose interleukin 2 preceded by low dose cyclophosphamide effectively induces LAK cells in vivo.	Cyclophosphamide	66-82	interleukin 2	Homo sapiens	31-44
1718146-2	1990	PSP 25 mg/kg ip into mice for 5 d antagonized the inhibition of IL-2 production by cyclophosphamide from activated T lymphocytes and restored the suppressed T-cell-mediated delayed, type hypersensitivity response to normal.	Cyclophosphamide	83-99	interleukin 2	Mus musculus	64-68
2129070-11	1990	Our results suggest that the principal target cell population of CY is the PNAhi, CD3- and DP immature cortical thymocytes as well as splenic B cells.	Cyclophosphamide	65-67	CD3 antigen, epsilon polypeptide	Mus musculus	82-85
2144844-2	1990	In normal mice and in mice pretreated with cyclophosphamide, hydrocortisone acetate, or sublethal total body irradiation, the outgrowth of Candida albicans in the kidney was significantly reduced by the administration of a single intraperitoneal dose of 80 ng of IL-1 (P less than 0.05).	Cyclophosphamide	43-59	interleukin 1 complex	Mus musculus	263-267
2144844-3	1990	In mice treated with either cyclophosphamide or irradiation, IL-1 also significantly reduced the outgrowth of C. albicans in the spleen.	Cyclophosphamide	28-44	interleukin 1 complex	Mus musculus	61-65
2144844-4	1990	The protective effect of IL-1 was present when given 24 h before injection of C. albicans but also when IL-1 was given simultaneously with or 6 h after injection of C. albicans in cyclophosphamide-treated mice.	Cyclophosphamide	180-196	interleukin 1 complex	Mus musculus	25-29
2144844-4	1990	The protective effect of IL-1 was present when given 24 h before injection of C. albicans but also when IL-1 was given simultaneously with or 6 h after injection of C. albicans in cyclophosphamide-treated mice.	Cyclophosphamide	180-196	interleukin 1 complex	Mus musculus	104-108
2400809-6	1990	Levels of aldehyde dehydrogenase (ALDH), which inactivates CY by prevention of formation of PhM, were significantly elevated in these CY-resistant AML cells: cytosolic and particulate ALDH fractions from these cells were 11 to 13 times control with NAD cofactor and propanal substrate and three to four times control with NADP cofactor and benzaldehyde substrate.	Cyclophosphamide	59-61	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	10-32
2400809-6	1990	Levels of aldehyde dehydrogenase (ALDH), which inactivates CY by prevention of formation of PhM, were significantly elevated in these CY-resistant AML cells: cytosolic and particulate ALDH fractions from these cells were 11 to 13 times control with NAD cofactor and propanal substrate and three to four times control with NADP cofactor and benzaldehyde substrate.	Cyclophosphamide	59-61	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	34-38
2400809-6	1990	Levels of aldehyde dehydrogenase (ALDH), which inactivates CY by prevention of formation of PhM, were significantly elevated in these CY-resistant AML cells: cytosolic and particulate ALDH fractions from these cells were 11 to 13 times control with NAD cofactor and propanal substrate and three to four times control with NADP cofactor and benzaldehyde substrate.	Cyclophosphamide	134-136	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	10-32
2400809-6	1990	Levels of aldehyde dehydrogenase (ALDH), which inactivates CY by prevention of formation of PhM, were significantly elevated in these CY-resistant AML cells: cytosolic and particulate ALDH fractions from these cells were 11 to 13 times control with NAD cofactor and propanal substrate and three to four times control with NADP cofactor and benzaldehyde substrate.	Cyclophosphamide	134-136	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	34-38
2400809-6	1990	Levels of aldehyde dehydrogenase (ALDH), which inactivates CY by prevention of formation of PhM, were significantly elevated in these CY-resistant AML cells: cytosolic and particulate ALDH fractions from these cells were 11 to 13 times control with NAD cofactor and propanal substrate and three to four times control with NADP cofactor and benzaldehyde substrate.	Cyclophosphamide	134-136	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	184-188
2400809-7	1990	Further studies with this animal model of AML, in which resistance to CY is mediated by elevated ALDH activity, may elucidate mechanisms for effective elimination of drug-resistant leukemic cells ex vivo and in vivo.	Cyclophosphamide	70-72	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	97-101
2121696-0	1990	Production and enhanced anti-tumor activity of tumor necrosis factor in mice treated with cyclophosphamide.	Cyclophosphamide	90-106	tumor necrosis factor	Mus musculus	47-68
2118418-8	1990	In contrast to the suppression of these testosterone-dependent P-450s, P-450 3 (IIA1), P-450j (IIE1), and the P-450-independent microsomal enzyme steroid 5 alpha-reductase were each elevated in rat liver following cyclophosphamide administration.	Cyclophosphamide	214-230	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	87-99
2118418-10	1990	In vitro experiments revealed that P-450j was severalfold more susceptible to inactivation by the cyclophosphamide metabolite acrolein as compared with P-450 3.	Cyclophosphamide	98-114	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	35-41
2118418-11	1990	These observations suggest that P-450j protein is induced by cyclophosphamide treatment but that the protein is inactivated by the cyclophosphamide metabolite acrolein.	Cyclophosphamide	61-77	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	32-38
2118418-11	1990	These observations suggest that P-450j protein is induced by cyclophosphamide treatment but that the protein is inactivated by the cyclophosphamide metabolite acrolein.	Cyclophosphamide	131-147	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	32-38
2145216-7	1990	Activation of these CD8+ T cells was indicated by the finding that they were rapidly converted from being cyclophosphamide (Cy) resistant to being highly Cy sensitive within 48 hr of giving Vb.	Cyclophosphamide	106-122	CD8a molecule	Homo sapiens	20-23
2145216-7	1990	Activation of these CD8+ T cells was indicated by the finding that they were rapidly converted from being cyclophosphamide (Cy) resistant to being highly Cy sensitive within 48 hr of giving Vb.	Cyclophosphamide	124-126	CD8a molecule	Homo sapiens	20-23
2145216-7	1990	Activation of these CD8+ T cells was indicated by the finding that they were rapidly converted from being cyclophosphamide (Cy) resistant to being highly Cy sensitive within 48 hr of giving Vb.	Cyclophosphamide	154-156	CD8a molecule	Homo sapiens	20-23
2121696-2	1990	In the present study, the ability of this treatment to induce the production of TNF in mice receiving cyclophosphamide (CY) was examined.	Cyclophosphamide	102-118	tumor necrosis factor	Mus musculus	80-83
2121696-2	1990	In the present study, the ability of this treatment to induce the production of TNF in mice receiving cyclophosphamide (CY) was examined.	Cyclophosphamide	120-122	tumor necrosis factor	Mus musculus	80-83
2121696-5	1990	TNF was also induced by the administration of MDP-GDP and LPS to Meth A sarcoma-bearing mice treated with this dose of CY.	Cyclophosphamide	119-121	tumor necrosis factor	Mus musculus	0-3
2121696-8	1990	These results demonstrated that the anti-tumor activity of endogenously induced TNF is potentiated by combined therapy with a high dose of CY.	Cyclophosphamide	139-141	tumor necrosis factor	Mus musculus	80-83
2246824-6	1990	After chemotherapy using adriamycin, cyclophosphamide, vincristine, and prednisolone (CHOP), lymphadenopathy and splenomegaly reduced and lymphoid blasts disappeared from the blood and bone marrow.	Cyclophosphamide	37-53	DNA damage inducible transcript 3	Homo sapiens	86-90
2389941-5	1990	Treatment with cultured killer cells and in vivo IL 2 after immunochemotherapy (immunostimulator followed by CPA) was the most effective protocol in which immunostimulator, chemotherapy, killer cells and IL 2 respectively seemed to induce, regulate, supplement and amplify anti-tumor effector cells.	Cyclophosphamide	109-112	interleukin 2	Mus musculus	49-53
2201427-7	1990	The authors" patient was correctly diagnosed during life and received considerable benefit from cyclophosphamide, doxorubicin, and vincristine (CAV) therapy and survived for 26 months after diagnosis.	Cyclophosphamide	96-112	caveolin 2	Homo sapiens	144-147
1966937-5	1990	Addition of serum CSFs as well as exogenous addition of interleukin 3 (IL-3) or G-CSF to BMC taken from mice 1 day after CY-treatment induced high activity to stimulate the proliferation of those cells.	Cyclophosphamide	121-123	colony stimulating factor 3 (granulocyte)	Mus musculus	80-85
1966937-6	1990	Production of interleukin 1 (IL-1) was also stimulated in sera of CY-treated and untreated mice by administration of GLA-60.	Cyclophosphamide	66-68	interleukin 1 complex	Mus musculus	14-33
1698897-2	1990	In the cyclophosphamide-treated neutropenic mice, the prophylactic administration of G-CSF (2 micrograms/day/mouse) yielded a lower incidence of infection than that of saline alone.	Cyclophosphamide	7-23	colony stimulating factor 3 (granulocyte)	Mus musculus	85-90
2385246-0	1990	Cytochrome P-450 and chromosome damage by cyclophosphamide in LEC strain rats predisposed to hereditary hepatitis and liver cancer.	Cyclophosphamide	42-58	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-16
2175049-0	1990	Treatment of small cell lung cancer with cyclophosphamide, adriamycin and vincristine (CAV) combination therapy: experience at University Hospital, Kuala Lumpur, Malaysia.	Cyclophosphamide	41-57	caveolin 2	Homo sapiens	87-90
2367754-1	1990	The uptake of cyclophosphamide (CTX) and its metabolites was evaluated by injecting adult female rats with 14C-CTX on the morning of metestrous or proestrus.	Cyclophosphamide	14-30	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	32-35
2367754-1	1990	The uptake of cyclophosphamide (CTX) and its metabolites was evaluated by injecting adult female rats with 14C-CTX on the morning of metestrous or proestrus.	Cyclophosphamide	14-30	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	111-114
2126987-4	1990	The same combination immunotherapy treatment strongly stimulated natural killer activity and cytotoxicity against autologus 3LL tumor cells in 3LL-tumor-bearing mice treated with cyclophosphamide, whereas treatments with each agent singly did not alter or only slightly modified the cytotoxic activity towards Yac-1 or 3LL target cells.	Cyclophosphamide	179-195	ADP-ribosyltransferase 1	Mus musculus	310-315
2258610-0	1990	Chemoprotective effects of recombinant human IL-1 alpha in cyclophosphamide-treated normal and tumor-bearing mice.	Cyclophosphamide	59-75	interleukin 1 alpha	Homo sapiens	45-55
2161174-1	1990	Chemotherapy with cisplatin (CDDP, 90 mg/m2) and cyclophosphamide (CTX, 600 mg/m2) was administered to 54 consecutive patients with advanced epithelial ovarian cancer (37 stage III and 17 stage IV).	Cyclophosphamide	49-65	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	67-70
2142603-0	1990	Protective effects of D-Trp6-luteinising hormone-releasing hormone microcapsules against cyclophosphamide-induced gonadotoxicity in female rats.	Cyclophosphamide	89-105	gonadotropin releasing hormone 1	Rattus norvegicus	29-66
2142603-1	1990	The possible protective effect of an agonist of luteinising hormone-releasing hormone (LH-RH) against the ovarian damage caused by cyclophosphamide was investigated in rats.	Cyclophosphamide	131-147	gonadotropin releasing hormone 1	Rattus norvegicus	48-85
2142603-1	1990	The possible protective effect of an agonist of luteinising hormone-releasing hormone (LH-RH) against the ovarian damage caused by cyclophosphamide was investigated in rats.	Cyclophosphamide	131-147	gonadotropin releasing hormone 1	Rattus norvegicus	87-92
2142603-9	1990	Thus, the treatment with D-Trp6-LH-RH microcapsules before and during chemotherapy prevented the ovarian injury inflicted by cyclophosphamide.	Cyclophosphamide	125-141	gonadotropin releasing hormone 1	Rattus norvegicus	32-37
2372503-0	1990	Stem cell recovery from cyclophosphamide-induced myelosuppression requires the presence of CD4+ cells.	Cyclophosphamide	24-40	CD4 antigen	Mus musculus	91-94
2111738-2	1990	Cyclophosphamide-treated mice received human rIL-1 beta at 7.0, 0.7, or 00.7 micrograms/kg, according to different regimens, to be challenged with a lethal ip inoculum of pseudomonas cells 5 days after myelosuppression.	Cyclophosphamide	0-16	interleukin 1 beta	Rattus norvegicus	45-55
2111738-7	1990	Assay of serum colony-stimulating activity (CSA) revealed that (a) cyclophosphamide treatment alone significantly increased the level of circulating CSA, (b) administration of a single dose of IL-1 to neutropenic mice induced an early, further increase in serum CSA, followed by depression, (c) a biphasic pattern of CSA response was also evident in mice repeatedly treated with IL-1.	Cyclophosphamide	67-83	interleukin 1 complex	Mus musculus	193-197
2111738-7	1990	Assay of serum colony-stimulating activity (CSA) revealed that (a) cyclophosphamide treatment alone significantly increased the level of circulating CSA, (b) administration of a single dose of IL-1 to neutropenic mice induced an early, further increase in serum CSA, followed by depression, (c) a biphasic pattern of CSA response was also evident in mice repeatedly treated with IL-1.	Cyclophosphamide	67-83	interleukin 1 complex	Mus musculus	379-383
2332628-3	1990	The resultant FBL-3-specific T cell lines were adoptively transferred into cyclophosphamide pretreated congenic hosts (B6/Thy-1.1), and restimulated every 14 days by an injection of irradiated FBL-3 plus a 7-day course of IL-2.	Cyclophosphamide	75-91	F-box and leucine rich repeat protein 2	Homo sapiens	14-19
2364257-1	1990	This article demonstrates the positive effect of thymostimulin (TP-1) on leucolymphopoiesis in dogs, based on its apparent ability to counteract the immunodepression induced by cyclophosphamide chemotherapy.	Cyclophosphamide	177-193	translocation protein SEC62	Canis lupus familiaris	64-68
2364257-3	1990	In a control group given a placebo instead of TP-1, the immune depression provoked by cyclophosphamide was maintained during all the therapeutic cycles.	Cyclophosphamide	86-102	translocation protein SEC62	Canis lupus familiaris	46-50
2185337-0	1990	Recombinant human granulocyte-macrophage colony-stimulating factor reduces hematologic toxicity and widens clinical applicability of high-dose cyclophosphamide treatment in breast cancer and non-Hodgkin"s lymphoma.	Cyclophosphamide	143-159	colony stimulating factor 2	Homo sapiens	18-66
2317752-4	1990	Continuous CHOP protocol consists of initial 8 weeks of intensive chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisolone, followed by local/cranial radiotherapy and maintenance therapy.	Cyclophosphamide	84-100	DNA damage inducible transcript 3	Homo sapiens	11-15
2317799-9	1990	Enhanced antibacterial resistance by IL-1 and OK432 was also observed in cyclophosphamide- and aminomethylpyrimidinylmethylchloroethylnitrosourea hydrochloride-pretreated (day -5) normal hosts and in cyclophosphamide-treated tumor-bearing hosts.	Cyclophosphamide	73-89	interleukin 1 complex	Mus musculus	37-41
2317799-9	1990	Enhanced antibacterial resistance by IL-1 and OK432 was also observed in cyclophosphamide- and aminomethylpyrimidinylmethylchloroethylnitrosourea hydrochloride-pretreated (day -5) normal hosts and in cyclophosphamide-treated tumor-bearing hosts.	Cyclophosphamide	200-216	interleukin 1 complex	Mus musculus	37-41
2317799-11	1990	or s.c.) (days -4 to -1), a statistical difference in survival rate between granulocyte colony-stimulating factor and its vehicle-treated groups was observed in cyclophosphamide-pretreated hosts, but not in normal hosts or aminomethylpyrimidinylmethylchloroethylnitrosourea hydrochloride-pretreated hosts.	Cyclophosphamide	161-177	colony stimulating factor 3 (granulocyte)	Mus musculus	76-113
1690032-0	1990	Quantitative in vivo assay of human granulocyte colony-stimulating factor using cyclophosphamide-induced neutropenic mice.	Cyclophosphamide	80-96	colony stimulating factor 3	Homo sapiens	36-73
1690032-1	1990	Administration of human granulocyte colony-stimulating factor (hG-CSF) to mice with cyclophosphamide (CPA)-induced neutropenia for 4 consecutive days from the day after the CPA dosing (100 mg/kg) resulted in a dose-dependent increase in the peripheral blood neutrophil count 6 hours after the final hG-CSF injection.	Cyclophosphamide	84-100	colony stimulating factor 3	Homo sapiens	24-61
1690032-1	1990	Administration of human granulocyte colony-stimulating factor (hG-CSF) to mice with cyclophosphamide (CPA)-induced neutropenia for 4 consecutive days from the day after the CPA dosing (100 mg/kg) resulted in a dose-dependent increase in the peripheral blood neutrophil count 6 hours after the final hG-CSF injection.	Cyclophosphamide	84-100	colony stimulating factor 3	Homo sapiens	63-69
1690032-1	1990	Administration of human granulocyte colony-stimulating factor (hG-CSF) to mice with cyclophosphamide (CPA)-induced neutropenia for 4 consecutive days from the day after the CPA dosing (100 mg/kg) resulted in a dose-dependent increase in the peripheral blood neutrophil count 6 hours after the final hG-CSF injection.	Cyclophosphamide	84-100	colony stimulating factor 3	Homo sapiens	299-305
1690032-1	1990	Administration of human granulocyte colony-stimulating factor (hG-CSF) to mice with cyclophosphamide (CPA)-induced neutropenia for 4 consecutive days from the day after the CPA dosing (100 mg/kg) resulted in a dose-dependent increase in the peripheral blood neutrophil count 6 hours after the final hG-CSF injection.	Cyclophosphamide	102-105	colony stimulating factor 3	Homo sapiens	24-61
1690032-4	1990	Such an association never occurred with intact mice, and 100 mg/kg of CPA induced the highest response to hG-CSF.	Cyclophosphamide	70-73	colony stimulating factor 3	Homo sapiens	106-112
1690032-6	1990	When assayed by this bioassay procedure, which we have termed CPA-mouse assay, natural hG-CSF and recombinant hG-CSF (produced by Chinese hamster ovary cells) were nearly equipotent in specific biologic activity.	Cyclophosphamide	62-65	colony stimulating factor 3	Homo sapiens	87-93
1690032-7	1990	These results confirm the CPA-mouse assay as an especially useful assay method for quantifying the in vivo activity of hG-CSF.	Cyclophosphamide	26-29	colony stimulating factor 3	Homo sapiens	119-125
2317946-5	1990	Elevated NK activity was Cy dose- and time-dependent, was evident within 7 days post Cy/ovalbumin and persisted for at least 28 days.	Cyclophosphamide	25-27	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	88-97
2153765-1	1990	The present randomized, prospective study was designed to assess whether alternating induction cyclophosphamide, doxorubicin, vincristine-altretamine (hexamethylmelamine), etoposide, and methotrexate (CAV-HEM) chemotherapy is better than standard chemotherapy (CAV) in improving response, survival, and remission time in 577 evaluable patients having extensive-disease small-cell lung cancer (SCLC).	Cyclophosphamide	95-111	caveolin 2	Homo sapiens	201-204
2106164-1	1990	In vitro and in vivo studies with N,N",N""-triethylene-thiophosphoramide (thiotepa) alone and in combination with cyclophosphamide (CTX) were carried out using the MCF-7 human breast carcinoma cell line and the EMT6 mouse mammary carcinoma cell line.	Cyclophosphamide	114-130	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	132-135
2154857-2	1990	Twenty-five patients had prior exposure to cisplatin plus etoposide, and 14 of the 26 patients (54%) had prior therapy with CAV (cyclophosphamide, doxorubicin, and vincristine).	Cyclophosphamide	129-145	caveolin 2	Homo sapiens	124-127
2144163-6	1990	The log leukaemic stem cell kill (LCK) values, as estimated by a survival assay, were 1.8, 0.7, and 5.4 for the leukaemic rats injected with cyclophosphamide (day 12), with daunorubicin (day 14), or with cyclophosphamide (day 12) plus daunorubicin (day 14), respectively).	Cyclophosphamide	141-157	LCK proto-oncogene, Src family tyrosine kinase	Rattus norvegicus	34-37
2144163-7	1990	The simultaneous administration of cyclophosphamide and daunorubicin at day 14, induced a LCK of 2.7, a value that was the sum of the LCKs of cyclophosphamide and daunorubicin alone.	Cyclophosphamide	35-51	LCK proto-oncogene, Src family tyrosine kinase	Rattus norvegicus	90-93
2144163-7	1990	The simultaneous administration of cyclophosphamide and daunorubicin at day 14, induced a LCK of 2.7, a value that was the sum of the LCKs of cyclophosphamide and daunorubicin alone.	Cyclophosphamide	142-158	LCK proto-oncogene, Src family tyrosine kinase	Rattus norvegicus	90-93
1972131-1	1990	Five patients with high risk multiple myeloma not responsive to standard chemotherapy were treated by high-dose chemotherapy (Melphalan, Cyclophosphamide) (HDC) and total body irradiation (TBI) followed by autografting with blood stem cells.	Cyclophosphamide	137-153	histidine decarboxylase	Homo sapiens	156-159
2190884-2	1990	We report that sizable numbers of CD34+ cells transiently circulate in the peripheral blood (PB) of patients treated with high-dose (7 g/sqm) cyclophosphamide (HD-CTX) with or without recombinant human glycosylated granulocyte macrophage colony stimulating factor (rhGM-CSF).	Cyclophosphamide	142-158	CD34 molecule	Homo sapiens	34-38
2190885-0	1990	High-dose cyclophosphamide in patients with operable breast cancer: recombinant human GM-CSF ameliorates drug-induced leukopenia and thrombocytopenia.	Cyclophosphamide	10-26	colony stimulating factor 2	Homo sapiens	86-92
1691246-1	1990	This manuscript summarizes our experience with recombinant human granulocyte colony-stimulating factor (rhG-CSF) with high-dose Cytoxan, carmustine and etoposide (CBV in Hodgkin"s disease).	Cyclophosphamide	128-135	colony stimulating factor 3	Homo sapiens	65-102
1704477-1	1990	Protective effect of recombinant human granulocyte colony-stimulating factor (rG-CSF) on microbial infections was studied in cyclophosphamide (CPA)-induced neutropenic mice.	Cyclophosphamide	125-141	colony stimulating factor 3	Rattus norvegicus	78-84
1704477-3	1990	When such mice were injected subcutaneously with rG-CSF on four consecutive days beginning the day after CPA injection, the decreased anti-microbial resistance of the mice was restored to the level of that in normal mice.	Cyclophosphamide	105-108	colony stimulating factor 3	Rattus norvegicus	49-55
33591324-1	2021	Rituximab plus cyclophosphamide-doxorubicin-vincristine-prednisone (R-CHOP) is the standard of care for untreated diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	15-31	DNA damage inducible transcript 3	Homo sapiens	70-74
2191233-3	1990	Treatment with intravenous corticosteroids and oral cyclophosphamide (CTX) failed to arrest the decline in renal function.	Cyclophosphamide	52-68	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	70-73
2134689-5	1990	The P-450 catalyzed benzo[a]pyrene and tolbutamide hydroxylations and cyclophosphamide oxidation, but showed low activity for the mutagenic activation of IQ (2-amino-3-methylimidazo [4, 5-f]quinoline).	Cyclophosphamide	70-86	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	4-9
2136026-1	1990	We investigated the mechanism of cyclophosphamide (CTX) induced ovarian toxicity by studying the effect of an activated form, 4-hydroperoxycyclophosphamide (PCTX), on human and rat granulosa cell function in vitro.	Cyclophosphamide	33-49	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	51-54
2136026-8	1990	The above findings demonstrate that cyclophosphamide metabolites, at concentrations achievable in vivo during CTX therapy, decrease rat and human granulosa cell function in vitro.	Cyclophosphamide	36-52	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	110-113
2076177-4	1990	Plasma IgG2a elevation after LDV infection was greatly delayed and reduced by depletion of the mice of CD4+, but not of CD8+, T cells by administration of protein-G-purified anti-CD4 or anti-CD8 mAbs, and completely inhibited by repeated treatment of the mice with cyclophosphamide.	Cyclophosphamide	265-281	immunoglobulin heavy variable V1-9	Mus musculus	7-12
2076177-4	1990	Plasma IgG2a elevation after LDV infection was greatly delayed and reduced by depletion of the mice of CD4+, but not of CD8+, T cells by administration of protein-G-purified anti-CD4 or anti-CD8 mAbs, and completely inhibited by repeated treatment of the mice with cyclophosphamide.	Cyclophosphamide	265-281	CD4 antigen	Mus musculus	103-106
2343578-5	1990	An increase of middle lifetime and recovery of 24% mice of C57BL/6 strain with leukosis EL-4 were observed after complex treatment of the animals with GMDP, lipopolysaccharide, cyclophosphane and indomethacin.	Cyclophosphamide	177-191	epilepsy 4	Mus musculus	88-92
33813365-17	2021	The astA gene was detected in 27 (41.5%) mcr-ESBL-Ec isolates demonstrating their potential virulence.	Cyclophosphamide	4-8	EsbL	Escherichia coli	45-49
33944646-5	2021	The main focus of this study was on newly diagnosed patients receiving cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) versus other chemotherapy.	Cyclophosphamide	71-87	DNA damage inducible transcript 3	Homo sapiens	131-135
33775207-0	2021	C-reactive protein and ground-glass opacity as predictors for intractable interstitial lung disease in patients with systemic sclerosis under cyclophosphamide treatment regardless of concomitant glucocorticoids.	Cyclophosphamide	142-158	C-reactive protein	Homo sapiens	0-18
33775207-11	2021	CONCLUSIONS: High CRP levels with non-widespread GGO predicted progressive ILD in patients with SSc treated with CYC.	Cyclophosphamide	113-116	C-reactive protein	Homo sapiens	18-21
33818020-1	2021	PURPOSE: This study aimed to investigate the changes in microRNA-130a (miR-130a) and its correlation with cardiotoxicity during epirubicin/cyclophosphamide followed by docetaxel plus trastuzumab (EC-D+T) adjuvant chemotherapy in human epidermal growth factor receptor-2-positive (HER2+) breast cancer patients.	Cyclophosphamide	139-155	microRNA 130a	Homo sapiens	56-69
33818020-1	2021	PURPOSE: This study aimed to investigate the changes in microRNA-130a (miR-130a) and its correlation with cardiotoxicity during epirubicin/cyclophosphamide followed by docetaxel plus trastuzumab (EC-D+T) adjuvant chemotherapy in human epidermal growth factor receptor-2-positive (HER2+) breast cancer patients.	Cyclophosphamide	139-155	microRNA 130a	Homo sapiens	71-79
33798588-6	2021	CSL-0.1 increased the spleen and thymus indices in a dose-dependent manner and conferred immunomodulation on reversing the Th1/Th2-related cytokine imbalance in cyclophosphamide (CP)-induced immunosuppressed mice.	Cyclophosphamide	161-177	citrate synthase like	Mus musculus	0-3
33770141-13	2021	Cyclophosphamide pretreatment eliminated the survival benefit of Cse+/+ mice, whereas BMT increased the survival of Cse-/- mice.	Cyclophosphamide	0-16	cystathionase (cystathionine gamma-lyase)	Mus musculus	65-68
33766090-9	2021	RESULTS: IRF8 expression can precisely predict the complete pathological response to monoclonal antibody therapy or to select combinations of chemotherapy such as FAC (fluorouracil, adriamycin, and cytoxan) in ER-negative BC subtypes.	Cyclophosphamide	198-205	interferon regulatory factor 8	Homo sapiens	9-13
33766090-9	2021	RESULTS: IRF8 expression can precisely predict the complete pathological response to monoclonal antibody therapy or to select combinations of chemotherapy such as FAC (fluorouracil, adriamycin, and cytoxan) in ER-negative BC subtypes.	Cyclophosphamide	198-205	epiregulin	Homo sapiens	210-212
33769265-9	2021	Former cyclophosphamide therapy, thus more severe type of the disease was referred to the increased thrombin generation.	Cyclophosphamide	7-23	coagulation factor II, thrombin	Homo sapiens	100-108
33763830-0	2021	Allicin mitigates hepatic injury following cyclophosphamide administration via activation of Nrf2/ARE pathways and through inhibition of inflammatory and apoptotic machinery.	Cyclophosphamide	43-59	NFE2 like bZIP transcription factor 2	Rattus norvegicus	93-97
33819481-0	2021	Feasibility and Efficacy of CD45RA+ Depleted Donor Lymphocytes Infusion After Haploidentical Transplantation With Post-Transplantation Cyclophosphamide in Patients With Hematological Malignancies.	Cyclophosphamide	135-151	protein tyrosine phosphatase receptor type C	Homo sapiens	28-34
33778186-2	2021	Cyclophosphamide (CTX) not only directly kills tumors but also causes immunogenic cell death, providing a promising source of antigens for cancer vaccines.	Cyclophosphamide	0-16	V-set and immunoglobulin domain containing 2	Mus musculus	18-21
33233444-2	2020	CHOP, consisting of cyclophosphamide (CPA), doxorubicin, vincristine, and prednisone, is a first-generation chemotherapy extensively used to treat NHL.	Cyclophosphamide	20-36	DNA-damage inducible transcript 3	Mus musculus	0-4
33233444-2	2020	CHOP, consisting of cyclophosphamide (CPA), doxorubicin, vincristine, and prednisone, is a first-generation chemotherapy extensively used to treat NHL.	Cyclophosphamide	38-41	DNA-damage inducible transcript 3	Mus musculus	0-4
33233444-4	2020	CPA, an integral component of CHOP, is a prodrug that requires CYP2B6-mediated bioactivation to 4-hydroxy-CPA (4-OH-CPA).	Cyclophosphamide	0-3	DNA damage inducible transcript 3	Homo sapiens	30-34
33233444-4	2020	CPA, an integral component of CHOP, is a prodrug that requires CYP2B6-mediated bioactivation to 4-hydroxy-CPA (4-OH-CPA).	Cyclophosphamide	0-3	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	63-69
30091025-1	2018	The standard treatment for diffuse large B cell lymphoma (DLBCL) is rituximab with CHOP (cyclophosphamide, doxorubicin, vincristine (VCR), and prednisone).	Cyclophosphamide	89-105	DNA damage inducible transcript 3	Homo sapiens	83-87
26159874-5	2015	The incidence of PM status by phenotype following administration of omeprazole/esomeprazole (known inhibitors of CYP2C19) was 10-fold higher than those who are genetically PMs in the general population, which could have critical clinical implications for personalizing medications primarily metabolized by CYP2C19, such as clopidogrel, PPI, cyclophosphamide, thalidomide, citalopram, clonazepam, diazepam, phenytoin, etc.	Cyclophosphamide	341-357	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	113-120
25589624-1	2015	PURPOSE: Veliparib, a PARP inhibitor, demonstrated clinical activity in combination with oral cyclophosphamide in patients with BRCA-mutant solid tumors in a phase I trial.	Cyclophosphamide	94-110	BRCA1 DNA repair associated	Homo sapiens	128-132
25589624-9	2015	CONCLUSION: This is the first trial that evaluated single-agent, low-dose cyclophosphamide in HGSOC, peritoneal, fallopian tube, and BRCA-mutant ovarian cancers.	Cyclophosphamide	74-90	BRCA1 DNA repair associated	Homo sapiens	133-137
24932293-5	2014	The effects of chemotherapy drugs, cyclophosphamide (CTX) and pirarubicin (THP), on the expression of these two genes were also investigated.	Cyclophosphamide	35-51	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	53-56
22357256-3	2012	PATIENTS AND METHODS: DNA was isolated and BRCA1-like status was assessed in 101 patients with early-stage TNBC receiving adjuvant cyclophosphamide-based chemotherapy.	Cyclophosphamide	131-147	BRCA1 DNA repair associated	Homo sapiens	43-48
34945585-1	2021	We previously reported that the immunostimulatory activity of heat-killed Latilactobacillus sakei K040706 in macrophages and cyclophosphamide (CTX)-treated mice.	Cyclophosphamide	125-141	V-set and immunoglobulin domain containing 2	Mus musculus	143-146
34160685-9	2022	However, additional combination with cyclophosphamide or axitinib, a vascular endothelial growth factor receptor inhibitor, induced complete regression in half of the RENCA/hCA9-bearing aged mice with increased expression of PD-L1 in tumor tissues.	Cyclophosphamide	37-53	carbonic anhydrase 9	Homo sapiens	173-177
34160685-9	2022	However, additional combination with cyclophosphamide or axitinib, a vascular endothelial growth factor receptor inhibitor, induced complete regression in half of the RENCA/hCA9-bearing aged mice with increased expression of PD-L1 in tumor tissues.	Cyclophosphamide	37-53	CD274 antigen	Mus musculus	225-230
34597426-1	2022	This study evaluated the mechanistic sequel of aldehyde dehyrogenase (ALDH2) and Klotho protein in cyclophosphamide (CP)-induced cardiotoxicity in rats and the protective effect of astaxanthin (AST) against that sequel.	Cyclophosphamide	99-115	aldehyde dehydrogenase 2 family member	Rattus norvegicus	70-75
34597426-1	2022	This study evaluated the mechanistic sequel of aldehyde dehyrogenase (ALDH2) and Klotho protein in cyclophosphamide (CP)-induced cardiotoxicity in rats and the protective effect of astaxanthin (AST) against that sequel.	Cyclophosphamide	99-115	Klotho	Rattus norvegicus	81-87
34843406-2	2022	Cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) therapy is widely used as first-line treatment of PTCL; however, it has limited efficacy.	Cyclophosphamide	0-16	DNA damage inducible transcript 3	Homo sapiens	60-64
34969250-6	2022	We then applied this method to evaluate endogenous DNA damage to human embryonic lung fibroblast cells exposed to five nitrogen mustards (NMs, i.e., HN1, HN2, HN3, chlorambucil (CB), and cyclophosphamide (CTX)), where curcumin exposure was used as a control due to its inability to induce the formation of endogenous DNA adducts.	Cyclophosphamide	187-203	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	205-208
34591162-0	2022	Long-term outcomes following the addition of granulocyte colony-stimulating factor-combined high-dose cytarabine to total body irradiation and cyclophosphamide conditioning in single-unit cord blood transplantation for myeloid malignancies.	Cyclophosphamide	143-159	colony stimulating factor 3	Homo sapiens	45-82
34580862-0	2022	Donor source and post-transplantation cyclophosphamide influence outcome in allogeneic stem cell transplantation for GATA2 deficiency.	Cyclophosphamide	38-54	GATA binding protein 2	Homo sapiens	117-122
34312098-2	2022	The aim of this study is to compare the efficacy and late-onset cardiac toxicity of neoadjuvant chemotherapy regimens, trastuzumab plus paclitaxel followed by 5-fluorouracil, epirubicin, and cyclophosphamide (PH-FECH) versus trastuzumab plus docetaxel and carboplatin (TCH), for human epidermal growth factor receptor 2-positive (HER2+) breast cancer (BC).	Cyclophosphamide	191-207	ferrochelatase	Homo sapiens	212-216
34312098-2	2022	The aim of this study is to compare the efficacy and late-onset cardiac toxicity of neoadjuvant chemotherapy regimens, trastuzumab plus paclitaxel followed by 5-fluorouracil, epirubicin, and cyclophosphamide (PH-FECH) versus trastuzumab plus docetaxel and carboplatin (TCH), for human epidermal growth factor receptor 2-positive (HER2+) breast cancer (BC).	Cyclophosphamide	191-207	erb-b2 receptor tyrosine kinase 2	Homo sapiens	285-319
34312098-2	2022	The aim of this study is to compare the efficacy and late-onset cardiac toxicity of neoadjuvant chemotherapy regimens, trastuzumab plus paclitaxel followed by 5-fluorouracil, epirubicin, and cyclophosphamide (PH-FECH) versus trastuzumab plus docetaxel and carboplatin (TCH), for human epidermal growth factor receptor 2-positive (HER2+) breast cancer (BC).	Cyclophosphamide	191-207	erb-b2 receptor tyrosine kinase 2	Homo sapiens	330-334
34813868-6	2022	IL-6 content in serum of mice was significantly higher than that of the control group provided with cyclophosphamide (CTX).	Cyclophosphamide	100-116	interleukin 6	Mus musculus	0-4
34592784-1	2022	AIM: To explore the effect of TEC chemotherapy regimen (Docetaxel + Epirubicin + Cyclophosphamide) on traditional cardiovascular risk factors, atherosclerotic cardiovascular disease and cardiac electrical activity.	Cyclophosphamide	81-97	tec protein tyrosine kinase	Homo sapiens	30-33
34622458-9	2022	CONCLUSIONS: Estrogen has a direct effect on the regulation of bladder overactivity in rats with cyclophosphamide-induced cystitis by downregulating the expression of bladder epithelial P2X3 receptors through ERbeta and reducing the adenosine triphosphate released from urothelium during bladder filling, thereby inhibiting the generation of the micturition reflex.	Cyclophosphamide	97-113	estrogen receptor 2	Rattus norvegicus	209-215
34607074-0	2022	Effect of donor NKG2D polymorphism on relapse after haploidentical transplantation with post-transplant cyclophosphamide.	Cyclophosphamide	104-120	killer cell lectin like receptor K1	Homo sapiens	16-21
34990525-1	2021	Purpose: Febrile neutropenia (FN) can cause suboptimal treatment and treatment-related mortality (TRM) in diffuse large B-cell lymphoma (DLBCL) patients treated with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP).	Cyclophosphamide	177-193	DNA damage inducible transcript 3	Homo sapiens	241-245
34987399-6	2021	The results showed that SA could alleviate the immunosuppression induced by cyclophosphamide in mice and regulate the protein expression of Jun, Trp53, and Creb1 in the spleen tissue of mice, together with the transcription factors Atf4 and E2f2.	Cyclophosphamide	76-92	transformation related protein 53	Mus musculus	145-150
34987399-6	2021	The results showed that SA could alleviate the immunosuppression induced by cyclophosphamide in mice and regulate the protein expression of Jun, Trp53, and Creb1 in the spleen tissue of mice, together with the transcription factors Atf4 and E2f2.	Cyclophosphamide	76-92	cAMP responsive element binding protein 1	Mus musculus	156-161
34987399-6	2021	The results showed that SA could alleviate the immunosuppression induced by cyclophosphamide in mice and regulate the protein expression of Jun, Trp53, and Creb1 in the spleen tissue of mice, together with the transcription factors Atf4 and E2f2.	Cyclophosphamide	76-92	activating transcription factor 4	Mus musculus	232-236
34949747-4	2022	In this study, crude polysaccharides (GBP) were isolated from Korean ginseng berries and their immunomodulatory activities were investigated using cyclophosphamide (CY)-induced immunosuppressive BALB/c mice.	Cyclophosphamide	147-163	protein inhibitor of activated STAT 1	Mus musculus	38-41
34949747-4	2022	In this study, crude polysaccharides (GBP) were isolated from Korean ginseng berries and their immunomodulatory activities were investigated using cyclophosphamide (CY)-induced immunosuppressive BALB/c mice.	Cyclophosphamide	165-167	protein inhibitor of activated STAT 1	Mus musculus	38-41
34949747-5	2022	In CY-treated mice, oral administration of GBP (50-500 mg/kg BW) remarkably increased their spleen sizes and spleen indices and activated NK cell activities.	Cyclophosphamide	3-5	protein inhibitor of activated STAT 1	Mus musculus	43-46
34949747-7	2022	In addition, GBP significantly stimulated mRNA expression levels of immune-associated genes including interleukin-1beta (IL-1beta), IL-2, IL-4, IL-6, tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), Toll-like receptor 4 (TLR-4), and cyclooxygenase-2 (COX-2) in CY-treated mice.	Cyclophosphamide	283-285	protein inhibitor of activated STAT 1	Mus musculus	13-16
34949747-7	2022	In addition, GBP significantly stimulated mRNA expression levels of immune-associated genes including interleukin-1beta (IL-1beta), IL-2, IL-4, IL-6, tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), Toll-like receptor 4 (TLR-4), and cyclooxygenase-2 (COX-2) in CY-treated mice.	Cyclophosphamide	283-285	interleukin 1 beta	Mus musculus	102-119
34949747-7	2022	In addition, GBP significantly stimulated mRNA expression levels of immune-associated genes including interleukin-1beta (IL-1beta), IL-2, IL-4, IL-6, tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), Toll-like receptor 4 (TLR-4), and cyclooxygenase-2 (COX-2) in CY-treated mice.	Cyclophosphamide	283-285	interleukin 1 alpha	Mus musculus	121-129
34949747-7	2022	In addition, GBP significantly stimulated mRNA expression levels of immune-associated genes including interleukin-1beta (IL-1beta), IL-2, IL-4, IL-6, tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), Toll-like receptor 4 (TLR-4), and cyclooxygenase-2 (COX-2) in CY-treated mice.	Cyclophosphamide	283-285	interleukin 2	Mus musculus	132-136
34949747-7	2022	In addition, GBP significantly stimulated mRNA expression levels of immune-associated genes including interleukin-1beta (IL-1beta), IL-2, IL-4, IL-6, tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), Toll-like receptor 4 (TLR-4), and cyclooxygenase-2 (COX-2) in CY-treated mice.	Cyclophosphamide	283-285	interleukin 4	Mus musculus	138-142
34949747-7	2022	In addition, GBP significantly stimulated mRNA expression levels of immune-associated genes including interleukin-1beta (IL-1beta), IL-2, IL-4, IL-6, tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), Toll-like receptor 4 (TLR-4), and cyclooxygenase-2 (COX-2) in CY-treated mice.	Cyclophosphamide	283-285	interleukin 6	Mus musculus	144-148
34949747-7	2022	In addition, GBP significantly stimulated mRNA expression levels of immune-associated genes including interleukin-1beta (IL-1beta), IL-2, IL-4, IL-6, tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), Toll-like receptor 4 (TLR-4), and cyclooxygenase-2 (COX-2) in CY-treated mice.	Cyclophosphamide	283-285	tumor necrosis factor	Mus musculus	150-177
34949747-7	2022	In addition, GBP significantly stimulated mRNA expression levels of immune-associated genes including interleukin-1beta (IL-1beta), IL-2, IL-4, IL-6, tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), Toll-like receptor 4 (TLR-4), and cyclooxygenase-2 (COX-2) in CY-treated mice.	Cyclophosphamide	283-285	tumor necrosis factor	Mus musculus	179-188
34949747-7	2022	In addition, GBP significantly stimulated mRNA expression levels of immune-associated genes including interleukin-1beta (IL-1beta), IL-2, IL-4, IL-6, tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), Toll-like receptor 4 (TLR-4), and cyclooxygenase-2 (COX-2) in CY-treated mice.	Cyclophosphamide	283-285	interferon gamma	Mus musculus	191-207
34949747-7	2022	In addition, GBP significantly stimulated mRNA expression levels of immune-associated genes including interleukin-1beta (IL-1beta), IL-2, IL-4, IL-6, tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), Toll-like receptor 4 (TLR-4), and cyclooxygenase-2 (COX-2) in CY-treated mice.	Cyclophosphamide	283-285	interferon gamma	Mus musculus	209-218
34949747-7	2022	In addition, GBP significantly stimulated mRNA expression levels of immune-associated genes including interleukin-1beta (IL-1beta), IL-2, IL-4, IL-6, tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), Toll-like receptor 4 (TLR-4), and cyclooxygenase-2 (COX-2) in CY-treated mice.	Cyclophosphamide	283-285	toll-like receptor 4	Mus musculus	221-241
34949747-7	2022	In addition, GBP significantly stimulated mRNA expression levels of immune-associated genes including interleukin-1beta (IL-1beta), IL-2, IL-4, IL-6, tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), Toll-like receptor 4 (TLR-4), and cyclooxygenase-2 (COX-2) in CY-treated mice.	Cyclophosphamide	283-285	prostaglandin-endoperoxide synthase 2	Mus musculus	255-271
34949747-7	2022	In addition, GBP significantly stimulated mRNA expression levels of immune-associated genes including interleukin-1beta (IL-1beta), IL-2, IL-4, IL-6, tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), Toll-like receptor 4 (TLR-4), and cyclooxygenase-2 (COX-2) in CY-treated mice.	Cyclophosphamide	283-285	prostaglandin-endoperoxide synthase 2	Mus musculus	273-278
34949747-8	2022	These results indicate that GBP is involved in immune effects against CY-induced immunosuppression.	Cyclophosphamide	70-72	protein inhibitor of activated STAT 1	Mus musculus	28-31
34921960-2	2022	The ECHELON-2 study demonstrated that brentuximab vedotin plus cyclophosphamide, doxorubicin, and prednisone (A+CHP) exhibited statistically superior progression-free survival (PFS) per independent central review and improvements in overall survival vs cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) for the frontline treatment of patients with systemic anaplastic large cell lymphoma or other CD30-positive PTCL.	Cyclophosphamide	63-79	ras homolog family member V	Homo sapiens	112-115
34921960-2	2022	The ECHELON-2 study demonstrated that brentuximab vedotin plus cyclophosphamide, doxorubicin, and prednisone (A+CHP) exhibited statistically superior progression-free survival (PFS) per independent central review and improvements in overall survival vs cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) for the frontline treatment of patients with systemic anaplastic large cell lymphoma or other CD30-positive PTCL.	Cyclophosphamide	63-79	TNF receptor superfamily member 8	Homo sapiens	413-417
34821227-1	2021	This work aimed to investigate the effects of a sulfated derivative of Cyclocarya paliurus polysaccharide (SCP3) on cyclophosphamide (CTX)-induced intestinal barrier damage and intestinal microbiota in mice.	Cyclophosphamide	116-132	synaptonemal complex protein 3	Mus musculus	107-111
34955900-5	2021	We previously showed that in the absence of AVP, sertraline, carbamazepine, haloperidol, and cyclophosphamide each increased vasopressin V2 receptor (V2R) mRNA and aquaporin-2 (AQP2) protein and mRNA expression in primary cultured inner medullary collecting duct cells.	Cyclophosphamide	93-109	arginine vasopressin receptor 2	Homo sapiens	125-148
34955900-5	2021	We previously showed that in the absence of AVP, sertraline, carbamazepine, haloperidol, and cyclophosphamide each increased vasopressin V2 receptor (V2R) mRNA and aquaporin-2 (AQP2) protein and mRNA expression in primary cultured inner medullary collecting duct cells.	Cyclophosphamide	93-109	arginine vasopressin receptor 2	Homo sapiens	150-153
34955900-5	2021	We previously showed that in the absence of AVP, sertraline, carbamazepine, haloperidol, and cyclophosphamide each increased vasopressin V2 receptor (V2R) mRNA and aquaporin-2 (AQP2) protein and mRNA expression in primary cultured inner medullary collecting duct cells.	Cyclophosphamide	93-109	aquaporin 2	Homo sapiens	164-175
34955900-5	2021	We previously showed that in the absence of AVP, sertraline, carbamazepine, haloperidol, and cyclophosphamide each increased vasopressin V2 receptor (V2R) mRNA and aquaporin-2 (AQP2) protein and mRNA expression in primary cultured inner medullary collecting duct cells.	Cyclophosphamide	93-109	aquaporin 2	Homo sapiens	177-181
34870568-0	2021	Underutilisation of prophylactic G-CSF in breast cancer patients receiving adjuvant docetaxel/cyclophosphamide chemotherapy.	Cyclophosphamide	94-110	colony stimulating factor 3	Homo sapiens	33-38
34699004-0	2021	Neoadjuvant Therapy with Concurrent Docetaxel, Epirubicin, and Cyclophosphamide (TEC) in High-Risk HER2-Negative Breast Cancers.	Cyclophosphamide	63-79	tec protein tyrosine kinase	Homo sapiens	81-84
34699004-0	2021	Neoadjuvant Therapy with Concurrent Docetaxel, Epirubicin, and Cyclophosphamide (TEC) in High-Risk HER2-Negative Breast Cancers.	Cyclophosphamide	63-79	erb-b2 receptor tyrosine kinase 2	Homo sapiens	99-103
34699004-2	2021	Data on efficacy and tolerance to 6 cycles of concurrent docetaxel, epirubicin, and cyclophosphamide (TEC) is limited.	Cyclophosphamide	84-100	tec protein tyrosine kinase	Homo sapiens	102-105
34854117-3	2022	Cyclophosphamide caused a significant increase in the activities of indoleamine 2, 3-dioxygenases (IDO), tryptophan 2, 3-dioxygenase (TDO), myeloperoxidase (MPO), and elevated the concentrations of interleukin 6 (IL-6) and interferon-gamma (IFN-gamma).	Cyclophosphamide	0-16	indoleamine 2,3-dioxygenase 1	Rattus norvegicus	68-97
34854117-3	2022	Cyclophosphamide caused a significant increase in the activities of indoleamine 2, 3-dioxygenases (IDO), tryptophan 2, 3-dioxygenase (TDO), myeloperoxidase (MPO), and elevated the concentrations of interleukin 6 (IL-6) and interferon-gamma (IFN-gamma).	Cyclophosphamide	0-16	indoleamine 2,3-dioxygenase 1	Rattus norvegicus	99-102
34854117-3	2022	Cyclophosphamide caused a significant increase in the activities of indoleamine 2, 3-dioxygenases (IDO), tryptophan 2, 3-dioxygenase (TDO), myeloperoxidase (MPO), and elevated the concentrations of interleukin 6 (IL-6) and interferon-gamma (IFN-gamma).	Cyclophosphamide	0-16	tryptophan 2,3-dioxygenase	Rattus norvegicus	105-132
34854117-3	2022	Cyclophosphamide caused a significant increase in the activities of indoleamine 2, 3-dioxygenases (IDO), tryptophan 2, 3-dioxygenase (TDO), myeloperoxidase (MPO), and elevated the concentrations of interleukin 6 (IL-6) and interferon-gamma (IFN-gamma).	Cyclophosphamide	0-16	tryptophan 2,3-dioxygenase	Rattus norvegicus	134-137
34854117-3	2022	Cyclophosphamide caused a significant increase in the activities of indoleamine 2, 3-dioxygenases (IDO), tryptophan 2, 3-dioxygenase (TDO), myeloperoxidase (MPO), and elevated the concentrations of interleukin 6 (IL-6) and interferon-gamma (IFN-gamma).	Cyclophosphamide	0-16	myeloperoxidase	Rattus norvegicus	140-155
34854117-3	2022	Cyclophosphamide caused a significant increase in the activities of indoleamine 2, 3-dioxygenases (IDO), tryptophan 2, 3-dioxygenase (TDO), myeloperoxidase (MPO), and elevated the concentrations of interleukin 6 (IL-6) and interferon-gamma (IFN-gamma).	Cyclophosphamide	0-16	myeloperoxidase	Rattus norvegicus	157-160
34854117-3	2022	Cyclophosphamide caused a significant increase in the activities of indoleamine 2, 3-dioxygenases (IDO), tryptophan 2, 3-dioxygenase (TDO), myeloperoxidase (MPO), and elevated the concentrations of interleukin 6 (IL-6) and interferon-gamma (IFN-gamma).	Cyclophosphamide	0-16	interleukin 6	Rattus norvegicus	198-211
34854117-3	2022	Cyclophosphamide caused a significant increase in the activities of indoleamine 2, 3-dioxygenases (IDO), tryptophan 2, 3-dioxygenase (TDO), myeloperoxidase (MPO), and elevated the concentrations of interleukin 6 (IL-6) and interferon-gamma (IFN-gamma).	Cyclophosphamide	0-16	interleukin 6	Rattus norvegicus	213-217
34854117-3	2022	Cyclophosphamide caused a significant increase in the activities of indoleamine 2, 3-dioxygenases (IDO), tryptophan 2, 3-dioxygenase (TDO), myeloperoxidase (MPO), and elevated the concentrations of interleukin 6 (IL-6) and interferon-gamma (IFN-gamma).	Cyclophosphamide	0-16	interferon gamma	Rattus norvegicus	223-239
34854117-3	2022	Cyclophosphamide caused a significant increase in the activities of indoleamine 2, 3-dioxygenases (IDO), tryptophan 2, 3-dioxygenase (TDO), myeloperoxidase (MPO), and elevated the concentrations of interleukin 6 (IL-6) and interferon-gamma (IFN-gamma).	Cyclophosphamide	0-16	interferon gamma	Rattus norvegicus	241-250
34854117-4	2022	Cyclophosphamide increased testis malondialdehyde (MDA) concentrations but depleted superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and glutathione (GSH).	Cyclophosphamide	0-16	catalase	Rattus norvegicus	112-120
34854117-4	2022	Cyclophosphamide increased testis malondialdehyde (MDA) concentrations but depleted superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and glutathione (GSH).	Cyclophosphamide	0-16	catalase	Rattus norvegicus	122-125
34854117-8	2022	Thus, quercetin protected the testes against cyclophosphamide-induced alterations in immunosuppressive IDO/TDO activities elicited by oxidative-inflammatory mediators.	Cyclophosphamide	45-61	indoleamine 2,3-dioxygenase 1	Rattus norvegicus	103-106
34854117-8	2022	Thus, quercetin protected the testes against cyclophosphamide-induced alterations in immunosuppressive IDO/TDO activities elicited by oxidative-inflammatory mediators.	Cyclophosphamide	45-61	tryptophan 2,3-dioxygenase	Rattus norvegicus	107-110
34565287-0	2021	Silencing aurora-kinase-A (AURKA) reinforced the sensitivity of diffuse large B-cell lymphoma cells to cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) via suppressing beta-Catenin and RAS-extracellular signal-regulated protein kinase (ERK1/2) pathway.	Cyclophosphamide	103-119	aurora kinase A	Homo sapiens	10-25
34565287-0	2021	Silencing aurora-kinase-A (AURKA) reinforced the sensitivity of diffuse large B-cell lymphoma cells to cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) via suppressing beta-Catenin and RAS-extracellular signal-regulated protein kinase (ERK1/2) pathway.	Cyclophosphamide	103-119	aurora kinase A	Homo sapiens	27-32
34565287-0	2021	Silencing aurora-kinase-A (AURKA) reinforced the sensitivity of diffuse large B-cell lymphoma cells to cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) via suppressing beta-Catenin and RAS-extracellular signal-regulated protein kinase (ERK1/2) pathway.	Cyclophosphamide	103-119	DNA damage inducible transcript 3	Homo sapiens	163-167
34565287-0	2021	Silencing aurora-kinase-A (AURKA) reinforced the sensitivity of diffuse large B-cell lymphoma cells to cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) via suppressing beta-Catenin and RAS-extracellular signal-regulated protein kinase (ERK1/2) pathway.	Cyclophosphamide	103-119	catenin beta 1	Homo sapiens	185-197
34565287-0	2021	Silencing aurora-kinase-A (AURKA) reinforced the sensitivity of diffuse large B-cell lymphoma cells to cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) via suppressing beta-Catenin and RAS-extracellular signal-regulated protein kinase (ERK1/2) pathway.	Cyclophosphamide	103-119	mitogen-activated protein kinase 3	Homo sapiens	253-259
34565287-1	2021	The therapeutic effects of standard cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) therapy for prevalent lymphoma diffuse large B-cell lymphoma (DLBC, DLBCL) still require improvement.	Cyclophosphamide	36-52	DNA damage inducible transcript 3	Homo sapiens	95-99
34482064-0	2021	Betulinic acid attenuates cyclophosphamide-induced intestinal mucosa injury by inhibiting the NF-kappaB/MAPK signalling pathways and activating the Nrf2 signalling pathway.	Cyclophosphamide	26-42	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	94-103
34482064-0	2021	Betulinic acid attenuates cyclophosphamide-induced intestinal mucosa injury by inhibiting the NF-kappaB/MAPK signalling pathways and activating the Nrf2 signalling pathway.	Cyclophosphamide	26-42	nuclear factor, erythroid derived 2, like 2	Mus musculus	148-152
34592197-12	2021	The Drug resistance analysis demonstrated ADAM12 and COL1A2 up-regulation among 66 overexpressed CSPs caused resistance to Venetoclax and Cyclophosphamide with a high estimate, respectively.	Cyclophosphamide	138-154	ADAM metallopeptidase domain 12	Homo sapiens	42-48
34592197-12	2021	The Drug resistance analysis demonstrated ADAM12 and COL1A2 up-regulation among 66 overexpressed CSPs caused resistance to Venetoclax and Cyclophosphamide with a high estimate, respectively.	Cyclophosphamide	138-154	collagen type I alpha 2 chain	Homo sapiens	53-59
34865774-0	2021	Sulfated modification enhances the immunomodulatory effect of Cyclocarya paliurus polysaccharide on cyclophosphamide-induced immunosuppressed mice through MyD88-dependent MAPK/NF-kappaB and PI3K-Akt signaling pathways.	Cyclophosphamide	100-116	myeloid differentiation primary response gene 88	Mus musculus	155-160
34865774-0	2021	Sulfated modification enhances the immunomodulatory effect of Cyclocarya paliurus polysaccharide on cyclophosphamide-induced immunosuppressed mice through MyD88-dependent MAPK/NF-kappaB and PI3K-Akt signaling pathways.	Cyclophosphamide	100-116	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	176-185
34865774-0	2021	Sulfated modification enhances the immunomodulatory effect of Cyclocarya paliurus polysaccharide on cyclophosphamide-induced immunosuppressed mice through MyD88-dependent MAPK/NF-kappaB and PI3K-Akt signaling pathways.	Cyclophosphamide	100-116	thymoma viral proto-oncogene 1	Mus musculus	195-198
34658283-0	2021	Cyclophosphamide inhibits Pax5 methylation to regulate the growth of retinoblastoma via the Notch1 pathway.	Cyclophosphamide	0-16	paired box 5	Homo sapiens	26-30
34658283-0	2021	Cyclophosphamide inhibits Pax5 methylation to regulate the growth of retinoblastoma via the Notch1 pathway.	Cyclophosphamide	0-16	notch receptor 1	Homo sapiens	92-98
34658283-7	2021	Cyclophosphamide inhibited cell proliferation, migration, and invasion, promoted cell apoptosis via the Notch1 pathway.	Cyclophosphamide	0-16	notch receptor 1	Homo sapiens	104-110
34774073-0	2021	Correction to: Normalization of magnesium deficiency attenuated mechanical allodynia, depressive-like behaviors, and memory deficits associated with cyclophosphamide-induced cystitis by inhibiting TNF-alpha/NF-kappaB signaling in female rats.	Cyclophosphamide	149-165	tumor necrosis factor	Rattus norvegicus	197-206
34815664-0	2021	Activation of GPR18 by Resolvin D2 Relieves Pain and Improves Bladder Function in Cyclophosphamide-Induced Cystitis Through Inhibiting TRPV1.	Cyclophosphamide	82-98	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	135-140
34815664-11	2021	The mRNA and protein expression of GPR18 was reduced in the bladder and dorsal root ganglia (DRG) in rats with CYP-induced cystitis.	Cyclophosphamide	111-114	G protein-coupled receptor 18	Rattus norvegicus	35-40
34815664-15	2021	Conclusion: Activation of GPR18 by RvD2 alleviated hyperalgesia and improved bladder function, possibly by inhibiting TRPV1 in rats with CYP-induced cystitis.	Cyclophosphamide	137-140	G protein-coupled receptor 18	Rattus norvegicus	26-31
34820026-4	2021	We sought to identify the effect of cyclophosphamide (CTX), a drug commonly used for LN treatment, on MC proliferation and explore its underlying mechanisms.	Cyclophosphamide	36-52	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	54-57
34710846-4	2021	Cyclophosphamide (CTX) and GM -CSF were used to inhibit and stimulate bone marrow hematopoiesis, respectively.	Cyclophosphamide	0-16	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	18-21
34939392-1	2021	OBJECTIVE: To investigate the efficacy of needling acupoins of Guanyuan (CV4), Sanyinjiao (SP6), Zusanli (ST36), Pishu (BL20), Shenshu (BL23), Zigong (EX-CA1) on the expression of p38 mitogen-activated protein kinase (p38MAPK) in ovarian tissue in rats with premature ovarian failure induced by cyclophosphamide, and to study the underlying mechanism.	Cyclophosphamide	295-311	Sp6 transcription factor	Rattus norvegicus	91-94
34939392-1	2021	OBJECTIVE: To investigate the efficacy of needling acupoins of Guanyuan (CV4), Sanyinjiao (SP6), Zusanli (ST36), Pishu (BL20), Shenshu (BL23), Zigong (EX-CA1) on the expression of p38 mitogen-activated protein kinase (p38MAPK) in ovarian tissue in rats with premature ovarian failure induced by cyclophosphamide, and to study the underlying mechanism.	Cyclophosphamide	295-311	mitogen activated protein kinase 14	Rattus norvegicus	180-216
34939392-1	2021	OBJECTIVE: To investigate the efficacy of needling acupoins of Guanyuan (CV4), Sanyinjiao (SP6), Zusanli (ST36), Pishu (BL20), Shenshu (BL23), Zigong (EX-CA1) on the expression of p38 mitogen-activated protein kinase (p38MAPK) in ovarian tissue in rats with premature ovarian failure induced by cyclophosphamide, and to study the underlying mechanism.	Cyclophosphamide	295-311	mitogen activated protein kinase 14	Rattus norvegicus	218-225
34939392-10	2021	CONCLUSIONS: Acupuncture has the same effect as estrogen in interfering POF caused by cyclophosphamide, and its mechanism may be related to inhibiting the expression of p38MAPK protein in ovarian tissue and affecting the activation of p38MAPK signaling pathway.	Cyclophosphamide	86-102	mitogen activated protein kinase 14	Rattus norvegicus	169-176
34939392-10	2021	CONCLUSIONS: Acupuncture has the same effect as estrogen in interfering POF caused by cyclophosphamide, and its mechanism may be related to inhibiting the expression of p38MAPK protein in ovarian tissue and affecting the activation of p38MAPK signaling pathway.	Cyclophosphamide	86-102	mitogen activated protein kinase 14	Rattus norvegicus	235-242
34435547-0	2021	Lower dose of ATG combined with post-transplant cyclophosphamide for HLA matched RIC alloHCT is associated with effective control of GVHD and less viral infections.	Cyclophosphamide	48-64	FXYD domain containing ion transport regulator 5	Homo sapiens	81-84
34900377-9	2021	However, it was notable that the concomitant treatment with DOX and CPS resulted in a significant increase in serum levels of aspartate aminotransferase (AST).	Cyclophosphamide	68-71	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	126-152
34900377-9	2021	However, it was notable that the concomitant treatment with DOX and CPS resulted in a significant increase in serum levels of aspartate aminotransferase (AST).	Cyclophosphamide	68-71	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	154-157
34900377-10	2021	Elevated serum AST levels were also associated with increased serum creatinine kinase (CK) levels, suggesting that the elevated serum AST levels are likely due to muscle injury following the co-administration of DOX and CPS.	Cyclophosphamide	220-223	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	15-18
34900377-10	2021	Elevated serum AST levels were also associated with increased serum creatinine kinase (CK) levels, suggesting that the elevated serum AST levels are likely due to muscle injury following the co-administration of DOX and CPS.	Cyclophosphamide	220-223	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	134-137
34693876-0	2021	Huaiqihuang (HQH) granule alleviates cyclophosphamide-induced nephrotoxicity via suppressing the MAPK/NF-kappaB pathway and NLRP3 inflammasome activation.	Cyclophosphamide	37-53	NLR family, pyrin domain containing 3	Rattus norvegicus	124-129
34693876-9	2021	Additionally, HQH decreased the production of MDA (37.02%, 46.18%) and increased the activities of antioxidant enzyme CAT (59.18%, 112.25%) and SOD (67.10%, 308.34%) after CYP treatment.	Cyclophosphamide	172-175	catalase	Rattus norvegicus	118-121
34693876-11	2021	Furthermore, the phosphorylation of the NF-kappaB/MAPK pathway and the activation of the NLRP3 inflammasome were significantly boosted in CYP-treated rats, which was also abrogated by HQH treatment.	Cyclophosphamide	138-141	NLR family, pyrin domain containing 3	Rattus norvegicus	89-94
34563457-4	2021	However, by adding plerixafor to bortezomib and cyclophosphamide, collected CD34-positive cells were increased six-fold compared to the previous day.	Cyclophosphamide	48-64	CD34 molecule	Homo sapiens	76-80
34748891-9	2021	CYP-induced increase in the activities of immunosuppressive indoleamine 2, 3-dioxygenase (IDO) and tryptophan 2, 3-dioxygenase (TDO) in the tissues was abated in quercetin co-treated rats.	Cyclophosphamide	0-3	indoleamine 2,3-dioxygenase 1	Rattus norvegicus	60-88
34748891-9	2021	CYP-induced increase in the activities of immunosuppressive indoleamine 2, 3-dioxygenase (IDO) and tryptophan 2, 3-dioxygenase (TDO) in the tissues was abated in quercetin co-treated rats.	Cyclophosphamide	0-3	indoleamine 2,3-dioxygenase 1	Rattus norvegicus	90-93
34748891-9	2021	CYP-induced increase in the activities of immunosuppressive indoleamine 2, 3-dioxygenase (IDO) and tryptophan 2, 3-dioxygenase (TDO) in the tissues was abated in quercetin co-treated rats.	Cyclophosphamide	0-3	tryptophan 2,3-dioxygenase	Rattus norvegicus	99-126
34748891-9	2021	CYP-induced increase in the activities of immunosuppressive indoleamine 2, 3-dioxygenase (IDO) and tryptophan 2, 3-dioxygenase (TDO) in the tissues was abated in quercetin co-treated rats.	Cyclophosphamide	0-3	tryptophan 2,3-dioxygenase	Rattus norvegicus	128-131
34748891-10	2021	In conclusion, Quercetin ameliorated deficits in the hepatic-renal function in CYP-exposed rats by lowering the activities/expression of immunosuppressive IDO and TDO via diminution of oxidative-inflammatory stress.	Cyclophosphamide	79-82	indoleamine 2,3-dioxygenase 1	Rattus norvegicus	155-158
34748891-10	2021	In conclusion, Quercetin ameliorated deficits in the hepatic-renal function in CYP-exposed rats by lowering the activities/expression of immunosuppressive IDO and TDO via diminution of oxidative-inflammatory stress.	Cyclophosphamide	79-82	tryptophan 2,3-dioxygenase	Rattus norvegicus	163-166
34884588-0	2021	Downregulation of MMP-9 Enhances the Anti-Migratory Effect of Cyclophosphamide in MDA-MB-231 and MCF-7 Breast Cancer Cell Lines.	Cyclophosphamide	62-78	matrix metallopeptidase 9	Homo sapiens	18-23
34840584-8	2021	CPP upregulated the contents of cytokines (IL-2, IL-6, IFN-gamma, and TNF-alpha) in serum, which were downregulated by cyclophosphamide.	Cyclophosphamide	119-135	interleukin 2	Mus musculus	43-47
34840584-8	2021	CPP upregulated the contents of cytokines (IL-2, IL-6, IFN-gamma, and TNF-alpha) in serum, which were downregulated by cyclophosphamide.	Cyclophosphamide	119-135	interleukin 6	Mus musculus	49-53
34840584-8	2021	CPP upregulated the contents of cytokines (IL-2, IL-6, IFN-gamma, and TNF-alpha) in serum, which were downregulated by cyclophosphamide.	Cyclophosphamide	119-135	interferon gamma	Mus musculus	55-64
34840584-8	2021	CPP upregulated the contents of cytokines (IL-2, IL-6, IFN-gamma, and TNF-alpha) in serum, which were downregulated by cyclophosphamide.	Cyclophosphamide	119-135	tumor necrosis factor	Mus musculus	70-79
34840584-10	2021	Cyclophosphamide upregulated the expressions of NF-kappaB p65, TLR4, and MyD88, suggesting that the NF-kappaB signaling pathway was activated by cyclophosphamide.	Cyclophosphamide	0-16	toll-like receptor 4	Mus musculus	63-67
34840584-10	2021	Cyclophosphamide upregulated the expressions of NF-kappaB p65, TLR4, and MyD88, suggesting that the NF-kappaB signaling pathway was activated by cyclophosphamide.	Cyclophosphamide	0-16	myeloid differentiation primary response gene 88	Mus musculus	73-78
34840584-10	2021	Cyclophosphamide upregulated the expressions of NF-kappaB p65, TLR4, and MyD88, suggesting that the NF-kappaB signaling pathway was activated by cyclophosphamide.	Cyclophosphamide	0-16	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	100-109
34840584-10	2021	Cyclophosphamide upregulated the expressions of NF-kappaB p65, TLR4, and MyD88, suggesting that the NF-kappaB signaling pathway was activated by cyclophosphamide.	Cyclophosphamide	145-161	toll-like receptor 4	Mus musculus	63-67
34840584-10	2021	Cyclophosphamide upregulated the expressions of NF-kappaB p65, TLR4, and MyD88, suggesting that the NF-kappaB signaling pathway was activated by cyclophosphamide.	Cyclophosphamide	145-161	myeloid differentiation primary response gene 88	Mus musculus	73-78
34840584-10	2021	Cyclophosphamide upregulated the expressions of NF-kappaB p65, TLR4, and MyD88, suggesting that the NF-kappaB signaling pathway was activated by cyclophosphamide.	Cyclophosphamide	145-161	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	100-109
34887762-4	2021	In vitro and in vivo metabolic activities of CYP2B10 were probed using cyclophosphamide (CPA) as a specific substrate.	Cyclophosphamide	71-87	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	45-52
34887762-4	2021	In vitro and in vivo metabolic activities of CYP2B10 were probed using cyclophosphamide (CPA) as a specific substrate.	Cyclophosphamide	89-92	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	45-52
34887762-9	2021	Decreased expression of CYP2B10 was translated to reduced metabolism and altered pharmacokinetics of CPA as well as attenuated CPA hepatotoxicity in Per2 Del4-6 mice.	Cyclophosphamide	101-104	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	24-31
34887762-9	2021	Decreased expression of CYP2B10 was translated to reduced metabolism and altered pharmacokinetics of CPA as well as attenuated CPA hepatotoxicity in Per2 Del4-6 mice.	Cyclophosphamide	127-130	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	24-31
34797531-1	2022	Patients with high-risk diffuse large B-cell lymphoma (DLBCL) have poor outcomes following first-line cyclophosphamide, doxorubicin, vincristine, prednisone, and rituximab (R-CHOP).	Cyclophosphamide	102-118	DNA damage inducible transcript 3	Homo sapiens	175-179
34737699-10	2021	The reduction of CD4+ and CD8+ T lymphocytes in CY-treated mice was also highly increased in XFBD groups.	Cyclophosphamide	48-50	CD4 antigen	Mus musculus	17-20
34507634-6	2021	Cyclophosphamide significantly increased tryptophan hydroxylase 1 (TPH1) mRNA expression, number of anti-TPH antibody-positive cells, and 5-HT content in the intestine.	Cyclophosphamide	0-16	tryptophan hydroxylase 1	Rattus norvegicus	41-65
34507634-6	2021	Cyclophosphamide significantly increased tryptophan hydroxylase 1 (TPH1) mRNA expression, number of anti-TPH antibody-positive cells, and 5-HT content in the intestine.	Cyclophosphamide	0-16	tryptophan hydroxylase 1	Rattus norvegicus	67-71
34507634-6	2021	Cyclophosphamide significantly increased tryptophan hydroxylase 1 (TPH1) mRNA expression, number of anti-TPH antibody-positive cells, and 5-HT content in the intestine.	Cyclophosphamide	0-16	tryptophan hydroxylase 1	Rattus norvegicus	105-108
34507634-7	2021	Cyclophosphamide also significantly increased the expression of Tac1 mRNA, encoding preprotachykinin-1, which is a preprotein of substance P, and the number of anti-substance P antibody-positive cells in the intestine.	Cyclophosphamide	0-16	tachykinin, precursor 1	Rattus norvegicus	64-68
34507634-8	2021	Cyclophosphamide significantly increased Lgr5, Bmi1, and Atoh1 mRNA levels, which are markers for the proliferation and differentiation of stem cells.	Cyclophosphamide	0-16	leucine rich repeat containing G protein coupled receptor 5	Rattus norvegicus	41-45
34507634-8	2021	Cyclophosphamide significantly increased Lgr5, Bmi1, and Atoh1 mRNA levels, which are markers for the proliferation and differentiation of stem cells.	Cyclophosphamide	0-16	BMI1 proto-oncogene, polycomb ring finger	Rattus norvegicus	47-51
34507634-8	2021	Cyclophosphamide significantly increased Lgr5, Bmi1, and Atoh1 mRNA levels, which are markers for the proliferation and differentiation of stem cells.	Cyclophosphamide	0-16	atonal bHLH transcription factor 1	Rattus norvegicus	57-62
34329754-0	2021	Increased infections and delayed CD4+ T-cell but faster B-cell Immune Reconstitution after Posttransplant Cyclophosphamide Compared to Conventional GVHD prophylaxis in Allogeneic Transplantation.	Cyclophosphamide	106-122	CD4 molecule	Homo sapiens	33-36
34745610-0	2021	Intratumoral T-cell receptor repertoire is predictive of interim PET scan results in patients with diffuse large B-cell lymphoma treated with rituximab/cyclophosphamide/doxorubicin/prednisolone/vincristine (R-CHOP) chemoimmunotherapy.	Cyclophosphamide	152-168	DNA damage inducible transcript 3	Homo sapiens	209-213
34745610-1	2021	Objectives: A diverse intratumoral T-cell receptor (TCR) repertoire is associated with improved survival in diffuse large B-cell lymphoma (DLBCL) treated with rituximab/cyclophosphamide/doxorubicin/prednisolone/vincristine (R-CHOP) chemoimmunotherapy.	Cyclophosphamide	169-185	DNA damage inducible transcript 3	Homo sapiens	226-230
34689333-0	2022	Laminaria japonica fucoidan ameliorates cyclophosphamide-induced liver and kidney injury possibly by regulating Nrf2/HO-1 and TLR4/NF-kappaB signaling pathways.	Cyclophosphamide	40-56	nuclear factor, erythroid derived 2, like 2	Mus musculus	112-116
34689333-0	2022	Laminaria japonica fucoidan ameliorates cyclophosphamide-induced liver and kidney injury possibly by regulating Nrf2/HO-1 and TLR4/NF-kappaB signaling pathways.	Cyclophosphamide	40-56	heme oxygenase 1	Mus musculus	117-121
34689333-0	2022	Laminaria japonica fucoidan ameliorates cyclophosphamide-induced liver and kidney injury possibly by regulating Nrf2/HO-1 and TLR4/NF-kappaB signaling pathways.	Cyclophosphamide	40-56	toll-like receptor 4	Mus musculus	126-130
34689333-0	2022	Laminaria japonica fucoidan ameliorates cyclophosphamide-induced liver and kidney injury possibly by regulating Nrf2/HO-1 and TLR4/NF-kappaB signaling pathways.	Cyclophosphamide	40-56	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	131-140
34676831-0	2021	Cyclophosphamide enhances the antitumor potency of GITR engagement by increasing oligoclonal cytotoxic T cell fitness.	Cyclophosphamide	0-16	TNF receptor superfamily member 18	Homo sapiens	51-55
34831388-11	2021	Treatment with ipilimumab, cyclophosphamide/GVAX/degarelix, or degarelix alone may increase PD-L1 expression.	Cyclophosphamide	27-43	CD274 molecule	Homo sapiens	92-97
34764434-3	2022	We aimed to evaluate the prognostic value of BCL2 expression determined by immunohistochemistry (IHC), incorporating both the staining intensity and proportion, in patients with de novo DLBCL who received rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) as first-line treatment.	Cyclophosphamide	216-232	BCL2 apoptosis regulator	Homo sapiens	45-49
34820430-0	2021	The Role of METTL3-Mediated N6-Methyladenosine (m6A) of JPH2 mRNA in Cyclophosphamide-Induced Cardiotoxicity.	Cyclophosphamide	69-85	methyltransferase 3, N6-adenosine-methyltransferase complex catalytic subunit	Homo sapiens	12-18
34820430-0	2021	The Role of METTL3-Mediated N6-Methyladenosine (m6A) of JPH2 mRNA in Cyclophosphamide-Induced Cardiotoxicity.	Cyclophosphamide	69-85	junctophilin 2	Homo sapiens	56-60
34820430-4	2021	Our data demonstrated that CYP-induced a prolonged cardiac QT interval and electromechanical coupling time courses accompanied by JPH2 downregulation.	Cyclophosphamide	27-30	junctophilin 2	Homo sapiens	130-134
34820430-7	2021	Our results revealed a novel mechanism for m6A methylation-dependent regulation of JPH2, which provides new strategies for the treatment and prevention of CYP-induced cardiotoxicity.	Cyclophosphamide	155-158	junctophilin 2	Homo sapiens	83-87
34818240-16	2022	Both cyclical cyclophosphamide/steroids (cCYC/GC) and rituximab were equally effective in inducing remission, but rituximab had a favourable adverse event profile compared to cCYC/GC.	Cyclophosphamide	14-30	RAD17 checkpoint clamp loader component	Homo sapiens	41-45
34514879-5	2021	The differences in mechanical pelvic sensitivity between wild type and Asic3 KO mice treated with CYP were ascribed to sensitized bladder C nociceptors.	Cyclophosphamide	98-101	acid-sensing (proton-gated) ion channel 3	Mus musculus	71-76
34732441-6	2021	Moreover, high risk, defined as co-expression of BTK and either or both BCL2/MYC, independently predicted shorter progression-free survival in patients treated with rituximab plus cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) (all R-CHOP-treated patients: hazard ratio=2.565, p=0.044; R-CHOP-treated non-GCB subgroup: HR=3.833, p=0.019).	Cyclophosphamide	180-196	Bruton tyrosine kinase	Homo sapiens	49-52
34732441-6	2021	Moreover, high risk, defined as co-expression of BTK and either or both BCL2/MYC, independently predicted shorter progression-free survival in patients treated with rituximab plus cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) (all R-CHOP-treated patients: hazard ratio=2.565, p=0.044; R-CHOP-treated non-GCB subgroup: HR=3.833, p=0.019).	Cyclophosphamide	180-196	BCL2 apoptosis regulator	Homo sapiens	72-76
34732441-6	2021	Moreover, high risk, defined as co-expression of BTK and either or both BCL2/MYC, independently predicted shorter progression-free survival in patients treated with rituximab plus cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) (all R-CHOP-treated patients: hazard ratio=2.565, p=0.044; R-CHOP-treated non-GCB subgroup: HR=3.833, p=0.019).	Cyclophosphamide	180-196	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	77-80
34732441-6	2021	Moreover, high risk, defined as co-expression of BTK and either or both BCL2/MYC, independently predicted shorter progression-free survival in patients treated with rituximab plus cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) (all R-CHOP-treated patients: hazard ratio=2.565, p=0.044; R-CHOP-treated non-GCB subgroup: HR=3.833, p=0.019).	Cyclophosphamide	180-196	DNA damage inducible transcript 3	Homo sapiens	241-245
34724567-0	2022	HLA Informs Risk Predictions after Haploidentical Stem Cell Transplantation with Post-transplantation Cyclophosphamide.	Cyclophosphamide	102-118	major histocompatibility complex, class II, DR beta 1	Homo sapiens	0-3
34667205-5	2021	However, intraperitoneal injection of cyclophosphamide suppressed IFN-gamma, TNF-alpha, and IL-10 expression.	Cyclophosphamide	38-54	interferon gamma	Mus musculus	66-75
34667205-5	2021	However, intraperitoneal injection of cyclophosphamide suppressed IFN-gamma, TNF-alpha, and IL-10 expression.	Cyclophosphamide	38-54	tumor necrosis factor	Mus musculus	77-86
34667205-5	2021	However, intraperitoneal injection of cyclophosphamide suppressed IFN-gamma, TNF-alpha, and IL-10 expression.	Cyclophosphamide	38-54	interleukin 10	Mus musculus	92-97
34667205-7	2021	However, LPS, ampicillin, cyclophosphamide all increased IIE and TNF-alpha to IL-10 expression (TIE) ratios.	Cyclophosphamide	26-42	tumor necrosis factor	Mus musculus	65-74
34667205-7	2021	However, LPS, ampicillin, cyclophosphamide all increased IIE and TNF-alpha to IL-10 expression (TIE) ratios.	Cyclophosphamide	26-42	interleukin 10	Mus musculus	78-83
34661507-0	2021	Rituximab, cyclophosphamide, doxorubicin, vincristine and prednisolone therapy increases carotid intima-media thickness and plaque score with von Willebrand factor activity elevation in patients with malignant lymphoma.	Cyclophosphamide	11-27	von Willebrand factor	Homo sapiens	142-163
34642909-11	2021	Additionally, pretreatment with 20 mg/kg melatonin regulated the PTEN/Akt/FOXO3a signaling pathway components after cyclophosphamide treatment.	Cyclophosphamide	116-132	phosphatase and tensin homolog	Mus musculus	65-69
34642909-11	2021	Additionally, pretreatment with 20 mg/kg melatonin regulated the PTEN/Akt/FOXO3a signaling pathway components after cyclophosphamide treatment.	Cyclophosphamide	116-132	thymoma viral proto-oncogene 1	Mus musculus	70-73
34642909-11	2021	Additionally, pretreatment with 20 mg/kg melatonin regulated the PTEN/Akt/FOXO3a signaling pathway components after cyclophosphamide treatment.	Cyclophosphamide	116-132	forkhead box O3	Mus musculus	74-80
34519276-2	2021	We aimed at describing the pattern of residual ovarian function in a cohort of survivors of hematological malignancies and/or hematopoietic stem cell transplantation (HSCT) and assessing the relationship between Cyclophosphamide Equivalent Dose (CED) and Anti-Mullerian Hormone (AMH).	Cyclophosphamide	212-228	anti-Mullerian hormone	Homo sapiens	279-282
34765356-4	2021	We report a case of a 65-year-old man who presented with acutely worsening dyspnoea and stridor following his fifth cycle of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP) chemotherapy for hematological malignancy.	Cyclophosphamide	136-152	DNA damage inducible transcript 3	Homo sapiens	200-204
34918136-8	2021	Young age, bloody sputum, low serum creatinine, and high C-reactive protein levels were independently associated with CY use in MPA.	Cyclophosphamide	118-120	C-reactive protein	Homo sapiens	57-75
34753632-0	2022	A Retrospective Analysis of Metronomic Cyclophosphamide, Methotrexate, and Fluorouracil (CMF) Versus Docetaxel and Cyclophosphamide (TC) as Adjuvant Treatment in Early Stage, Hormone Receptor Positive, HER2 Negative Breast Cancer.	Cyclophosphamide	115-131	nuclear receptor subfamily 4 group A member 1	Homo sapiens	175-191
34611276-9	2021	In conclusion, present findings identified Ppia as the best housekeeping gene for CY + NC and SC + CO groups, while Hprt was the best for the HT + WT group.	Cyclophosphamide	82-84	peptidylprolyl isomerase A	Mus musculus	43-47
34606555-9	2021	Also, a significant prophylactic effect against liver, kidney, and heart injuries induced by CYP via decreasing inflammation (serum TNF-alpha, IL-1beta & IL-6) and lipid peroxidation (MDA) was also revealed.	Cyclophosphamide	93-96	tumor necrosis factor	Rattus norvegicus	132-141
34606555-9	2021	Also, a significant prophylactic effect against liver, kidney, and heart injuries induced by CYP via decreasing inflammation (serum TNF-alpha, IL-1beta & IL-6) and lipid peroxidation (MDA) was also revealed.	Cyclophosphamide	93-96	interleukin 1 alpha	Rattus norvegicus	143-151
34606555-9	2021	Also, a significant prophylactic effect against liver, kidney, and heart injuries induced by CYP via decreasing inflammation (serum TNF-alpha, IL-1beta & IL-6) and lipid peroxidation (MDA) was also revealed.	Cyclophosphamide	93-96	interleukin 6	Rattus norvegicus	154-158
34746455-0	2021	The correlation between the level of 3-hydroxypropyl mercapturic acid, CYP2B6 polymorphisms, and hematuria occurrences after cyclophosphamide administration and its bioanalytical methods: A systematic review.	Cyclophosphamide	125-141	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	71-77
34746455-1	2021	Background: Cyclophosphamide (CPA) is a cytotoxic prodrug that needs to be metabolized by cytochrome P450 enzymes, like CYP2B6.	Cyclophosphamide	12-28	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	120-126
34746455-1	2021	Background: Cyclophosphamide (CPA) is a cytotoxic prodrug that needs to be metabolized by cytochrome P450 enzymes, like CYP2B6.	Cyclophosphamide	30-33	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	120-126
34746455-4	2021	Also, this review was written to examine the relationship between levels of 3-HPMA in urine, polymorphisms of CYP2B6 enzymes, and the incidence of hematuria after cyclophosphamide administration in cancer patients.	Cyclophosphamide	163-179	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	110-116
34746455-18	2021	Also, there is a relationship between 3-HPMA levels, CYP2B6 polymorphisms, and the occurrences of hematuria after the administration of cyclophosphamide, which is a type of CYP2B6 polymorph, namely CYP2B6*6, can increase cyclophosphamide hydroxylation so that it can increase the levels of acrolein and 3-HPMA, as its metabolites, and risk of hematuria.	Cyclophosphamide	136-152	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	53-59
34746455-18	2021	Also, there is a relationship between 3-HPMA levels, CYP2B6 polymorphisms, and the occurrences of hematuria after the administration of cyclophosphamide, which is a type of CYP2B6 polymorph, namely CYP2B6*6, can increase cyclophosphamide hydroxylation so that it can increase the levels of acrolein and 3-HPMA, as its metabolites, and risk of hematuria.	Cyclophosphamide	136-152	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	173-179
34746455-18	2021	Also, there is a relationship between 3-HPMA levels, CYP2B6 polymorphisms, and the occurrences of hematuria after the administration of cyclophosphamide, which is a type of CYP2B6 polymorph, namely CYP2B6*6, can increase cyclophosphamide hydroxylation so that it can increase the levels of acrolein and 3-HPMA, as its metabolites, and risk of hematuria.	Cyclophosphamide	136-152	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	198-204
34746455-18	2021	Also, there is a relationship between 3-HPMA levels, CYP2B6 polymorphisms, and the occurrences of hematuria after the administration of cyclophosphamide, which is a type of CYP2B6 polymorph, namely CYP2B6*6, can increase cyclophosphamide hydroxylation so that it can increase the levels of acrolein and 3-HPMA, as its metabolites, and risk of hematuria.	Cyclophosphamide	221-237	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	53-59
34746455-18	2021	Also, there is a relationship between 3-HPMA levels, CYP2B6 polymorphisms, and the occurrences of hematuria after the administration of cyclophosphamide, which is a type of CYP2B6 polymorph, namely CYP2B6*6, can increase cyclophosphamide hydroxylation so that it can increase the levels of acrolein and 3-HPMA, as its metabolites, and risk of hematuria.	Cyclophosphamide	221-237	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	173-179
34746455-18	2021	Also, there is a relationship between 3-HPMA levels, CYP2B6 polymorphisms, and the occurrences of hematuria after the administration of cyclophosphamide, which is a type of CYP2B6 polymorph, namely CYP2B6*6, can increase cyclophosphamide hydroxylation so that it can increase the levels of acrolein and 3-HPMA, as its metabolites, and risk of hematuria.	Cyclophosphamide	221-237	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	198-204
34646085-0	2021	Notch1 Signaling Contributes to Mechanical Allodynia Associated with Cyclophosphamide-Induced Cystitis by Promoting Microglia Activation and Neuroinflammation.	Cyclophosphamide	69-85	notch receptor 1	Rattus norvegicus	0-6
34720803-3	2021	Methods: IGKC expression was immunohistochemically analyzed in 193 breast cancer patients who were treated with adjuvant chemotherapy, either with cyclophosphamide, methotrexate, and 5-fluorouracil (CMF) or 5-fluorouracil, epirubicin, and cyclophosphamide (FEC) between 1993 and 2001 with a median follow-up of 11 years.	Cyclophosphamide	147-163	immunoglobulin kappa constant	Homo sapiens	9-13
34658764-16	2021	Conclusions: Low-dose CYP treatment was confirmed to induce nerve injury, which leading to bladder pain and overactive bladder in female rats, and the up-regulation of Nlrp6 and Casp11 may contribute to these pathological changes.	Cyclophosphamide	22-25	NLR family, pyrin domain containing 6	Rattus norvegicus	168-173
34658764-16	2021	Conclusions: Low-dose CYP treatment was confirmed to induce nerve injury, which leading to bladder pain and overactive bladder in female rats, and the up-regulation of Nlrp6 and Casp11 may contribute to these pathological changes.	Cyclophosphamide	22-25	caspase 4	Rattus norvegicus	178-184
34175195-6	2021	CE was superior to cyclophosphamide mono with a significantly higher number of collected CD34+ cells (15.46 x 106 CD34+ cells/kg vs. 9.92 x 106 CD34+ cells/kg), significantly faster engraftment of granulocytes after stem cell transplantation (day 10.5 vs. day 11.6), shorter duration of the inpatient stay (17.47 days vs. 19.16 days) and significantly less transfusions (8.82 % vs. 30.61 % patients receiving transfusions).	Cyclophosphamide	19-35	CD34 molecule	Homo sapiens	89-93
34175195-6	2021	CE was superior to cyclophosphamide mono with a significantly higher number of collected CD34+ cells (15.46 x 106 CD34+ cells/kg vs. 9.92 x 106 CD34+ cells/kg), significantly faster engraftment of granulocytes after stem cell transplantation (day 10.5 vs. day 11.6), shorter duration of the inpatient stay (17.47 days vs. 19.16 days) and significantly less transfusions (8.82 % vs. 30.61 % patients receiving transfusions).	Cyclophosphamide	19-35	CD34 molecule	Homo sapiens	114-118
34175195-6	2021	CE was superior to cyclophosphamide mono with a significantly higher number of collected CD34+ cells (15.46 x 106 CD34+ cells/kg vs. 9.92 x 106 CD34+ cells/kg), significantly faster engraftment of granulocytes after stem cell transplantation (day 10.5 vs. day 11.6), shorter duration of the inpatient stay (17.47 days vs. 19.16 days) and significantly less transfusions (8.82 % vs. 30.61 % patients receiving transfusions).	Cyclophosphamide	19-35	CD34 molecule	Homo sapiens	144-148
34455128-9	2021	The immunoreactivity for Ly6G-positive cells, intracellular histone H3, and released histone H3 in thrombi was significantly reduced in the cyclophosphamide group by 92.8%, 50.2%, and 34.3%, respectively.	Cyclophosphamide	140-156	lymphocyte antigen 6 complex, locus G	Mus musculus	25-29
34382487-4	2021	Metabolic activity of CYP2B10 was probed using cyclophosphamide (CPA) as a specific substrate.	Cyclophosphamide	47-63	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	22-29
34382487-4	2021	Metabolic activity of CYP2B10 was probed using cyclophosphamide (CPA) as a specific substrate.	Cyclophosphamide	65-68	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	22-29
34363824-4	2021	AL1-1"s in vivo immunomodulatory activity on cyclophosphamide (CY)-treated mice was investigated and it was shown that it could strongly enhance Sig A levels, promote the total antioxidant capacity (T-AOC), and reduce malondialdehyde (MDA) level in the intestine.	Cyclophosphamide	45-61	ephrin A5	Mus musculus	0-3
34363824-4	2021	AL1-1"s in vivo immunomodulatory activity on cyclophosphamide (CY)-treated mice was investigated and it was shown that it could strongly enhance Sig A levels, promote the total antioxidant capacity (T-AOC), and reduce malondialdehyde (MDA) level in the intestine.	Cyclophosphamide	63-65	ephrin A5	Mus musculus	0-3
34753632-0	2022	A Retrospective Analysis of Metronomic Cyclophosphamide, Methotrexate, and Fluorouracil (CMF) Versus Docetaxel and Cyclophosphamide (TC) as Adjuvant Treatment in Early Stage, Hormone Receptor Positive, HER2 Negative Breast Cancer.	Cyclophosphamide	115-131	erb-b2 receptor tyrosine kinase 2	Homo sapiens	202-206
34193553-9	2021	Lastly, in a cyclophosphamide cystitis model of bladder overactivity, optogenetic activation of CRH-PMC neurons returned the voiding pattern to normal.	Cyclophosphamide	13-29	corticotropin releasing hormone	Mus musculus	96-99
34665971-9	2022	LDH, cTn1, cK-Mb, AST, ALT, ALP, MDA, creatinine, and BUN were found to be high in the cyclophosphamide group, however, these values were reduced with apelin-13 administration.	Cyclophosphamide	87-103	PDZ and LIM domain 3	Rattus norvegicus	28-31
34665971-10	2022	Antioxidant enzymes such as SOD, GPx, CAT, and GSH decreased in the cyclophosphamide group, apelin-13 increased these enzyme activities.	Cyclophosphamide	68-84	catalase	Rattus norvegicus	38-41
34621832-9	2021	CONCLUSION: The treatment of CD57-negative gammadeltaT-LGLL with PRCA with cyclophosphamide helps to improve prognosis.	Cyclophosphamide	75-91	beta-1,3-glucuronyltransferase 1	Homo sapiens	29-33
34114066-1	2021	PURPOSE: Genetic variation in the activation of the prodrug cyclophosphamide (CP) by cytochrome P450 (CYP) enzymes has been shown to influence outcomes.	Cyclophosphamide	60-76	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	85-100
34114066-1	2021	PURPOSE: Genetic variation in the activation of the prodrug cyclophosphamide (CP) by cytochrome P450 (CYP) enzymes has been shown to influence outcomes.	Cyclophosphamide	60-76	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	102-105
34114066-9	2021	CONCLUSION: Comedications may be the cause for this inter-occasion variation in bioactivation of cyclophosphamide and the ensuing phenoconversion may account for the conflicting reports in the literature about the relationship between CYP2C19 genotype and CP bioactivation pharmacokinetics.	Cyclophosphamide	97-113	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	235-242
34252986-4	2021	Presently we identified that pyruvate dehydrogenase kinase 4 (PDK4) is markedly elevated in DLBCL cells derived from both the patients and cell lines with R-CHOP (rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone regimen) resistant.	Cyclophosphamide	178-194	pyruvate dehydrogenase kinase 4	Homo sapiens	29-60
34252986-4	2021	Presently we identified that pyruvate dehydrogenase kinase 4 (PDK4) is markedly elevated in DLBCL cells derived from both the patients and cell lines with R-CHOP (rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone regimen) resistant.	Cyclophosphamide	178-194	pyruvate dehydrogenase kinase 4	Homo sapiens	62-66
34282601-0	2021	Hepatoprotective Impact of Ghrelin against Cyclophosphamide-Induced Toxicity in the Male Mice.	Cyclophosphamide	43-59	ghrelin	Mus musculus	27-34
34586105-2	2021	The current first-line regimen for the treatment of DLBCL is R-CHOP, which is the combination of rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone.	Cyclophosphamide	108-124	DNA damage inducible transcript 3	Homo sapiens	63-67
34089986-7	2021	Total ten selective ALDH1A1 inhibitors with diverse scaffolds and appropriate ADMET were identified that can be further developed as adjuvant therapy in cyclophosphamide and cisplatin resistance cancer.	Cyclophosphamide	153-169	aldehyde dehydrogenase 1 family member A1	Homo sapiens	20-27
34193553-12	2021	Moreover, engaging this inhibitory function of CRH can ameliorate bladder hyperexcitability induced by cyclophosphamide in a model of cystitis.	Cyclophosphamide	103-119	corticotropin releasing hormone	Mus musculus	47-50
34489928-1	2021	Introduction: Animal studies and preclinical studies in cancer patients suggest that the induction of immunogenic cell death (ICD) by neoadjuvant chemotherapy with doxorubicin and cyclophosphamide (NAC-AC) recovers the functional performance of the immune system.	Cyclophosphamide	180-196	synuclein alpha	Homo sapiens	198-201
34378880-0	2021	Cyclophosphamide abrogates the expansion of CD4+Foxp3+ regulatory T cells and enhances the efficacy of bleomycin in the treatment of mouse B16-F10 melanomas.	Cyclophosphamide	0-16	CD4 antigen	Mus musculus	44-47
34378880-0	2021	Cyclophosphamide abrogates the expansion of CD4+Foxp3+ regulatory T cells and enhances the efficacy of bleomycin in the treatment of mouse B16-F10 melanomas.	Cyclophosphamide	0-16	forkhead box P3	Mus musculus	48-53
34355022-2	2021	Aberrant expression of ANXA3 promotes tumor cell proliferation, invasion, metastasis, angiogenesis, and therapy resistance to multiple chemotherapeutic drugs including platinum-based agents, fluoropyrimidines, cyclophosphamide, doxorubicin, and docetaxel.	Cyclophosphamide	210-226	annexin A3	Homo sapiens	23-28
34349169-3	2021	In this study, the investigation of NK receptors on T lymphocytes during immune reconstitution after T-cell-replete haploidentical HSCT with Post-Transplant Cyclophosphamide (PTCy) has shown a significant increase of KIR2DL2/3+ T cell frequency at day 25.	Cyclophosphamide	157-173	killer cell immunoglobulin like receptor, two Ig domains and long cytoplasmic tail 2	Homo sapiens	217-226
34128029-4	2021	The results demonstrated that treatment with AH could prevent the reduction in spleen and thymus indices as well as body weight, and significantly increase the Peyer"s patch count in CY-induced mice and the levels of IL-2, IL-6, and TNF-alpha in serum, suggesting the role of Alhagi honey polysaccharides in alleviating the immunosuppression induced by CY.	Cyclophosphamide	353-355	interleukin 2	Mus musculus	217-221
34128029-4	2021	The results demonstrated that treatment with AH could prevent the reduction in spleen and thymus indices as well as body weight, and significantly increase the Peyer"s patch count in CY-induced mice and the levels of IL-2, IL-6, and TNF-alpha in serum, suggesting the role of Alhagi honey polysaccharides in alleviating the immunosuppression induced by CY.	Cyclophosphamide	353-355	interleukin 6	Mus musculus	223-227
34128029-4	2021	The results demonstrated that treatment with AH could prevent the reduction in spleen and thymus indices as well as body weight, and significantly increase the Peyer"s patch count in CY-induced mice and the levels of IL-2, IL-6, and TNF-alpha in serum, suggesting the role of Alhagi honey polysaccharides in alleviating the immunosuppression induced by CY.	Cyclophosphamide	353-355	tumor necrosis factor	Mus musculus	233-242
34128029-5	2021	Moreover, administration of AH significantly increased the SOD activity and the expression level of beta-defensin while decreasing the MDA content and DAO activity in CY-treated mice, which suggested a protective effect of AH on the intestinal barrier.	Cyclophosphamide	167-169	D-amino acid oxidase	Mus musculus	151-154
34128029-6	2021	Simultaneously, a CY-induced decrease in the ratio of villi length/crypt depth and the number of intraepithelial lymphocytes and goblet cells was reversed by AH treatment, as were the alterations in the expression of ZO-1, mucin-2, E-cadherin and occludin in the intestine and the concentrations of SCFAs in the colon.	Cyclophosphamide	18-20	tight junction protein 1	Mus musculus	217-221
34128029-6	2021	Simultaneously, a CY-induced decrease in the ratio of villi length/crypt depth and the number of intraepithelial lymphocytes and goblet cells was reversed by AH treatment, as were the alterations in the expression of ZO-1, mucin-2, E-cadherin and occludin in the intestine and the concentrations of SCFAs in the colon.	Cyclophosphamide	18-20	mucin 2	Mus musculus	223-230
34128029-6	2021	Simultaneously, a CY-induced decrease in the ratio of villi length/crypt depth and the number of intraepithelial lymphocytes and goblet cells was reversed by AH treatment, as were the alterations in the expression of ZO-1, mucin-2, E-cadherin and occludin in the intestine and the concentrations of SCFAs in the colon.	Cyclophosphamide	18-20	cadherin 1	Mus musculus	232-242
34128029-6	2021	Simultaneously, a CY-induced decrease in the ratio of villi length/crypt depth and the number of intraepithelial lymphocytes and goblet cells was reversed by AH treatment, as were the alterations in the expression of ZO-1, mucin-2, E-cadherin and occludin in the intestine and the concentrations of SCFAs in the colon.	Cyclophosphamide	18-20	occludin	Mus musculus	247-255
34128029-7	2021	Furthermore, AH have the ability to regulate the MAPK pathway in CY-mice models to reduce CY-induced toxicity, evidenced by the increased expression of p-ERK and inhibited production of both p-JNK and p-p38.	Cyclophosphamide	65-67	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	152-157
34128029-7	2021	Furthermore, AH have the ability to regulate the MAPK pathway in CY-mice models to reduce CY-induced toxicity, evidenced by the increased expression of p-ERK and inhibited production of both p-JNK and p-p38.	Cyclophosphamide	65-67	mitogen-activated protein kinase 8	Mus musculus	193-196
34128029-7	2021	Furthermore, AH have the ability to regulate the MAPK pathway in CY-mice models to reduce CY-induced toxicity, evidenced by the increased expression of p-ERK and inhibited production of both p-JNK and p-p38.	Cyclophosphamide	65-67	mitogen-activated protein kinase 14	Mus musculus	203-206
34128029-7	2021	Furthermore, AH have the ability to regulate the MAPK pathway in CY-mice models to reduce CY-induced toxicity, evidenced by the increased expression of p-ERK and inhibited production of both p-JNK and p-p38.	Cyclophosphamide	90-92	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	152-157
34128029-7	2021	Furthermore, AH have the ability to regulate the MAPK pathway in CY-mice models to reduce CY-induced toxicity, evidenced by the increased expression of p-ERK and inhibited production of both p-JNK and p-p38.	Cyclophosphamide	90-92	mitogen-activated protein kinase 8	Mus musculus	193-196
34062413-3	2021	The aim of this study was to investigate the synergistic anti-tumor activity of SBD with cyclophosphamide (CTX) and the possibly underlying mechanisms in treating the hepatoma 22 (H22) -bearing mice.	Cyclophosphamide	89-105	V-set and immunoglobulin domain containing 2	Mus musculus	107-110
34895738-7	2021	CASE SUMMARY: An 81-year-old female patient received her first cycle of R-CHOP (rituximab, cyclophosphamide, vincristine, and prednisolone) treatment after being diagnosed with high- grade B-cell lymphoma.	Cyclophosphamide	91-107	DNA damage inducible transcript 3	Homo sapiens	74-78
34254266-1	2022	PURPOSE: Comprehensive geriatric assessment (CGA) has been used to help identify elderly patients with diffuse large B-cell lymphoma (DLBCL) who were suitable for rituximab combined with CHOP therapy (cyclophosphamide, Adriamycin, vincristine, and prednisolone), but there are few reports of CGA for elderly patients with DLBCL who received R-mini-CHOP.	Cyclophosphamide	201-217	DNA damage inducible transcript 3	Homo sapiens	187-191
34124276-1	2021	The majority of diffuse large B-cell lymphoma (DLBCL) patients develop relapsed or refractory disease after standard ruxolitinib, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) chemotherapy, which is partly related to a dysregulated tumor immune microenvironment.	Cyclophosphamide	130-146	DNA damage inducible transcript 3	Homo sapiens	192-196
34245022-13	2021	Cyclophosphamide significantly increased p53 and decreased Bcl-2 expression compared to the control group.	Cyclophosphamide	0-16	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	41-44
34245022-13	2021	Cyclophosphamide significantly increased p53 and decreased Bcl-2 expression compared to the control group.	Cyclophosphamide	0-16	BCL2, apoptosis regulator	Rattus norvegicus	59-64
34245022-15	2021	Moreover, S. platensis co-treated groups displayed a significant decreasing in p53 and increasing in Bcl-2 expression compared to the Cyclophosphamide group.	Cyclophosphamide	134-150	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	79-82
34245022-15	2021	Moreover, S. platensis co-treated groups displayed a significant decreasing in p53 and increasing in Bcl-2 expression compared to the Cyclophosphamide group.	Cyclophosphamide	134-150	BCL2, apoptosis regulator	Rattus norvegicus	101-106
34245022-20	2021	Co-administration of Spirulina plantesis with Cyclophosphamide reduces sperm apoptosis also decreases P53 protein expression and increases Bcl-2 protein expression.	Cyclophosphamide	46-62	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	102-105
34245022-20	2021	Co-administration of Spirulina plantesis with Cyclophosphamide reduces sperm apoptosis also decreases P53 protein expression and increases Bcl-2 protein expression.	Cyclophosphamide	46-62	BCL2, apoptosis regulator	Rattus norvegicus	139-144
34893156-7	2021	The polymorphism rs1695 of the GSTP1 gene has been associated with the effectiveness and toxicity of fluorouracil, cyclophosphamide and epirubicin therapy.	Cyclophosphamide	115-131	glutathione S-transferase pi 1	Homo sapiens	31-36
34306306-0	2021	Nrf2 Pathway Ameliorates Bladder Dysfunction in Cyclophosphamide-Induced Cystitis via Suppression of Oxidative Stress.	Cyclophosphamide	48-64	nuclear factor, erythroid derived 2, like 2	Mus musculus	0-4
34209690-5	2021	CYP administration caused macroscopic and histological bladder changes, inflammatory infiltrates, increased mast cell numbers, oxidative stress, decreased expression of the tight endothelial junction (e.g., zonula occludens-1 (ZO-1) and occludin), and bladder pain.	Cyclophosphamide	0-3	tight junction protein 1	Homo sapiens	207-225
34209690-5	2021	CYP administration caused macroscopic and histological bladder changes, inflammatory infiltrates, increased mast cell numbers, oxidative stress, decreased expression of the tight endothelial junction (e.g., zonula occludens-1 (ZO-1) and occludin), and bladder pain.	Cyclophosphamide	0-3	tight junction protein 1	Homo sapiens	227-231
34209690-5	2021	CYP administration caused macroscopic and histological bladder changes, inflammatory infiltrates, increased mast cell numbers, oxidative stress, decreased expression of the tight endothelial junction (e.g., zonula occludens-1 (ZO-1) and occludin), and bladder pain.	Cyclophosphamide	0-3	occludin	Homo sapiens	237-245
34173661-7	2022	KEY FINDINGS: CPA acutely elevated then reduced hepatic microsomal cytochrome P450 2B6 (CYP2B6) content and significantly suppressed bladder and lung glutathione-S-transferase activity.	Cyclophosphamide	14-17	cytochrome P450, family 2, subfamily b, polypeptide 3	Rattus norvegicus	88-94
34173661-8	2022	Furthermore, CPA elevated lung myeloperoxidase activity, DNA content and hydroxyproline level and bladder blood content.	Cyclophosphamide	13-16	myeloperoxidase	Rattus norvegicus	31-46
34173661-9	2022	AE ameliorated CPA-induced derangements through suppression of CYP2B6 and myeloperoxidase and augmentation of glutathione-S-transferase activity in CPA-treated rats.	Cyclophosphamide	15-18	cytochrome P450, family 2, subfamily b, polypeptide 3	Rattus norvegicus	63-69
34201565-8	2021	Current data suggest that patients with the mutated variable region of the immunoglobulin heavy chain (IGHV) achieve fairly durable remissions, especially when treated with fludarabine, cyclophosphamide, and rituximab (FCR) regimen.	Cyclophosphamide	186-202	immunoglobulin heavy variable 3/OR16-7 (pseudogene)	Homo sapiens	75-101
34201565-8	2021	Current data suggest that patients with the mutated variable region of the immunoglobulin heavy chain (IGHV) achieve fairly durable remissions, especially when treated with fludarabine, cyclophosphamide, and rituximab (FCR) regimen.	Cyclophosphamide	186-202	immunoglobulin heavy variable 3/OR16-7 (pseudogene)	Homo sapiens	103-107
34224377-0	2021	Correction: Cyclophosphamide and Vinorelbine Activate Stem-Like CD8+ T Cells and Improve Anti-PD-1 Efficacy in Triple-Negative Breast Cancer.	Cyclophosphamide	12-28	CD8a molecule	Homo sapiens	64-67
34224377-0	2021	Correction: Cyclophosphamide and Vinorelbine Activate Stem-Like CD8+ T Cells and Improve Anti-PD-1 Efficacy in Triple-Negative Breast Cancer.	Cyclophosphamide	12-28	programmed cell death 1	Homo sapiens	94-98
34211480-7	2021	The results indicated that CBLEB treatment reduced cyclophosphamide-induced death, weight loss, and damage to the gut, liver, spleen, and lungs and eliminated a cyclophosphamide-induced increase in the mean hemoglobin content and GGT, M-CSF, and MIP-3alpha levels and a decrease in the red blood cell distribution width and total protein and creatinine levels in the blood.	Cyclophosphamide	161-177	gamma-glutamyltransferase 1	Rattus norvegicus	230-233
34211480-7	2021	The results indicated that CBLEB treatment reduced cyclophosphamide-induced death, weight loss, and damage to the gut, liver, spleen, and lungs and eliminated a cyclophosphamide-induced increase in the mean hemoglobin content and GGT, M-CSF, and MIP-3alpha levels and a decrease in the red blood cell distribution width and total protein and creatinine levels in the blood.	Cyclophosphamide	161-177	colony stimulating factor 1	Rattus norvegicus	235-240
34211480-7	2021	The results indicated that CBLEB treatment reduced cyclophosphamide-induced death, weight loss, and damage to the gut, liver, spleen, and lungs and eliminated a cyclophosphamide-induced increase in the mean hemoglobin content and GGT, M-CSF, and MIP-3alpha levels and a decrease in the red blood cell distribution width and total protein and creatinine levels in the blood.	Cyclophosphamide	161-177	C-C motif chemokine ligand 20	Rattus norvegicus	246-256
34164401-1	2021	Cyclophosphamide (CTX) is widely used in various cancer therapies and in immunosuppression, and patients can still have babies after CTX chemotherapy.	Cyclophosphamide	0-16	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	18-21
34164401-1	2021	Cyclophosphamide (CTX) is widely used in various cancer therapies and in immunosuppression, and patients can still have babies after CTX chemotherapy.	Cyclophosphamide	0-16	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	133-136
34068924-0	2021	Hidrox  Counteracts Cyclophosphamide-Induced Male Infertility through NRF2 Pathways in a Mouse Model.	Cyclophosphamide	20-36	nuclear factor, erythroid derived 2, like 2	Mus musculus	70-74
34922405-11	2021	CONCLUSION: High CRP levels with non-widespread GGO predicted progressive ILD in patients with SSc treated with CYC.	Cyclophosphamide	112-115	C-reactive protein	Homo sapiens	17-20
34268990-0	2021	Sequential anthracycline and weekly paclitaxel might be more effective compared to docetaxel and cyclophosphamide in the adjuvant treatment of HER2-negative breast cancer patients.	Cyclophosphamide	97-113	erb-b2 receptor tyrosine kinase 2	Homo sapiens	143-147
34922405-0	2021	C-reactive protein and ground-glass opacity as predictors for intractable interstitial lung disease in patients with systemic sclerosis under cyclophosphamide treatment regardless of concomitant glucocorticoids.	Cyclophosphamide	142-158	C-reactive protein	Homo sapiens	0-18
34175846-0	2021	Neuronal Dual Leucine Zipper Kinase Mediates Inflammatory and Nociceptive Responses in Cyclophosphamide-Induced Cystitis.	Cyclophosphamide	87-103	mitogen-activated protein kinase kinase kinase 12	Mus musculus	9-35
34175846-8	2021	Deletion of neuronal DLK attenuated CYP-induced pain-like nociceptive behavior and suppressed histamine release from mast cells, neuronal activation in the spinal cord, and bladder pathology.	Cyclophosphamide	36-39	mitogen-activated protein kinase kinase kinase 12	Mus musculus	21-24
35636581-10	2022	KEY FINDINGS: Cyclo administration resulted in deterioration of serum liver function tests and elevation of hepatic tissue concentration of P53, Nf-kbeta, apoptosis-inducing factor-1, NLRP3 inflammasome, Bax; gene expression of receptor-induced protein-1 along with reduction of hepatic Bcl-2 concentration.	Cyclophosphamide	14-19	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	140-182
35636581-10	2022	KEY FINDINGS: Cyclo administration resulted in deterioration of serum liver function tests and elevation of hepatic tissue concentration of P53, Nf-kbeta, apoptosis-inducing factor-1, NLRP3 inflammasome, Bax; gene expression of receptor-induced protein-1 along with reduction of hepatic Bcl-2 concentration.	Cyclophosphamide	14-19	NLR family, pyrin domain containing 3	Rattus norvegicus	184-189
35636581-10	2022	KEY FINDINGS: Cyclo administration resulted in deterioration of serum liver function tests and elevation of hepatic tissue concentration of P53, Nf-kbeta, apoptosis-inducing factor-1, NLRP3 inflammasome, Bax; gene expression of receptor-induced protein-1 along with reduction of hepatic Bcl-2 concentration.	Cyclophosphamide	14-19	BCL2 associated X, apoptosis regulator	Rattus norvegicus	204-207
35636581-10	2022	KEY FINDINGS: Cyclo administration resulted in deterioration of serum liver function tests and elevation of hepatic tissue concentration of P53, Nf-kbeta, apoptosis-inducing factor-1, NLRP3 inflammasome, Bax; gene expression of receptor-induced protein-1 along with reduction of hepatic Bcl-2 concentration.	Cyclophosphamide	14-19	BCL2, apoptosis regulator	Rattus norvegicus	287-292
35636581-12	2022	Cyclo administration also resulted in a severe deterioration of the hepatic histopathological picture and significant immunohistochemical expression of caspase-3, tumor necrosis factor-alpha (TNF-alpha) and Cyclooxygenase-2 (COX-2) in hepatic tissues versus the normal group.	Cyclophosphamide	0-5	caspase 3	Rattus norvegicus	152-161
35636581-12	2022	Cyclo administration also resulted in a severe deterioration of the hepatic histopathological picture and significant immunohistochemical expression of caspase-3, tumor necrosis factor-alpha (TNF-alpha) and Cyclooxygenase-2 (COX-2) in hepatic tissues versus the normal group.	Cyclophosphamide	0-5	tumor necrosis factor	Rattus norvegicus	163-190
35636581-12	2022	Cyclo administration also resulted in a severe deterioration of the hepatic histopathological picture and significant immunohistochemical expression of caspase-3, tumor necrosis factor-alpha (TNF-alpha) and Cyclooxygenase-2 (COX-2) in hepatic tissues versus the normal group.	Cyclophosphamide	0-5	tumor necrosis factor	Rattus norvegicus	192-201
35636581-12	2022	Cyclo administration also resulted in a severe deterioration of the hepatic histopathological picture and significant immunohistochemical expression of caspase-3, tumor necrosis factor-alpha (TNF-alpha) and Cyclooxygenase-2 (COX-2) in hepatic tissues versus the normal group.	Cyclophosphamide	0-5	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	207-223
35636581-12	2022	Cyclo administration also resulted in a severe deterioration of the hepatic histopathological picture and significant immunohistochemical expression of caspase-3, tumor necrosis factor-alpha (TNF-alpha) and Cyclooxygenase-2 (COX-2) in hepatic tissues versus the normal group.	Cyclophosphamide	0-5	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	225-230
35489561-11	2022	After controlling for gender, age and education level, the BDNF gene rs16917237 polymorphism did not affect job burnout, but it interacted with job stress to influence EE and CY (both p < 0.05), indicating that individuals with TT genotype were more susceptible to higher levels of job stress, resulting in job burnout symptoms.	Cyclophosphamide	175-177	brain derived neurotrophic factor	Homo sapiens	59-63
35504331-0	2022	Trimetazidine attenuates cyclophosphamide-induced cystitis by inhibiting TLR4-mediated NFkappaB signaling in mice.	Cyclophosphamide	25-41	toll-like receptor 4	Mus musculus	73-77
35504331-0	2022	Trimetazidine attenuates cyclophosphamide-induced cystitis by inhibiting TLR4-mediated NFkappaB signaling in mice.	Cyclophosphamide	25-41	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	87-95
35293071-0	2022	Activation of translocator protein alleviates mechanical allodynia and bladder dysfunction in cyclophosphamide-induced cystitis through repression of BDNF-mediated neuroinflammation.	Cyclophosphamide	94-110	brain-derived neurotrophic factor	Rattus norvegicus	150-154
35293071-3	2022	Moreover, we previously demonstrated that brain-derived neurotrophic factor (BDNF) regulates neuroinflammation and mechanical allodynia in cyclophosphamide (CYP)-induced cystitis through activation of glial cells.	Cyclophosphamide	139-155	brain-derived neurotrophic factor	Rattus norvegicus	42-75
35293071-3	2022	Moreover, we previously demonstrated that brain-derived neurotrophic factor (BDNF) regulates neuroinflammation and mechanical allodynia in cyclophosphamide (CYP)-induced cystitis through activation of glial cells.	Cyclophosphamide	139-155	brain-derived neurotrophic factor	Rattus norvegicus	77-81
35293071-3	2022	Moreover, we previously demonstrated that brain-derived neurotrophic factor (BDNF) regulates neuroinflammation and mechanical allodynia in cyclophosphamide (CYP)-induced cystitis through activation of glial cells.	Cyclophosphamide	157-160	brain-derived neurotrophic factor	Rattus norvegicus	42-75
35293071-3	2022	Moreover, we previously demonstrated that brain-derived neurotrophic factor (BDNF) regulates neuroinflammation and mechanical allodynia in cyclophosphamide (CYP)-induced cystitis through activation of glial cells.	Cyclophosphamide	157-160	brain-derived neurotrophic factor	Rattus norvegicus	77-81
35293071-10	2022	RESULTS: TSPO was activated in the SDH after CYP injection and was primarily colocalised with astrocytes.	Cyclophosphamide	45-48	translocator protein	Rattus norvegicus	9-13
34997322-11	2022	Further re-intensification of IA and addition of cyclophosphamide improved proteinuria again with reduced IgG-IgA.	Cyclophosphamide	49-65	CD79a molecule	Homo sapiens	110-113
35525311-0	2022	Vitexin-2-O-rhamnoside improves immunosuppression, oxidative stress, and phosphorylation of PI3K/Akt signal pathway in cyclophosphamide treated mice.	Cyclophosphamide	119-135	thymoma viral proto-oncogene 1	Mus musculus	97-100
35525311-5	2022	Moreover, it can upregulate the phosphorylation level of PI3K/Akt signaling pathway in mice immunosuppressed by CY, increase the activities of glutathione peroxidase (GSH-Px), chloramphenicol acetyltransferase (CAT), superoxide dismutase (SOD), and total antioxidant capacity (T-AOC), and decrease the level of malondialdehyde (MDA).	Cyclophosphamide	112-114	thymoma viral proto-oncogene 1	Mus musculus	62-65
35143644-2	2022	We performed a prospective randomized, multicenter, phase III trial to study whether posttransplant cyclophosphamide (PT-Cy) combined with a short course of cyclosporine A (CsA) would result in a reduction of severe GVHD and improvement of GVHD-free, relapse free survival (GRFS) as compared to the combination of CsA and mycophenolic acid (MPA) after non-myeloablative (NMA) matched related and unrelated peripheral blood alloHSCT.	Cyclophosphamide	100-116	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	314-317
35339754-0	2022	Cyclophosphamide-induced GPX4 degradation triggers parthanatos by activating AIFM1.	Cyclophosphamide	0-16	glutathione peroxidase 4	Homo sapiens	25-29
35339754-0	2022	Cyclophosphamide-induced GPX4 degradation triggers parthanatos by activating AIFM1.	Cyclophosphamide	0-16	apoptosis inducing factor mitochondria associated 1	Homo sapiens	77-82
35339754-2	2022	Here, we show a previously unrecognized role of cyclophosphamide in triggering the protein degradation of glutathione peroxidase 4 (GPX4), a phospholipid hydroperoxidase that protects cells from oxidative damage.	Cyclophosphamide	48-64	glutathione peroxidase 4	Homo sapiens	106-130
35339754-2	2022	Here, we show a previously unrecognized role of cyclophosphamide in triggering the protein degradation of glutathione peroxidase 4 (GPX4), a phospholipid hydroperoxidase that protects cells from oxidative damage.	Cyclophosphamide	48-64	glutathione peroxidase 4	Homo sapiens	132-136
35339754-2	2022	Here, we show a previously unrecognized role of cyclophosphamide in triggering the protein degradation of glutathione peroxidase 4 (GPX4), a phospholipid hydroperoxidase that protects cells from oxidative damage.	Cyclophosphamide	48-64	glutathione peroxidase 4	Homo sapiens	141-169
35339754-3	2022	Mechanistically, we found that the ubiquitin-proteasome system, but not autophagy, mediates cyclophosphamide-induced degradation of GPX4 in human leukemia cell lines.	Cyclophosphamide	92-108	glutathione peroxidase 4	Homo sapiens	132-136
35339754-4	2022	Surprisingly, cyclophosphamide-induced degradation of GPX4 leads to caspase-independent parthanatos, but not lipid peroxidation-mediated ferroptosis, through the nuclear translocation of apoptosis-inducing factor mitochondria-associated 1 (AIFM1).	Cyclophosphamide	14-30	glutathione peroxidase 4	Homo sapiens	54-58
35339754-4	2022	Surprisingly, cyclophosphamide-induced degradation of GPX4 leads to caspase-independent parthanatos, but not lipid peroxidation-mediated ferroptosis, through the nuclear translocation of apoptosis-inducing factor mitochondria-associated 1 (AIFM1).	Cyclophosphamide	14-30	apoptosis inducing factor mitochondria associated 1	Homo sapiens	187-238
35339754-4	2022	Surprisingly, cyclophosphamide-induced degradation of GPX4 leads to caspase-independent parthanatos, but not lipid peroxidation-mediated ferroptosis, through the nuclear translocation of apoptosis-inducing factor mitochondria-associated 1 (AIFM1).	Cyclophosphamide	14-30	apoptosis inducing factor mitochondria associated 1	Homo sapiens	240-245
35339754-5	2022	Consequently, the overexpression of GPX4 or the knockdown of AIFM1 limits the anticancer activity of cyclophosphamide in vitro and in xenograft tumor models.	Cyclophosphamide	101-117	glutathione peroxidase 4	Homo sapiens	36-40
35339754-5	2022	Consequently, the overexpression of GPX4 or the knockdown of AIFM1 limits the anticancer activity of cyclophosphamide in vitro and in xenograft tumor models.	Cyclophosphamide	101-117	apoptosis inducing factor mitochondria associated 1	Homo sapiens	61-66
35618489-1	2022	Aldehyde dehydrogenase 1 (ALDH1A1), an oxidoreductase class of enzymes, is overexpressed in various types of cancer cell lines and is the major cause of resistance to the Food and Drug Administration (FDA)-approved drug, cyclophosphamide (CP).	Cyclophosphamide	221-237	aldehyde dehydrogenase 1 family member A1	Homo sapiens	26-33
35613889-10	2022	Taxifolin reduced the cyclophosphamide-induced increases in the MDA, TNF-alpha, IL-1beta, and IL-6 levels and the TOS and OSI values; it decreased the tGSH and TAS levels and reduced histopathological damage (P<0.001).	Cyclophosphamide	22-38	tumor necrosis factor	Rattus norvegicus	69-78
35613889-10	2022	Taxifolin reduced the cyclophosphamide-induced increases in the MDA, TNF-alpha, IL-1beta, and IL-6 levels and the TOS and OSI values; it decreased the tGSH and TAS levels and reduced histopathological damage (P<0.001).	Cyclophosphamide	22-38	interleukin 1 alpha	Rattus norvegicus	80-88
35613889-10	2022	Taxifolin reduced the cyclophosphamide-induced increases in the MDA, TNF-alpha, IL-1beta, and IL-6 levels and the TOS and OSI values; it decreased the tGSH and TAS levels and reduced histopathological damage (P<0.001).	Cyclophosphamide	22-38	interleukin 6	Rattus norvegicus	94-98
35614109-4	2022	Apigenin when combined with etoposide or cyclophosphamide-induced apoptosis via the mitochondrial pathway, increasing the expression of pro-apoptotic cytochrome c, SMAC/DIABLO, and HTRA2/OMI, which promoted caspase-9 and -3 activation.	Cyclophosphamide	41-57	cytochrome c, somatic	Homo sapiens	150-162
35614109-4	2022	Apigenin when combined with etoposide or cyclophosphamide-induced apoptosis via the mitochondrial pathway, increasing the expression of pro-apoptotic cytochrome c, SMAC/DIABLO, and HTRA2/OMI, which promoted caspase-9 and -3 activation.	Cyclophosphamide	41-57	diablo IAP-binding mitochondrial protein	Homo sapiens	164-168
35614109-4	2022	Apigenin when combined with etoposide or cyclophosphamide-induced apoptosis via the mitochondrial pathway, increasing the expression of pro-apoptotic cytochrome c, SMAC/DIABLO, and HTRA2/OMI, which promoted caspase-9 and -3 activation.	Cyclophosphamide	41-57	diablo IAP-binding mitochondrial protein	Homo sapiens	169-175
35614109-4	2022	Apigenin when combined with etoposide or cyclophosphamide-induced apoptosis via the mitochondrial pathway, increasing the expression of pro-apoptotic cytochrome c, SMAC/DIABLO, and HTRA2/OMI, which promoted caspase-9 and -3 activation.	Cyclophosphamide	41-57	HtrA serine peptidase 2	Homo sapiens	181-190
35597840-2	2022	The current study aims to identify and validate reliable markers that can predict pathological complete response (pCR) in fluorouracil, epirubicin, and cyclophosphamide (FEC)-based neoadjuvant therapy with (NACT/RT) and without concurrent radiation (NACT).	Cyclophosphamide	152-168	solute carrier family 13 member 5	Homo sapiens	207-211
35606478-5	2022	The a priori selected primary hypothesis was that patients who have CYP2B6 reduced metabolizer activity (poor or intermediate (PM/IM) vs. normal (NM) metabolizer) have lower risk of severe toxicity or cyclophosphamide treatment modification due to toxicity.	Cyclophosphamide	201-217	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	68-74
35606478-9	2022	CONCLUSION: The finding that patients who carry ALDH1A1 rs8187996 may have a lower risk of cyclophosphamide toxicity than wild-type patients contradicts a prior finding for this variant and should be viewed with skepticism.	Cyclophosphamide	91-107	aldehyde dehydrogenase 1 family member A1	Homo sapiens	48-55
35597840-2	2022	The current study aims to identify and validate reliable markers that can predict pathological complete response (pCR) in fluorouracil, epirubicin, and cyclophosphamide (FEC)-based neoadjuvant therapy with (NACT/RT) and without concurrent radiation (NACT).	Cyclophosphamide	152-168	solute carrier family 13 member 5	Homo sapiens	250-254
35582850-6	2022	RESULTS: Compared to controls, cyclophosphamide induced a shorter intercontraction interval, lower bladder compliance, increased number of non-voiding contractions, and increased pathological scores and myeloperoxidase expression in the bladder.	Cyclophosphamide	31-47	myeloperoxidase	Rattus norvegicus	203-218
35582850-8	2022	In addition, cyclophosphamide-induced decreases in bladder compliance and increases in myeloperoxidase were not detected with 5-aminolevulinic acid hydrochloride combined with sodium ferrous citrate pretreatment.	Cyclophosphamide	13-29	myeloperoxidase	Rattus norvegicus	87-102
35579950-0	2022	Targeting CAR-Nrf2 improves cyclophosphamide bioactivation while reducing doxorubicin-induced cardiotoxicity in triple-negative breast cancer treatment.	Cyclophosphamide	28-44	nuclear receptor subfamily 1 group I member 3	Homo sapiens	10-13
35579950-0	2022	Targeting CAR-Nrf2 improves cyclophosphamide bioactivation while reducing doxorubicin-induced cardiotoxicity in triple-negative breast cancer treatment.	Cyclophosphamide	28-44	NFE2 like bZIP transcription factor 2	Homo sapiens	14-18
35579950-3	2022	CN06 enhances CAR-induced bioactivation of CPA (a prodrug) by provoking hepatic expression of CYP2B6, while repressing DOX-induced cytotoxicity in cardiomyocytes in vitro via stimulating Nrf2-antioxidant signaling.	Cyclophosphamide	43-46	nuclear receptor subfamily 1 group I member 3	Homo sapiens	14-17
35579950-3	2022	CN06 enhances CAR-induced bioactivation of CPA (a prodrug) by provoking hepatic expression of CYP2B6, while repressing DOX-induced cytotoxicity in cardiomyocytes in vitro via stimulating Nrf2-antioxidant signaling.	Cyclophosphamide	43-46	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	94-100
35579950-3	2022	CN06 enhances CAR-induced bioactivation of CPA (a prodrug) by provoking hepatic expression of CYP2B6, while repressing DOX-induced cytotoxicity in cardiomyocytes in vitro via stimulating Nrf2-antioxidant signaling.	Cyclophosphamide	43-46	NFE2 like bZIP transcription factor 2	Homo sapiens	187-191
35579950-4	2022	Utilizing a multicellular co-culture model incorporating human primary hepatocytes, TNBC cells, and cardiomyocytes, we show that CN06 increased CPA/DOX-mediated TNBC cell death via CAR-dependent CYP2B6 induction and subsequent conversion of CPA to its active metabolite 4-hydroxy-CPA, while protecting against DOX-induced cardiotoxicity by selectively activating Nrf2-antioxidant signaling in cardiomyocytes but not in TNBC cells.	Cyclophosphamide	144-147	nuclear receptor subfamily 1 group I member 3	Homo sapiens	181-184
35579950-4	2022	Utilizing a multicellular co-culture model incorporating human primary hepatocytes, TNBC cells, and cardiomyocytes, we show that CN06 increased CPA/DOX-mediated TNBC cell death via CAR-dependent CYP2B6 induction and subsequent conversion of CPA to its active metabolite 4-hydroxy-CPA, while protecting against DOX-induced cardiotoxicity by selectively activating Nrf2-antioxidant signaling in cardiomyocytes but not in TNBC cells.	Cyclophosphamide	144-147	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	195-201
35579950-4	2022	Utilizing a multicellular co-culture model incorporating human primary hepatocytes, TNBC cells, and cardiomyocytes, we show that CN06 increased CPA/DOX-mediated TNBC cell death via CAR-dependent CYP2B6 induction and subsequent conversion of CPA to its active metabolite 4-hydroxy-CPA, while protecting against DOX-induced cardiotoxicity by selectively activating Nrf2-antioxidant signaling in cardiomyocytes but not in TNBC cells.	Cyclophosphamide	144-147	NFE2 like bZIP transcription factor 2	Homo sapiens	363-367
35579950-4	2022	Utilizing a multicellular co-culture model incorporating human primary hepatocytes, TNBC cells, and cardiomyocytes, we show that CN06 increased CPA/DOX-mediated TNBC cell death via CAR-dependent CYP2B6 induction and subsequent conversion of CPA to its active metabolite 4-hydroxy-CPA, while protecting against DOX-induced cardiotoxicity by selectively activating Nrf2-antioxidant signaling in cardiomyocytes but not in TNBC cells.	Cyclophosphamide	241-244	nuclear receptor subfamily 1 group I member 3	Homo sapiens	181-184
35579950-6	2022	Collectively, our findings identify CAR and Nrf2 as novel combined therapeutic targets whereby CN06 holds the potential to improve the efficacy:toxicity ratio of CPA/DOX-containing chemotherapy.	Cyclophosphamide	162-165	nuclear receptor subfamily 1 group I member 3	Homo sapiens	36-39
35579950-6	2022	Collectively, our findings identify CAR and Nrf2 as novel combined therapeutic targets whereby CN06 holds the potential to improve the efficacy:toxicity ratio of CPA/DOX-containing chemotherapy.	Cyclophosphamide	162-165	NFE2 like bZIP transcription factor 2	Homo sapiens	44-48
35551214-4	2022	PCNA in D8 and D10 granulosa cells and ERalpha in D10 granulosa cells of follicles in BPA+Asta group were significantly higher.	Cyclophosphamide	90-94	proliferating cell nuclear antigen	Homo sapiens	0-4
35576032-0	2022	Ameliorative effect of flavocoxid on cyclophosphamide-induced cardio and neurotoxicity via targeting the GM-CSF/NF-kappaB signaling pathway.	Cyclophosphamide	37-53	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	105-111
35576032-0	2022	Ameliorative effect of flavocoxid on cyclophosphamide-induced cardio and neurotoxicity via targeting the GM-CSF/NF-kappaB signaling pathway.	Cyclophosphamide	37-53	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	112-121
35437281-7	2022	Notably, CXCL13 deficiency further improved the efficacy of a traditional chemotherapeutic drug (cyclophosphamide), as well as that of anti-programmed death receptor-1 immunotherapy.	Cyclophosphamide	97-113	chemokine (C-X-C motif) ligand 13	Mus musculus	9-15
35551214-4	2022	PCNA in D8 and D10 granulosa cells and ERalpha in D10 granulosa cells of follicles in BPA+Asta group were significantly higher.	Cyclophosphamide	90-94	estrogen receptor 1	Homo sapiens	39-46
35551214-5	2022	The levels of malondialdehyde in the follicle culture medium, levels of ROS in the oocytes, the expression levels of caspase 3 and cathepsin B in the oocytes of the BPA+Asta group were significantly lower.	Cyclophosphamide	169-173	caspase 3	Homo sapiens	117-126
35551214-5	2022	The levels of malondialdehyde in the follicle culture medium, levels of ROS in the oocytes, the expression levels of caspase 3 and cathepsin B in the oocytes of the BPA+Asta group were significantly lower.	Cyclophosphamide	169-173	cathepsin B	Homo sapiens	131-142
35551214-6	2022	However, the mitochondrial membrane potential, and the expression levels of antioxidant genes (CAT, SOD1 and SOD2) and anti-apoptotic gene Bcl-2 in the oocytes in the BPA+Asta group were significantly higher.	Cyclophosphamide	171-175	BCL2 apoptosis regulator	Homo sapiens	139-144
35513252-1	2022	With the use of post-transplantation cyclophosphamide (PTCy), the outcomes of mismatched related donor hematopoietic cell transplantation (HCT) are now approaching that of matched donors.	Cyclophosphamide	37-53	solute carrier family 35 member G1	Homo sapiens	16-20
35508891-9	2022	Although urine beta2-microglobulin significantly decreased following 2 months of treatment with all medications, efficacy was greater with tacrolimus than with cyclophosphamide and MMF (P < 0.001).	Cyclophosphamide	160-176	beta-2-microglobulin	Homo sapiens	15-34
34997774-6	2022	The results revealed that CYP exposure affected functional and structural integrities of the testes, by depleting sperm count and motility, testosterone, LH, spermatogenic and mature sperm cell population, Leydig cells and PCNA immunoreactive proliferating cells.	Cyclophosphamide	26-29	proliferating cell nuclear antigen	Rattus norvegicus	223-227
35283102-8	2022	During acute cyclophosphamide-induced bladder injury, Arid1a knockouts develop hyperproliferative and hyperinflammatory phenotypes and exhibit a severe loss of urothelial cells.	Cyclophosphamide	13-29	AT rich interactive domain 1A (SWI-like)	Mus musculus	54-60
35436749-6	2022	Results revealed that CYP treatment alone significantly provoked an oxidative-inflammatory response, increased serum kynurenine concentration, and concomitantly increased immunosuppressive IDO and tryptophan 2, 3-dioxygenase (TDO), in the spleen as well as altering hematological indices.	Cyclophosphamide	22-25	indoleamine 2,3-dioxygenase 1	Rattus norvegicus	189-192
35216831-3	2022	Modeled AMH patterns were compared among cyclophosphamide-based chemotherapy, non-cyclophosphamide-based chemotherapy, no chemotherapy, and no breast cancer groups.	Cyclophosphamide	41-57	anti-Mullerian hormone	Homo sapiens	8-11
35216831-12	2022	In contrast, among those who received cyclophosphamide-based and noncyclophosphamide-based chemotherapy, a nonlinear pattern of AMH level of initial fall during chemotherapy, followed by an increase over 2-4 years, and then by a plateau over 1-2 years before a decline was observed.	Cyclophosphamide	38-54	anti-Mullerian hormone	Homo sapiens	128-131
35227076-5	2022	AR- status predicted the failure of adjuvant endocrine therapy with aromatase inhibitors and of adjuvant chemotherapy with docetaxel plus cyclophosphamide.	Cyclophosphamide	138-154	androgen receptor	Homo sapiens	0-2
35436749-6	2022	Results revealed that CYP treatment alone significantly provoked an oxidative-inflammatory response, increased serum kynurenine concentration, and concomitantly increased immunosuppressive IDO and tryptophan 2, 3-dioxygenase (TDO), in the spleen as well as altering hematological indices.	Cyclophosphamide	22-25	tryptophan 2,3-dioxygenase	Rattus norvegicus	197-224
35436749-6	2022	Results revealed that CYP treatment alone significantly provoked an oxidative-inflammatory response, increased serum kynurenine concentration, and concomitantly increased immunosuppressive IDO and tryptophan 2, 3-dioxygenase (TDO), in the spleen as well as altering hematological indices.	Cyclophosphamide	22-25	tryptophan 2,3-dioxygenase	Rattus norvegicus	226-229
35436750-2	2022	Low-dose cyclophosphamide (CTX) can inhibit the number and function of Tregs.	Cyclophosphamide	9-25	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	27-30
35563427-4	2022	PMF90 also reduced the upregulation of connexin 43 (Cx43), a major component of gap junction channels, in the bladder mucosa of CYP-treated mice.	Cyclophosphamide	128-131	gap junction protein, alpha 1	Mus musculus	39-50
35563427-4	2022	PMF90 also reduced the upregulation of connexin 43 (Cx43), a major component of gap junction channels, in the bladder mucosa of CYP-treated mice.	Cyclophosphamide	128-131	gap junction protein, alpha 1	Mus musculus	52-56
35563427-4	2022	PMF90 also reduced the upregulation of connexin 43 (Cx43), a major component of gap junction channels, in the bladder mucosa of CYP-treated mice.	Cyclophosphamide	128-131	RAS p21 protein activator 1	Mus musculus	80-83
35563427-6	2022	In urothelium-specific Cx43 knockout (uCx43KO) mice, macroscopic signs of bladder inflammation and changes in voiding behavior induced by CYP treatment were significantly attenuated when compared to controls.	Cyclophosphamide	138-141	gap junction protein, alpha 1	Mus musculus	23-27
35563427-7	2022	These findings indicate the participation of urothelial Cx43 in the development of bladder inflammation and urinary symptoms in CYP-treated mice and provide pre-clinical evidence for the preventive potential of NOB through its anti-inflammatory effects on IL-1beta signaling and urothelial Cx43 expression.	Cyclophosphamide	128-131	gap junction protein, alpha 1	Mus musculus	56-60
35199314-8	2022	RESULTS: Cyclophosphamide had uncertain effects on inducing complete remission when compared to rituximab (OR 0.35, CI 0.10-1.24, low certainty evidence), mycophenolate mofetil (OR 1.81, CI 0.69-4.71, low certainty), calcineurin inhibitor (OR 1.26, CI 0.61-2.63, low certainty) or steroid monotherapy (OR 2.31, CI 0.62-8.52, low certainty).	Cyclophosphamide	9-25	calcineurin binding protein 1	Homo sapiens	217-238
35571333-2	2022	This study aimed to investigate the immunostimulatory activity of GLP-1 in vitro and in vivo by using RAW264.7 macrophages and cyclophosphamide-induced immunosuppressed mice model.	Cyclophosphamide	127-143	glucagon	Mus musculus	66-71
35571333-5	2022	Furthermore, GLP-1 increased the thymus index, serum immunoglobulin levels, and percentage of CD3+ T lymphocytes in cyclophosphamide-induced immunosuppressed mice.	Cyclophosphamide	116-132	glucagon	Mus musculus	13-18
35468783-1	2022	BACKGROUND: Rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) has been used to treat patients with diffuse large B-cell lymphoma (DLBCL) under National Health Insurance (NHI) scheme in Indonesia.	Cyclophosphamide	27-43	DNA damage inducible transcript 3	Homo sapiens	89-93
35621844-0	2022	beta-Caryophyllene Ameliorates Cyclophosphamide Induced Cardiac Injury: The Association of TLR4/NFkappaB and Nrf2/HO1/NQO1 Pathways.	Cyclophosphamide	31-47	toll-like receptor 4	Rattus norvegicus	91-95
35621844-0	2022	beta-Caryophyllene Ameliorates Cyclophosphamide Induced Cardiac Injury: The Association of TLR4/NFkappaB and Nrf2/HO1/NQO1 Pathways.	Cyclophosphamide	31-47	NFE2 like bZIP transcription factor 2	Rattus norvegicus	109-113
35621844-0	2022	beta-Caryophyllene Ameliorates Cyclophosphamide Induced Cardiac Injury: The Association of TLR4/NFkappaB and Nrf2/HO1/NQO1 Pathways.	Cyclophosphamide	31-47	heme oxygenase 1	Rattus norvegicus	114-117
35621844-0	2022	beta-Caryophyllene Ameliorates Cyclophosphamide Induced Cardiac Injury: The Association of TLR4/NFkappaB and Nrf2/HO1/NQO1 Pathways.	Cyclophosphamide	31-47	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	118-122
35493453-0	2022	Commentary: Post-Transplantation Cyclophosphamide Uniquely Restrains Alloreactive CD4+ T-Cell Proliferation and Differentiation After Murine MHC-Haploidentical Hematopoietic Cell Transplantation.	Cyclophosphamide	33-49	CD4 antigen	Mus musculus	82-85
35528149-9	2022	Imatinib prevention and treatment significantly (0.0001 <= p <= 0.05) reduced pERK and pAKT expression in the upper LP (U. LP) and deeper LP (D. LP) in female mice with 4 h CYP-induced cystitis.	Cyclophosphamide	173-176	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	78-82
35411376-7	2022	Antibody levels were significantly lower in the groups treated with TNF inhibitor (TNFi) with methotrexate (MTX), abatacept, mycophenolate mofetil (MMF), MMF or mizoribine (MMF/MZR) combined with calcineurin inhibitor (CNI), and rituximab or cyclophosphamide (RTX/CPA) compared with those treated with sulfasalazine and/or bucillamine or CNI (p<0.01).	Cyclophosphamide	242-258	tumor necrosis factor	Homo sapiens	68-71
35385034-2	2022	The aim of this observational retrospective study was to evaluate the efficacy of non-pegylated liposomal doxorubicin (Myocet ) and cyclophosphamide in elderly women as HER2 negative first-line MBC treatment.	Cyclophosphamide	132-148	erb-b2 receptor tyrosine kinase 2	Homo sapiens	169-173
34986233-9	2022	When CD45-ADC was combined with pre-transplant TBI (50cGy) and post-transplant Rapamycin, Cytoxan or a JAK inhibitor, 90-100% of recipients achieved stable chimerism (mean: 77%, 59%, 78%, respectively).	Cyclophosphamide	90-97	protein tyrosine phosphatase, receptor type, C	Mus musculus	5-9
35063403-0	2022	AKT signaling downstream of KGF is necessary and sufficient for blocking cyclophosphamide bladder injury.	Cyclophosphamide	73-89	thymoma viral proto-oncogene 1	Mus musculus	0-3
35063403-0	2022	AKT signaling downstream of KGF is necessary and sufficient for blocking cyclophosphamide bladder injury.	Cyclophosphamide	73-89	fibroblast growth factor 7	Mus musculus	28-31
35063403-1	2022	Keratinocyte growth factor (KGF) drives phosphorylated (activated) AKT (pAKT) in bladder urothelium which correlates with cytoprotection from cyclophosphamide.	Cyclophosphamide	142-158	fibroblast growth factor 7	Mus musculus	0-26
35063403-1	2022	Keratinocyte growth factor (KGF) drives phosphorylated (activated) AKT (pAKT) in bladder urothelium which correlates with cytoprotection from cyclophosphamide.	Cyclophosphamide	142-158	fibroblast growth factor 7	Mus musculus	28-31
35063403-1	2022	Keratinocyte growth factor (KGF) drives phosphorylated (activated) AKT (pAKT) in bladder urothelium which correlates with cytoprotection from cyclophosphamide.	Cyclophosphamide	142-158	thymoma viral proto-oncogene 1	Mus musculus	67-70
35063403-6	2022	Indeed, KGF induced pBAD urothelial staining and prevented cyclophosphamide-induced loss of urothelial pS6 staining (likely stabilizing mTORC1 activity).	Cyclophosphamide	59-75	CREB regulated transcription coactivator 1	Mus musculus	136-142
35063403-7	2022	Moreover, co-administration of KGF and AKTi blocked KGF-driven urothelial cytoprotection from cyclophosphamide and prevented pAKT, pBAD and pS6 urothelial expression.	Cyclophosphamide	94-110	fibroblast growth factor 7	Mus musculus	31-34
35063403-7	2022	Moreover, co-administration of KGF and AKTi blocked KGF-driven urothelial cytoprotection from cyclophosphamide and prevented pAKT, pBAD and pS6 urothelial expression.	Cyclophosphamide	94-110	fibroblast growth factor 7	Mus musculus	52-55
35063403-9	2022	Thus, the KGF-AKT signaling axis appears to phosphorylate (suppress) BAD and prevents cyclophosphamide-induced loss of mTOC1 signaling, both of which likely suppresses apoptosis.	Cyclophosphamide	86-102	fibroblast growth factor 7	Mus musculus	10-13
35063403-9	2022	Thus, the KGF-AKT signaling axis appears to phosphorylate (suppress) BAD and prevents cyclophosphamide-induced loss of mTOC1 signaling, both of which likely suppresses apoptosis.	Cyclophosphamide	86-102	thymoma viral proto-oncogene 1	Mus musculus	14-17
35063403-11	2022	Thus, AKT may be a therapeutic target to block urothelial apoptosis form cyclophosphamide.	Cyclophosphamide	73-89	thymoma viral proto-oncogene 1	Mus musculus	6-9
34995765-11	2022	Cyclophosphamide exposure (CYC) and its cumulative dose influenced gonadal function in SLE women, leading to amenorrhoea and POF, as reported in 19 studies.	Cyclophosphamide	0-16	POF1B actin binding protein	Homo sapiens	125-128
35433455-14	2022	CellMinor analysis showed that the CD4 mRNA expression level dramatically climbed with increased sensitivity of tumor cells to NAC drugs such as cyclophosphamide, cisplatin, and carboplatin (p"s < 0.05).	Cyclophosphamide	145-161	CD4 molecule	Homo sapiens	35-38
35531104-2	2022	Numerous studies have shown that traditional HER2 inhibitors and chemotherapeutics such as albumin-paclitaxel, liposomal doxorubicin, and cyclophosphamide (TAC regimen) have different degrees of cardiotoxicity.	Cyclophosphamide	138-154	erb-b2 receptor tyrosine kinase 2	Homo sapiens	45-49
35119651-0	2022	Possible prognostic impact of WT1 mRNA expression at day + 30 after haploidentical peripheral blood stem cell transplantation with posttransplant cyclophosphamide for patients with myeloid neoplasm: a multicenter study from the Okayama Hematological Study Group.	Cyclophosphamide	146-162	WT1 transcription factor	Homo sapiens	30-33
35247119-0	2022	Protective effects of a SIRT1 inhibitor on primordial follicle activation and growth induced by cyclophosphamide: insights from a bovine in vitro folliculogenesis system.	Cyclophosphamide	96-112	sirtuin 1	Bos taurus	24-29
35573753-3	2022	We report a case of a 67-year-old woman with a story of non-Hodgkin lymphoma treated with R-CHOP (rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone), who got a severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection while being totally depleted of B cells.	Cyclophosphamide	113-129	DNA damage inducible transcript 3	Homo sapiens	92-96
35388988-0	2022	FGF7 peptide (FGF7p) mimetic mitigates bladder urothelial injury from cyclophosphamide.	Cyclophosphamide	70-86	fibroblast growth factor 7	Mus musculus	0-4
35388988-0	2022	FGF7 peptide (FGF7p) mimetic mitigates bladder urothelial injury from cyclophosphamide.	Cyclophosphamide	70-86	fibroblast growth factor 7	Mus musculus	14-19
35388988-1	2022	Although full-length fibroblast growth factor 7 (FGF7) blocks cyclophosphamide-induced urothelial apoptosis in mice, limitations include high production costs because of its large size.	Cyclophosphamide	62-78	fibroblast growth factor 7	Mus musculus	21-47
35388988-1	2022	Although full-length fibroblast growth factor 7 (FGF7) blocks cyclophosphamide-induced urothelial apoptosis in mice, limitations include high production costs because of its large size.	Cyclophosphamide	62-78	fibroblast growth factor 7	Mus musculus	49-53
35093504-0	2022	High plasma IL-6 levels following haploidentical allogeneic hematopoietic stem cell transplantation post-transplant cyclophosphamide as predictor of early death with worse outcome.	Cyclophosphamide	116-132	interleukin 6	Homo sapiens	12-16
35344582-5	2022	We demonstrate via in vivo cyclophosphamide treatment using the Emicro-TCL1 mouse model that loss of macrophage phagocytic capacity in Tp53-deleted leukemia is driven by a significant downregulation of a phagocytic transcriptomic signature using scRNA-Seq.	Cyclophosphamide	27-43	T cell lymphoma breakpoint 1	Mus musculus	71-75
35332235-4	2022	We hypothesized that down-regulation of the regulatory functions of PDGFRalpha+ cells and/or loss of PDGFRalpha+ cells generates the DO in CYP-treated mice.	Cyclophosphamide	139-142	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	68-78
35332235-4	2022	We hypothesized that down-regulation of the regulatory functions of PDGFRalpha+ cells and/or loss of PDGFRalpha+ cells generates the DO in CYP-treated mice.	Cyclophosphamide	139-142	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	101-111
35332235-5	2022	After CYP treatment, transcripts of Pdgfralpha and Kcnn3 and PDGFRalpha and SK3 protein were reduced in detrusor muscle extracts.	Cyclophosphamide	6-9	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	36-46
35332235-5	2022	After CYP treatment, transcripts of Pdgfralpha and Kcnn3 and PDGFRalpha and SK3 protein were reduced in detrusor muscle extracts.	Cyclophosphamide	6-9	potassium intermediate/small conductance calcium-activated channel, subfamily N, member 3	Mus musculus	51-56
35332235-5	2022	After CYP treatment, transcripts of Pdgfralpha and Kcnn3 and PDGFRalpha and SK3 protein were reduced in detrusor muscle extracts.	Cyclophosphamide	6-9	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	61-71
35332235-5	2022	After CYP treatment, transcripts of Pdgfralpha and Kcnn3 and PDGFRalpha and SK3 protein were reduced in detrusor muscle extracts.	Cyclophosphamide	6-9	potassium intermediate/small conductance calcium-activated channel, subfamily N, member 3	Mus musculus	76-79
35332235-9	2022	This response was significantly depressed in PDGFRalpha+ cells from CYP-treated bladders.	Cyclophosphamide	68-71	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	45-55
35332235-10	2022	Contractile experiments and ex vivo cystometry showed increased spontaneous contractions and transient contractions, respectively in CYP-treated bladders with a reduction of apamin sensitivity, that could be attributable to the reduction in the SK conductance expressed by PDGFRalpha+ cells.	Cyclophosphamide	133-136	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	273-283
35332235-11	2022	In summary, PDGFRalpha+ cells were reduced and the SK3 conductance was downregulated in CYP-treated bladders.	Cyclophosphamide	88-91	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	12-22
35332235-11	2022	In summary, PDGFRalpha+ cells were reduced and the SK3 conductance was downregulated in CYP-treated bladders.	Cyclophosphamide	88-91	potassium intermediate/small conductance calcium-activated channel, subfamily N, member 3	Mus musculus	51-54
35297262-13	2022	The patient received treatment with mini-CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine, and prednisolone) plus rituximab with partial response after the third cycle.	Cyclophosphamide	60-76	DNA damage inducible transcript 3	Homo sapiens	41-45
35451406-1	2022	ABSTRACT: Maintaining relative dose intensity (RDI) of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) improves the prognosis of patients with diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	66-82	DNA damage inducible transcript 3	Homo sapiens	128-132
35268821-3	2022	Cyclophosphamide (CTX) is a commonly used chemotherapeutic drug that suppresses the host immune system, intestinal mucosa inflammation, and dysbiosis of the intestinal flora.	Cyclophosphamide	0-16	V-set and immunoglobulin domain containing 2	Mus musculus	18-21
35146537-6	2022	Meanwhile, we found several VIP variants that might alter the drug metabolism of cisplatin-cyclophosphamide (CYP2E1), vitamin E (CYP4F2), asthma amlodipine, chlorthalidone, and lisinopril (ACE) through PharmGKB.	Cyclophosphamide	91-107	cytochrome P450 family 2 subfamily E member 1	Homo sapiens	109-115
35244050-4	2022	PATIENT CONCERNS: A 48-year-old Chinese male patient with MALT lymphoma and API2/MALT received 2 courses of standard-dose rituximab, cyclophosphamide, vincristine, prednisone regimen chemotherapy combined with Helicobacter pylori eradication therapy.	Cyclophosphamide	133-149	baculoviral IAP repeat containing 3	Homo sapiens	76-80
35218068-10	2022	RESULTS: Our study noted a higher total and day one CD34+ count in the two groups utilizing cyclophosphamide in mobilization.	Cyclophosphamide	92-108	CD34 molecule	Homo sapiens	52-56
35218068-3	2022	Cyclophosphamide/GCSF is an effective regimen, although reported associated toxicities include risk of febrile neutropenia (FN).	Cyclophosphamide	0-16	colony stimulating factor 3	Homo sapiens	17-21
35194103-1	2022	Human CYP2B6 enzyme although constitutes relatively low proportion (1-4%) of hepatic cytochrome P450 content, it is the major catalyst of metabolism of several clinically important drugs (efavirenz, cyclophosphamide, bupropion, methadone).	Cyclophosphamide	199-215	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	6-12
35194103-1	2022	Human CYP2B6 enzyme although constitutes relatively low proportion (1-4%) of hepatic cytochrome P450 content, it is the major catalyst of metabolism of several clinically important drugs (efavirenz, cyclophosphamide, bupropion, methadone).	Cyclophosphamide	199-215	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	85-100
35177657-3	2022	In both natural aging and cyclophosphamide-induced POF models, treatment with Ab4B19 completely reverses the reduction of pre-antral and antral follicles, and normalizes gonadal hormone.	Cyclophosphamide	26-42	POF1B actin binding protein	Homo sapiens	51-54
35205845-1	2022	BACKGROUND: The two most noteworthy strategies for haploidentical stem cell transplantation (haplo-HSCT) are posttransplantation cyclophosphamide (PTCy) with or without thymoglobulin (ATG) and granulocyte colony stimulating factor-primed bone marrow plus peripheral blood stem cells (GIAC).	Cyclophosphamide	129-145	colony stimulating factor 3	Homo sapiens	193-230
35413036-0	2022	Upregulation of transient receptor potential cation channel subfamily M member-3 in bladder afferents is involved in chronic pain in cyclophosphamide-induced cystitis.	Cyclophosphamide	133-149	transient receptor potential cation channel, subfamily M, member 3	Rattus norvegicus	16-80
35413036-9	2022	Cyclophosphamide-induced cystitis was associated with TRPM3 upregulation at the mRNA, protein, and functional levels in bladder afferent neurons.	Cyclophosphamide	0-16	transient receptor potential cation channel, subfamily M, member 3	Rattus norvegicus	54-59
35413036-10	2022	Our results suggest that upregulation of TRPM3 channels is involved in the development of chronic pain in CYP-induced cystitis, and targeting TRPM3 may be a pharmacological strategy for treating bladder pain in IC/PBS.	Cyclophosphamide	106-109	transient receptor potential cation channel, subfamily M, member 3	Rattus norvegicus	41-46
35413036-10	2022	Our results suggest that upregulation of TRPM3 channels is involved in the development of chronic pain in CYP-induced cystitis, and targeting TRPM3 may be a pharmacological strategy for treating bladder pain in IC/PBS.	Cyclophosphamide	106-109	transient receptor potential cation channel, subfamily M, member 3	Rattus norvegicus	142-147
35242129-0	2022	Post-Transplantation Cyclophosphamide Uniquely Restrains Alloreactive CD4+ T-Cell Proliferation and Differentiation After Murine MHC-Haploidentical Hematopoietic Cell Transplantation.	Cyclophosphamide	21-37	CD4 antigen	Mus musculus	70-73
35242129-7	2022	However, cyclophosphamide was unique in consistently reducing proliferation and expression of the activation marker CD25 by alloreactive CD4+Foxp3- conventional T cells at day +7.	Cyclophosphamide	9-25	forkhead box P3	Mus musculus	141-146
35242129-7	2022	However, cyclophosphamide was unique in consistently reducing proliferation and expression of the activation marker CD25 by alloreactive CD4+Foxp3- conventional T cells at day +7.	Cyclophosphamide	9-25	interleukin 2 receptor, alpha chain	Mus musculus	116-120
35242129-8	2022	Furthermore, cyclophosphamide restrained the differentiation of alloreactive CD4+Foxp3- conventional T cells at both days +7 and +21, whereas methotrexate and cytarabine only restrained differentiation at day +7.	Cyclophosphamide	13-29	CD4 antigen	Mus musculus	77-80
35242129-8	2022	Furthermore, cyclophosphamide restrained the differentiation of alloreactive CD4+Foxp3- conventional T cells at both days +7 and +21, whereas methotrexate and cytarabine only restrained differentiation at day +7.	Cyclophosphamide	13-29	forkhead box P3	Mus musculus	81-86
35242129-7	2022	However, cyclophosphamide was unique in consistently reducing proliferation and expression of the activation marker CD25 by alloreactive CD4+Foxp3- conventional T cells at day +7.	Cyclophosphamide	9-25	CD4 antigen	Mus musculus	137-140
35112552-2	2022	The TACL2014-001 phase 1 trial of the mTOR inhibitor temsirolimus in combination with cyclophosphamide and etoposide was performed in children and adolescents with relapsed/refractory ALL.	Cyclophosphamide	86-102	mechanistic target of rapamycin kinase	Homo sapiens	38-42
35156781-16	2022	RESULTS: Thiamine pyrophosphate significantly decreased the cyclophosphamide-induced increase in the levels of the oxidant parameter malondialdehyde (MDA), proinflammatory nuclear factor kappa B (NF-kappaB), tumor necrosis factor alpha (TNF-alpha), and interleukin 1 beta (IL-1beta).	Cyclophosphamide	60-76	tumor necrosis factor	Rattus norvegicus	208-235
35156781-16	2022	RESULTS: Thiamine pyrophosphate significantly decreased the cyclophosphamide-induced increase in the levels of the oxidant parameter malondialdehyde (MDA), proinflammatory nuclear factor kappa B (NF-kappaB), tumor necrosis factor alpha (TNF-alpha), and interleukin 1 beta (IL-1beta).	Cyclophosphamide	60-76	tumor necrosis factor	Rattus norvegicus	237-246
35156781-16	2022	RESULTS: Thiamine pyrophosphate significantly decreased the cyclophosphamide-induced increase in the levels of the oxidant parameter malondialdehyde (MDA), proinflammatory nuclear factor kappa B (NF-kappaB), tumor necrosis factor alpha (TNF-alpha), and interleukin 1 beta (IL-1beta).	Cyclophosphamide	60-76	interleukin 1 beta	Rattus norvegicus	253-271
35156781-16	2022	RESULTS: Thiamine pyrophosphate significantly decreased the cyclophosphamide-induced increase in the levels of the oxidant parameter malondialdehyde (MDA), proinflammatory nuclear factor kappa B (NF-kappaB), tumor necrosis factor alpha (TNF-alpha), and interleukin 1 beta (IL-1beta).	Cyclophosphamide	60-76	interleukin 1 alpha	Rattus norvegicus	273-281
35096395-6	2022	She received six cycles R-CHOP chemotherapy (rituximab, cyclophosphamide, epirubicin, vincristine, and prednisone) with complete resolution of the mass.	Cyclophosphamide	56-72	DNA damage inducible transcript 3	Homo sapiens	26-30
35101364-1	2022	INTRODUCTION: European Organisation for Research and Treatment of Cancer (EORTC) phase II trial (75111-10114) demonstrated that combining pertuzumab with trastuzumab plus cyclophosphamide (TPM) improved median progression-free survival by seven months compared with pertuzumab and trastuzumab (TP) in older/frail patients with HER2-positive metastatic breast cancer (MBC).	Cyclophosphamide	171-187	erb-b2 receptor tyrosine kinase 2	Homo sapiens	327-331
35145514-1	2021	Even with high-dose post-transplant cyclophosphamide (PT-Cy) which was initially introduced for graft-versus-host disease (GvHD) prevention in the setting of HLA-haploidentical transplantation, both acute and chronic GvHDs remain a major clinical challenge.	Cyclophosphamide	36-52	interleukin 10	Homo sapiens	217-222
35054804-4	2022	This study aimed to identify the immunomodulatory effects, and underlying mechanisms thereof, of submerged cultures of CLM using RAW264.7 macrophages and cyclophosphamide (CTX)-induced immunosuppression in mice.	Cyclophosphamide	154-170	CD300C molecule 2	Mus musculus	119-122
35582170-9	2022	Cyclophosphamide treatment significantly improved kidney function as determined by the fold-change of eGFR during the observation period.	Cyclophosphamide	0-16	epidermal growth factor receptor	Homo sapiens	102-106
35039063-3	2022	METHODS: Firstly, blood tonic efficacies of the stems of K. interior (KIS) and its closely related species were compared using BD mouse model induced by 1-acetyl-2-phenylhydrazine (APH) and cyclophosphamide (CTX).	Cyclophosphamide	190-206	U2AF homology motif (UHM) kinase 1	Mus musculus	70-73
35371455-1	2022	Background: A randomized controlled trial demonstrated a beneficial effect of corticosteroids (CS) + cyclophosphamide followed by azathioprine in progressive immunoglobulin A nephropathy (IgAN).	Cyclophosphamide	101-117	IGAN1	Homo sapiens	188-192
35045923-7	2022	Regulating the levels of haematopoietic cytokines, the balance of Bcl-2/Bax, and the inhibition of caspase-3 expression may be the mechanisms of action of ICS I and ICS II against cyclophosphamide-induced bone marrow suppression in mice.	Cyclophosphamide	180-196	B cell leukemia/lymphoma 2	Mus musculus	66-71
35045923-7	2022	Regulating the levels of haematopoietic cytokines, the balance of Bcl-2/Bax, and the inhibition of caspase-3 expression may be the mechanisms of action of ICS I and ICS II against cyclophosphamide-induced bone marrow suppression in mice.	Cyclophosphamide	180-196	caspase 3	Mus musculus	99-108
35044836-1	2022	PURPOSE: Rituximab with cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP) represents the standard of care for first-line treatment of diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	24-40	DNA damage inducible transcript 3	Homo sapiens	88-92
2736513-10	1989	The timing of Cy and TNF administration was critical since administration of Cy prior to or concurrent with rhTNF was not effective in reducing tumor area or increasing cure rates over those achieved with either agent alone.	Cyclophosphamide	77-79	tumor necrosis factor	Mus musculus	21-24
2479801-6	1989	The prolongation of the survival time by rG-CSF was more evident when rG-CSF was administered in therapeutic combination with cyclophosphamide.	Cyclophosphamide	126-142	colony stimulating factor 3	Rattus norvegicus	41-47
2479801-6	1989	The prolongation of the survival time by rG-CSF was more evident when rG-CSF was administered in therapeutic combination with cyclophosphamide.	Cyclophosphamide	126-142	colony stimulating factor 3	Rattus norvegicus	70-76
2806435-1	1989	Previous reports have shown that interleukin 1 (IL-1) has radioprotective effects when given to mice 20 h before a lethal dose of irradiation and enhances granulocyte recovery in mice treated with cyclophosphamide.	Cyclophosphamide	197-213	interleukin 1 complex	Mus musculus	33-52
2676137-2	1989	Adjuvant therapy consisted of 5-fluorouracil, doxorubicin (Adriamycin, Adria Laboratories, Columbus, OH), and cyclophosphamide (FAC) in ten patients and cyclophosphamide, methotrexate, and 5-fluorouracil (CMF) in one patient.	Cyclophosphamide	110-126	FA complementation group C	Homo sapiens	128-131
2795457-6	1989	Collectively, these results indicate that the glutathione-acrolein adduct formed after exposure to acrolein, or as a result of allyl alcohol oxidation and cyclophosphamide metabolism, can be oxidized by hepatic ALDH or ADH, respectively.	Cyclophosphamide	155-171	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	211-215
2570283-1	1989	Granulocyte-macrophage colony-stimulating factor (GM-CSF), given to accelerate recovery from cytopenia induced by high-dose (7 g/m2) cyclophosphamide, reproducibly brought about a dramatic increase (up to 1000-fold) in the number of peripheral blood granulocyte-macrophage colony-forming units (CFU-GM).	Cyclophosphamide	133-149	colony stimulating factor 2	Homo sapiens	0-48
2570283-1	1989	Granulocyte-macrophage colony-stimulating factor (GM-CSF), given to accelerate recovery from cytopenia induced by high-dose (7 g/m2) cyclophosphamide, reproducibly brought about a dramatic increase (up to 1000-fold) in the number of peripheral blood granulocyte-macrophage colony-forming units (CFU-GM).	Cyclophosphamide	133-149	colony stimulating factor 2	Homo sapiens	50-56
2504842-1	1989	The ability of cyclophosphamide (CTX) and mitomycin C (MMC) to modify the expression of thermotolerance in vivo at 43.5 degrees C was investigated in a transplantable C3H mouse mammary carcinoma grown s.c. in feet of C3D2F1/Bom mice.	Cyclophosphamide	15-31	V-set and immunoglobulin domain containing 2	Mus musculus	33-36
2505070-2	1989	The present study, which used cyclophosphamide as a positive control, shows that one planar PCB congener, 3,4,3",4"-tetrachlorobiphenyl, caused dose-related chromosome breakage in human lymphocytes exposed in vitro to 0.1-10(-4) micrograms/ml.	Cyclophosphamide	30-46	pyruvate carboxylase	Homo sapiens	92-95
2682131-19	1989	Succinylcholine is hydrolysed by plasma cholinesterase, and drugs which decrease the activity of this enzyme may produce a prolonged block, i.e. contraceptive pills, cyclophosphamide, echothiopate and organophosphate.	Cyclophosphamide	166-182	butyrylcholinesterase	Homo sapiens	40-54
2787959-0	1989	Marrow hypoplasia associated with a monoclonal CD8 large granular lymphocyte proliferation: reversal with cyclophosphamide and prednisone.	Cyclophosphamide	106-122	CD8a molecule	Homo sapiens	47-50
2554602-1	1989	The restoration of resistance by N alpha-acetylmuramyl-L-alanyl-D-isoglutaminyl-N epsilon-stearoyl-L-lysine [MDP-Lys(L18)] on herpes simplex virus (HSV) type-1 infection was examined in cyclophosphamide (CY)-treated mice.	Cyclophosphamide	186-202	ribosomal protein L18	Mus musculus	117-120
2554602-1	1989	The restoration of resistance by N alpha-acetylmuramyl-L-alanyl-D-isoglutaminyl-N epsilon-stearoyl-L-lysine [MDP-Lys(L18)] on herpes simplex virus (HSV) type-1 infection was examined in cyclophosphamide (CY)-treated mice.	Cyclophosphamide	204-206	ribosomal protein L18	Mus musculus	117-120
2554602-2	1989	MDP-Lys(L18) was shown to restore the resistance to HSV infection in CY-treated mice when it was injected either subcutaneously, intravenously, or intraperitoneally before infection.	Cyclophosphamide	69-71	ribosomal protein L18	Mus musculus	8-11
2554602-3	1989	Treatment with MDP-Lys(L18) in CY-treated mice restored impaired activity for inhibiting HSV growth in the liver.	Cyclophosphamide	31-33	ribosomal protein L18	Mus musculus	23-26
2606575-1	1989	The sensitivity of a cyclophosphamide (CP)-resistant MIR rat mammary carcinoma cell variant (MIRCPr) in monolayer culture towards the cytotoxic effect of mafosfamide (an analogue of "activated" CP) was measured as a function of extracellular pH (pHe).	Cyclophosphamide	21-37	membrane associated ring-CH-type finger 8	Rattus norvegicus	53-56
2573634-5	1989	IFN-alpha/beta in turn activates a cyclophosphamide-sensitive NK-like cell that is the effector cell for HR (effector phase).	Cyclophosphamide	35-51	interferon alpha	Mus musculus	0-9
2478216-0	1989	Circulation of CD34+ hematopoietic stem cells in the peripheral blood of high-dose cyclophosphamide-treated patients: enhancement by intravenous recombinant human granulocyte-macrophage colony-stimulating factor.	Cyclophosphamide	83-99	CD34 molecule	Homo sapiens	15-19
2478216-0	1989	Circulation of CD34+ hematopoietic stem cells in the peripheral blood of high-dose cyclophosphamide-treated patients: enhancement by intravenous recombinant human granulocyte-macrophage colony-stimulating factor.	Cyclophosphamide	83-99	colony stimulating factor 2	Homo sapiens	163-211
2478216-1	1989	We report that hematopoietic progenitor cells expressing the CD34 antigen (CD34+ cells) transiently circulate in the peripheral blood (PB) of cancer patients treated with 7 g/m2 cyclophosphamide (HD-CTX) with or without recombinant human granulocyte macrophage-colony stimulating factor (rHuGM-CSF).	Cyclophosphamide	178-194	CD34 molecule	Homo sapiens	61-65
2478216-1	1989	We report that hematopoietic progenitor cells expressing the CD34 antigen (CD34+ cells) transiently circulate in the peripheral blood (PB) of cancer patients treated with 7 g/m2 cyclophosphamide (HD-CTX) with or without recombinant human granulocyte macrophage-colony stimulating factor (rHuGM-CSF).	Cyclophosphamide	178-194	CD34 molecule	Homo sapiens	75-79
2787754-0	1989	A single low dose of human recombinant interleukin 1 accelerates the recovery of neutrophils in mice with cyclophosphamide-induced neutropenia.	Cyclophosphamide	106-122	interleukin 1 alpha	Homo sapiens	39-52
2672132-1	1989	Intravenous cyclophosphamide therapy of severe systemic lupus is associated with reduction in the numbers of circulating T and B lymphocytes, suppression of T11 (CD2) receptor-mediated responses, and suppression of autoantibody production.	Cyclophosphamide	12-28	CD2 molecule	Homo sapiens	157-160
2672132-1	1989	Intravenous cyclophosphamide therapy of severe systemic lupus is associated with reduction in the numbers of circulating T and B lymphocytes, suppression of T11 (CD2) receptor-mediated responses, and suppression of autoantibody production.	Cyclophosphamide	12-28	CD2 molecule	Homo sapiens	162-165
2507490-2	1989	Recently we observed that the antitumor efficacy of various antitumor agents (5-fluorouracil, tegafur, adriamycin, mitomycin C, cyclophosphamide, and cisplatin) against experimental solid tumors was enhanced by prior or simultaneous administration of human epidermal growth factor (EGF).	Cyclophosphamide	128-144	epidermal growth factor	Homo sapiens	257-280
2507490-2	1989	Recently we observed that the antitumor efficacy of various antitumor agents (5-fluorouracil, tegafur, adriamycin, mitomycin C, cyclophosphamide, and cisplatin) against experimental solid tumors was enhanced by prior or simultaneous administration of human epidermal growth factor (EGF).	Cyclophosphamide	128-144	epidermal growth factor	Homo sapiens	282-285
2666309-4	1989	Detectable levels of IL-2 in these mitogen-stimulated supernatants began to rise after Day 25, which was temporally associated with a gradual shift from active immunity, to immunity mediated by cyclophosphamide-resistant memory T cells, which did not absorb IL-2 in vitro.	Cyclophosphamide	194-210	interleukin 2	Mus musculus	21-25
2471557-1	1989	Pretreatment of mice with recombinant murine (rM) colony-stimulating factor-granulocyte-macrophage (CSF-gm) or recombinant human (rH) CSF-g provides partial protection from the lethal effects of ionizing radiation or the alkylating agent cyclophosphamide (CTX).	Cyclophosphamide	238-254	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	50-106
2656523-7	1989	In GM-CSF-treated mice, the neutrophil levels in peripheral blood started to increase 5 days after CPA administration and were consistently higher than those in controls.	Cyclophosphamide	99-102	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	3-9
2785408-2	1989	In addition, rH IL-2 was able to accelerate host recovery from cyclophosphamide (CTX)- or radiation-induced bone marrow depression and peripheral blood leukopenia.	Cyclophosphamide	63-79	interleukin 2	Homo sapiens	16-20
2787392-0	1989	Tumor-infiltrating lymphocytes cultured in recombinant interleukin-2: enhancement of growth, cytotoxicity, and phenotypic expression of cytotoxic T-cell antigens by cyclophosphamide given intravenously prior to tumor harvest.	Cyclophosphamide	165-181	interleukin 2	Homo sapiens	55-68
2545164-2	1989	The intrinsic antiviral activity of macrophages against herpes simplex virus type 1 (HSV-1) as well as natural killer (NK) activity against YAC-1 target cells was stimulated by administration of GLA-60 to CY-immunosuppressed mice.	Cyclophosphamide	205-207	ADP-ribosyltransferase 1	Mus musculus	140-145
2476892-7	1989	When each of the cytokines was administered subcutaneously four times daily into cyclophosphamide-treated mice before intravenous infection with HSV, only GM-CSF revealed any protective activity.	Cyclophosphamide	81-97	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	155-161
2534133-9	1989	The in vivo anti-tumor activity of spleen cells of mice in regression was nullified by treatment with anti-Thy 1 and anti-Lyt 1 plus C, but not anti-Lyt 2 plus C. These results indicate that CY administration results in only a transient decrease of tumor cell number and that an induction of Lyt 1 +, Lyt 2 + T cells in the peritoneal cavity and Lyt 1 + T cells in spleen may be responsible for a complete disappearance of tumor cells.	Cyclophosphamide	191-193	CD5 antigen	Mus musculus	292-297
2706622-1	1989	Cytochrome P-450-catalyzed activation of cyclophosphamide to alkylating metabolites was studied in isolated rat liver microsomes and purified, reconstituted P-450 enzyme systems in order to identify the major enzymatic catalysts of drug activation in both uninduced and drug-induced liver tissue.	Cyclophosphamide	41-57	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-16
2706622-4	1989	Cyclophosphamide activation catalyzed by uninduced adult male rat liver microsomes (specific activity, 0.68 nmol/min/mg), although not inhibited by anti-P-450 PB-4 antibodies, was partially inhibited (approximately 60%) by antibodies to P-450 PB-1 (gene IIC6) and more completely inhibited (greater than 95%) by antibodies reactive with both P-450 PB-1 and P-450 2c (gene IIC11).	Cyclophosphamide	0-16	cytochrome P450, family 2, subfamily c, polypeptide 12	Rattus norvegicus	237-247
2706622-4	1989	Cyclophosphamide activation catalyzed by uninduced adult male rat liver microsomes (specific activity, 0.68 nmol/min/mg), although not inhibited by anti-P-450 PB-4 antibodies, was partially inhibited (approximately 60%) by antibodies to P-450 PB-1 (gene IIC6) and more completely inhibited (greater than 95%) by antibodies reactive with both P-450 PB-1 and P-450 2c (gene IIC11).	Cyclophosphamide	0-16	cytochrome P450, family 2, subfamily c, polypeptide 12	Rattus norvegicus	342-352
2706622-5	1989	Consistent with these observations, P-450 PB-1 and P-450 2c both activated cyclophosphamide at moderate rates in reconstituted systems (turnover, 1.6-2.7 nmol metabolite/min/nmol P-450), while seven other purified hepatic P-450 forms exhibited significantly lower activities (turnover less than or equal to 0.5 nmol metabolite/min/nmol P-450).	Cyclophosphamide	75-91	cytochrome P450, family 2, subfamily c, polypeptide 12	Rattus norvegicus	36-46
2534133-9	1989	The in vivo anti-tumor activity of spleen cells of mice in regression was nullified by treatment with anti-Thy 1 and anti-Lyt 1 plus C, but not anti-Lyt 2 plus C. These results indicate that CY administration results in only a transient decrease of tumor cell number and that an induction of Lyt 1 +, Lyt 2 + T cells in the peritoneal cavity and Lyt 1 + T cells in spleen may be responsible for a complete disappearance of tumor cells.	Cyclophosphamide	191-193	CD8 antigen, alpha chain	Mus musculus	301-306
2534133-9	1989	The in vivo anti-tumor activity of spleen cells of mice in regression was nullified by treatment with anti-Thy 1 and anti-Lyt 1 plus C, but not anti-Lyt 2 plus C. These results indicate that CY administration results in only a transient decrease of tumor cell number and that an induction of Lyt 1 +, Lyt 2 + T cells in the peritoneal cavity and Lyt 1 + T cells in spleen may be responsible for a complete disappearance of tumor cells.	Cyclophosphamide	191-193	CD5 antigen	Mus musculus	292-297
2702696-7	1989	We now show that the ability of v-p97NY to induce delayed-type hypersensitivity to p97 improved if the vaccinated mice were given cyclophosphamide (Cy) on the day of vaccination.	Cyclophosphamide	130-146	growth factor receptor bound protein 2-associated protein 2	Mus musculus	34-37
2655227-5	1989	In contrast, cyclophosphamide (CyP) treatment led to acute (less than 4 weeks) destruction of both 1st- and 2nd-set allografts; breaking of tolerance was regularly seen when donor and host differed by two MHC haplotypes, but occurred infrequently in semiallogeneic combinations.	Cyclophosphamide	13-29	major histocompatibility complex, class I, C	Homo sapiens	205-208
2702696-7	1989	We now show that the ability of v-p97NY to induce delayed-type hypersensitivity to p97 improved if the vaccinated mice were given cyclophosphamide (Cy) on the day of vaccination.	Cyclophosphamide	148-150	growth factor receptor bound protein 2-associated protein 2	Mus musculus	34-37
2496686-11	1989	Taken together, our results imply that the vigorous T cell proliferation during cyclophosphamide-induced lymphatic regeneration is independent of the IL-2/IL-2R hormone system, like T-cell precursor proliferation in the thymus, and is characterized by both high c-myb expression typical for thymocytes and high c-myc expression typical for in vitro proliferation-activated T cells.	Cyclophosphamide	80-96	myeloblastosis oncogene	Mus musculus	262-267
2705401-5	1989	The fluorouracil, doxorubicin (Adriamycin), and cyclophosphamide (FAC) regimen was effective in improving disease and overall survival regardless of age of the patient, stage of disease, or extent of nodal involvement in comparison with the historical control patients treated with similar local therapy.	Cyclophosphamide	48-64	FA complementation group C	Homo sapiens	66-69
2730016-8	1989	In patients with preoperative treatment of PSK and cyclophosphamide, the decreases in helper and cytotoxic T cells and the increase in suppressor inducer T cells were significantly blocked during the postoperative course.	Cyclophosphamide	51-67	TAO kinase 2	Homo sapiens	43-46
2785489-2	1989	Adoptively transferred Thy-1.1+ H-2b (KbDb) LCM virus-immune T cells are inhibited in cyclophosphamide (Cy)-suppressed, virus-infected mice that are heterozygous for H-2Db (e.g. H-2k x b F1).	Cyclophosphamide	86-102	thymus cell antigen 1, theta	Mus musculus	23-30
2785489-2	1989	Adoptively transferred Thy-1.1+ H-2b (KbDb) LCM virus-immune T cells are inhibited in cyclophosphamide (Cy)-suppressed, virus-infected mice that are heterozygous for H-2Db (e.g. H-2k x b F1).	Cyclophosphamide	104-106	thymus cell antigen 1, theta	Mus musculus	23-30
2709334-7	1989	The ratio of fibronectin mRNA to polyadenylated RNA was elevated to a similar extent in both murine strains during the 1st week after cyclophosphamide treatment.	Cyclophosphamide	134-150	fibronectin 1	Mus musculus	13-24
2784143-1	1989	Based on recently published data, IL-1 has been shown to provide radioprotective effects when given to mice 20 h before a lethal dose of irradiation and to enhance granulocyte recovery in mice treated with cyclophosphamide.	Cyclophosphamide	206-222	interleukin 1 complex	Mus musculus	34-38
2784143-2	1989	In this study, we have investigated whether IL-1 can provide protection for human bone marrow colony-forming cells treated with high doses of 4-hydroperoxycyclophosphamide (4-HC), a potent derivative of cyclophosphamide.	Cyclophosphamide	155-171	interleukin 1 alpha	Homo sapiens	44-48
2784067-0	1989	Interleukin-1 accelerates murine granulocyte recovery following treatment with cyclophosphamide.	Cyclophosphamide	79-95	interleukin 1 alpha	Homo sapiens	0-13
2713472-3	1989	Combined injection of thymectomized (CBA X C57B1/6)F1 mice with a massive dose of rat spleen cells and cyclophosphamide induced in animals stable tolerance to rat cells.	Cyclophosphamide	103-119	complement component 6	Mus musculus	43-53
2521829-1	1989	Treatment of murine CBA splenocytes with Vibrio cholerae neuraminidase (VCN) prior to engraftment into cyclophosphamide (CY) immunosuppressed Balb/c x CBA mice reduced the incidence of acute lethal graft-versus-host disease (GvHD) and delayed mortality in the later phase of the disease.	Cyclophosphamide	103-119	neuraminidase 1	Homo sapiens	57-70
2643663-1	1989	Human rIL-1 alpha was shown to be a potent stimulus of granulopoiesis in mice that have been myelosuppressed with cyclophosphamide.	Cyclophosphamide	114-130	interleukin 1 alpha	Rattus norvegicus	6-17
2643663-7	1989	IL-1 effects were observed in mice treated with a wide dose range (50 to 300 mg/kg) of cyclophosphamide, with optimal effects occurring at a dose of 200 mg/kg.	Cyclophosphamide	87-103	interleukin 1 complex	Mus musculus	0-4
2473150-4	1989	In the cyclophosphamide-treated group, the prophylactic administration of G-CSF (2 micrograms/day/mouse) yielded a lower incidence of infection and of infection-induced mortality than that of saline alone.	Cyclophosphamide	7-23	colony stimulating factor 3 (granulocyte)	Mus musculus	74-79
2502309-1	1989	The present study was designed to examine whether cyclophosphamide augmented induction of antitumor cells and antitumor resistance in C57BL/6 mice pretreated with mitomycin-C-treated EL4 cells (EL4MMC) plus OK-432, a streptococcal preparation.	Cyclophosphamide	50-66	epilepsy 4	Mus musculus	183-186
2502309-10	1989	Despite the fact that cyclophosphamide effectively augmented induction of antitumor cells in C57BL/6 mice pretreated with EL4MMC plus OK-432, it diminished rather than augmented, under all conditions tested, the ability of the mice to resist a challenge of live EL4 cells.	Cyclophosphamide	22-38	epilepsy 4	Mus musculus	122-125
2502309-11	1989	Reduction of antitumor resistance by cyclophosphamide was also observed in an experimental system of a semi-syngeneic host (BDF1) tumor (EL4).	Cyclophosphamide	37-53	epilepsy 4	Mus musculus	137-140
2513138-1	1989	The effects of Fluosol-DA, an oxygen-carrying perfluorochemical emulsion, and carbogen breathing alone or in combination on the antitumor activity of cyclophosphamide (CTX) in vivo were investigated.	Cyclophosphamide	150-166	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	168-171
2518399-0	1989	The CD4 cell dependency of SJL/J B-cell lymphomas as a target for cyclophosphamide therapy.	Cyclophosphamide	66-82	CD4 antigen	Mus musculus	4-7
2518399-2	1989	We sought to determine whether cyclophosphamide (CY) treatment of tumor-bearing mice would be successful through effects on tumor cells, CD4 cells, or both.	Cyclophosphamide	31-47	CD4 antigen	Mus musculus	137-140
2518399-2	1989	We sought to determine whether cyclophosphamide (CY) treatment of tumor-bearing mice would be successful through effects on tumor cells, CD4 cells, or both.	Cyclophosphamide	49-51	CD4 antigen	Mus musculus	137-140
2518399-5	1989	We concluded that CY affected the tumor-stimulated environment of SJL/J mice by killing CD4 cells that had been activated by a pre-existing tumor stimulus and by promoting the appearance of a population of CD8 cells that suppressed the ability of residual or recovering CD4 cells to proliferate in response to tumor.	Cyclophosphamide	18-20	CD4 antigen	Mus musculus	88-91
2518399-5	1989	We concluded that CY affected the tumor-stimulated environment of SJL/J mice by killing CD4 cells that had been activated by a pre-existing tumor stimulus and by promoting the appearance of a population of CD8 cells that suppressed the ability of residual or recovering CD4 cells to proliferate in response to tumor.	Cyclophosphamide	18-20	CD4 antigen	Mus musculus	270-273
2525078-1	1989	The novel 5HT3 receptor antagonist GR38032F was evaluated in the control of emesis induced by the cyclophosphamide analogue ifosfamide.	Cyclophosphamide	98-114	5-hydroxytryptamine receptor 3A	Homo sapiens	10-14
2624921-2	1989	Cyclophosphamide, combined with lymphokine-activated killer (LAK) cells and recombinant interleukin-2 (rIL-2), is known to mediate regression of tumors, but the effects of cyclophosphamide on the subsequent generation of LAK cells are unclear.	Cyclophosphamide	172-188	interleukin 2	Rattus norvegicus	103-108
2624921-3	1989	It was the aim of the experiments in this paper to determine whether fresh splenocytes cultured with rIL-2 would maintain or regain their cytotoxicity in vitro after being exposed to the cytotoxic agent cyclophosphamide in vivo.	Cyclophosphamide	203-219	interleukin 2	Rattus norvegicus	101-106
2624921-8	1989	It is concluded that murine splenocytes can demonstrate cytotoxicity after exposure to cyclophosphamide, through prolonged continuous in vitro culture with rIL-2.	Cyclophosphamide	87-103	interleukin 2	Rattus norvegicus	156-161
2785003-6	1989	A synergistic therapeutic effect was achieved in mice with the solid tumors, but not in mice with the lymphoma, only when IL-2 was given 1-4 days after cyclophosphamide (100-200 mg/kg).	Cyclophosphamide	152-168	interleukin 2	Mus musculus	122-126
2785003-7	1989	Conversely, administration of IL-2 1-4 days prior to cyclophosphamide resulted, in all three tumor systems, in enhanced tumor growth and in decreased survival as compared with mice receiving cyclophosphamide alone.	Cyclophosphamide	53-69	interleukin 2	Mus musculus	30-34
2785003-7	1989	Conversely, administration of IL-2 1-4 days prior to cyclophosphamide resulted, in all three tumor systems, in enhanced tumor growth and in decreased survival as compared with mice receiving cyclophosphamide alone.	Cyclophosphamide	191-207	interleukin 2	Mus musculus	30-34
2785003-8	1989	Similarly, treatment with IL-2 both before and after cyclophosphamide was less efficacious than a single course of IL-2 given afterwards.	Cyclophosphamide	53-69	interleukin 2	Mus musculus	26-30
2766862-2	1989	A randomized clinical study of patients with advanced epithelial ovarian cancer after debulking surgery showed that high-dose (120 mg/m2) cis-platinum (DDP) in combination with cyclophosphamide (600 mg/m2) had a significantly higher response and survival rate than the low-dose DDP (60 mg/m2) and cyclophosphamide combination.	Cyclophosphamide	177-193	translocase of inner mitochondrial membrane 8A	Homo sapiens	278-281
2766862-2	1989	A randomized clinical study of patients with advanced epithelial ovarian cancer after debulking surgery showed that high-dose (120 mg/m2) cis-platinum (DDP) in combination with cyclophosphamide (600 mg/m2) had a significantly higher response and survival rate than the low-dose DDP (60 mg/m2) and cyclophosphamide combination.	Cyclophosphamide	297-313	translocase of inner mitochondrial membrane 8A	Homo sapiens	152-155
2697584-6	1989	In the Vth MRC myelomatosis trial, patients treated with a combination of adriamycin, carmustine, cyclophosphamide and melphalan are living significantly longer than those treated with melphalan alone, and this survival advantage persists after correction for the most important prognostic factor, beta 2 microglobulin.	Cyclophosphamide	98-114	beta-2-microglobulin	Homo sapiens	298-318
2707426-1	1989	In experiments on CBA/Lac J mice it was found that the course administration of adriamycin (0.95 mg/kg), vinblastine (0.24 mg/kg) and cyclophosphan (27 mg/kg) in 1/10 LD50.10 causes persistent disturbances of the functional activity of the lymphoid tissue manifesting by inhibition of the proliferative response of the spleen lymphocytes to T- and B-cell mitogens one month and to a lesser extent three months after cytostatic action.	Cyclophosphamide	134-147	lactase	Mus musculus	22-25
2530180-9	1989	Flow cytometric analysis indicated a quantitative depletion of all T-lymphocytes, including Thy-1.2(+), Lyt-1(+), Lyt-2(+) and L3T4(+) subsets in the spleens of CY-treated mice; however, a population of Mac-1(+) cells was markedly expanded.	Cyclophosphamide	161-163	thymus cell antigen 1, theta	Mus musculus	92-99
2695567-9	1989	Cyclophosphamide, dexamethasone and anti-ASGM1 antibody were most effective in increasing survival and inhibiting immune enhancement but differentially effective in inhibiting TNF induction (or in certain cases gamma interferon induction), decreasing ascites or hydrothorax or affecting lymphoid proliferation in the lungs and spleen.	Cyclophosphamide	0-16	tumor necrosis factor	Homo sapiens	176-179
2783314-6	1989	Both neutrophilia and augmented resistance to infection were eliminated by a second dose of cyclophosphamide administered during the IL-1 treatments.	Cyclophosphamide	92-108	interleukin 1 complex	Mus musculus	133-137
2785972-3	1989	The footpad reaction to the purified protein derivative of tuberculin (PPD) was enhanced remarkably by Cy pretreatment in both MRL-lpr and MRL-+/+ mice.	Cyclophosphamide	103-105	Fas (TNF receptor superfamily member 6)	Mus musculus	131-134
2785972-4	1989	In addition, the lymph node cells obtained from nonpretreated MRL-lpr and MRL-+/+ mice at 7 days after BCG CW immunization suppressed the DTH induction of Cy-pretreated MRL-+/+ mice.	Cyclophosphamide	155-157	Fas (TNF receptor superfamily member 6)	Mus musculus	66-69
2785972-5	1989	On the other hand, a positive proliferative response to PPD in vitro was seen only in the cells from Cy-pretreated MRL-+/+ and younger MRL-lpr mice, but not in the cells of nonpretreated MRL-+/+ or both pretreated and nonpretreated older MRL-lpr mice.	Cyclophosphamide	101-103	Fas (TNF receptor superfamily member 6)	Mus musculus	139-142
2785972-5	1989	On the other hand, a positive proliferative response to PPD in vitro was seen only in the cells from Cy-pretreated MRL-+/+ and younger MRL-lpr mice, but not in the cells of nonpretreated MRL-+/+ or both pretreated and nonpretreated older MRL-lpr mice.	Cyclophosphamide	101-103	Fas (TNF receptor superfamily member 6)	Mus musculus	242-245
2534133-9	1989	The in vivo anti-tumor activity of spleen cells of mice in regression was nullified by treatment with anti-Thy 1 and anti-Lyt 1 plus C, but not anti-Lyt 2 plus C. These results indicate that CY administration results in only a transient decrease of tumor cell number and that an induction of Lyt 1 +, Lyt 2 + T cells in the peritoneal cavity and Lyt 1 + T cells in spleen may be responsible for a complete disappearance of tumor cells.	Cyclophosphamide	191-193	thymus cell antigen 1, theta	Mus musculus	107-112
2534133-9	1989	The in vivo anti-tumor activity of spleen cells of mice in regression was nullified by treatment with anti-Thy 1 and anti-Lyt 1 plus C, but not anti-Lyt 2 plus C. These results indicate that CY administration results in only a transient decrease of tumor cell number and that an induction of Lyt 1 +, Lyt 2 + T cells in the peritoneal cavity and Lyt 1 + T cells in spleen may be responsible for a complete disappearance of tumor cells.	Cyclophosphamide	191-193	CD5 antigen	Mus musculus	122-127
2785972-6	1989	Removal of B220-positive cells from the lymph node cell populations of Cy-pretreated MRL-lpr mice restored PPD responsiveness, but the same treatment had no effect on the cells from nonpretreated MRL-lpr mice.	Cyclophosphamide	71-73	Fas (TNF receptor superfamily member 6)	Mus musculus	89-92
2785972-6	1989	Removal of B220-positive cells from the lymph node cell populations of Cy-pretreated MRL-lpr mice restored PPD responsiveness, but the same treatment had no effect on the cells from nonpretreated MRL-lpr mice.	Cyclophosphamide	71-73	Fas (TNF receptor superfamily member 6)	Mus musculus	200-203
2642487-5	1989	After the patient had received immunosuppressive therapy with prednisone and cyclophosphamide for 3 months, her insulin resistance remitted, and she developed hypoglycemia.	Cyclophosphamide	77-93	insulin	Homo sapiens	112-119
3263325-4	1988	Augmentation by interleukin-1 alpha of resistance to infection was also observed in P. aeruginosa-infected mice in a state of cyclophosphamide-induced leucopenia.	Cyclophosphamide	126-142	interleukin 1 alpha	Homo sapiens	16-35
2473363-6	1989	Eighty-six of 137 patients (63%) treated according to the HD3 protocol achieved complete remission after induction chemotherapy with COPP + ABVD.	Cyclophosphamide	133-137	histone deacetylase 3	Homo sapiens	58-61
2688030-10	1989	TNF cytotoxic effects appeared to be amplified by pretreatment of cells with chemotherapeutic agents such as Actinomycin D, Adriamycin, and Cytoxan as well as to have synergistic effects with gamma interferon, alpha interferon, and IL-2.	Cyclophosphamide	140-147	tumor necrosis factor	Homo sapiens	0-3
2799726-4	1989	The experimental data are also provided concerning the influence of a single oral cyclophosphamide administration on the morphologic signs of nephritis in GBA and C57BL mice.	Cyclophosphamide	82-98	glucosidase, beta, acid	Mus musculus	155-158
2593878-4	1989	The isolated strain, named TK-1, caused no symptoms in ddY and BALB/c mice except when the mice were treated with cyclophosphamide.	Cyclophosphamide	114-130	thymidine kinase 1	Mus musculus	27-31
2772560-3	1989	Treatment with steroids and cyclophosphamide reduced the IGF-I immunoreactivity.	Cyclophosphamide	28-44	insulin like growth factor 1	Homo sapiens	57-62
20702290-8	1989	The b and e forms of cytochrome P-450 were non-inducible but it is highly likely that the c form was both inducible (by 3MC and betaNF) and functional, the latter being assessed by modulation of DPH toxicity and CPA activation.	Cyclophosphamide	212-215	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	21-37
3233147-0	1988	The ratio of two isozyme groups in microsomal cytochrome P-450 under exogenous influence of carbon tetrachloride and cyclophosphamide.	Cyclophosphamide	117-133	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	46-62
2459064-4	1988	Recombinant human granulocyte colony-stimulating factor hastened the recovery of peripheral neutrophil counts in animals made leukopenic by prior treatment with cyclophosphamide.	Cyclophosphamide	161-177	colony stimulating factor 3	Homo sapiens	18-55
3167803-6	1988	Employing CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine, prednisone) and consolidation radiation therapy in most cases, 80% achieved a complete remission and 59% survive failure-free at 5 years by actuarial calculation.	Cyclophosphamide	29-45	DNA damage inducible transcript 3	Homo sapiens	10-14
3264714-10	1988	The effect was further enhanced by a second dose of CY at the end of a course of IL-2.	Cyclophosphamide	52-54	interleukin 2	Mus musculus	81-85
3199515-0	1988	[Experimental study on the effectiveness of BRM in radiation therapy--OK-432 and cyclophosphamide].	Cyclophosphamide	81-97	SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 2	Mus musculus	44-47
3145205-6	1988	For cyclophosphamide (CTX) and mitomycin C (MMC) both DER and TER (thermal enhancement ratio) were significantly larger than 1.0.	Cyclophosphamide	4-20	V-set and immunoglobulin domain containing 2	Mus musculus	22-25
2467649-2	1988	Induction of severe neutropenia was prevented by repeated daily injections of h G-CSF at a dose of 2.5 micrograms/day for 4 days after the CPA treatment.	Cyclophosphamide	139-142	colony stimulating factor 3 (granulocyte)	Mus musculus	80-85
3143703-6	1988	Natural killer cell and LAK precursor cell activities in the spleen cells from the treated mice were found to be restored by IL-2 alone or CY + IL-2, whereas they were suppressed by CY alone.	Cyclophosphamide	139-141	alpha-kinase 1	Mus musculus	24-27
3192382-7	1988	About 30% of leukemia-bearing mice receiving cyclophosphamide and L1210-Maf cells after L1210 inoculation were able to reject the leukemia (as compared with 0% after injection of L1210-Maf cells only or 5% after cyclophosphamide administration).	Cyclophosphamide	45-61	avian musculoaponeurotic fibrosarcoma oncogene homolog	Mus musculus	185-188
3192382-7	1988	About 30% of leukemia-bearing mice receiving cyclophosphamide and L1210-Maf cells after L1210 inoculation were able to reject the leukemia (as compared with 0% after injection of L1210-Maf cells only or 5% after cyclophosphamide administration).	Cyclophosphamide	212-228	avian musculoaponeurotic fibrosarcoma oncogene homolog	Mus musculus	72-75
3192382-13	1988	Cyclophosphamide not only reduces the tumor burden but probably can potentiate the L1210-Maf dependent antitumor immunity as well.	Cyclophosphamide	0-16	avian musculoaponeurotic fibrosarcoma oncogene homolog	Mus musculus	89-92
2467644-5	1988	In both, cyclophosphamide and busulfan induced myelosuppression, G-CSF in doses between 10 and 30 micrograms/kg/d was able to significantly shorten the time of neutropenia.	Cyclophosphamide	9-25	colony stimulating factor 3	Homo sapiens	65-70
3169807-1	1988	We have analyzed the expression of cyclophosphamide (CY) resistance in somatic cell hybrids of mouse LPC-1/CY-R plasmacytoma and P3-X63-Ag8.653 (Ag8) myeloma cells.	Cyclophosphamide	35-51	annexin A1	Mus musculus	101-106
3169807-1	1988	We have analyzed the expression of cyclophosphamide (CY) resistance in somatic cell hybrids of mouse LPC-1/CY-R plasmacytoma and P3-X63-Ag8.653 (Ag8) myeloma cells.	Cyclophosphamide	53-55	annexin A1	Mus musculus	101-106
3138120-4	1988	When a combination chemotherapy consisting of cisplatin, adriamycin and cyclophosphamide was given to these ovarian cancer patients, the IL-2 production was markedly depressed.	Cyclophosphamide	72-88	interleukin 2	Homo sapiens	137-141
3259600-4	1988	IL-1 can also significantly increase survival and can "rescue" a number of animals if administered either before or after lethal doses of cyclophosphamide or gamma-irradiation.	Cyclophosphamide	138-154	interleukin 1 beta	Homo sapiens	0-4
2896209-6	1988	Cyclophosphamide treatment could reconstitute CHS responsiveness of the vit/vit mice to the allergen dinitrofluorobenzene.	Cyclophosphamide	0-16	vitrin	Mus musculus	72-75
2896209-6	1988	Cyclophosphamide treatment could reconstitute CHS responsiveness of the vit/vit mice to the allergen dinitrofluorobenzene.	Cyclophosphamide	0-16	vitrin	Mus musculus	76-79
3389749-3	1988	An attempt to potentiate IFNa action with Zymozan or Cyclophosphamide did not succeed.	Cyclophosphamide	53-69	interferon alpha 1	Homo sapiens	25-29
3356000-17	1988	Thus, IFN-alpha/beta potentiated suboptimal CY effects for P388 leukemia, had neutral effects when injected before CY treatment, and inhibited antitumor activity of curative CY or nitrosourea schedules.	Cyclophosphamide	44-46	interferon alpha	Mus musculus	6-15
3356000-17	1988	Thus, IFN-alpha/beta potentiated suboptimal CY effects for P388 leukemia, had neutral effects when injected before CY treatment, and inhibited antitumor activity of curative CY or nitrosourea schedules.	Cyclophosphamide	115-117	interferon alpha	Mus musculus	6-15
3356000-17	1988	Thus, IFN-alpha/beta potentiated suboptimal CY effects for P388 leukemia, had neutral effects when injected before CY treatment, and inhibited antitumor activity of curative CY or nitrosourea schedules.	Cyclophosphamide	115-117	interferon alpha	Mus musculus	6-15
3385205-7	1988	Chronic immunosuppressive therapy with cyclophosphamide at most only attenuated the development of renal infarct hypertension associated with this transient renin elevation.	Cyclophosphamide	39-55	renin	Rattus norvegicus	157-162
3258182-19	1988	IL-2 inhibitor activity of the sera from the tumor-bearing rats was greater than that of normal rats (P less than 0.001), but it was depressed markedly by cyclophosphamide (P less than 0.01).	Cyclophosphamide	155-171	interleukin 2	Rattus norvegicus	0-4
2839116-6	1988	A current study comparing the standard chemotherapy with cyclophosphamide, adriamycin and vincristine (CAV) to alternating CAV with etoposide (E) and cisplatin (P) has suggested an advantage for alternating chemotherapy, with a statistically superior response rate and survival.	Cyclophosphamide	57-73	caveolin 2	Homo sapiens	103-106
2842488-1	1988	The mechanism of reduction in cyclophosphamide (CPA)-induced toxicity by diethyldithiocarbamate (DTC) and carbon disulfide (CS2) was examined in relation to CPA metabolism in mice.	Cyclophosphamide	30-46	calsyntenin 2	Mus musculus	124-127
2842488-1	1988	The mechanism of reduction in cyclophosphamide (CPA)-induced toxicity by diethyldithiocarbamate (DTC) and carbon disulfide (CS2) was examined in relation to CPA metabolism in mice.	Cyclophosphamide	48-51	calsyntenin 2	Mus musculus	124-127
2842488-8	1988	These results suggested that the reduction of CPA-induced toxicity in mice pretreated with DTC or CS2 was due to the inhibition of activation of CPA and reduced formation of alkylating metabolites.	Cyclophosphamide	46-49	calsyntenin 2	Mus musculus	98-101
2842488-8	1988	These results suggested that the reduction of CPA-induced toxicity in mice pretreated with DTC or CS2 was due to the inhibition of activation of CPA and reduced formation of alkylating metabolites.	Cyclophosphamide	145-148	calsyntenin 2	Mus musculus	98-101
2830969-0	1988	Effect of low dose cyclophosphamide on the immune system of cancer patients: depletion of CD4+, 2H4+ suppressor-inducer T-cells.	Cyclophosphamide	19-35	CD4 molecule	Homo sapiens	90-93
2830969-6	1988	Treatment of melanoma patients with CY plus vaccine resulted in a progressive fall in the proportion of CD4+ T-cells expressing the 2H4 (CD45) antigen, which identifies inducers of suppression.	Cyclophosphamide	36-38	CD4 molecule	Homo sapiens	104-107
2830969-6	1988	Treatment of melanoma patients with CY plus vaccine resulted in a progressive fall in the proportion of CD4+ T-cells expressing the 2H4 (CD45) antigen, which identifies inducers of suppression.	Cyclophosphamide	36-38	protein tyrosine phosphatase receptor type C	Homo sapiens	137-141
2830969-7	1988	The reduction of CD4+, 2H4+ T-cells did not become apparent until day 28 after the first dose of CY and reached statistical significance only on days 49 (21 days after the second dose) and 105 (21 days after the fourth dose) (mean changes +/- SE: day 49, -5.4 +/- 1.4%, P less than 0.01; day 105, -9.1 +/- 2.2%, P less than 0.01; t test for nonindependent samples).	Cyclophosphamide	97-99	CD4 molecule	Homo sapiens	17-20
2895062-0	1988	Lethal vaccinia infection in cyclophosphamide-suppressed mice is associated with decreased expression of Thy-1, Lyt-2 and L3T4 and diminished IL-2 production in surviving T cells.	Cyclophosphamide	29-45	thymus cell antigen 1, theta	Mus musculus	105-110
2895062-0	1988	Lethal vaccinia infection in cyclophosphamide-suppressed mice is associated with decreased expression of Thy-1, Lyt-2 and L3T4 and diminished IL-2 production in surviving T cells.	Cyclophosphamide	29-45	CD8 antigen, alpha chain	Mus musculus	112-117
2895062-0	1988	Lethal vaccinia infection in cyclophosphamide-suppressed mice is associated with decreased expression of Thy-1, Lyt-2 and L3T4 and diminished IL-2 production in surviving T cells.	Cyclophosphamide	29-45	CD4 antigen	Mus musculus	122-126
2895062-0	1988	Lethal vaccinia infection in cyclophosphamide-suppressed mice is associated with decreased expression of Thy-1, Lyt-2 and L3T4 and diminished IL-2 production in surviving T cells.	Cyclophosphamide	29-45	interleukin 2	Mus musculus	142-146
2979834-6	1988	Although cyclophosphamide alone and radiotherapy plus cyclophosphamide demonstrated antitumour activity, the number of tumour nodules and the nodule diameter were reduced most effectively in group 8 (receiving MTP, radiotherapy and cyclophosphamide).	Cyclophosphamide	54-70	lysosomal-associated protein transmembrane 4A	Mus musculus	210-213
2979834-6	1988	Although cyclophosphamide alone and radiotherapy plus cyclophosphamide demonstrated antitumour activity, the number of tumour nodules and the nodule diameter were reduced most effectively in group 8 (receiving MTP, radiotherapy and cyclophosphamide).	Cyclophosphamide	54-70	lysosomal-associated protein transmembrane 4A	Mus musculus	210-213
3384743-8	1988	In contrast, there were significant effects of cyclophosphamide on carnitine acetyltransferase and acid phosphatase specific activity.	Cyclophosphamide	47-63	carnitine O-acetyltransferase	Rattus norvegicus	67-94
3384743-10	1988	After 6 weeks of treatment with the high dose of cyclophosphamide, carnitine acetyltransferase specific activity in the initial segment and the corpus epididymidis was elevated to 165 and 140%, respectively, as compared with the 1-week high dose values.	Cyclophosphamide	49-65	carnitine O-acetyltransferase	Rattus norvegicus	67-94
3263471-0	1988	Phase I trial of recombinant interleukin-2 and cyclophosphamide: augmentation of cellular immunity and T-cell mitogenic response with long-term administration of rIL-2.	Cyclophosphamide	47-63	interleukin 2	Rattus norvegicus	162-167
3409214-1	1988	In vivo 31P nuclear magnetic resonance spectroscopy has been used to examine the RIF-1 fibrosarcoma in mice during untreated growth and following chemotherapy with cyclophosphamide.	Cyclophosphamide	164-180	replication timing regulatory factor 1	Mus musculus	81-86
2970969-7	1988	mAb 14-12 can convert nonresponder mice into responders for the Ir gene-controlled response to the random terpolymer L-glutamic acid60-L-alanine30-L-tyrosine 10 (GAT), and can substitute for cyclophosphamide in overcoming a suppressor barrier in the adoptive transfer of contact sensitivity.	Cyclophosphamide	191-207	glycine-N-acyltransferase	Mus musculus	162-165
2838358-0	1988	Administration of silica particles or anti-Lyt2 antibody prevents beta-cell destruction in NOD mice given cyclophosphamide.	Cyclophosphamide	106-122	CD8 antigen, alpha chain	Mus musculus	43-47
2838358-4	1988	After administration of cyclophosphamide, 10 of 26 untreated mice and 1 of 21 anti-Lyt2-treated mice became diabetic.	Cyclophosphamide	24-40	CD8 antigen, alpha chain	Mus musculus	83-87
3265631-10	1988	IL-2 inhibitor activity of the sera from the tumor-bearers was greater than that of normal rats, while it was depressed markedly by cyclophosphamide (60 mg/kg i.p.).	Cyclophosphamide	132-148	interleukin 2	Rattus norvegicus	0-4
3289548-1	1988	By cloning T cells, mutations at the hypoxanthine-guanine phosphoribosyltransferase locus were quantified in peripheral blood lymphocytes of 12 patients with connective tissue diseases receiving long-term cyclophosphamide.	Cyclophosphamide	205-221	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	37-83
3365687-1	1988	The cytosolic aldehyde dehydrogenase (ALDH) isozyme from cyclophosphamide (CPA) resistant L1210 cells (L1210/CPA) was purified to apparent homogeneity using ternary enzyme complex-dye ligand chromatography.	Cyclophosphamide	57-73	aldehyde dehydrogenase family 3, subfamily A1	Mus musculus	38-42
3365687-1	1988	The cytosolic aldehyde dehydrogenase (ALDH) isozyme from cyclophosphamide (CPA) resistant L1210 cells (L1210/CPA) was purified to apparent homogeneity using ternary enzyme complex-dye ligand chromatography.	Cyclophosphamide	75-78	aldehyde dehydrogenase family 3, subfamily A1	Mus musculus	38-42
3365687-6	1988	Thus, the increased levels of only the cytosolic ALDH isoform in L1210/CPA cells appear to be the single phenotypic difference necessary for conferring resistance to CPA.	Cyclophosphamide	71-74	aldehyde dehydrogenase family 3, subfamily A1	Mus musculus	49-53
3420943-7	1988	Microsomal fractions provided greater cytochrome P-450 dependent activation of cyclophosphamide and were less cytotoxic than S9.	Cyclophosphamide	79-95	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	38-54
3135686-0	1988	Granulopoietic effects of colony-stimulating factor obtained from urine of patients with aplastic anemia on normal and cyclophosphamide-treated mice.	Cyclophosphamide	119-135	colony stimulating factor 2	Homo sapiens	26-51
3135686-3	1988	In addition, this CSF induced faster recoveries of neutrophils in the peripheral blood and progenitor spleen cells of cyclophosphamide (CY)-treated mice.	Cyclophosphamide	118-134	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	18-21
3135686-3	1988	In addition, this CSF induced faster recoveries of neutrophils in the peripheral blood and progenitor spleen cells of cyclophosphamide (CY)-treated mice.	Cyclophosphamide	136-138	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	18-21
2464358-5	1988	The DBCG trial 80-R2 is the largest randomized trial of CAF (cyclophosphamide, doxorubicin, 5-fluorouracil) versus CMF (cyclophosphamide, methotrexate, 5-fluorouracil) in recurrent breast cancer.	Cyclophosphamide	61-77	lysine acetyltransferase 2B	Homo sapiens	56-59
3203011-0	1988	Treatment of diffuse histiocytic and diffuse mixed non-Hodgkin lymphomas with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP).	Cyclophosphamide	78-94	DNA damage inducible transcript 3	Homo sapiens	137-141
3190440-0	1988	Activation of cyclophosphamide in mouse limb bud cultures using a reconstituted cytochrome P-450 system.	Cyclophosphamide	14-30	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	80-96
3260132-0	1988	Improved therapeutic effects of interleukin 2 after the accumulation of lymphokine-activated killer cells in tumor tissue of mice previously treated with cyclophosphamide.	Cyclophosphamide	154-170	interleukin 2	Mus musculus	32-45
3260132-6	1988	Satisfactory effects from the combination of CY and IL-2 were also obtained by 5 days administration of IL-2 between days 11 and 15, initiated 6 days after CY treatment, but not by that given before CY (days 1-5) or 1 day after CY (days 6-10).	Cyclophosphamide	45-47	interleukin 2	Mus musculus	104-108
3260132-6	1988	Satisfactory effects from the combination of CY and IL-2 were also obtained by 5 days administration of IL-2 between days 11 and 15, initiated 6 days after CY treatment, but not by that given before CY (days 1-5) or 1 day after CY (days 6-10).	Cyclophosphamide	156-158	interleukin 2	Mus musculus	52-56
3260132-6	1988	Satisfactory effects from the combination of CY and IL-2 were also obtained by 5 days administration of IL-2 between days 11 and 15, initiated 6 days after CY treatment, but not by that given before CY (days 1-5) or 1 day after CY (days 6-10).	Cyclophosphamide	156-158	interleukin 2	Mus musculus	104-108
3260132-6	1988	Satisfactory effects from the combination of CY and IL-2 were also obtained by 5 days administration of IL-2 between days 11 and 15, initiated 6 days after CY treatment, but not by that given before CY (days 1-5) or 1 day after CY (days 6-10).	Cyclophosphamide	156-158	interleukin 2	Mus musculus	52-56
3260132-6	1988	Satisfactory effects from the combination of CY and IL-2 were also obtained by 5 days administration of IL-2 between days 11 and 15, initiated 6 days after CY treatment, but not by that given before CY (days 1-5) or 1 day after CY (days 6-10).	Cyclophosphamide	156-158	interleukin 2	Mus musculus	104-108
3260132-6	1988	Satisfactory effects from the combination of CY and IL-2 were also obtained by 5 days administration of IL-2 between days 11 and 15, initiated 6 days after CY treatment, but not by that given before CY (days 1-5) or 1 day after CY (days 6-10).	Cyclophosphamide	156-158	interleukin 2	Mus musculus	52-56
3260132-6	1988	Satisfactory effects from the combination of CY and IL-2 were also obtained by 5 days administration of IL-2 between days 11 and 15, initiated 6 days after CY treatment, but not by that given before CY (days 1-5) or 1 day after CY (days 6-10).	Cyclophosphamide	156-158	interleukin 2	Mus musculus	104-108
3257158-0	1988	Effect of continuous administration of interleukin 2 on active specific chemoimmunotherapy with extracted tumor-specific transplantation antigen and cyclophosphamide.	Cyclophosphamide	149-165	interleukin 2	Homo sapiens	39-52
3257158-1	1988	Injection of purified human interleukin 2 (IL-2) directly into the spleen has been shown to potentiate the effect of specific chemoimmunotherapy, using butanol-extracted tumor-specific transplantation antigen (TSTA) and cyclophosphamide (CY) in a C3H/HeJ murine methylcholanthrene-induced fibrosarcoma model.	Cyclophosphamide	220-236	interleukin 2	Homo sapiens	28-41
3257158-1	1988	Injection of purified human interleukin 2 (IL-2) directly into the spleen has been shown to potentiate the effect of specific chemoimmunotherapy, using butanol-extracted tumor-specific transplantation antigen (TSTA) and cyclophosphamide (CY) in a C3H/HeJ murine methylcholanthrene-induced fibrosarcoma model.	Cyclophosphamide	220-236	interleukin 2	Homo sapiens	43-47
3257158-1	1988	Injection of purified human interleukin 2 (IL-2) directly into the spleen has been shown to potentiate the effect of specific chemoimmunotherapy, using butanol-extracted tumor-specific transplantation antigen (TSTA) and cyclophosphamide (CY) in a C3H/HeJ murine methylcholanthrene-induced fibrosarcoma model.	Cyclophosphamide	238-240	interleukin 2	Homo sapiens	28-41
3257158-1	1988	Injection of purified human interleukin 2 (IL-2) directly into the spleen has been shown to potentiate the effect of specific chemoimmunotherapy, using butanol-extracted tumor-specific transplantation antigen (TSTA) and cyclophosphamide (CY) in a C3H/HeJ murine methylcholanthrene-induced fibrosarcoma model.	Cyclophosphamide	238-240	interleukin 2	Homo sapiens	43-47
3257158-7	1988	IL-2 delivered by all routes either by continuous infusion or by bolus injection augmented the chemoimmunotherapeutic efficacy of TSTA/CY against 7-day established tumors.	Cyclophosphamide	135-137	interleukin 2	Homo sapiens	0-4
3257158-15	1988	Thus continuous i.s.-IL-2 infusion appears to augment cytotoxic T-cell induction in tumor-bearing hosts undergoing stimulation of helper elements by TSTA and inhibition of suppressor cells by CY.	Cyclophosphamide	192-194	interleukin 2	Homo sapiens	21-25
3257159-3	1988	Cy at doses of 100 mg/kg and 150 mg/kg completely protected mice from a 100% lethal dose of IL-2, and doses of 50 mg/kg and 150 mg/kg allowed the administration of a median of 4.5 and 10.0 more doses of IL-2, respectively, before death from IL-2 toxicity occurred.	Cyclophosphamide	0-2	interleukin 2	Mus musculus	92-96
3257159-3	1988	Cy at doses of 100 mg/kg and 150 mg/kg completely protected mice from a 100% lethal dose of IL-2, and doses of 50 mg/kg and 150 mg/kg allowed the administration of a median of 4.5 and 10.0 more doses of IL-2, respectively, before death from IL-2 toxicity occurred.	Cyclophosphamide	0-2	interleukin 2	Mus musculus	203-207
3257159-3	1988	Cy at doses of 100 mg/kg and 150 mg/kg completely protected mice from a 100% lethal dose of IL-2, and doses of 50 mg/kg and 150 mg/kg allowed the administration of a median of 4.5 and 10.0 more doses of IL-2, respectively, before death from IL-2 toxicity occurred.	Cyclophosphamide	0-2	interleukin 2	Mus musculus	203-207
3257159-5	1988	In mice bearing pulmonary metastases of the weakly immunogenic MCA-105 sarcoma, IL-2 increased median survival time from 33 (no IL-2) to greater than 60 days for all doses of IL-2 tested when combined with a single injection of Cy at 75 mg/kg (P less than 0.002).	Cyclophosphamide	228-230	interleukin 2	Mus musculus	80-84
3128500-4	1988	When a combination chemotherapy of cisplatin, adriamycin and cyclophosphamide was given, the OKT 4/OKT 8 cell ratio was significantly increased with a significant decrease of the absolute number of the OKT 8 cell subset, while the expression of IL-2 receptor and the absolute number of the OKT 4 cell subset remained unchanged.	Cyclophosphamide	61-77	interleukin 2 receptor subunit beta	Homo sapiens	245-258
3500254-4	1987	In vitro studies of the direct effects of CY metabolites (mafosfamide and 4-hydroperoxycyclophosphamide) on human monocytes showed only concomitant decreases in production of IL-1 and TNF-like molecules.	Cyclophosphamide	42-44	interleukin 1 alpha	Homo sapiens	175-179
3435704-6	1987	Correlation of in vitro sensitivity to cis-platinum with clinical response to cis-platinum assessed using CT scan and second-look laparotomy, showed positive correlation in 9/11 (89%) patients (8 = S/S; 1 = R/R); positive correlation between in vitro sensitivity to phosphoramide mustard and clinical response was also found in 4/6 patients receiving cyclophosphamide (3 = S/S; 1 = R/R).	Cyclophosphamide	351-367	cytokine inducible SH2 containing protein	Homo sapiens	39-42
3435704-6	1987	Correlation of in vitro sensitivity to cis-platinum with clinical response to cis-platinum assessed using CT scan and second-look laparotomy, showed positive correlation in 9/11 (89%) patients (8 = S/S; 1 = R/R); positive correlation between in vitro sensitivity to phosphoramide mustard and clinical response was also found in 4/6 patients receiving cyclophosphamide (3 = S/S; 1 = R/R).	Cyclophosphamide	351-367	cytokine inducible SH2 containing protein	Homo sapiens	78-81
3500254-4	1987	In vitro studies of the direct effects of CY metabolites (mafosfamide and 4-hydroperoxycyclophosphamide) on human monocytes showed only concomitant decreases in production of IL-1 and TNF-like molecules.	Cyclophosphamide	42-44	tumor necrosis factor	Homo sapiens	184-187
3501452-3	1987	When a combination chemotherapy which consisted of cisplatin, adriamycin and cyclophosphamide was given to these ovarian cancer patients, the OKT 4/8 cell ratio was significantly increased while the IL-2 production was markedly inhibited.	Cyclophosphamide	77-93	interleukin 2	Mus musculus	199-203
2444540-3	1987	When mice were injected subcutaneously once a day with 2.5 micrograms of hG-CSF beginning on the day after CPA injection, the reduction was prevented markedly, even 4 days later.	Cyclophosphamide	107-110	colony stimulating factor 3	Homo sapiens	73-79
2820571-2	1987	The effectiveness of both cyclophosphamide, doxorubicin, and vincristine (CAV) and etoposide and cisplatin (VPP) in previously untreated patients with small cell lung cancer has been well-documented.	Cyclophosphamide	26-42	caveolin 2	Homo sapiens	74-77
3744939-1	1986	Low dose cyclophosphamide (CTX) is protective against a subsequent challenge with a lethal dose of the same drug administered 5 days later.	Cyclophosphamide	9-25	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	27-30
3117468-6	1987	The higher metastatic capacity of B16-A cells with induced high levels of H-2 antigens was observed also in adult mice and in young mice pretreated with cyclophosphamide.	Cyclophosphamide	153-169	histocompatibility-2, MHC	Mus musculus	74-77
2436816-6	1987	The antigen-nonspecific suppressor T cells generated by SAP were sensitive to cyclophosphamide.	Cyclophosphamide	78-94	amyloid P component, serum	Mus musculus	56-59
2960008-3	1987	It appears that Cyclophosphamide is able to correct the CD4/CD8 ratio imbalance observed in most MS patients and that this correction is generally associated with a beneficial effect on the disease.	Cyclophosphamide	16-32	CD4 molecule	Homo sapiens	56-59
2960008-3	1987	It appears that Cyclophosphamide is able to correct the CD4/CD8 ratio imbalance observed in most MS patients and that this correction is generally associated with a beneficial effect on the disease.	Cyclophosphamide	16-32	CD8a molecule	Homo sapiens	60-63
2950845-1	1987	Cyclophosphamide was administered to 14 patients with chronic progressive multiple sclerosis on an intermittent escalating dosage schedule adjusted to maintain numbers of peripheral blood B lymphocytes and helper/inducer (CD4) T cells below the fifth percentile of the normal population.	Cyclophosphamide	0-16	CD4 molecule	Homo sapiens	222-225
3494816-7	1987	Lymphocyte proliferative responses to myelin basic protein (BP) and concanavalin A (Con A) and antibody titers to BP were preserved in CY-treated rats.	Cyclophosphamide	135-137	myelin basic protein	Rattus norvegicus	38-58
3815352-9	1987	These data suggest that the albumin-catalyzed reaction of cis-4-OHCP in plasma represents an important pathway for the transformation of cyclophosphamide metabolites and further emphasize the importance of considering phosphoramide mustard generated extracellularly versus intracellularly and the respective contributions of extracellular and intracellular phosphoramide mustard to cyclophosphamide cytotoxicity in vivo.	Cyclophosphamide	137-153	suppressor of cytokine signaling 6	Mus musculus	58-63
3815352-9	1987	These data suggest that the albumin-catalyzed reaction of cis-4-OHCP in plasma represents an important pathway for the transformation of cyclophosphamide metabolites and further emphasize the importance of considering phosphoramide mustard generated extracellularly versus intracellularly and the respective contributions of extracellular and intracellular phosphoramide mustard to cyclophosphamide cytotoxicity in vivo.	Cyclophosphamide	382-398	suppressor of cytokine signaling 6	Mus musculus	58-63
3542201-1	1987	Protection of testicular integrity against damage from cyclophosphamide (CY) by simultaneous treatment with a gonadotropin-releasing hormone (GnRH) analogue was reported in BALB/c mice (L.M.	Cyclophosphamide	55-71	gonadotropin releasing hormone 1	Mus musculus	110-140
3542201-1	1987	Protection of testicular integrity against damage from cyclophosphamide (CY) by simultaneous treatment with a gonadotropin-releasing hormone (GnRH) analogue was reported in BALB/c mice (L.M.	Cyclophosphamide	55-71	gonadotropin releasing hormone 1	Mus musculus	142-146
3542201-1	1987	Protection of testicular integrity against damage from cyclophosphamide (CY) by simultaneous treatment with a gonadotropin-releasing hormone (GnRH) analogue was reported in BALB/c mice (L.M.	Cyclophosphamide	73-75	gonadotropin releasing hormone 1	Mus musculus	110-140
3542201-1	1987	Protection of testicular integrity against damage from cyclophosphamide (CY) by simultaneous treatment with a gonadotropin-releasing hormone (GnRH) analogue was reported in BALB/c mice (L.M.	Cyclophosphamide	73-75	gonadotropin releasing hormone 1	Mus musculus	142-146
2949833-6	1987	The in vivo treatment with Cy decreased the total number of lymphoid cells in the spleens, as well as the proportion of B lymphocytes; however, it increased the percentage of both Lyt2+ and L3T4+ lymphocytes.	Cyclophosphamide	27-29	CD8 antigen, alpha chain	Mus musculus	180-184
2949833-9	1987	After Cy treatment, the proliferative ability of spleen cells in response to interleukin-2 (IL-2) was substantially impaired.	Cyclophosphamide	6-8	interleukin 2	Mus musculus	77-90
2949833-9	1987	After Cy treatment, the proliferative ability of spleen cells in response to interleukin-2 (IL-2) was substantially impaired.	Cyclophosphamide	6-8	interleukin 2	Mus musculus	92-96
2949833-10	1987	Using monoclonal antibodies to the IL-2 receptor, we found that Cy-treated T lymphocytes failed to fully express the IL-2 receptor following in vitro stimulation with irradiated tumor cells.	Cyclophosphamide	64-66	interleukin 2	Mus musculus	35-39
3594490-3	1987	In this communication we show that ABPP, when used in combination with low or moderate doses of cyclophosphamide, can be quite effective against early established (day 3) tumor as well as against advanced, grossly visible (day 8-10) tumor in both the i.p.	Cyclophosphamide	96-112	amyloid beta (A4) precursor protein	Mus musculus	35-39
3570504-4	1987	It was found that CY treatment diminished the formation of glycosylation inhibiting factor (GIF) and enhanced the formation of glycosylation enhancing factor (GEF).	Cyclophosphamide	18-20	rho/rac guanine nucleotide exchange factor (GEF) 2	Mus musculus	127-157
3570504-4	1987	It was found that CY treatment diminished the formation of glycosylation inhibiting factor (GIF) and enhanced the formation of glycosylation enhancing factor (GEF).	Cyclophosphamide	18-20	rho/rac guanine nucleotide exchange factor (GEF) 2	Mus musculus	159-162
3570504-5	1987	The results suggest that the enhancement of the IgE antibody response by CY treatment is due not only to elimination of suppressor T cells but also to the activation of GEF-forming lymphocytes.	Cyclophosphamide	73-75	rho/rac guanine nucleotide exchange factor (GEF) 2	Mus musculus	169-172
3151500-14	1987	Aflatoxin B1, cyclophosphamide, dibutylnitrosamine, and benzo[a]pyrene mutated SD1 and/or XEM1 and XEM2 cells, but were inactive in parental V79 cells.	Cyclophosphamide	14-30	CUP2Q35	Homo sapiens	79-82
3550612-5	1987	We are currently testing this hypothesis in a randomized clinical trial of women with advanced breast cancer who are randomized to receive 5FU, doxorubicin, and cyclophosphamide (FAC) or FAC plus ICRF-187.	Cyclophosphamide	161-177	FA complementation group C	Homo sapiens	179-182
2877222-5	1986	Administration of cyclophosphamide to patients with AILD was followed by return to normal of both N-ras and c-fos expression.	Cyclophosphamide	18-34	NRAS proto-oncogene, GTPase	Homo sapiens	98-103
2877222-5	1986	Administration of cyclophosphamide to patients with AILD was followed by return to normal of both N-ras and c-fos expression.	Cyclophosphamide	18-34	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	108-113
2875791-12	1986	Furthermore, chemoimmunotherapy including intrasplenic IL-2 injection potentiated the antitumor immunity achieved with combined tumor-specific transplantation antigen and cyclophosphamide.	Cyclophosphamide	171-187	interleukin 2	Mus musculus	55-59
3019517-2	1986	Statistically significant potentiation of cis-platinum (CDDP) and cyclophosphamide (CY) given weekly in a low dose was seen when human lymphoblastoid interferon (IFN-alpha nl) (2 X 10(5) mu/mouse/day) was administered simultaneously.	Cyclophosphamide	66-82	interferon alpha 1	Homo sapiens	162-171
3019517-2	1986	Statistically significant potentiation of cis-platinum (CDDP) and cyclophosphamide (CY) given weekly in a low dose was seen when human lymphoblastoid interferon (IFN-alpha nl) (2 X 10(5) mu/mouse/day) was administered simultaneously.	Cyclophosphamide	84-86	interferon alpha 1	Homo sapiens	162-171
3019517-4	1986	A similar though less marked effect was seen with CY (median doubling time increased from 21.5, 19.5, and 27 days to 32, 27, and 35 days with the addition of IFN-alpha nl).	Cyclophosphamide	50-52	interferon alpha 1	Homo sapiens	158-167
3020701-1	1986	Cisplatin plus VP-16 has become a widely used salvage regimen for CAV (cyclophosphamide, doxorubicin [Adriamycin], and vincristine) failures.	Cyclophosphamide	71-87	host cell factor C1	Homo sapiens	15-20
2427212-4	1986	The suppressive potential was then tested in mice previously primed for delayed-type hypersensitivity responses which were also treated with cyclophosphamide to deplete Ts3 and other drug-sensitive Ts cell types.	Cyclophosphamide	141-157	Trichinella spiralis resistance 3	Mus musculus	169-172
2873885-4	1986	In contrast, anti-Thy 1.1 antibody therapy of mice in remission following treatment with cyclophosphamide prolonged remission duration (P less than 0.001) and modestly prolonged survival (P less than 0.01) compared to treatment with irrelevant antibody or chemotherapy alone.	Cyclophosphamide	89-105	thymus cell antigen 1, theta	Mus musculus	18-25
2425812-2	1986	The genotoxic activities of cyclophosphamide and its direct acting metabolite, phosphoramide mustard, were studied in the hepatoma cells as cyclophosphamide is known to be metabolized by phenobarbital-inducible cytochrome P-450-associated metabolic activity.	Cyclophosphamide	28-44	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	211-227
2425812-2	1986	The genotoxic activities of cyclophosphamide and its direct acting metabolite, phosphoramide mustard, were studied in the hepatoma cells as cyclophosphamide is known to be metabolized by phenobarbital-inducible cytochrome P-450-associated metabolic activity.	Cyclophosphamide	140-156	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	211-227
2425812-5	1986	The cytochrome P-450-associated enzyme inhibitors, SKF-525A and metyrapone, were found to reduce the level of cyclophosphamide-induced sister chromatid exchanges in HepG2 and H4-II-E, suggesting that cyclophosphamide was activated by this pathway in both hepatoma lines.	Cyclophosphamide	110-126	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	4-20
2425812-5	1986	The cytochrome P-450-associated enzyme inhibitors, SKF-525A and metyrapone, were found to reduce the level of cyclophosphamide-induced sister chromatid exchanges in HepG2 and H4-II-E, suggesting that cyclophosphamide was activated by this pathway in both hepatoma lines.	Cyclophosphamide	200-216	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	4-20
3708572-4	1986	CY increased also the sensitivity of the residual MBL-2 tumor cells to Mo-mediated immunotherapy.	Cyclophosphamide	0-2	mannose-binding lectin (protein C) 2	Mus musculus	50-55
3742481-1	1986	Differentially radiolabeled cyclophosphamide (CP) was metabolized with a reconstituted cytochrome P-450 system in the presence of calf thymus DNA or plasmid pBR-322 DNA.	Cyclophosphamide	28-44	translocator protein	Bos taurus	157-160
2455481-12	1988	When mice were treated with 5-fluorouracil, cyclophosphamide or irradiation, the period of granulocytopenia was significantly shortened by subcutaneous injection of Re Hu G-CSF.	Cyclophosphamide	44-60	colony stimulating factor 3 (granulocyte)	Mus musculus	171-176
22358448-2	1987	The subline R16, which is resistant to cyclophosphamide, was obtained by treating M5 mice repeatedly with this compound and subsequently transplanting the regrowing tumor for 16 passages.	Cyclophosphamide	39-55	solute carrier family 1 (neutral amino acid transporter), member 5	Mus musculus	12-15
2887298-5	1987	Also pretreatment with cyclophosphamide or irradiation abolished the capacity of adult mice to increase cell surface H-2 on YAC-1 cells.	Cyclophosphamide	23-39	histocompatibility-2, MHC	Mus musculus	117-120
2887298-5	1987	Also pretreatment with cyclophosphamide or irradiation abolished the capacity of adult mice to increase cell surface H-2 on YAC-1 cells.	Cyclophosphamide	23-39	ADP-ribosyltransferase 1	Mus musculus	124-129
3505758-2	1987	The presence of lymphoproliferation in MRL-lpr/lpr mice was associated with poorer taste aversion learning and varied as a function of the dose of cyclophosphamide.	Cyclophosphamide	147-163	Fas (TNF receptor superfamily member 6)	Mus musculus	43-46
3505758-2	1987	The presence of lymphoproliferation in MRL-lpr/lpr mice was associated with poorer taste aversion learning and varied as a function of the dose of cyclophosphamide.	Cyclophosphamide	147-163	Fas (TNF receptor superfamily member 6)	Mus musculus	47-50
3687583-4	1987	Regarding the acute phase response, dexamethasone and D-penicillamine appeared to lower and indomethacin and cyclophosphamide to elevate, serum levels of haptoglobin, but these effects were not statistically significant.	Cyclophosphamide	109-125	haptoglobin	Mus musculus	154-165
2957983-3	1987	Cyclophosphamide was administered at monthly intervals, escalating the dose until there was a significant reduction in both the number of blood B lymphocytes and helper/inducer (CD4) T cells of 14 patients with chronic progressive MS.	Cyclophosphamide	0-16	CD4 molecule	Homo sapiens	178-181
2444243-5	1987	High doses of IL-2 or pretreatment with cyclophosphamide restored the efficacy of IL-2 and LAK cell immunotherapy.	Cyclophosphamide	40-56	interleukin 2	Mus musculus	82-86
3127325-6	1987	On the other hand, CY was more effective than PT on the production of interleukin-3 (IL-3).	Cyclophosphamide	19-21	interleukin 3	Mus musculus	70-83
3127325-6	1987	On the other hand, CY was more effective than PT on the production of interleukin-3 (IL-3).	Cyclophosphamide	19-21	interleukin 3	Mus musculus	85-89
3450167-0	1987	[The preparation of liposome entrapment of cyclophosphamide (CPL) in its reconstituted form and the properties and antitumor activities of reconstituted CPL].	Cyclophosphamide	43-59	hephaestin	Homo sapiens	61-64
3450167-0	1987	[The preparation of liposome entrapment of cyclophosphamide (CPL) in its reconstituted form and the properties and antitumor activities of reconstituted CPL].	Cyclophosphamide	43-59	hephaestin	Homo sapiens	153-156
3581030-0	1987	Cyclophosphamide, vincristine, adriamycin, and prednisone (CHOP) with and without intermediate dose methotrexate for the treatment of non-Hodgkin"s lymphomas of diffuse histology.	Cyclophosphamide	0-16	DNA damage inducible transcript 3	Homo sapiens	59-63
3610214-8	1987	Furthermore, the effect of short-term deprivation on tolerance for DTH responses was similar to that observed after cyclophosphamide pretreatment of OVA-fed mice.	Cyclophosphamide	116-132	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	149-152
3496854-4	1987	Combination therapy with lentinan, cyclophosphamide and IL-2 may well be documented as a new rational chemo-immunotherapy in place of adoptive LAK therapy and the infusion of large amounts of IL-2 causing frequent detrimental side effects.	Cyclophosphamide	35-51	interleukin 2	Homo sapiens	192-196
3108445-5	1987	In addition, the T lymphocytes in CSF of cyclophosphamide-suppressed, virus-infected recipients that had been injected 4 d previously with LCMV-immune spleen cells were almost entirely donor Lyt-2+ cells, while the nonlymphoid elements were exclusively of host origin.	Cyclophosphamide	41-57	CD8 antigen, alpha chain	Mus musculus	191-196
3576380-5	1987	All patients were subsequently treated with combination intravenous chemotherapy consisting of cis-platinum, doxorubicin and cyclophosphamide (PAC 1).	Cyclophosphamide	125-141	dual specificity phosphatase 2	Homo sapiens	143-148
3107475-8	1987	rhG-CSF was demonstrated to accelerate the recovery from neutropenia induced in mice and monkeys by 5-fluorouracil or cyclophosphamide.	Cyclophosphamide	118-134	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	4-7
3325740-1	1987	Cyclophosphamide (CP)-induced micronuclei were evaluated in females of two strains of mice (C57BL and CD1), in F1 hybrid females and in fetuses (day 13 of gestation) obtained from different crosses.	Cyclophosphamide	0-16	CD1 antigen complex	Mus musculus	102-105
3106196-4	1987	The optimal times for the inhibitory effect of anti-L3T4 Mab was 7 days after Cy treatment, when the number of spleen cells increased to a maximum following a regenerative phase.	Cyclophosphamide	78-80	CD4 antigen	Mus musculus	52-56
3106196-6	1987	A short time exposure of the Cy-SCs to the anti-L3T4 Mabs was sufficient to decrease the response to Con A.	Cyclophosphamide	29-31	CD4 antigen	Mus musculus	48-52
3804497-6	1987	The strongest anti-tumor effects in normal BALB/c mice were observed when TNF was combined with the following doses of chemotherapeutic agents: cyclophosphamide 100 mg/kg, adriamycin 5 mg/kg, 5-FU 30-100 mg/kg.	Cyclophosphamide	144-160	tumor necrosis factor	Mus musculus	74-77
3804497-12	1987	Histological analysis revealed a potentiation of the TNF-induced necrosis by cyclophosphamide.	Cyclophosphamide	77-93	tumor necrosis factor	Mus musculus	53-56
3493003-4	1987	It is possible that repeated G-CSF injections after administration of cyclophosphamide (CY) in mice could accelerate recovery of granulopoiesis with a rather transient rise in blood neutrophil counts.	Cyclophosphamide	70-86	colony stimulating factor 3 (granulocyte)	Mus musculus	29-34
3493003-4	1987	It is possible that repeated G-CSF injections after administration of cyclophosphamide (CY) in mice could accelerate recovery of granulopoiesis with a rather transient rise in blood neutrophil counts.	Cyclophosphamide	88-90	colony stimulating factor 3 (granulocyte)	Mus musculus	29-34
2445487-3	1987	In contrast, the immunosuppressive drug cyclophosphamide inhibited the IL-2 release from spleen cells under the same conditions.	Cyclophosphamide	40-56	interleukin 2	Rattus norvegicus	71-75
3500779-4	1987	CSF induction by BRMs increased myelopoiesis and counteracted the myelosuppressive and immunosuppressive effects of cyclophosphamide.	Cyclophosphamide	116-132	colony stimulating factor 2	Homo sapiens	0-3
3815421-7	1987	Parallel in vitro studies showed that the inhibitory effect on NKA provoked by CMF is due to cyclophosphamide present in the association and is effectively antagonized by IF.	Cyclophosphamide	93-109	tachykinin precursor 1	Homo sapiens	63-66
2448255-4	1987	Cytotoxic antitumor agents of 5-fluorouracil (5-FU), cyclophosphamide (CY) and bleomycin (BLM) suppressed TNF production in mice primed with CP and challenged with LPS.	Cyclophosphamide	53-69	tumor necrosis factor	Mus musculus	106-109
2448255-4	1987	Cytotoxic antitumor agents of 5-fluorouracil (5-FU), cyclophosphamide (CY) and bleomycin (BLM) suppressed TNF production in mice primed with CP and challenged with LPS.	Cyclophosphamide	71-73	tumor necrosis factor	Mus musculus	106-109
2448255-5	1987	TNF production suppressed by 5-FU, CY and BLM was partially restored by the combined treatment with OK-432 or PSK.	Cyclophosphamide	35-37	tumor necrosis factor	Mus musculus	0-3
3490700-0	1986	Cyclophosphamide therapy for Weber-Christian disease associated with alpha 1-antitrypsin deficiency.	Cyclophosphamide	0-16	serpin family A member 1	Homo sapiens	69-88
3490700-4	1986	We have reported the case of a young man with life-threatening Weber-Christian disease associated with alpha 1-antitrypsin deficiency unresponsive to corticosteroids who responded to cyclophosphamide.	Cyclophosphamide	183-199	serpin family A member 1	Homo sapiens	103-122
3489753-6	1986	However, although clones remained MEL-14 negative, they were able to disseminate widely after subcutaneous adoptive transfer in the presence of clone-specific antigen and rIL 2 into Thy-1.1 mice pretreated with cyclophosphamide.	Cyclophosphamide	211-227	interleukin 2	Rattus norvegicus	171-176
3489753-6	1986	However, although clones remained MEL-14 negative, they were able to disseminate widely after subcutaneous adoptive transfer in the presence of clone-specific antigen and rIL 2 into Thy-1.1 mice pretreated with cyclophosphamide.	Cyclophosphamide	211-227	thymus cell antigen 1, theta	Mus musculus	182-189
3489291-4	1986	The combination of TIL and cyclophosphamide was further potentiated by the simultaneous administration of IL-2.	Cyclophosphamide	27-43	interleukin 2	Mus musculus	106-110
3709709-3	1986	Studies are described that demonstrate the ability of lithium (Li) to enhance the recovery of the total peripheral blood neutrophil and pluripotential stem cell (CFU-S and CFU-Mix) populations per femur from mice administered cyclophosphamide (CTX)(200 mg/kg body weight).	Cyclophosphamide	226-242	V-set and immunoglobulin domain containing 2	Mus musculus	244-247
3948164-1	1986	A series of experiments in DBA/2J mice evaluated the biological and pharmacokinetic interactions of the alkylating agent cyclophosphamide (CTX) and the histamine-H2 antagonists cimetidine (CMT) and ranitidine (RNT).	Cyclophosphamide	121-137	V-set and immunoglobulin domain containing 2	Mus musculus	139-142
3485563-1	1986	Normal and cyclophosphamide (Cy)-enhanced delayed-type hypersensitivity (DTH) reactions to sheep red blood cells (SRBC) were severely impaired in CD1 mice injected with 10(6) viable Landschutz ascites carcinoma (LAC) cells at the time of immunization.	Cyclophosphamide	11-27	T-cell surface glycoprotein CD1b-1	Ovis aries	146-149
3485563-1	1986	Normal and cyclophosphamide (Cy)-enhanced delayed-type hypersensitivity (DTH) reactions to sheep red blood cells (SRBC) were severely impaired in CD1 mice injected with 10(6) viable Landschutz ascites carcinoma (LAC) cells at the time of immunization.	Cyclophosphamide	29-31	T-cell surface glycoprotein CD1b-1	Ovis aries	146-149
3158396-1	1985	It was found earlier that nonspecific suppressor cells obtained from the spleen of mice injected with cyclophosphamide (Cy) at a dose of 200 mg/kg body wt are nonadherent, surface Ig negative, and Thy-1 negative.	Cyclophosphamide	102-118	thymus cell antigen 1, theta	Mus musculus	197-202
3020704-5	1986	In addition, combination chemotherapy studies using etoposide have yielded toxicity equivalent to IV administered programs such as CAV (cyclophosphamide, doxorubicin, vincristine).	Cyclophosphamide	136-152	caveolin 2	Homo sapiens	131-134
3079800-7	1986	We obtained an extremely homogeneous population of cells in the early stage of macrophage differentiation that is responsible for all the candidacidal activity and for a major part of the NK activity observed in the spleen of Cy-treated mice, and which is extremely sensitive to CSF-1 induction.	Cyclophosphamide	226-228	colony stimulating factor 1 (macrophage)	Mus musculus	279-284
3945239-1	1986	This study reports the influence of acute starvation on spontaneous and cyclophosphamide (CP) induced micronucleus (MN) frequencies in the bone marrow polychromatic erythrocytes (PCE) of CD-1 mice.	Cyclophosphamide	72-88	CD1 antigen complex	Mus musculus	187-191
3592938-1	1986	The studies concerned the effect of cyclophosphamide on immunological and biochemical indices of MBP-induced encephalomyelitis.	Cyclophosphamide	36-52	myelin basic protein	Gallus gallus	97-100
2419260-1	1986	Complete Freund"s adjuvant (CFA) administered before sensitization dampened the normal and cyclophosphamide-enhanced response of high and moderate IgE responder phenotype mice (CAF1 and C57B1/6J, respectively).	Cyclophosphamide	91-107	chromatin assembly factor 1, subunit A (p150)	Mus musculus	177-181
2428762-6	1986	Administration of isoprinosine every day (50 mg/kg) augmented Con A induced mitogenesis, IL-2 production and NK activity in animals treated with cyclophosphamide, but not in normal mice.	Cyclophosphamide	145-161	interleukin 2	Mus musculus	89-93
2416810-7	1986	Lyt-2+, L3T4- T cells from the peripheral lymphoid organs of nephritic kdkd mice, after adoptive transfer into cyclophosphamide-pretreated CBA/Ca recipients, mediate an antigen-specific delayed-type hypersensitivity response to renal tubular basement membrane antigens.	Cyclophosphamide	111-127	CD8 antigen, alpha chain	Mus musculus	0-5
4027979-3	1985	Here we show that the CY-induced immunopotentiating T-cells express the Lyt 1, Lyt 2, and L3T4 phenotypes.	Cyclophosphamide	22-24	CD5 antigen	Mus musculus	72-77
4027979-3	1985	Here we show that the CY-induced immunopotentiating T-cells express the Lyt 1, Lyt 2, and L3T4 phenotypes.	Cyclophosphamide	22-24	CD8 antigen, alpha chain	Mus musculus	79-84
4027979-4	1985	The phenotype of the immunopotentiating T-cells was deduced from our observations that depletion of Lyt 1+, Lyt 2+, or L3T4+ cells from the Sephadex G-10-adherent spleen cell population of CY-treated tumor bearers abolished the ability of the adherent cells to enhance the generation of antitumor cytotoxicity when added to the in vitro immunization culture of normal spleen cells.	Cyclophosphamide	189-191	CD5 antigen	Mus musculus	100-105
3843325-0	1985	Studies with MPG against the side effects of cyclophosphamide (Endoxan)--a preliminary study.	Cyclophosphamide	45-61	N-methylpurine DNA glycosylase	Homo sapiens	13-16
3843325-0	1985	Studies with MPG against the side effects of cyclophosphamide (Endoxan)--a preliminary study.	Cyclophosphamide	63-70	N-methylpurine DNA glycosylase	Homo sapiens	13-16
4025847-1	1985	Cyclophosphamide (CFA) is one of the alkylating agents which has now been used with some success in the treatment of human neoplasias and renal disease.	Cyclophosphamide	0-16	tubulin folding cofactor A	Homo sapiens	18-21
2859929-4	1985	The in vivo inhibitory effect is apparently unrelated to preferential induction of suppressor T cells as GK1.5 inhibited DTH induction in cyclophosphamide-treated as well as normal recipients.	Cyclophosphamide	138-154	kallikrein 1-related peptidase b1	Mus musculus	105-108
4040585-5	1985	On the other hand, the prolongation of life span induced by AP-M on S-180 ascites type tumor-bearing mice was markedly minimized or abolished by the pretreatment of cyclophosphamide.	Cyclophosphamide	165-181	alanyl (membrane) aminopeptidase	Mus musculus	60-64
3754070-2	1986	We describe a case of a 68-year-old man with an immunoblastic primary cerebral lymphoma first treated with surgery and radiotherapy and subsequently with chemotherapy consisting of cyclophosphamide, adriamycin, vincristine and prednisone (CHOP).	Cyclophosphamide	181-197	DNA damage inducible transcript 3	Homo sapiens	239-243
3940219-5	1986	In vivo total-body plasma clearance of cyclophosphamide, a drug metabolized by hepatic cytochrome P-450, was decreased to 53 ml/min/kg in mice that had received P388 cells 8 days earlier, as against 97.2 ml/min/kg in control mice.	Cyclophosphamide	39-55	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	87-103
3698367-5	1986	However, this activity of alpha A/D in the mice pretreated with CY was abrogated by inoculation of anti-asialo GM1 serum but not by i-carrageenan.	Cyclophosphamide	64-66	coenzyme Q10A	Mus musculus	111-114
2420733-9	1986	Cyclophosphamide-treated rats had significantly reduced spleen and thymus weights, antibody synthesis, DTH reactions, NKC cytotoxicity and IL2 production, but IL1 and PGE2 synthesis were significantly elevated.	Cyclophosphamide	0-16	interleukin 2	Rattus norvegicus	139-142
2932218-5	1985	They were resistant to treatment of mice with high-dose cyclophosphamide (CTX).	Cyclophosphamide	56-72	V-set and immunoglobulin domain containing 2	Mus musculus	74-77
3931471-4	1985	After the addition of cyclophosphamide for one week, the anti-insulin receptor autoantibody titer dropped from greater than 1:1,000 to 1:1.	Cyclophosphamide	22-38	insulin receptor	Homo sapiens	62-78
4031495-0	1985	Modulation of c-myb transcription in autoimmune disease by cyclophosphamide.	Cyclophosphamide	59-75	myeloblastosis oncogene	Mus musculus	14-19
4031495-4	1985	Both lpr/lpr and gld/gld mice and an AILD patient with lymphadenopathy and high myb RNA in peripheral blood cells were treated with cyclophosphamide (CY).	Cyclophosphamide	132-148	MYB proto-oncogene, transcription factor	Homo sapiens	80-83
4031495-9	1985	Consistent with these clinical findings, LN myb was normalized in gld/gld mice by a single injection of CY, whereas there was no effect on myb expression in lpr/lpr mice.	Cyclophosphamide	104-106	myeloblastosis oncogene	Mus musculus	44-47
4031495-11	1985	The lymphadenopathy and high levels of LN myb mRNA of the lpr/lpr mice could be normalized; this occurred only after long-term treatment with CY.	Cyclophosphamide	142-144	myeloblastosis oncogene	Mus musculus	42-45
4031495-11	1985	The lymphadenopathy and high levels of LN myb mRNA of the lpr/lpr mice could be normalized; this occurred only after long-term treatment with CY.	Cyclophosphamide	142-144	Fas (TNF receptor superfamily member 6)	Mus musculus	58-61
4031495-11	1985	The lymphadenopathy and high levels of LN myb mRNA of the lpr/lpr mice could be normalized; this occurred only after long-term treatment with CY.	Cyclophosphamide	142-144	Fas (TNF receptor superfamily member 6)	Mus musculus	62-65
3840280-2	1985	We have reported a case of diffuse, poorly differentiated lymphocytic lymphoma, stage IIIa, in a patient whose disease went into remission after she received six courses of CHOP therapy (cyclophosphamide, doxorubicin, vincristine, and prednisolone).	Cyclophosphamide	187-203	DNA damage inducible transcript 3	Homo sapiens	173-177
3888386-1	1985	The purpose of this study was to determine if tamoxifen added to the efficacy of a CFP (cyclophosphamide, 5-FU, and prednisone) regimen.	Cyclophosphamide	88-104	complement factor properdin	Homo sapiens	83-86
3158396-1	1985	It was found earlier that nonspecific suppressor cells obtained from the spleen of mice injected with cyclophosphamide (Cy) at a dose of 200 mg/kg body wt are nonadherent, surface Ig negative, and Thy-1 negative.	Cyclophosphamide	120-122	thymus cell antigen 1, theta	Mus musculus	197-202
4004283-5	1985	Indomethacin or cyclophosphamide administered intraperitoneally at a dose at which, although not directly effective against tumor growth, both were expected to stimulate the host immune system by inhibiting suppressor macrophage function or suppressor T cells, respectively, showed neither enhancing nor suppressing effect on the above mentioned strong antitumor effect of locally administered IFN-alpha A/D.	Cyclophosphamide	16-32	interferon alpha	Mus musculus	394-403
3871661-1	1985	Treatment of normal or MBL-2 tumor-bearing mice with cyclophosphamide (CY) caused severe suppression of myelopoiesis and macrophage (M phi) functions, both of which may limit further use of chemotherapy.	Cyclophosphamide	53-69	mannose-binding lectin (protein C) 2	Mus musculus	23-28
3871661-1	1985	Treatment of normal or MBL-2 tumor-bearing mice with cyclophosphamide (CY) caused severe suppression of myelopoiesis and macrophage (M phi) functions, both of which may limit further use of chemotherapy.	Cyclophosphamide	71-73	mannose-binding lectin (protein C) 2	Mus musculus	23-28
3871661-4	1985	Injection of MBL-2 tumor-bearing mice with MVE-2, at 3 days after Cy treatment, caused a decrease in tumor burden and a significant increase in median survival time as compared to treatment with CY alone.	Cyclophosphamide	195-197	mannose-binding lectin (protein C) 2	Mus musculus	13-18
3156110-2	1985	Using the growth delay assay, the therapeutic response was enhanced by prior TBX: for example, in mice receiving 3000 rad TBX 1 day before fibrosarcoma cell inoculation, the growth delay from 8 to 12 mm produced by CY (150 mg/kg) was 18.8 days compared with 9.4 days without prior TBX.	Cyclophosphamide	215-217	T-box 1	Mus musculus	122-127
3921421-7	1985	High background levels of IL2, presumably induced by KLH injections shortly before termination, were significantly suppressed in PCB-, Pb-, and CY-treated rats.	Cyclophosphamide	144-146	interleukin 2	Rattus norvegicus	26-29
3921421-6	1985	CY-injected rats had significantly reduced IL2 activity, NKC cytotoxicity, and Ab levels.	Cyclophosphamide	0-2	interleukin 2	Rattus norvegicus	43-46
3833119-2	1985	The results presented in this study indicate that treatment of mice with Cyclophosphamide prior to Lewis lung carcinoma (LL2) cells inoculation enhanced the formation of artificial lung metastases in a dose-dependent manner.	Cyclophosphamide	73-89	peroxiredoxin 2, pseudogene 1	Mus musculus	121-124
3833119-5	1985	Treatment of mice with Cyclophosphamide after LL2 cells inoculation did not enhance formation of tumor metastases.	Cyclophosphamide	23-39	peroxiredoxin 2, pseudogene 1	Mus musculus	46-49
3914253-3	1985	Cyclophosphamide-induced enhancement of artificial lung metastasis of LL2 could be partly abolished by reconstituting of mice with spleen, lymph nodes or bone marrow cells but not with thymus cells.	Cyclophosphamide	0-16	peroxiredoxin 2, pseudogene 1	Mus musculus	70-73
3921421-9	1985	These results indicate that PCB, Pb, and CY alter IL2 synthesis and adversely affect NKC cytotoxicity and Ab synthesis following in vivo or in vitro exposure.	Cyclophosphamide	41-43	interleukin 2	Rattus norvegicus	50-53
4038650-1	1985	The Authors describe their experience with a combination therapy with carmustine (BCNU), cyclophosphamide (CTX) plus adriamycin (ADM) in the treatment of advanced ovarian cancer.	Cyclophosphamide	89-105	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	107-110
2931383-3	1985	This resistance of T helper cells was observed in unimmunized mice and in mice injected with SRBC two days prior to Cy administration.	Cyclophosphamide	116-118	caveolae associated 3	Mus musculus	93-97
2412956-4	1985	A single injection of IL-2 was sufficient to reverse the effect of cyclophosphamide treatment, while additional injections with as little as 8 micrograms of protein ablated the steroid-induced suppression.	Cyclophosphamide	67-83	interleukin 2	Homo sapiens	22-26
3886553-5	1985	In mice immunocompromised with cyclophosphamide, treatment with IgG still exerted protection against low challenge inocula.	Cyclophosphamide	31-47	immunoglobulin heavy chain (V7183 family)	Mus musculus	64-67
2931385-1	1985	4-Hydroperoxycyclophosphamide (4-OOH-CYP) is spontaneously converted in aqueous solution to 4-hydroxycyclophosphamide (4-OH-CYP), the major active metabolic of cyclophosphamide.	Cyclophosphamide	13-29	peptidylprolyl isomerase G	Homo sapiens	37-40
3880810-2	1985	CBP (cyclophosphamide, bleomycin, and cisplatin) and AFP (doxorubicin, 5-fluorouracil, and cisplatin) had shown activity in generation II of this study (EST 2575).	Cyclophosphamide	5-21	CREB binding protein	Homo sapiens	0-3
2931385-1	1985	4-Hydroperoxycyclophosphamide (4-OOH-CYP) is spontaneously converted in aqueous solution to 4-hydroxycyclophosphamide (4-OH-CYP), the major active metabolic of cyclophosphamide.	Cyclophosphamide	13-29	peptidylprolyl isomerase G	Homo sapiens	124-127
2411821-2	1985	This dose of CY increased the cytotoxic response to DAC on L1210 tumor in mice by an additional 4 logs of L1210 cell kill or an approximate doubling of the response to DAC alone.	Cyclophosphamide	13-15	dachshund family transcription factor 1	Mus musculus	52-55
3965629-16	1985	The recommended starting doses for misonidazole and cyclophosphamide in phase II trials using this schedule of administration should be 2 g/m2 and 1 g/m2, respectively, with escalation for cyclophosphamide to individual tolerance.	Cyclophosphamide	52-68	myoregulin	Homo sapiens	140-148
3155471-9	1985	This report provides data that demonstrate that the Ts2 cells were induced in spleens from cyclophosphamide (Cy)-resistant precursors in response to cryptococcal Ts1 cells or TsF1 and that a proliferative process sensitive to Cy was not required for Ts2 induction.	Cyclophosphamide	91-107	Trichinella spiralis resistance 2	Mus musculus	52-55
3155471-9	1985	This report provides data that demonstrate that the Ts2 cells were induced in spleens from cyclophosphamide (Cy)-resistant precursors in response to cryptococcal Ts1 cells or TsF1 and that a proliferative process sensitive to Cy was not required for Ts2 induction.	Cyclophosphamide	91-107	Trichinella spiralis resistance 1	Mus musculus	162-165
2411821-2	1985	This dose of CY increased the cytotoxic response to DAC on L1210 tumor in mice by an additional 4 logs of L1210 cell kill or an approximate doubling of the response to DAC alone.	Cyclophosphamide	13-15	dachshund family transcription factor 1	Mus musculus	168-171
2411821-3	1985	These data support the hypothesis that CY at this low dose selectively inhibits suppressor t-cells which normally function to prevent the full cytotoxic potential of DAC from being realized.	Cyclophosphamide	39-41	dachshund family transcription factor 1	Mus musculus	166-169
3155471-9	1985	This report provides data that demonstrate that the Ts2 cells were induced in spleens from cyclophosphamide (Cy)-resistant precursors in response to cryptococcal Ts1 cells or TsF1 and that a proliferative process sensitive to Cy was not required for Ts2 induction.	Cyclophosphamide	91-107	serine/threonine kinase 16	Homo sapiens	175-179
3155471-9	1985	This report provides data that demonstrate that the Ts2 cells were induced in spleens from cyclophosphamide (Cy)-resistant precursors in response to cryptococcal Ts1 cells or TsF1 and that a proliferative process sensitive to Cy was not required for Ts2 induction.	Cyclophosphamide	109-111	Trichinella spiralis resistance 2	Mus musculus	52-55
6239664-2	1984	It was revealed that low MIF production in response to this antigen is determined by the existence of specific suppressors which are inhibited by cyclophosphamide.	Cyclophosphamide	146-162	macrophage migration inhibitory factor (glycosylation-inhibiting factor)	Mus musculus	25-28
3155471-9	1985	This report provides data that demonstrate that the Ts2 cells were induced in spleens from cyclophosphamide (Cy)-resistant precursors in response to cryptococcal Ts1 cells or TsF1 and that a proliferative process sensitive to Cy was not required for Ts2 induction.	Cyclophosphamide	109-111	Trichinella spiralis resistance 1	Mus musculus	162-165
3155471-9	1985	This report provides data that demonstrate that the Ts2 cells were induced in spleens from cyclophosphamide (Cy)-resistant precursors in response to cryptococcal Ts1 cells or TsF1 and that a proliferative process sensitive to Cy was not required for Ts2 induction.	Cyclophosphamide	109-111	serine/threonine kinase 16	Homo sapiens	175-179
3155471-9	1985	This report provides data that demonstrate that the Ts2 cells were induced in spleens from cyclophosphamide (Cy)-resistant precursors in response to cryptococcal Ts1 cells or TsF1 and that a proliferative process sensitive to Cy was not required for Ts2 induction.	Cyclophosphamide	109-111	Trichinella spiralis resistance 2	Mus musculus	250-253
3155471-9	1985	This report provides data that demonstrate that the Ts2 cells were induced in spleens from cyclophosphamide (Cy)-resistant precursors in response to cryptococcal Ts1 cells or TsF1 and that a proliferative process sensitive to Cy was not required for Ts2 induction.	Cyclophosphamide	226-228	Trichinella spiralis resistance 2	Mus musculus	52-55
3937032-6	1985	Noteworthily, IFN-alpha/beta, but not IFN-gamma, was produced even 6 hr after stimulation with LPS in cyclophosphamide- or antithymocyte serum-treated mice.	Cyclophosphamide	102-118	interferon alpha	Mus musculus	14-23
6396563-2	1984	Chemotherapy with cyclophosphamide, vincristine and prednisone (COP) yielded partial response, but the addition of adriamycin (CHOP) a complete remission.	Cyclophosphamide	18-34	caspase recruitment domain family member 16	Homo sapiens	64-67
6548630-1	1984	Administration to hamsters of a highly purified human leukocyte interferon subtype, IFN-alpha A, obtained by recombinant DNA methods, abolished the efficacy of high doses of cyclophosphamide (2.5 mg/hamster) against the TBD 932 lymphosarcoma.	Cyclophosphamide	174-190	interferon alpha 2	Homo sapiens	54-95
6487517-9	1984	Similar experiments were performed to test the combination of cyclophosphamide (Cy) and MISO (0.5 mg g-1) in the RIF-1 tumour; again chemopotentiation was maintained with increasing fractionation.	Cyclophosphamide	62-78	replication timing regulatory factor 1	Mus musculus	113-118
6487517-9	1984	Similar experiments were performed to test the combination of cyclophosphamide (Cy) and MISO (0.5 mg g-1) in the RIF-1 tumour; again chemopotentiation was maintained with increasing fractionation.	Cyclophosphamide	80-82	replication timing regulatory factor 1	Mus musculus	113-118
6334134-1	1984	Precursors of antigen-specific cytotoxic T cells from mice pretreated with immunosuppressive doses of cyclophosphamide can be expanded in vitro and in vivo by low doses of human interleukin-2.	Cyclophosphamide	102-118	interleukin 2	Homo sapiens	178-191
6380709-0	1984	Metabolism and binding of cyclophosphamide and its metabolite acrolein to rat hepatic microsomal cytochrome P-450.	Cyclophosphamide	26-42	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	97-113
6206958-7	1984	IFN-gamma production was abrogated completely by cyclophosphamide and antithymocyte serum, and partially by hydrocortisone and carrageenan, but not by anti-asialo GM1 antibody in Listeria-infected mice treated with these agents before induction of IFN-gamma by LCWF.	Cyclophosphamide	49-65	interferon gamma	Mus musculus	0-9
6236881-1	1984	The activation of cytotoxic T lymphocytes (CTL) in vivo after immunization of normal or cyclophosphamide-treated mice with allogeneic cells was strongly augmented by the administration of mitomycin C-treated or irradiated concanavalin A-activated spleen cells (Con A-spl).	Cyclophosphamide	88-104	plasma serotonin level	Mus musculus	247-250
6334134-3	1984	High doses of human interleukin-2 in vitro can expand both normal and cyclophosphamide-resistant T cell precursors into effector cells capable of lysing both natural killer cell-sensitive and -insensitive target cells in the absence of antigen.	Cyclophosphamide	70-86	interleukin 2	Homo sapiens	20-33
6334139-2	1984	Treatment of conventional mice implanted with lung and mammary carcinomas by repeated administration of low-dose cyclophosphamide (CY), IL-2, and tumor-sensitized CTC resulted in delayed tumor onset, retarded tumor growth rate, prolonged survival, and a higher cure rate as compared with mice receiving only CY.	Cyclophosphamide	308-310	interleukin 2	Mus musculus	136-140
6334139-6	1984	IL-2 injections into normal, untreated, as well as X-irradiated or CY-treated mice, resulted in enhanced natural cytotoxicity and cytotoxic responsiveness in vitro to syngeneic tumors, greater proliferative response to phytohemagglutinin, and a tendency toward depressed proliferative responses to concanavalin A and to allogeneic leukocytes.	Cyclophosphamide	67-69	interleukin 2	Mus musculus	0-4
6334140-8	1984	Elevated quantities of TCGF (up to threefold) were generated by TBS of mice pretreated in vivo 1-4 days previously with low doses of either cyclophosphamide or X-irradiation, with or without IND.	Cyclophosphamide	140-156	interleukin 2	Mus musculus	23-27
6386629-2	1984	In the Ames test in Salmonella typhimurium TA1535 with mouse-liver S-9 mix, the addition of retinol, retinyl acetate or retinyl palmitate caused a dose-dependent inhibition of cyclophosphamide mutagenicity.	Cyclophosphamide	176-192	proteasome (prosome, macropain) 26S subunit, non-ATPase, 11	Mus musculus	67-70
6442929-1	1984	In ACI/N rats pretreated with cyclophosphamide (CY) growth of the bladder cancer, BC-47, and adenosine deaminase (ADA) and purine nucleoside phosphorylase (PNP) activities in lymphocytes were investigated to clarify the possible antitumor effect via the immune system of the chemotherapeutic agent.	Cyclophosphamide	30-46	adenosine deaminase	Rattus norvegicus	93-112
6442929-1	1984	In ACI/N rats pretreated with cyclophosphamide (CY) growth of the bladder cancer, BC-47, and adenosine deaminase (ADA) and purine nucleoside phosphorylase (PNP) activities in lymphocytes were investigated to clarify the possible antitumor effect via the immune system of the chemotherapeutic agent.	Cyclophosphamide	48-50	adenosine deaminase	Rattus norvegicus	93-112
6611201-6	1984	The immunopotentiating activity was abolished when the Sephadex G-10-adherent spleen cell population from CY-treated tumor-bearing mice was depleted of T-cells by anti-Thy 1.2 plus complement but not when this adherent spleen cell population was depleted of macrophages by carbonyl iron and magnet.	Cyclophosphamide	106-108	thymus cell antigen 1, theta	Mus musculus	168-175
6610060-3	1984	The low cytotoxic T-lymphocyte activity in the lungs and spleens of cyclophosphamide-treated mice could be partially restored in vitro by human interleukin 2.	Cyclophosphamide	68-84	interleukin 2	Homo sapiens	144-157
6205065-5	1984	A cyclophosphamide-sensitive, I-J+, Ly-2 T transducer cell is required in the immune donor cell population for contrasuppression to be induced by the TcsF plus specific antigen.	Cyclophosphamide	2-18	basigin (Ok blood group)	Homo sapiens	150-154
6090736-6	1984	Complete remission was obtained by CHOP therapy (consisting of cyclophosphamide, adriamycin, vincristine, and prednisolone) combined with cervical irradiation.	Cyclophosphamide	63-79	DNA damage inducible transcript 3	Homo sapiens	35-39
6235832-4	1984	The findings of the present study demonstrate that Ts1 and Ts2 cells are CY-insensitive while T3 cells are CY-sensitive.	Cyclophosphamide	73-75	Trichinella spiralis resistance 2	Mus musculus	59-62
6607893-9	1984	The overall data indicated that the ultimate rejection of those tumor cells remaining after the direct anti-tumor action of CY had been dissipated was probably mediated by the combined action of TAL and TAM.	Cyclophosphamide	124-126	talipes	Mus musculus	195-198
6697295-4	1984	A few hours after initiation of chemotherapy with cyclophosphamide, Adriamycin (doxorubicin), vincristine, and prednisolone (CHOP regimen), the patient developed an acute ascending paralysis.	Cyclophosphamide	50-66	DNA damage inducible transcript 3	Homo sapiens	125-129
6205109-2	1984	In spite of a series of postoperative chemotherapeutic programs reported to be effective against gonadal germ cell tumors, the patient"s condition continued to worsen even though the level of AFP had decreased to the normal range after the first line therapy with vincristine, actinomycin D and cyclophosphamide.	Cyclophosphamide	295-311	alpha fetoprotein	Homo sapiens	192-195
6713344-3	1984	Seventeen patients were treated with the cyclophosphamide (CTX) L2 protocol which included maintenance chemotherapy for 3 years.	Cyclophosphamide	41-57	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	59-62
6479366-3	1984	Cyclophosphane induced both the decrease of Ach content in the heart and the simultaneous reduction of ChE activity.	Cyclophosphamide	0-14	butyrylcholinesterase	Homo sapiens	103-106
6732764-0	1984	Metabolism of cyclophosphamide by purified cytochrome P-450 from microsomes of phenobarbital-treated rats.	Cyclophosphamide	14-30	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	43-59
6732764-2	1984	These results indicate that phenobarbital-inducible cytochrome P-450 is able to dechlorinate CPA and may account, in part, for the inability of phenobarbital to enhance the therapeutic activity and toxicity of this important anticancer and immunosuppressive agent.	Cyclophosphamide	93-96	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	52-68
6608425-3	1984	Weekly injections of cyclophosphamide (Cy) at a dose of 20 mg/kg body weight prevented IgM to IgG class switch of serum anti-DNA antibodies and also immunoglobulin secreting cells in the spleen of MRL/Mp-lpr/lpr (MRL/1) mice.	Cyclophosphamide	21-37	Fas (TNF receptor superfamily member 6)	Mus musculus	201-211
6608425-3	1984	Weekly injections of cyclophosphamide (Cy) at a dose of 20 mg/kg body weight prevented IgM to IgG class switch of serum anti-DNA antibodies and also immunoglobulin secreting cells in the spleen of MRL/Mp-lpr/lpr (MRL/1) mice.	Cyclophosphamide	39-41	Fas (TNF receptor superfamily member 6)	Mus musculus	201-211
6191677-0	1983	[Cyclophosphamide, adriamycin, vincristine, bleomycin and prednisolone (CHOP-Bleo) combination chemotherapy for advanced non-Hodgkin"s lymphoma].	Cyclophosphamide	1-17	DNA damage inducible transcript 3	Homo sapiens	72-76
6202228-0	1983	Augmentation of delayed-type hypersensitivity reactions to ovalbumin by cyclophosphamide in the mouse: strain variability, antigen specificity and nature of the suppressor cell.	Cyclophosphamide	72-88	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	59-68
6202228-1	1983	The use of complete Freund"s adjuvant (CFA) or pretreatment with cyclophosphamide (Cy) resulted in augmented delayed-type hypersensitivity (DTH) reactions in mice immunized with ovalbumin (OVA) and challenged 8 days later with heat-aggregated antigen.	Cyclophosphamide	65-81	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	178-187
6202228-1	1983	The use of complete Freund"s adjuvant (CFA) or pretreatment with cyclophosphamide (Cy) resulted in augmented delayed-type hypersensitivity (DTH) reactions in mice immunized with ovalbumin (OVA) and challenged 8 days later with heat-aggregated antigen.	Cyclophosphamide	83-85	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	178-187
6347997-1	1983	The combination of cyclophosphamide, adriamycin, vincristine, and prednisone (CHOP) alternating with total body irradiation (TBI) has been shown earlier to be effective therapy in patients with malignant lymphoma who have received prior chemotherapy and/or radiation therapy.	Cyclophosphamide	19-35	DNA damage inducible transcript 3	Homo sapiens	78-82
6347997-4	1983	CHOP was given in the following manner: cyclophosphamide 400 mg/M2 IV day 1, adriamycin 40 mg/M2 IV day 1, vincristine 2 mg IV day 1, and Prednisone 100 mg po daily X 5.	Cyclophosphamide	40-56	DNA damage inducible transcript 3	Homo sapiens	0-4
6134774-0	1983	Expansion of cyclophosphamide-resistant cytotoxic precursors in vitro and in vivo by purified human interleukin 2.	Cyclophosphamide	13-29	interleukin 2	Homo sapiens	100-113
6134774-1	1983	Precursors of cytotoxic lymphoid cells obtained from mice treated with cyclophosphamide (CY) can be expanded in culture by alloantigens in the presence of purified human interleukin 2 (IL 2).	Cyclophosphamide	71-87	interleukin 2	Homo sapiens	170-183
6134774-1	1983	Precursors of cytotoxic lymphoid cells obtained from mice treated with cyclophosphamide (CY) can be expanded in culture by alloantigens in the presence of purified human interleukin 2 (IL 2).	Cyclophosphamide	71-87	interleukin 2	Homo sapiens	185-189
6134774-1	1983	Precursors of cytotoxic lymphoid cells obtained from mice treated with cyclophosphamide (CY) can be expanded in culture by alloantigens in the presence of purified human interleukin 2 (IL 2).	Cyclophosphamide	89-91	interleukin 2	Homo sapiens	170-183
6134774-2	1983	Similarly, IL 2 delivered in vivo in a rate-controlled manner enhances cytotoxic activity in mice that are immunosuppressed by high doses of CY.	Cyclophosphamide	141-143	interleukin 2	Mus musculus	11-15
6688200-0	1983	Cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) in patients with advanced Hodgkin"s disease: a Southwest Oncology Group Phase II Study.	Cyclophosphamide	0-16	DNA damage inducible transcript 3	Homo sapiens	60-64
6884701-0	1983	Antitumor effect and metabolic activation of cyclophosphamide and 4-hydroperoxycyclophosphamide in the human breast carcinoma (MX-1)-nude mouse system.	Cyclophosphamide	45-61	MX dynamin like GTPase 1	Homo sapiens	127-131
6600950-1	1983	Purified human lactoferrin was assessed for its influence in vivo in untreated mice and in mice undergoing rebound myelopoiesis after sublethal dosages of Cytoxan.	Cyclophosphamide	155-162	lactotransferrin	Mus musculus	15-26
6600950-10	1983	Titration of the effects of lactoferrin in Cytoxan-treated mice demonstrated a plateau curve of suppression of nucleated cells and CFU-GM per femur with dosages ranging from 100 micrograms to 10(-4) micrograms lactoferrin per mouse, with loss of activity at 10(-5) micrograms.	Cyclophosphamide	43-50	lactotransferrin	Mus musculus	28-39
6600950-10	1983	Titration of the effects of lactoferrin in Cytoxan-treated mice demonstrated a plateau curve of suppression of nucleated cells and CFU-GM per femur with dosages ranging from 100 micrograms to 10(-4) micrograms lactoferrin per mouse, with loss of activity at 10(-5) micrograms.	Cyclophosphamide	43-50	lactotransferrin	Mus musculus	210-221
6472248-13	1984	Leukocyte migration was inhibited by injection of PSK after treatment of CPA at a dose of 50 mg/kg, while in the case of CPA at a dose of 200 mg/kg, preinjection of PSK inhibited leukocyte migration.	Cyclophosphamide	73-76	TAO kinase 2	Mus musculus	50-53
6472248-13	1984	Leukocyte migration was inhibited by injection of PSK after treatment of CPA at a dose of 50 mg/kg, while in the case of CPA at a dose of 200 mg/kg, preinjection of PSK inhibited leukocyte migration.	Cyclophosphamide	121-124	TAO kinase 2	Mus musculus	165-168
6607792-3	1984	Weekly injection of cyclophosphamide (Cy) into MRL/Mp-lpr/lpr (MRL/l) mice, at a dose of 10-20 mg/kg, from 1 month of age prevented the development of generalized lymph node enlargement, decreased serum levels of anti-DNA antibodies and immune complexes, and markedly prolonged their life span.	Cyclophosphamide	20-36	Fas (TNF receptor superfamily member 6)	Mus musculus	47-61
6607792-3	1984	Weekly injection of cyclophosphamide (Cy) into MRL/Mp-lpr/lpr (MRL/l) mice, at a dose of 10-20 mg/kg, from 1 month of age prevented the development of generalized lymph node enlargement, decreased serum levels of anti-DNA antibodies and immune complexes, and markedly prolonged their life span.	Cyclophosphamide	38-40	Fas (TNF receptor superfamily member 6)	Mus musculus	47-61
6607792-5	1984	Cy was also shown to suppress abnormal expansion of Thy-1 positive cells in lymphoid organs of MRL/1 mice.	Cyclophosphamide	0-2	thymus cell antigen 1, theta	Mus musculus	52-57
6712177-2	1984	Digestion of the 3H-CPA-treated nuclei with DNase I and micrococcal nuclease, respectively, showed that the CPA-modified DNA apparently has become resistant against such enzymatic attack.	Cyclophosphamide	20-23	deoxyribonuclease 1	Rattus norvegicus	44-51
6705134-2	1984	Cyclophosphamide is an anticancer drug that is activated by hepatic microsomal cytochrome P-450, while the products of cyclophosphamide metabolism by cytochrome P-450 can be metabolized by other hepatic enzymes.	Cyclophosphamide	0-16	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	79-95
6705134-2	1984	Cyclophosphamide is an anticancer drug that is activated by hepatic microsomal cytochrome P-450, while the products of cyclophosphamide metabolism by cytochrome P-450 can be metabolized by other hepatic enzymes.	Cyclophosphamide	119-135	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	150-166
6607794-0	1984	Cyclophosphamide-induced changes in the MRL-lpr/lpr mouse: effects upon cellular composition, immune function, and disease.	Cyclophosphamide	0-16	Fas (TNF receptor superfamily member 6)	Mus musculus	44-47
6607794-0	1984	Cyclophosphamide-induced changes in the MRL-lpr/lpr mouse: effects upon cellular composition, immune function, and disease.	Cyclophosphamide	0-16	Fas (TNF receptor superfamily member 6)	Mus musculus	48-51
6607794-2	1984	To examine whether to not the disease process is intrinsic and irreversible, an immunomodulatory drug, cyclophosphamide, was administered to 16-week-old, sick MRL-lpr/lpr mice.	Cyclophosphamide	103-119	Fas (TNF receptor superfamily member 6)	Mus musculus	163-166
6607794-2	1984	To examine whether to not the disease process is intrinsic and irreversible, an immunomodulatory drug, cyclophosphamide, was administered to 16-week-old, sick MRL-lpr/lpr mice.	Cyclophosphamide	103-119	Fas (TNF receptor superfamily member 6)	Mus musculus	167-170
6607794-3	1984	Analysis of lymph node cells by flow cytometry from injected and control MRL-lpr/lpr mice indicated that cyclophosphamide had a marked effect upon the lymphoid cellular composition.	Cyclophosphamide	105-121	Fas (TNF receptor superfamily member 6)	Mus musculus	77-80
6607794-3	1984	Analysis of lymph node cells by flow cytometry from injected and control MRL-lpr/lpr mice indicated that cyclophosphamide had a marked effect upon the lymphoid cellular composition.	Cyclophosphamide	105-121	Fas (TNF receptor superfamily member 6)	Mus musculus	81-84
6468474-3	1984	The half-life (t1/2) of cyclophosphamide following intravenous administration in patients with liver failure was 12.5 +/- 1.0 h (m +/- SD), which was significantly longer than in the normal controls in whom it was 7.6 +/- 1.4 h (p less than 0.001).	Cyclophosphamide	24-40	MSD	Homo sapiens	129-137
6233223-8	1984	Cyclophosphamide treatment of nonresponders (to eliminate Ts activity) as well as immunization with GAT coupled to the immunogenic carrier MBSA result in the development of GAT-specific humoral, but not CMI responses.	Cyclophosphamide	0-16	glycine-N-acyltransferase	Mus musculus	173-176
6201567-1	1984	Grivet monkeys immunosuppressed with either cyclophosphamide or methylprednisolone retain their capacity to produce interferon in response to poly I:C/poly-L-lysine (poly ICL).	Cyclophosphamide	44-60	interferon alpha 1	Homo sapiens	116-126
6357429-1	1983	Resistance of mouse M5076 (M5) ovarian reticular cell sarcoma to cyclophosphamide (CTX) was obtained in vivo by repeated drug treatment followed by transplantation of the regrowing tumor.	Cyclophosphamide	65-81	V-set and immunoglobulin domain containing 2	Mus musculus	83-86
6644020-3	1983	IgE antibody to picryl or oxazolone determinants was induced by immunizing Hartley strain guinea pigs pretreated with cyclophosphamide.	Cyclophosphamide	118-134	immunoglobulin heavy constant epsilon	Homo sapiens	0-3
6368346-0	1983	[Effect of cyclophosphamide on neuroblastoma and the bone marrow function in the experimental studies].	Cyclophosphamide	11-27	Rho guanine nucleotide exchange factor (GEF) 16	Mus musculus	31-44
6368346-1	1983	The potential difference in survival and antitumor effect due to different dosage schedules of cyclophosphamide (CPM) treatment was analyzed in A/J mice inoculated with mouse neuroblastoma C 1300 Cells, which closely resembles the human neuroblastoma in its capacity of cathecolamin secretion and in response to chemotherapy.	Cyclophosphamide	95-111	Rho guanine nucleotide exchange factor (GEF) 16	Mus musculus	175-188
6368346-1	1983	The potential difference in survival and antitumor effect due to different dosage schedules of cyclophosphamide (CPM) treatment was analyzed in A/J mice inoculated with mouse neuroblastoma C 1300 Cells, which closely resembles the human neuroblastoma in its capacity of cathecolamin secretion and in response to chemotherapy.	Cyclophosphamide	95-111	Rho guanine nucleotide exchange factor (GEF) 16	Mus musculus	237-250
6368346-1	1983	The potential difference in survival and antitumor effect due to different dosage schedules of cyclophosphamide (CPM) treatment was analyzed in A/J mice inoculated with mouse neuroblastoma C 1300 Cells, which closely resembles the human neuroblastoma in its capacity of cathecolamin secretion and in response to chemotherapy.	Cyclophosphamide	113-116	Rho guanine nucleotide exchange factor (GEF) 16	Mus musculus	175-188
6649341-8	1983	High levels of dietary T-2 toxin appeared to be more immunosuppressive than cyclophosphamide because only one mouse died after treatment with HSV-1 and cyclophosphamide.	Cyclophosphamide	152-168	brachyury 2	Mus musculus	23-26
6354071-2	1983	Rats with EAMG were treated with a protocol consisting of three components: (1) A single high dose of cyclophosphamide (200 mg/kg) was used to produce a rapid and sustained fall in the anti-AChR antibody levels by preferential destruction of antibody-producing B-lymphocytes.	Cyclophosphamide	102-118	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	190-194
6871076-9	1983	The response of the RIF-1 sarcoma to cyclophosphamide was not enhanced by the lipophilic sensitizers at the doses previously stated.	Cyclophosphamide	37-53	replication timing regulatory factor 1	Homo sapiens	20-25
6617839-0	1983	[Reciprocal effect of cyclophosphane on the liver cytochrome P-450 and immunity system].	Cyclophosphamide	22-36	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	50-66
6617839-1	1983	It has been demonstrated in experiments on mice that administration of cyclophosphamide in a dose of 50 mg/kg for 3 days provokes marked induction of liver cytochrome P-450.	Cyclophosphamide	71-87	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	156-172
6617839-4	1983	The induction of liver cytochrome P-450 by cyclophosphamide or 3-methylcholanthrene is accompanied by pronounced inhibition of immunoreactivity.	Cyclophosphamide	43-59	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	23-39
6617839-6	1983	Apparently, the reciprocal action of cyclophosphamide and 3-methylcholanthrene on cytochrome P-450 and immunity is a consequence of intense formation with the involvement of cytochrome P-450 of highly reactive metabolites interfering with the function of immunocompetent cells.	Cyclophosphamide	37-53	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	82-98
6617839-6	1983	Apparently, the reciprocal action of cyclophosphamide and 3-methylcholanthrene on cytochrome P-450 and immunity is a consequence of intense formation with the involvement of cytochrome P-450 of highly reactive metabolites interfering with the function of immunocompetent cells.	Cyclophosphamide	37-53	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	174-190
6683184-7	1983	Clinical trials previously performed by our group comparing cyclophosphamide alone, either vs cis-platinum, adriamycin and hexamethylmelamine or vs Hexa-CAF, showed a better remission rate with the use of moderate-dose cyclophosphamide alone.	Cyclophosphamide	219-235	lysine acetyltransferase 2B	Homo sapiens	153-156
6339628-1	1983	Mice carrying the B cell leukemia (BCL1)+ were successfully treated by total lymphoid irradiation (TLI), cyclophosphamide, and allogeneic bone marrow (BM) transplantation.	Cyclophosphamide	105-121	cyclin D1	Mus musculus	35-39
6343182-4	1983	Cyclophosphamide was activated to induce reversions of an ochre mutation and heteroallelic reversion in yeast tester strains r2089-15V-P4 and P3288, respectively.	Cyclophosphamide	0-16	ochre	Mus musculus	58-63
6217254-2	1983	Specific hapten- and I-J-driven liberation of an inhibitor of cell proliferation by Lyt-1-2+ cyclophosphamide-sensitive T acceptor cells armed with a product of Lyt-1+2+-specific suppressor cells.	Cyclophosphamide	93-109	CD5 antigen	Mus musculus	84-89
6217254-2	1983	Specific hapten- and I-J-driven liberation of an inhibitor of cell proliferation by Lyt-1-2+ cyclophosphamide-sensitive T acceptor cells armed with a product of Lyt-1+2+-specific suppressor cells.	Cyclophosphamide	93-109	CD5 antigen	Mus musculus	161-166
6217254-4	1983	Stimulation by painting with contact sensitizer (which need not be specific) gives rise to Lyt-1-2+, I-J+, cyclophosphamide-sensitive T acceptor cells (Tacc).	Cyclophosphamide	107-123	CD5 antigen	Mus musculus	91-96
6294517-5	1983	In the ACTH group, the number of patients stabilized or improved was 8 of 20 at six months and 4 of 20 at one year; in the cyclophosphamide-ACTH group, 18 of 20 at six months and 16 of 20 at one year; and in the plasma exchange group, 11 of 18 at six months and 9 of 18 at one year.	Cyclophosphamide	123-139	proopiomelanocortin	Homo sapiens	140-144
6294517-6	1983	High-dose cyclophosphamide plus ACTH was most effective in halting progression of the disease at both 6 and 12 months (at 12 months, cyclophosphamide-ACTH vs. ACTH, P = 0.0004; cyclophosphamide-ACTH vs. plasma exchange, P = 0.087).	Cyclophosphamide	10-26	proopiomelanocortin	Homo sapiens	150-154
6294517-6	1983	High-dose cyclophosphamide plus ACTH was most effective in halting progression of the disease at both 6 and 12 months (at 12 months, cyclophosphamide-ACTH vs. ACTH, P = 0.0004; cyclophosphamide-ACTH vs. plasma exchange, P = 0.087).	Cyclophosphamide	10-26	proopiomelanocortin	Homo sapiens	150-154
6294517-6	1983	High-dose cyclophosphamide plus ACTH was most effective in halting progression of the disease at both 6 and 12 months (at 12 months, cyclophosphamide-ACTH vs. ACTH, P = 0.0004; cyclophosphamide-ACTH vs. plasma exchange, P = 0.087).	Cyclophosphamide	10-26	proopiomelanocortin	Homo sapiens	150-154
6294517-6	1983	High-dose cyclophosphamide plus ACTH was most effective in halting progression of the disease at both 6 and 12 months (at 12 months, cyclophosphamide-ACTH vs. ACTH, P = 0.0004; cyclophosphamide-ACTH vs. plasma exchange, P = 0.087).	Cyclophosphamide	133-149	proopiomelanocortin	Homo sapiens	32-36
6294517-6	1983	High-dose cyclophosphamide plus ACTH was most effective in halting progression of the disease at both 6 and 12 months (at 12 months, cyclophosphamide-ACTH vs. ACTH, P = 0.0004; cyclophosphamide-ACTH vs. plasma exchange, P = 0.087).	Cyclophosphamide	133-149	proopiomelanocortin	Homo sapiens	150-154
6294517-6	1983	High-dose cyclophosphamide plus ACTH was most effective in halting progression of the disease at both 6 and 12 months (at 12 months, cyclophosphamide-ACTH vs. ACTH, P = 0.0004; cyclophosphamide-ACTH vs. plasma exchange, P = 0.087).	Cyclophosphamide	133-149	proopiomelanocortin	Homo sapiens	150-154
6294517-6	1983	High-dose cyclophosphamide plus ACTH was most effective in halting progression of the disease at both 6 and 12 months (at 12 months, cyclophosphamide-ACTH vs. ACTH, P = 0.0004; cyclophosphamide-ACTH vs. plasma exchange, P = 0.087).	Cyclophosphamide	133-149	proopiomelanocortin	Homo sapiens	150-154
6294517-6	1983	High-dose cyclophosphamide plus ACTH was most effective in halting progression of the disease at both 6 and 12 months (at 12 months, cyclophosphamide-ACTH vs. ACTH, P = 0.0004; cyclophosphamide-ACTH vs. plasma exchange, P = 0.087).	Cyclophosphamide	133-149	proopiomelanocortin	Homo sapiens	32-36
6294517-6	1983	High-dose cyclophosphamide plus ACTH was most effective in halting progression of the disease at both 6 and 12 months (at 12 months, cyclophosphamide-ACTH vs. ACTH, P = 0.0004; cyclophosphamide-ACTH vs. plasma exchange, P = 0.087).	Cyclophosphamide	133-149	proopiomelanocortin	Homo sapiens	150-154
6294517-6	1983	High-dose cyclophosphamide plus ACTH was most effective in halting progression of the disease at both 6 and 12 months (at 12 months, cyclophosphamide-ACTH vs. ACTH, P = 0.0004; cyclophosphamide-ACTH vs. plasma exchange, P = 0.087).	Cyclophosphamide	133-149	proopiomelanocortin	Homo sapiens	150-154
6294517-6	1983	High-dose cyclophosphamide plus ACTH was most effective in halting progression of the disease at both 6 and 12 months (at 12 months, cyclophosphamide-ACTH vs. ACTH, P = 0.0004; cyclophosphamide-ACTH vs. plasma exchange, P = 0.087).	Cyclophosphamide	133-149	proopiomelanocortin	Homo sapiens	150-154
6761307-5	1982	Three immunosuppressive drugs, HCA, cyclophosphamide, and Ara-C, depleted the thymus of cells expressing a large quantity of Thy-1.	Cyclophosphamide	36-52	thymus cell antigen 1, theta	Mus musculus	125-130
6819097-6	1982	The results suggest that NADPH-cytochrome P-450 reductase, which is decreased 40% by cyclophosphamide pretreatment, is not rate-limiting in elimination of adriamycin.	Cyclophosphamide	85-101	cytochrome p450 oxidoreductase	Rattus norvegicus	25-57
6761307-14	1982	The proportion of cells bearing Lyt-2 was altered by only two drugs; cyclophosphamide increased both Lyt-1+2+ and Lyt-1-2+ spleen cells and ABPP (an interferon inducer which stimulates antibody formation) decreased both Lyt-2+ subpopulations.	Cyclophosphamide	69-85	CD8 antigen, alpha chain	Mus musculus	32-37
6761307-14	1982	The proportion of cells bearing Lyt-2 was altered by only two drugs; cyclophosphamide increased both Lyt-1+2+ and Lyt-1-2+ spleen cells and ABPP (an interferon inducer which stimulates antibody formation) decreased both Lyt-2+ subpopulations.	Cyclophosphamide	69-85	CD5 antigen	Mus musculus	101-106
6761307-14	1982	The proportion of cells bearing Lyt-2 was altered by only two drugs; cyclophosphamide increased both Lyt-1+2+ and Lyt-1-2+ spleen cells and ABPP (an interferon inducer which stimulates antibody formation) decreased both Lyt-2+ subpopulations.	Cyclophosphamide	69-85	CD5 antigen	Mus musculus	114-119
6130913-1	1982	Iminocyclophosphamide has been identified among the metabolites produced by incubation of cyclophosphamide with cytochrome P-450 mono-oxygenase immobilized on beaded Sepharose.	Cyclophosphamide	5-21	cytochrome P450 family 20 subfamily A member 1	Homo sapiens	112-143
6809312-3	1982	Administration of 180 or 200 mg cyclophosphamide per kg to Wistar rats caused 41 to 67% decrease in aryl hydrocarbon hydroxylase activity, a 21 to 54% decrease in aminopyrine demethylase activity, and a 34 to 40% decrease in cytochrome P-450 content.	Cyclophosphamide	32-48	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	225-241
6179592-2	1982	After modified VAC chemotherapy (vincristine, dactinomycin, and cyclophosphamide), AFP and HCG levels in the serum were reduced significantly, while serum CEA increased gradually to the level of 6.5 ng/ml.	Cyclophosphamide	64-80	alpha fetoprotein	Homo sapiens	83-86
6179592-2	1982	After modified VAC chemotherapy (vincristine, dactinomycin, and cyclophosphamide), AFP and HCG levels in the serum were reduced significantly, while serum CEA increased gradually to the level of 6.5 ng/ml.	Cyclophosphamide	64-80	CEA cell adhesion molecule 3	Homo sapiens	155-158
6286112-1	1982	Human colon tumor cells (cell line LS174T) retain a cytochrome P-450-containing drug metabolism system capable of hydroxylating polycyclic hydrocarbons and the anticancer drug cyclophosphamide.	Cyclophosphamide	176-192	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	52-68
7093969-1	1982	Murine LPC-1 plasmacytoma is sensitive to treatment with cyclophosphamide (CY), and animals bearing this tumor in advanced stages can be cured with doses as small as 60 mg/kg.	Cyclophosphamide	57-73	annexin A1	Mus musculus	7-12
7093969-1	1982	Murine LPC-1 plasmacytoma is sensitive to treatment with cyclophosphamide (CY), and animals bearing this tumor in advanced stages can be cured with doses as small as 60 mg/kg.	Cyclophosphamide	75-77	annexin A1	Mus musculus	7-12
7093969-2	1982	With repeated transfer of LPC-1 cells followed by subcurative CY therapy, we have developed from this CY-sensitive parent line (CY-S) a stable CY-resistant subline (CY-R) that is unaffected by doses as large as 250 mg/kg.	Cyclophosphamide	128-132	annexin A1	Mus musculus	26-31
7093969-2	1982	With repeated transfer of LPC-1 cells followed by subcurative CY therapy, we have developed from this CY-sensitive parent line (CY-S) a stable CY-resistant subline (CY-R) that is unaffected by doses as large as 250 mg/kg.	Cyclophosphamide	102-104	annexin A1	Mus musculus	26-31
6964039-3	1982	Cyclophosphamide and mechlorethamine inhibited human plasma pseudocholinesterase most strongly, followed by thiotepa, ACNU, DTIC, ifosfamide and BCNU.	Cyclophosphamide	0-16	butyrylcholinesterase	Homo sapiens	60-80
6950800-5	1982	Combination chemotherapy with cyclophosphamide, Doxorubicin, vincristine, and prednisone (CHOP) has produced impressive clinical responses in patients with PL.	Cyclophosphamide	30-46	DNA damage inducible transcript 3	Homo sapiens	90-94
6177358-0	1982	[Changes in the rhythms of the alpha-fetoprotein content of the blood serum of mice with hepatoma 22A and of tumor cell proliferation depending on the time of cyclophosphane administration].	Cyclophosphamide	159-173	alpha fetoprotein	Mus musculus	31-48
7066863-2	1982	Twenty-seven patients were treated with the cyclophosphamide (CTX) L2 protocol, which included maintenance chemotherapy for three years.	Cyclophosphamide	44-60	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	62-65
6177358-1	1982	A study was made of the content of alpha-fetoprotein (alpha-FP) in the blood serum and of proliferative processes in hepatoma 22A-bearing mice after injection of cyclophosphamide in a dose of 150 mg/kg at varying time of 4-day tumor growth.	Cyclophosphamide	162-178	alpha fetoprotein	Mus musculus	35-52
6177358-1	1982	A study was made of the content of alpha-fetoprotein (alpha-FP) in the blood serum and of proliferative processes in hepatoma 22A-bearing mice after injection of cyclophosphamide in a dose of 150 mg/kg at varying time of 4-day tumor growth.	Cyclophosphamide	162-178	alpha fetoprotein	Mus musculus	54-62
6177358-3	1982	Besides, cyclophosphamide exerts a more powerful inhibitory effect on the content of alpha-FP in the blood serum and less powerful on the proliferative processes in hepatoma 22A.	Cyclophosphamide	9-25	alpha fetoprotein	Mus musculus	85-93
6277454-6	1982	From accumulated treatment experience of small cell carcinoma with vincristine alone or with vincristine, Adriamycin, cyclophosphamide combinations, the authors feel that the severe neuropathy observed was due to an interaction of vincristine and VP-16.	Cyclophosphamide	118-134	host cell factor C1	Homo sapiens	247-252
7073938-0	1982	Effect of misonidazole or metronidazole pretreatment on the response of the RIF-1 mouse sarcoma to melphalan, cyclophosphamide, chlorambucil and CCNU.	Cyclophosphamide	110-126	replication timing regulatory factor 1	Mus musculus	76-81
6980279-0	1982	Early appearance of abnormally migrating serum IgM in control and cyclophosphamide-treated NZB/NZW mice.	Cyclophosphamide	66-82	immunoglobulin heavy constant mu	Mus musculus	47-50
6178678-1	1982	This brief review of our experiments concerning the in vivo activity of crude Il-2 led us to the following conclusion: The first is the existence, in vivo, of a cyclophosphamide-sensitive T-cell controlling the activity of a serum born Il-2 inhibitor in thymus-bearing normal mice.	Cyclophosphamide	161-177	interleukin 2	Mus musculus	78-82
6178678-1	1982	This brief review of our experiments concerning the in vivo activity of crude Il-2 led us to the following conclusion: The first is the existence, in vivo, of a cyclophosphamide-sensitive T-cell controlling the activity of a serum born Il-2 inhibitor in thymus-bearing normal mice.	Cyclophosphamide	161-177	interleukin 2	Mus musculus	236-240
6980279-7	1982	In 1 instance, an IgM paraprotein appeared and persisted in a mouse receiving prolonged treatment with a high dose of cyclophosphamide.	Cyclophosphamide	118-134	immunoglobulin heavy constant mu	Mus musculus	18-21
6803060-1	1982	Donor pretreatment of 100 mg/kg each of cyclophosphamide (CY) and methylprednisolone (P) infused 5 hours before nephrectomy invariably prolongs the survival of DLA mismatched, MLC incompatible nonlittermate Beagle renal allografts as well as the survival of mongrel renal allografts.	Cyclophosphamide	40-56	modulator of VRAC current 1	Homo sapiens	176-179
7034931-1	1982	Using the MOPC 104E murine plasmacytoma model, Ghanta et al have shown major synergism when cisplatin was added to a treatment program with BCNU and cyclophosphamide (CTX).	Cyclophosphamide	149-165	V-set and immunoglobulin domain containing 2	Mus musculus	167-170
6276303-3	1982	Cyclophosphamide and cimetidine treatments of mice, which augment delayed-type hypersensitivity reactions, enhanced liver granuloma size and decreased granuloma ACE activity.	Cyclophosphamide	0-16	angiotensin I converting enzyme (peptidyl-dipeptidase A) 1	Mus musculus	161-164
6175364-0	1982	[Effect of cyclophosphamide on alpha-fetoprotein content in the blood serum of mice with hepatoma 22a depending upon the period of tumor development].	Cyclophosphamide	11-27	alpha fetoprotein	Mus musculus	31-48
6173311-2	1982	Reversal of oral tolerance to ovalbumin by cyclophosphamide.	Cyclophosphamide	43-59	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	30-39
7053252-0	1982	Combination chemotherapy with cyclophosphamide, vincristine, and prednisone (CVP) in TNM-classified stage IV mycosis fungoides.	Cyclophosphamide	30-46	teneurin transmembrane protein 1	Homo sapiens	85-88
7053258-0	1982	Combination chemotherapy for bronchogenic carcinoma with doxorubicin, BCNU, and cyclophosphamide (ABC): a pilot study of the Southeastern Cancer Study Group.	Cyclophosphamide	80-96	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	98-101
6813749-1	1982	E-N-L-trimethyl lysine (TML) decreases the toxicity of Vincristin, Cyclophosphamide and Doxorubicin (Adriamycin) when administered simultaneously to healthy mice.	Cyclophosphamide	67-83	myeloid/lymphoid or mixed-lineage leukemia; translocated to, 1	Mus musculus	0-5
7058064-4	1982	The immunodepression to SRBC in Trichinella-infected mice was removed by treating mice with low doses of cyclophosphamide (CY).	Cyclophosphamide	105-121	caveolae associated 3	Mus musculus	24-28
7058064-4	1982	The immunodepression to SRBC in Trichinella-infected mice was removed by treating mice with low doses of cyclophosphamide (CY).	Cyclophosphamide	123-125	caveolae associated 3	Mus musculus	24-28
7337762-2	1981	The two schemes involve the administration of cyclophosphamide that, as has already been proved, significantly lowers serum cholinesterase level after only a few hours.	Cyclophosphamide	46-62	butyrylcholinesterase	Homo sapiens	124-138
7310817-1	1981	Hydrogenolysis of 3-(benzyloxy)cyclophosphamide (10) using Pd/C catalyst and ethyl acetate as solvent leads to the formation of 3-hydroxycyclophosphamide (3, approximately 20%) and cyclophosphamide (1, approximately 10%), accompanied by regioselective hydrogen-exchange reactions at the C-4 and C-5 positions in 3 and 1.	Cyclophosphamide	31-47	complement component 4B (Chido blood group)	Mus musculus	287-290
7310817-1	1981	Hydrogenolysis of 3-(benzyloxy)cyclophosphamide (10) using Pd/C catalyst and ethyl acetate as solvent leads to the formation of 3-hydroxycyclophosphamide (3, approximately 20%) and cyclophosphamide (1, approximately 10%), accompanied by regioselective hydrogen-exchange reactions at the C-4 and C-5 positions in 3 and 1.	Cyclophosphamide	31-47	hemolytic complement	Mus musculus	295-298
7337763-1	1981	As the Authors and Others have already demonstrated, cyclophosphamide leads to a rapid and prolonged decrease in the serum cholinesterase activity.	Cyclophosphamide	53-69	butyrylcholinesterase	Homo sapiens	123-137
7298626-0	1981	Studies on the mechanism of denaturation of cytochrome P-450 by cyclophosphamide and its metabolites.	Cyclophosphamide	64-80	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	44-60
6167628-6	1981	The induction of unresponsiveness that was abrogated by pretreatment with cyclophosphamide suggests the development of an S79-sensitive lymphocyte subset that regulates MBP-induced EAE in Lewis rats.	Cyclophosphamide	74-90	myelin basic protein	Rattus norvegicus	169-172
6790656-0	1981	Lyt-23+ cyclophosphamide-sensitive T cells regulate the activity of an interleukin 2 inhibitor in vivo.	Cyclophosphamide	8-24	nuclear factor of kappa light polypeptide gene enhancer in B cells 2, p49/p100	Mus musculus	0-3
7272187-0	1981	Enhancing effect of misonidazole on the response of the RIF-1 tumour to cyclophosphamide.	Cyclophosphamide	72-88	replication timing regulatory factor 1	Mus musculus	56-61
7272187-14	1981	From experiments performed to investigated the possible mechanisms involved, we conclude that for the RIF-1 tumour the major effect of MISO is to inhibit the repair from CY-induced potentially lethal damage.	Cyclophosphamide	170-172	replication timing regulatory factor 1	Mus musculus	102-107
6271847-1	1981	We studied the effect of THC upon the pharmacokinetics of cyclophosphamide (CTX) and doxorubicin (ADR).	Cyclophosphamide	58-74	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	76-79
6790656-0	1981	Lyt-23+ cyclophosphamide-sensitive T cells regulate the activity of an interleukin 2 inhibitor in vivo.	Cyclophosphamide	8-24	interleukin 2	Mus musculus	71-84
6790656-2	1981	Evidence is presented that cyclophosphamide-sensitive Lyt-23+ T cells induce high II-2 inhibitor activity in the recipient nu/nu mice in the course of a graft-vs.-host reaction.	Cyclophosphamide	27-43	nuclear factor of kappa light polypeptide gene enhancer in B cells 2, p49/p100	Mus musculus	54-57
6790656-2	1981	Evidence is presented that cyclophosphamide-sensitive Lyt-23+ T cells induce high II-2 inhibitor activity in the recipient nu/nu mice in the course of a graft-vs.-host reaction.	Cyclophosphamide	27-43	interleukin 2	Mus musculus	82-86
6972410-4	1981	A single injection of cyclophosphamide (CY) given to chronically infected mice with diminished granulomas and impaired ability to produce MIF restored the enhanced granulomatous response and lymphokine production by spleen cells.	Cyclophosphamide	22-38	macrophage migration inhibitory factor (glycosylation-inhibiting factor)	Mus musculus	138-141
7029774-6	1981	Cyclophosphamide was activated to mutagenic metabolites to the same extent (on a tissue wet weight basis) by enzyme fractions from maternal liver, kidney and placenta, despite differences in cytochrome P-450 content.	Cyclophosphamide	0-16	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	191-207
6972410-4	1981	A single injection of cyclophosphamide (CY) given to chronically infected mice with diminished granulomas and impaired ability to produce MIF restored the enhanced granulomatous response and lymphokine production by spleen cells.	Cyclophosphamide	40-42	macrophage migration inhibitory factor (glycosylation-inhibiting factor)	Mus musculus	138-141
6972410-6	1981	After CY treatment, spleen cells were still capable of adoptively suppressing the vigorous granulomatous response and MIF production in acutely infected recipients.	Cyclophosphamide	6-8	macrophage migration inhibitory factor (glycosylation-inhibiting factor)	Mus musculus	118-121
6264941-2	1981	In RIF-1, the growth delay due to CY was increased by the addition of 1 mg/g of MISO.	Cyclophosphamide	34-36	replication timing regulatory factor 1	Mus musculus	3-8
6113038-5	1981	In addition, when mice were immunosuppressed by cyclophosphamide, TH activity was relatively preserved early in the course of infection despite high viral titers in the ganglion and the presence of viral antigen and histopathological alterations in nearly 100% of neurons.	Cyclophosphamide	48-64	tyrosine hydroxylase	Mus musculus	66-68
6112490-0	1981	Protection from cyclophosphamide-induced testicular damage with an analogue of gonadotropin-releasing hormone.	Cyclophosphamide	16-32	gonadotropin releasing hormone 1	Homo sapiens	79-109
6167301-0	1981	[Increase in the concentration of alpha-fetoprotein in the blood of mice following a single dose of cyclophosphane].	Cyclophosphamide	100-114	alpha fetoprotein	Mus musculus	34-51
7015852-7	1981	Treatment with melphalan or cyclophosphamide resulted in a decrease in the serum IgE level and in the level of Bence Jones protein in the urine.	Cyclophosphamide	28-44	immunoglobulin heavy constant epsilon	Homo sapiens	81-84
6167301-1	1981	Activation of extramedullar hemopoiesis in the liver together with an appreciable elevation of the alpha-fetoprotein (alpha-FP) level in the blood were observed in CBA, C3H/HeJ, DD, C57BL/6 and CC57BR/Mv mice after a single injection of cyclophosphane in a dose of 200 mg/kg bw.	Cyclophosphamide	237-251	alpha fetoprotein	Mus musculus	99-116
6167301-1	1981	Activation of extramedullar hemopoiesis in the liver together with an appreciable elevation of the alpha-fetoprotein (alpha-FP) level in the blood were observed in CBA, C3H/HeJ, DD, C57BL/6 and CC57BR/Mv mice after a single injection of cyclophosphane in a dose of 200 mg/kg bw.	Cyclophosphamide	237-251	alpha fetoprotein	Mus musculus	118-126
6167301-2	1981	The alpha-FP concentration reached maximum days 2-4 after cyclophosphane administration, amounting of 290-560 ng/ml which surpasses 2-5-fold the basal level of the protein.	Cyclophosphamide	58-72	alpha fetoprotein	Mus musculus	4-12
7214354-1	1981	The addition of diethylnitrosamine or cyclophosphamide in cultures of hepatocytes overlaid on confluent diploid human fibroblasts resulted in a dose-dependent increase in the frequency of hypoxanthine-guanine phosphoribosyl transferase human fibroblast mutants with both chemicals.	Cyclophosphamide	38-54	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	188-235
7194923-3	1981	All 3 drugs (60 mg./m.2 cis-platinum, 40 mg./m.2 doxorubicin hydrochloride and 400 mg./m.2 cyclophosphamide) were given as a single dose every 4 weeks.	Cyclophosphamide	91-107	paired box 5	Homo sapiens	0-5
7262052-2	1981	CY at concentrations from 1 x 10(-5) M to 1 x 10(-3) M with S-9 mix increased the number of SCEs per cell in a dose-dependent manner.	Cyclophosphamide	0-2	ribosomal protein S9	Homo sapiens	60-63
7314093-1	1981	It was already reported that a masked compound, cyclophosphamide (Endoxan, EX) undergoes the first step metabolism by a drug-metabolizing enzyme in liver microsomes, cytochrome P-450.	Cyclophosphamide	48-64	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	166-182
7314093-1	1981	It was already reported that a masked compound, cyclophosphamide (Endoxan, EX) undergoes the first step metabolism by a drug-metabolizing enzyme in liver microsomes, cytochrome P-450.	Cyclophosphamide	66-73	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	166-182
6786291-0	1981	Inhibition of NADPH-cytochrome P450 reductase by cyclophosphamide and its metabolites.	Cyclophosphamide	49-65	cytochrome p450 oxidoreductase	Homo sapiens	14-45
7245091-7	1981	Since 4-OH-CPA decomposes into acrolein and PAM in vivo and in vitro and since PAM and 4-OH-CPA exhibit identical embryotoxicity towards preimplantation embryos in vitro, PAM probably also is an active embryotoxic CPA metabolite in vivo before implantation.	Cyclophosphamide	11-14	peptidylglycine alpha-amidating monooxygenase	Mus musculus	44-47
6794303-0	1981	Effect of erythropoietin on erythropoietin-responsive cell regeneration in polycythemic mice treated with cyclophosphamide.	Cyclophosphamide	106-122	erythropoietin	Mus musculus	28-42
6455653-0	1980	Different results of micronucleus test with cyclophosphamide in SPF and conventional mice and rats.	Cyclophosphamide	44-60	SEC14-like lipid binding 4	Mus musculus	64-67
7015645-1	1980	In CMF regimen, gastric disturbances secondary to oral administration of cyclophosphamide (CTX) frequently induce many patients to take the drug erratically, to lower the daily dose, or to divide it in many administrations.	Cyclophosphamide	73-89	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	91-94
7233568-0	1980	Combination chemotherapy with cyclophosphamide, adriamycin, vincristine and prednisone (CHOP) for non-Hodgkin"s lymphomas with unfavorable histology: preliminary results.	Cyclophosphamide	30-46	DNA damage inducible transcript 3	Homo sapiens	88-92
7459899-1	1980	Fifty-eight patients with non-small cell carcinoma of the lung (33 with epidermoid carcinoma, 22 with adenocarcinoma, and three with large cell anaplastic carcinoma) were treated with high-dose cyclophosphamide (CTX) or, alternatively, with CTX, methotrexate, 5-FU, and hydroxyurea (CMFH) in a controlled study.	Cyclophosphamide	194-210	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	212-215
7397660-7	1980	The program that we have come to regard as our standard program in controlled clinical trials (CFP) employs cyclophosphamide, 5-fluorouracil, and prednisone.	Cyclophosphamide	108-124	complement factor properdin	Homo sapiens	95-98
7448029-0	1980	[Administration of cyclophosphamide determines the lowering of serum cholinesterase levels].	Cyclophosphamide	19-35	butyrylcholinesterase	Homo sapiens	69-83
7448029-2	1980	Cyclophosphamide administration, even at low dose, causes a prolonged fall of serum cholinesterase levels.	Cyclophosphamide	0-16	butyrylcholinesterase	Homo sapiens	84-98
6966663-4	1980	The Lyt 1 cells that transferred the suppression were resistant to low (20 mg/kg) doses of cyclophosphamide (Cy) but required a Cy-sensitive precursor and/or amplifier cell to be activated.	Cyclophosphamide	91-107	CD5 antigen	Mus musculus	4-9
6966663-4	1980	The Lyt 1 cells that transferred the suppression were resistant to low (20 mg/kg) doses of cyclophosphamide (Cy) but required a Cy-sensitive precursor and/or amplifier cell to be activated.	Cyclophosphamide	109-111	CD5 antigen	Mus musculus	4-9
6966663-4	1980	The Lyt 1 cells that transferred the suppression were resistant to low (20 mg/kg) doses of cyclophosphamide (Cy) but required a Cy-sensitive precursor and/or amplifier cell to be activated.	Cyclophosphamide	128-130	CD5 antigen	Mus musculus	4-9
6966663-5	1980	Once activated, they required a Cy-sensitive Lyt 1 2 3 acceptor cell in the normal recipient to effectively suppress the adoptive host"s macrophages.	Cyclophosphamide	32-34	CD5 antigen	Mus musculus	45-50
6966663-6	1980	Our results indicative that immune complexes in concert with a Cy-sensitive T cell generate Cy-resistant Lyt 1 inducers of suppression.	Cyclophosphamide	63-65	CD5 antigen	Mus musculus	105-110
6966663-6	1980	Our results indicative that immune complexes in concert with a Cy-sensitive T cell generate Cy-resistant Lyt 1 inducers of suppression.	Cyclophosphamide	92-94	CD5 antigen	Mus musculus	105-110
7387676-0	1980	Protection by N-acetylcysteine of cyclophosphamide metabolism - related in vivo depression of mixed function oxygenase activity and in vitro denaturation of cytochrome P-450.	Cyclophosphamide	34-50	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	157-173
7193030-2	1980	With pathologically reduced serum cholinesterase activity the half-life of the drug increases from normally 4.3 h to 6.7 h. These patients show significantly lower peak levels of activated cyclophosphamide (4-hydroxy-cyclophosphamide + aldophosphamide).	Cyclophosphamide	189-205	butyrylcholinesterase	Homo sapiens	34-48
7386308-4	1980	Low doses of cyclophosphamide (CY) administered after antigen sensitization were found to enhance DTH to methylated bovine serum albumin (MBSA).	Cyclophosphamide	13-29	albumin	Mus musculus	123-136
7386308-4	1980	Low doses of cyclophosphamide (CY) administered after antigen sensitization were found to enhance DTH to methylated bovine serum albumin (MBSA).	Cyclophosphamide	31-33	albumin	Mus musculus	123-136
6931740-1	1980	The effect of cyclophosphamide and N-nitrosomethylurea(NMU) was intensified by combining these alkylizing substances.	Cyclophosphamide	14-30	neuromedin U	Rattus norvegicus	55-58
6776030-3	1980	Pretreatment with 100 mg/kg of cyclophosphamide (CTX) 3 d before antigen failed to alter this pattern, but treatment 3 d after antigen administration abrogated both DTH and DCMC.	Cyclophosphamide	31-47	V-set and immunoglobulin domain containing 2	Mus musculus	49-52
6966256-3	1980	In mice made granulocytopenic with cyclophosphamide and subsequently infected with a variety of garm-negative pathogens or with Candida albicans, PSK prolonged the average survival time of the animals.	Cyclophosphamide	35-51	TAO kinase 2	Mus musculus	146-149
6970728-0	1980	Recovery of the capacity for cytotoxic T cell generation in cyclophosphamide-treated mice by the addition of LYT-1/2- helper cells.	Cyclophosphamide	60-76	CD5 antigen	Mus musculus	109-114
6970728-2	1980	The reduced response of spleen cells from cyclophosphamide-treated mice is not due to the elimination of cytotoxic T cell precursors because normal responses are obtained by the addition of Lyt-1+2- T helper cells to the culture system.	Cyclophosphamide	42-58	CD5 antigen	Mus musculus	190-195
7462295-4	1980	Cyclophosphamide proved to be the most effective among the drugs studied (Cyclophosphamide, 5-FU, DBD, CCNU, Adriamycin, Vincristin, Hexyldeoxyuridine).	Cyclophosphamide	0-16	cyclin O	Mus musculus	103-107
7374015-2	1980	The association of HLA-B12 with short time-to-relapse after cyclophosphamide treatment of SRNS was also confirmed, but that with atopy in SRNS children was not, though we observed a similarly high incidence of atopy in them as before.	Cyclophosphamide	60-76	major histocompatibility complex, class I, B	Homo sapiens	19-24
7464688-0	1980	Studies on the antidiuretic effect of cyclophosphamide: vasopressin release and sodium excretion.	Cyclophosphamide	38-54	arginine vasopressin	Homo sapiens	56-67
7455636-1	1980	Six months" cyclophosphamide treatment significantly increased the sulfhydryl (SH) serum levels in all 12 rheumatoid arthritis (RA) patients studied and significantly decreased the PIP joints" technetium index (Tc-index), the erythrocyte sedimentation rate (ESR), and the joint count.	Cyclophosphamide	12-28	prolactin induced protein	Homo sapiens	181-184
6965827-0	1980	Effects of cyclophosphamide, levamisole and concanavalin A on the in vitro IgE biosynthesis.	Cyclophosphamide	11-27	immunoglobulin heavy constant epsilon	Homo sapiens	75-78
6965827-1	1980	The effects of cyclophosphamide (200 microgram/ml), levamisole (1 microgram/ml) and Concanavalin A (10 microgram/ml) on the in vitro IgE biosynthesis of lymphocytes from 2 allergic children and six healthy adults were studied.	Cyclophosphamide	15-31	immunoglobulin heavy constant epsilon	Homo sapiens	133-136
6965827-2	1980	The capability of the IgE biosynthesis was enhanced by cyclophosphamide in nine allergic children, suppressed by levamisole in three and not changed by Concanavalin A.	Cyclophosphamide	55-71	immunoglobulin heavy constant epsilon	Homo sapiens	22-25
479593-5	1979	By contrast, FTS has a depressive effect on the contact sensitivity response to DNFB of normal mice through a cyclophosphamide-sensitive T cell subset.	Cyclophosphamide	110-126	AKT interacting protein	Mus musculus	13-16
479593-6	1979	These results suggest that FTS regulates DNFB contact sensitivity by acting on a cyclophosphamide-sensitive T cell subset, still present 9 weeks after ATX but absent after 16 weeks.	Cyclophosphamide	81-97	AKT interacting protein	Mus musculus	27-30
479593-6	1979	These results suggest that FTS regulates DNFB contact sensitivity by acting on a cyclophosphamide-sensitive T cell subset, still present 9 weeks after ATX but absent after 16 weeks.	Cyclophosphamide	81-97	diencephalon/mesencephalon homeobox 1	Mus musculus	151-154
230674-5	1979	A significant decrease of MIF-activity was noted when the tumor-inoculated mice were treated with ds-RNA, antithymocyte serum and cyclophosphamide, respectively.	Cyclophosphamide	130-146	macrophage migration inhibitory factor (glycosylation-inhibiting factor)	Mus musculus	26-29
88878-1	1979	A significant in vivo activation of cytotoxic T-lymphocytes (CTL) against trinitrophenyl (TNP)-modified autologous cells and of a DNA-synthesis response in the peripheral lymphnodes is observed in cyclophosphamide (CyP) treated mice after skinpainting with trinitrochlorbenzene (TNCB) or after injection of TNP-coupled spleen cells (TNP-Spl) into the footpads.	Cyclophosphamide	197-213	plasma serotonin level	Mus musculus	337-340
507741-1	1979	A case of localized lymphomatous polyposis of the rectum successfully treated with a combination of cyclophosphamide, vincristine and prednisone (COP regimen) is reported and the literature is briefly reviewed.	Cyclophosphamide	100-116	caspase recruitment domain family member 16	Homo sapiens	146-149
369682-1	1979	A combination of 5-fluorouracil (5-FU), adriamycin, and cyclophosphamide (FAC) was compared to a combination of 5-FU, adriamycin, and ifosfamide (FAI) in the treatment of metastatic breast cancer.	Cyclophosphamide	56-72	FA complementation group C	Homo sapiens	74-77
363314-4	1978	The mitogenic response to these factors by spleen cells from athymic mice was highly significant, whereas the response of spleen cells taken from CD-1 mice which had been pre-treated with cyclophosphamide was much less, suggesting that the B cell was the major target of the trypanosome-derived mitogen.	Cyclophosphamide	188-204	CD1 antigen complex	Mus musculus	146-150
671649-0	1978	An approach to the control of massive hemorrhage in cyclophosphamide-induced cystitis by intravenous vasopressin: a case report.	Cyclophosphamide	52-68	arginine vasopressin	Homo sapiens	101-112
367261-6	1978	Adjuvant action of EBP was different of those of endotoxin, since the later suppresses the DTH response to optimal dose of SRBC, this effect being abolished with cyclophosphamide pretreatment.	Cyclophosphamide	162-178	phenylalkylamine Ca2+ antagonist (emopamil) binding protein	Mus musculus	19-22
27021-0	1978	[On the binding of cyclophosphamide and cyclophosphamide-metabolites to serum-albumin (author"s transl)].	Cyclophosphamide	19-35	albumin	Homo sapiens	72-85
27021-0	1978	[On the binding of cyclophosphamide and cyclophosphamide-metabolites to serum-albumin (author"s transl)].	Cyclophosphamide	40-56	albumin	Homo sapiens	72-85
305933-5	1978	Furthermore, the enhancing effect of CY pretreatment was abolished by passively transferred normal syngeneic thymocyreated with ATS and guinea pig C.	Cyclophosphamide	37-39	phosphatidylinositol N-acetylglucosaminyltransferase subunit C	Cavia porcellus	143-148
96959-0	1978	[Variation in delayed hypersensitivity to methylated bovine serum albumin as as function of the dose and time of administration of cyclophosphamide].	Cyclophosphamide	131-147	albumin	Homo sapiens	60-73
307938-9	1978	If MBP is administered after a 3-day action of CY, the number of these cells till the 7th day after the antigen challenge is strongly reduced, then surpasses the normal value about the 10th day and comes back to it towards the 20th day.	Cyclophosphamide	47-49	myelin basic protein	Cavia porcellus	3-6
348078-3	1978	The most important observations on resistance and cross-resistance reported are: (a) L1210 cells selected for complete resistance to cyclophosphamide (CPA) retain full sensitivity to selected nitrosoureas (BCNU, CCNU, MeCCNU), chlorozotocin), dianhydrogalactitol, and cis-DDPt, while retaining marked but somewhat reduced sensitivity to L-PAM, piperazinedione, and thioTEPA.	Cyclophosphamide	133-149	peptidylglycine alpha-amidating monooxygenase	Mus musculus	339-342
364284-1	1978	The results of a chemotherapy regimen utilizing adriamycin in combination with vincristine, prednisone plus or minus cyclophosphamide (CHOP-HOP) for the treatment of non-Hodgkin lymphoma are compared to those of a non-adriamycin containing combination (COP).	Cyclophosphamide	117-133	DNA damage inducible transcript 3	Homo sapiens	135-139
313902-0	1979	Cyclophosphamide intensifies the acquisition of allergic contact dermatitis in mice rendered B-cell deficient by heterologous anti-IgM antisera.	Cyclophosphamide	0-16	immunoglobulin heavy constant mu	Mus musculus	131-134
312893-2	1979	DH to methylated human serum albumin (MHSA) could be enhanced with CY in young mice but not in aged ones.	Cyclophosphamide	67-69	albumin	Mus musculus	23-36
698922-1	1978	Multicellular tumor spheroids (MTS) have been exposed to chemotherapeutic agents in vitro (nitrogen mustard) or in vivo (cyclophosphamide) and analyzed in vitro in terms of altered growth patterns.	Cyclophosphamide	121-137	MLRL	Homo sapiens	0-29
698922-4	1978	injection cyclophosphamide results in patterns similar to the in vitro exposure system, except that a host anti-MTS reaction was detected.	Cyclophosphamide	10-26	MLRL	Homo sapiens	112-115
728894-1	1978	One hundred and fourteen evaluable patients with measurable metastatic breast cancer were treated with a combination chemoimmunotherapy program (5-fluorouracil, adriamycin, and cyclophosphamide [FAC-levamisole [LSM]).	Cyclophosphamide	177-193	FA complementation group C	Homo sapiens	195-198
623430-5	1978	Against MX-1 tumor, both cyclophosphamide and melphalan induced tumor regressions with no recurrence.	Cyclophosphamide	25-41	MX dynamin-like GTPase 1	Mus musculus	8-12
658001-2	1978	The tumour myosarcoma ISM showed high sensitivity to cyclophosphamide, administration of which caused complete inhibition of tumour growth and regression of tumours.	Cyclophosphamide	53-69	isthmin 1, angiogenesis inhibitor	Mus musculus	22-25
922753-4	1977	When given together with noncurative doses of cyclophosphamide (CTX), ALK-NABS acts synergistically.	Cyclophosphamide	46-62	V-set and immunoglobulin domain containing 2	Mus musculus	64-67
922753-4	1977	When given together with noncurative doses of cyclophosphamide (CTX), ALK-NABS acts synergistically.	Cyclophosphamide	46-62	anaplastic lymphoma kinase	Mus musculus	70-73
72778-4	1977	Pretreatment of mice with cyclophosphamide prevents the high dose inhibition of T-RFC.	Cyclophosphamide	26-42	solute carrier family 19 (folate transporter), member 1	Mus musculus	82-85
588482-0	1977	Compared effects of irradiation and cyclophosphamide induced erythroid aplasia on the catabolism of exogenous erythropoietin.	Cyclophosphamide	36-52	erythropoietin	Rattus norvegicus	110-124
890694-4	1977	Furthermore, the estrogen and progesterone receptor contents of the residual tumor masses after cyclophosphamide treatment were about the same as those of untreated tumors.	Cyclophosphamide	96-112	progesterone receptor	Mus musculus	30-51
409523-1	1977	Delayed hypersensitivity to methylated bovine serum albumin may be induced in Mice without adjuvant, by injecting the antigen either with sensitized T lymphocytes, or by injecting just the antigen in Mice preptreated with Cyclophosphamid.	Cyclophosphamide	222-237	albumin	Mus musculus	46-59
403484-2	1977	The patients were treated with ciclophosphamide (CTX) (500 mg i.v.)	Cyclophosphamide	31-47	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	49-52
403484-4	1977	(TSPA) every 4 weeks associated with cyclophosphamide as follows: CTX--CTX--CTX--CTX+TSPA.	Cyclophosphamide	37-53	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	66-69
403484-4	1977	(TSPA) every 4 weeks associated with cyclophosphamide as follows: CTX--CTX--CTX--CTX+TSPA.	Cyclophosphamide	37-53	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	71-74
403484-4	1977	(TSPA) every 4 weeks associated with cyclophosphamide as follows: CTX--CTX--CTX--CTX+TSPA.	Cyclophosphamide	37-53	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	71-74
403484-4	1977	(TSPA) every 4 weeks associated with cyclophosphamide as follows: CTX--CTX--CTX--CTX+TSPA.	Cyclophosphamide	37-53	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	71-74
577161-0	1977	Influence of cortisone and cyclophosphamide on xanthine oxidase bacterial activation.	Cyclophosphamide	27-43	xanthine dehydrogenase	Mus musculus	47-63
577161-1	1977	The xanthine oxidase increase in mice liver as response to infection was studied as a possible parameter useful for a better understanding of theimmunosuppression due to cyclophosphamide and cortisone.	Cyclophosphamide	170-186	xanthine dehydrogenase	Mus musculus	4-20
10711-3	1976	dose of cyclophosphamide (100 mg/kg body weight) the activity of different "brush border enzymes" (maltase, sucrase lactase, alkaline phosphatase, gamma-glutamyl transferase) and of a lysosomal enzyme (acid phosphatase) did not change.	Cyclophosphamide	8-24	gamma-glutamyltransferase 1	Rattus norvegicus	147-173
781416-9	1976	A cytotoxic immunoglobulin inhibitor of the marrow erythroid cells or erythropoietin has been described and these patients may respond to prednisone and/or to cytotoxic immunosuppressive drugs such as cyclophosphamide and 6-mercaptopurine.	Cyclophosphamide	201-217	erythropoietin	Homo sapiens	70-84
1003701-4	1976	High doses of 5-fluorouracil (5-FU) and cyclophosphamide (CP) given parenterally for 6 days caused a partial decrease in whole body weight and the microsomal enzyme content such as cytochrome P-450 and cytochrome b5.	Cyclophosphamide	40-56	cytochrome b5 type A	Rattus norvegicus	202-215
132786-1	1976	In a prospective study eleven patients with metastasizing breast cancer were treated with 5-fluorouracil, adriamycin, and cyclophosphamide )FAC).	Cyclophosphamide	122-138	FA complementation group C	Homo sapiens	140-143
33146835-0	2021	Febrile neutropenia and role of prophylactic granulocyte colony-stimulating factor in docetaxel and cyclophosphamide chemotherapy for breast cancer.	Cyclophosphamide	100-116	colony stimulating factor 3	Homo sapiens	45-82
1081076-4	1976	More evidence for the (partial) T-cell dependence of MS-2 was obtained from experiments with anti-thymocyte serum or cyclophosphamide-treated mice.	Cyclophosphamide	117-133	minisatellites detected by probe MMS2	Mus musculus	53-57
1056807-2	1975	Cyclophosphamide, cytosine arabinoside and vincristine (CAV) therapy resulted in complete remission in 23 of 50 previously untreated patients with AML and in 3 of the 11 patients with CML.	Cyclophosphamide	0-16	caveolin 2	Homo sapiens	56-59
1131420-1	1975	A patient, CAL, with gamma heavy chain disease is presented who has had a complete remission lasting over 2 yr with combination chemotherapy consisting of pulsatile cyclophosphamide and prednisone.	Cyclophosphamide	165-181	filamin binding LIM protein 1	Homo sapiens	11-14
4135071-4	1974	Intermittent therapy with prednisone and cyclophosphamide together with antibiotics was followed by clinical recovery, return of histological appearances of the small intestine to normal, and disappearance of free alpha-chain protein from the serum.	Cyclophosphamide	41-57	Fc gamma receptor and transporter	Homo sapiens	214-225
4545635-0	1974	Proceedings: Relationship between aldehyde oxidase activity and biological activity of cyclophosphamide.	Cyclophosphamide	87-103	aldehyde oxidase 1	Homo sapiens	34-50
4576753-0	1972	Cyclophosphamide inhibition of insulin antibody production, insulin resistance and experimental immunodiabetes.	Cyclophosphamide	0-16	insulin	Homo sapiens	31-38
5921530-0	1966	The diuretic effects of cyclophosphamide and nor-nitrogen mustard: relationship to antidiuretic hormone.	Cyclophosphamide	24-40	arginine vasopressin	Homo sapiens	83-103
5946779-0	1966	Comparative effects of cyclophosphamide and total body irradiation on erythropoietin production in rats.	Cyclophosphamide	23-39	erythropoietin	Rattus norvegicus	70-84
5842374-0	1965	[Inhibition of serum cholinesterase by cyclophosphamide (endoxan)].	Cyclophosphamide	39-55	butyrylcholinesterase	Homo sapiens	21-35
5842374-0	1965	[Inhibition of serum cholinesterase by cyclophosphamide (endoxan)].	Cyclophosphamide	57-64	butyrylcholinesterase	Homo sapiens	21-35
1259925-2	1976	Two patients with pure red cell aplasia, whose marrow cells were capable of increasing their rate of haem synthesis when incubated in vitro with erythropoietin concentrate, had a complete remission associated with the administration of cyclophosphamide and prednisone.	Cyclophosphamide	236-252	erythropoietin	Homo sapiens	145-159
130494-7	1976	Marked reduction in this formation was observed when five daily doses of PS-K were administered simultaneously with cyclophosphamide.	Cyclophosphamide	116-132	TAO kinase 2	Mus musculus	73-77
1167458-0	1975	Cyclophosphamide, 2,2-dimethylaziridines and other alkylating agents as inhibitors of serum cholinesterase.	Cyclophosphamide	0-16	butyrylcholinesterase	Homo sapiens	92-106
1232533-2	1975	This study was conducted to determine whether cyclophosphamide (CTX) as an adjuvant to estrogen therapy might (1) prevent induced hypercalcemia or (2) achieve a higher tumoricidal effect during the phase of tumor stimulation.	Cyclophosphamide	46-62	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	64-67
4432244-0	1974	Increased antitumor activity of cyclophosphamide (Endoxan) following pretreatment with inducer of drug-metabolizing enzymes (cytochrome P-450).	Cyclophosphamide	32-48	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	125-141
4432244-0	1974	Increased antitumor activity of cyclophosphamide (Endoxan) following pretreatment with inducer of drug-metabolizing enzymes (cytochrome P-450).	Cyclophosphamide	50-57	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	125-141
4368615-0	1974	Effect of cyclophosphamide on ACTH-induced kidney disease.	Cyclophosphamide	10-26	proopiomelanocortin	Homo sapiens	30-34
4261840-1	1972	Pretreatment with pregnenolone-16a-carbonitrile (PCN) protects the rat against the toxic effects of indomethacin, digitoxin, cyclophosphamide and many other injurious agents.	Cyclophosphamide	125-141	plectin	Rattus norvegicus	18-47
5364896-0	1969	Uptake of P32-labelled cyclophosphamide from arthritic knee joints.	Cyclophosphamide	23-39	inhibitor of growth family member 2	Homo sapiens	10-13
5884968-0	1965	[A study of the effect of endoxan on the serum cholinesterase activity in gynecologic carcinomas].	Cyclophosphamide	26-33	butyrylcholinesterase	Homo sapiens	47-61
33737012-0	2021	Selective blockade of transient receptor potential vanilloid 4 reduces cyclophosphamide-induced bladder pain in mice.	Cyclophosphamide	71-87	transient receptor potential cation channel, subfamily V, member 4	Mus musculus	22-62
33716060-0	2021	Ligustrazine alleviates cyclophosphamide-induced hepatotoxicity via the inhibition of Txnip/Trx/NF-kappaB pathway.	Cyclophosphamide	24-40	thioredoxin interacting protein	Mus musculus	86-91
33716060-0	2021	Ligustrazine alleviates cyclophosphamide-induced hepatotoxicity via the inhibition of Txnip/Trx/NF-kappaB pathway.	Cyclophosphamide	24-40	thioredoxin 1	Mus musculus	92-95
33716060-0	2021	Ligustrazine alleviates cyclophosphamide-induced hepatotoxicity via the inhibition of Txnip/Trx/NF-kappaB pathway.	Cyclophosphamide	24-40	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	96-105
34047951-9	2021	Additionally, MCF-7/Wnt5a (+) cells displayed reduced sensitivity to the metabolic substrates of CYP, tamoxifen (P < 0.001), paclitaxel (P < 0.001), and cyclophosphamide (P < 0.001).	Cyclophosphamide	153-169	Wnt family member 5A	Homo sapiens	20-25
34047951-11	2021	CONCLUSIONS: In ER-positive breast cancer, Wnt5a upregulates the CYP metabolic pathway and suppresses tamoxifen, paclitaxel, and cyclophosphamide resistance, all of the three, standard treatment methods for ER-positive breast cancer.	Cyclophosphamide	129-145	estrogen receptor 1	Homo sapiens	16-18
34047951-11	2021	CONCLUSIONS: In ER-positive breast cancer, Wnt5a upregulates the CYP metabolic pathway and suppresses tamoxifen, paclitaxel, and cyclophosphamide resistance, all of the three, standard treatment methods for ER-positive breast cancer.	Cyclophosphamide	129-145	Wnt family member 5A	Homo sapiens	43-48
34057116-0	2021	Increased aldehyde dehydrogenase 1 (ALDH1) levels are associated with chemo-responsiveness in breast cancer patients treated with taxane-adriamycin-cyclophosphamide regimen.	Cyclophosphamide	148-164	aldehyde dehydrogenase 1 family member A1	Homo sapiens	10-34
34057116-0	2021	Increased aldehyde dehydrogenase 1 (ALDH1) levels are associated with chemo-responsiveness in breast cancer patients treated with taxane-adriamycin-cyclophosphamide regimen.	Cyclophosphamide	148-164	aldehyde dehydrogenase 1 family member A1	Homo sapiens	36-41
34057116-3	2021	OBJECTIVE: This study aimed to investigate the correlation between plasma levels of ALDH1 and chemotherapy responses to the taxane-adriamycin-cyclophosphamide (TAC) regimen in breast cancer patients.	Cyclophosphamide	142-158	aldehyde dehydrogenase 1 family member A1	Homo sapiens	84-89
34044030-2	2021	In this study, RAP"s effects to enhance the recovery of cyclophosphamide (Cy)-suppressed bone marrow and blood cells is confirmed in vivo first.	Cyclophosphamide	56-72	LDL receptor related protein associated protein 1	Homo sapiens	15-18
34044030-2	2021	In this study, RAP"s effects to enhance the recovery of cyclophosphamide (Cy)-suppressed bone marrow and blood cells is confirmed in vivo first.	Cyclophosphamide	74-76	LDL receptor related protein associated protein 1	Homo sapiens	15-18
33872945-1	2021	Human hepatic cytochrome P450 2B6 (CYP2B6) expressed is responsible for the metabolism of many drugs, such as cyclophosphamide, ifosfamid, and efavirenz.	Cyclophosphamide	110-126	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	14-33
33872945-1	2021	Human hepatic cytochrome P450 2B6 (CYP2B6) expressed is responsible for the metabolism of many drugs, such as cyclophosphamide, ifosfamid, and efavirenz.	Cyclophosphamide	110-126	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	35-41
33615710-8	2021	Cells with aberrations in CRLF2 were more resistant to cyclophosphamide and drugs commonly used during treatment than cells in the vector group.	Cyclophosphamide	55-71	cytokine receptor like factor 2	Homo sapiens	26-31
33216292-0	2021	Sesamol Alleviates the Cytotoxic Effect of Cyclophosphamide on Normal Human Lung WI-38 Cells via Suppressing RAGE/NF-kappaB/Autophagy Signaling.	Cyclophosphamide	43-59	advanced glycosylation end-product specific receptor	Homo sapiens	109-113
33216292-0	2021	Sesamol Alleviates the Cytotoxic Effect of Cyclophosphamide on Normal Human Lung WI-38 Cells via Suppressing RAGE/NF-kappaB/Autophagy Signaling.	Cyclophosphamide	43-59	nuclear factor kappa B subunit 1	Homo sapiens	114-123
33216292-11	2021	Thus, we concluded that SES offered a protective role against CYL-induced lung injury via suppressing oxidative stress and RAGE/NF-kappaB/Autophagy signaling, which is a natural safe therapeutic option against CYL toxicities.	Cyclophosphamide	62-65	advanced glycosylation end-product specific receptor	Homo sapiens	123-127
33216292-11	2021	Thus, we concluded that SES offered a protective role against CYL-induced lung injury via suppressing oxidative stress and RAGE/NF-kappaB/Autophagy signaling, which is a natural safe therapeutic option against CYL toxicities.	Cyclophosphamide	62-65	nuclear factor kappa B subunit 1	Homo sapiens	128-137
34053364-1	2021	Systemic lupus erythematosus (SLE) often affects females of reproductive age and Cyclophosphamide, an alkylating agent leading to premature ovarian insufficiency (POF) and labelled category D for pregnancy is used as induction therapy for severe manifestations of lupus.	Cyclophosphamide	81-97	POF1B actin binding protein	Homo sapiens	163-166
34053364-7	2021	The average cumulative dose of cyclophosphamide in the patients who had successful pregnancy was 4080.37 mg compared to 2806.25 mg in those who had a miscarriage (p 0.164) and 5526.47 mg in those who developed POF (p 0.046).	Cyclophosphamide	31-47	POF1B actin binding protein	Homo sapiens	210-213
34039551-9	2021	Our case highlights the importance of starting combined corticosteroids and cyclophosphamide early in crescentic IgAN and that corticosteroid monotherapy is insufficient in controlling disease progression.	Cyclophosphamide	76-92	IGAN1	Homo sapiens	113-117
33582440-0	2021	Spectroscopic studies of simultaneous binding of cyclophosphamide and imatinib mesylate to human holo-transferrin.	Cyclophosphamide	49-65	transferrin	Homo sapiens	102-113
33989716-1	2021	The aim of the present study is to assess whether low level laser therapy (LLLT) can protect ovaries from chemotherapy-induced gonadotoxicity using a mice model of premature ovarian failure induced by cyclophosphamide (CTX).	Cyclophosphamide	201-217	V-set and immunoglobulin domain containing 2	Mus musculus	219-222
33969557-0	2021	Acetovanillone prevents cyclophosphamide-induced acute lung injury by modulating PI3K/Akt/mTOR and Nrf2 signaling in rats.	Cyclophosphamide	24-40	AKT serine/threonine kinase 1	Rattus norvegicus	86-89
33969557-0	2021	Acetovanillone prevents cyclophosphamide-induced acute lung injury by modulating PI3K/Akt/mTOR and Nrf2 signaling in rats.	Cyclophosphamide	24-40	mechanistic target of rapamycin kinase	Rattus norvegicus	90-94
33969557-0	2021	Acetovanillone prevents cyclophosphamide-induced acute lung injury by modulating PI3K/Akt/mTOR and Nrf2 signaling in rats.	Cyclophosphamide	24-40	NFE2 like bZIP transcription factor 2	Rattus norvegicus	99-103
33992719-9	2021	Pretreatment with naringin significantly (p < 0.05) abolish CYCP-induced changes in the activities of serum and hepatic ALT, AST, GGT, ALP, and LDH.	Cyclophosphamide	60-64	gamma-glutamyltransferase 1	Rattus norvegicus	130-133
33992719-9	2021	Pretreatment with naringin significantly (p < 0.05) abolish CYCP-induced changes in the activities of serum and hepatic ALT, AST, GGT, ALP, and LDH.	Cyclophosphamide	60-64	PDZ and LIM domain 3	Rattus norvegicus	135-138
33966140-8	2021	BRCA2 high expression significantly correlated with response to olaparib, a PARP inhibitor, and inversely with cyclophosphamide in ER-positive/HER2-negative tumors, but not in TNBC.	Cyclophosphamide	111-127	BRCA2 DNA repair associated	Homo sapiens	0-5
33966140-8	2021	BRCA2 high expression significantly correlated with response to olaparib, a PARP inhibitor, and inversely with cyclophosphamide in ER-positive/HER2-negative tumors, but not in TNBC.	Cyclophosphamide	111-127	erb-b2 receptor tyrosine kinase 2	Homo sapiens	143-147
33582440-5	2021	In this study the effect of cyclophosphamide on the interaction of imatinib mesylate with human holo-transferrin has been investigated.	Cyclophosphamide	28-44	transferrin	Homo sapiens	101-112
33545713-0	2021	A combination of cyclophosphamide, interleukin-2 allow CD4+ T cells converted to Tregs to control scurfy syndrome.	Cyclophosphamide	17-33	CD4 molecule	Homo sapiens	55-58
30889984-5	2021	HSN significantly reduced the CPE-induced increments of serum creatinine and cystatin C.	Cyclophosphamide	30-33	cystatin C	Mus musculus	77-87
34025161-0	2021	Lucrative antioxidant effect of metformin against cyclophosphamide induced nephrotoxicity.	Cyclophosphamide	50-66	MET proto-oncogene, receptor tyrosine kinase	Rattus norvegicus	32-41
34025161-2	2021	This work was applied to study the lucrative antioxidant influence of metformin as co-therapy on the nephrotoxicity induced by cyclophosphamide in the treatment of different cancer diseases.	Cyclophosphamide	127-143	MET proto-oncogene, receptor tyrosine kinase	Rattus norvegicus	70-79
33580280-2	2021	A calcineurin inhibitor is initiated after cyclophosphamide administration in the commonly used PT/CY regimens.	Cyclophosphamide	43-59	calcineurin binding protein 1	Homo sapiens	2-23
33447883-7	2021	SAA mouse model was induced with cyclophosphamide and busulfan, and intravenous injection of LV inhibitor NC and LV-miR-150-5p inhibitor.	Cyclophosphamide	33-49	serum amyloid A1 cluster	Homo sapiens	0-3
33980589-14	2021	Notably, cyclophosphamide elevated serum Flt3L levels and, in combination with the absence of DNGR-1, synergized against tumor growth.	Cyclophosphamide	9-25	fms related receptor tyrosine kinase 3 ligand	Homo sapiens	41-46
33900636-0	2021	Cyclophosphamide suppresses spermatogenesis in the testis of mice through downregulation of miR-34b and miR-34c.	Cyclophosphamide	0-16	microRNA 34b	Mus musculus	92-99
33905145-0	2021	Protection by ginseng saponins against cyclophosphamide-induced liver injuries in rats by induction of cytochrome P450 expression and mediation of the l-arginine/nitric oxide pathway based on metabolomics.	Cyclophosphamide	39-55	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	103-118
33911199-7	2021	G-CSF + CY mobilisation generated higher median CD34 + yields (8.6 vs. 5.5 x 106/kg, p < 0.001).	Cyclophosphamide	8-10	CD34 molecule	Homo sapiens	48-52
33900636-0	2021	Cyclophosphamide suppresses spermatogenesis in the testis of mice through downregulation of miR-34b and miR-34c.	Cyclophosphamide	0-16	microRNA 34c	Mus musculus	104-111
33385344-0	2021	Loss of fibroblast growth factor receptor 2 (FGFR2) leads to defective bladder urothelial regeneration after Cyclophosphamide injury.	Cyclophosphamide	109-125	fibroblast growth factor receptor 2	Mus musculus	8-43
33864816-9	2021	Montelukast preconditioning offset the up-regulation of transient receptor potential vanilloid 4 (TRPV4) in urothelial tissue of CPA-treated rats, to greater extent than MESNA.	Cyclophosphamide	129-132	transient receptor potential cation channel, subfamily V, member 4	Rattus norvegicus	56-96
33864816-9	2021	Montelukast preconditioning offset the up-regulation of transient receptor potential vanilloid 4 (TRPV4) in urothelial tissue of CPA-treated rats, to greater extent than MESNA.	Cyclophosphamide	129-132	transient receptor potential cation channel, subfamily V, member 4	Rattus norvegicus	98-103
33880064-2	2021	In this study, we aimed to evaluate the efficacy of polyethylene glycol recombinant granulocyte colony-stimulating factor (PEG-rhG-CSF) compared with short-acting rhG-CSF in the dose-adjusted etoposide, prednisone, vincristine, cyclophosphamide, and doxorubicin (DA-EPOCH) regimen.	Cyclophosphamide	228-244	colony stimulating factor 3	Homo sapiens	84-121
33992954-0	2021	Plausible drug interaction between cyclophosphamide and voriconazole via inhibition of CYP2B6.	Cyclophosphamide	35-51	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	87-93
33992954-5	2021	Surveys of adverse event reporting databases in Japan (JADER) and the U.S. (FAERS) showed that the proportional reporting ratios of neutropenia, hemorrhagic cystitis, and alopecia for cyclophosphamide, which is principally activated by CYP2B6 in humans, were mostly reduced, or tended to be reduced when azoles, including voriconazole, were prescribed in combination.	Cyclophosphamide	184-200	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	236-242
33840704-8	2021	RESULTS: CY/ZA significantly increased the relative expression levels of IL-6 and decreased those of IL-10 and IGF-1 when compared with those in VC.	Cyclophosphamide	9-11	interleukin 6	Mus musculus	73-77
33840704-8	2021	RESULTS: CY/ZA significantly increased the relative expression levels of IL-6 and decreased those of IL-10 and IGF-1 when compared with those in VC.	Cyclophosphamide	9-11	interleukin 10	Mus musculus	101-106
33840704-8	2021	RESULTS: CY/ZA significantly increased the relative expression levels of IL-6 and decreased those of IL-10 and IGF-1 when compared with those in VC.	Cyclophosphamide	9-11	insulin-like growth factor 1	Mus musculus	111-116
33840704-9	2021	Moreover, CY/ZA significantly reduced the relative expression levels of CCR-7, cxcl12, cxcr4, and CD105 when compared with those in VC, whereas the level of F4/80 was significantly increased by CY/ZA.	Cyclophosphamide	10-12	chemokine (C-C motif) receptor 7	Mus musculus	72-77
33840704-9	2021	Moreover, CY/ZA significantly reduced the relative expression levels of CCR-7, cxcl12, cxcr4, and CD105 when compared with those in VC, whereas the level of F4/80 was significantly increased by CY/ZA.	Cyclophosphamide	10-12	chemokine (C-X-C motif) ligand 12	Mus musculus	79-85
33840704-9	2021	Moreover, CY/ZA significantly reduced the relative expression levels of CCR-7, cxcl12, cxcr4, and CD105 when compared with those in VC, whereas the level of F4/80 was significantly increased by CY/ZA.	Cyclophosphamide	10-12	chemokine (C-X-C motif) receptor 4	Mus musculus	87-92
33840704-9	2021	Moreover, CY/ZA significantly reduced the relative expression levels of CCR-7, cxcl12, cxcr4, and CD105 when compared with those in VC, whereas the level of F4/80 was significantly increased by CY/ZA.	Cyclophosphamide	10-12	endoglin	Mus musculus	98-103
33840704-9	2021	Moreover, CY/ZA significantly reduced the relative expression levels of CCR-7, cxcl12, cxcr4, and CD105 when compared with those in VC, whereas the level of F4/80 was significantly increased by CY/ZA.	Cyclophosphamide	194-196	adhesion G protein-coupled receptor E1	Mus musculus	157-162
33840704-10	2021	Furthermore, CY/ZA significantly decreased the relative expression levels of VEGFA, VEGFB, and VEGFC at 72 h postextraction compared with those in VC.	Cyclophosphamide	13-15	vascular endothelial growth factor A	Mus musculus	77-82
33840704-10	2021	Furthermore, CY/ZA significantly decreased the relative expression levels of VEGFA, VEGFB, and VEGFC at 72 h postextraction compared with those in VC.	Cyclophosphamide	13-15	vascular endothelial growth factor B	Mus musculus	84-89
33840704-10	2021	Furthermore, CY/ZA significantly decreased the relative expression levels of VEGFA, VEGFB, and VEGFC at 72 h postextraction compared with those in VC.	Cyclophosphamide	13-15	vascular endothelial growth factor C	Mus musculus	95-100
33897897-5	2021	Meanwhile, chemical immunomodulatory drug cyclophosphamide (CP) was also encapsulated in the vesicle (CD64-NVs-aPD-L1-CP), to simultaneously restrain the regulatory T cells (Tregs) and invigorate Ki67+CD8+ T cells, then further enhance their anti-tumor ability.	Cyclophosphamide	42-58	Fc gamma receptor Ia	Homo sapiens	102-106
33897897-5	2021	Meanwhile, chemical immunomodulatory drug cyclophosphamide (CP) was also encapsulated in the vesicle (CD64-NVs-aPD-L1-CP), to simultaneously restrain the regulatory T cells (Tregs) and invigorate Ki67+CD8+ T cells, then further enhance their anti-tumor ability.	Cyclophosphamide	42-58	CD8a molecule	Homo sapiens	201-204
33916864-6	2021	Rapidly progressive DM/CADM-ILD with the anti-MDA5 antibody is the most intractable condition, which requires immediate combined immunosuppressive therapy with GCs, CNIs, and intravenous cyclophosphamide.	Cyclophosphamide	187-203	interferon induced with helicase C domain 1	Homo sapiens	46-50
33385344-5	2021	Three days after Cyclophosphamide, Fgfr2KO urothelium had defective regeneration, fewer cells, larger Basal cell bodies and nuclei, paradoxical increases in proliferation markers and excessive replication stress versus controls.	Cyclophosphamide	17-33	fibroblast growth factor receptor 2	Mus musculus	35-42
33385344-7	2021	Mice with conditional deletion of Fgfr2 in urothelium enriched for KRT14+ cells reproduced Fgfr2KO abnormalities after Cyclophosphamide.	Cyclophosphamide	119-135	fibroblast growth factor receptor 2	Mus musculus	34-39
33385344-7	2021	Mice with conditional deletion of Fgfr2 in urothelium enriched for KRT14+ cells reproduced Fgfr2KO abnormalities after Cyclophosphamide.	Cyclophosphamide	119-135	keratin 14	Mus musculus	67-72
33385344-9	2021	Mice missing one allele of Fgfr2 also had (less severe) regeneration defects and Basal cell endoreplication three days after Cyclophosphamide versus controls.	Cyclophosphamide	125-141	fibroblast growth factor receptor 2	Mus musculus	27-32
33385344-10	2021	Thus, reduced FGFR2/ERK signaling apparently leads to abnormal urothelial repair after Cyclophosphamide from pathological Basal cell endoreplication.	Cyclophosphamide	87-103	fibroblast growth factor receptor 2	Mus musculus	14-19
33385344-10	2021	Thus, reduced FGFR2/ERK signaling apparently leads to abnormal urothelial repair after Cyclophosphamide from pathological Basal cell endoreplication.	Cyclophosphamide	87-103	mitogen-activated protein kinase 1	Mus musculus	20-23
33583301-7	2021	In addition, puerarin enhanced the immunologic activity of cyclophosphamide-induced immunosuppression mice by increasing the secretion of NO, IFN-gamma, and IL-4, the serum half hemolysis value (HC50), the spleen and thymus index, and proliferation for splenic lymphocytes.	Cyclophosphamide	59-75	interferon gamma	Mus musculus	142-151
33583301-7	2021	In addition, puerarin enhanced the immunologic activity of cyclophosphamide-induced immunosuppression mice by increasing the secretion of NO, IFN-gamma, and IL-4, the serum half hemolysis value (HC50), the spleen and thymus index, and proliferation for splenic lymphocytes.	Cyclophosphamide	59-75	interleukin 4	Mus musculus	157-161
33892727-0	2021	Quercetin prevents primordial follicle loss via suppression of PI3K/Akt/Foxo3a pathway activation in cyclophosphamide-treated mice.	Cyclophosphamide	101-117	thymoma viral proto-oncogene 1	Mus musculus	68-71
33892727-0	2021	Quercetin prevents primordial follicle loss via suppression of PI3K/Akt/Foxo3a pathway activation in cyclophosphamide-treated mice.	Cyclophosphamide	101-117	forkhead box O3	Mus musculus	72-78
33892727-11	2021	Analysis of the PI3K/Akt/Foxo3a pathway showed that quercetin decreased the phosphorylation of proteins that stimulate follicle activation in cyclophosphamide-induced ovaries.	Cyclophosphamide	142-158	thymoma viral proto-oncogene 1	Mus musculus	21-24
33892727-11	2021	Analysis of the PI3K/Akt/Foxo3a pathway showed that quercetin decreased the phosphorylation of proteins that stimulate follicle activation in cyclophosphamide-induced ovaries.	Cyclophosphamide	142-158	forkhead box O3	Mus musculus	25-31
33892727-12	2021	Furthermore, quercetin prevented cyclophosphamide-induced apoptosis in early growing follicles and early antral follicles, maintained anti-Mullerian hormone levels secreted by these follicles, and preserved the quiescence of the primordial follicle pool, as determined by intranuclear Foxo3a staining.	Cyclophosphamide	33-49	forkhead box O3	Mus musculus	285-291
33892727-13	2021	CONCLUSIONS: Quercetin attenuates cyclophosphamide-induced follicle loss by preventing the phosphorylation of PI3K/Akt/Foxo3a pathway members and maintaining the anti-Mullerian hormone level through reduced apoptosis in growing follicles.	Cyclophosphamide	34-50	thymoma viral proto-oncogene 1	Mus musculus	115-118
33892727-13	2021	CONCLUSIONS: Quercetin attenuates cyclophosphamide-induced follicle loss by preventing the phosphorylation of PI3K/Akt/Foxo3a pathway members and maintaining the anti-Mullerian hormone level through reduced apoptosis in growing follicles.	Cyclophosphamide	34-50	forkhead box O3	Mus musculus	119-125
33864237-4	2021	THP-COP (pirarubicin, cyclophosphamide, vincristine, and prednisone) is sometimes used for elderly patients with non-Hodgkin"s lymphoma in Japan.	Cyclophosphamide	22-38	caspase recruitment domain family member 16	Homo sapiens	4-7
33927422-11	2021	Therefore, in accordance with international guidelines, we will add a neurokinin-1 antagonist to the antiemetic regimens for patients receiving carboplatin-based chemotherapy AUC>=4, and olanzapine for those receiving combination anthracycline/cyclophosphamide chemotherapy, in an attempt to improve the rates of CINV in these groups.	Cyclophosphamide	244-260	tachykinin precursor 1	Homo sapiens	70-82
33846825-11	2021	Chemotherapy protocols using MTX-HD, MTX-HD associated with doxorubicin and cyclophosphamide, and MTX-HD and cyclophosphamide a have higher incidence of severe grades of OM.	Cyclophosphamide	76-92	metaxin 1	Homo sapiens	37-40
33846825-11	2021	Chemotherapy protocols using MTX-HD, MTX-HD associated with doxorubicin and cyclophosphamide, and MTX-HD and cyclophosphamide a have higher incidence of severe grades of OM.	Cyclophosphamide	76-92	metaxin 1	Homo sapiens	37-40
33576458-6	2021	The results demonstrated that 2-week CY treatment attenuated the neurological deficit score, brain water content and infarct area, and increased MAP-2 immunoreactivity in the cortex in MCAO model rats.	Cyclophosphamide	37-39	microtubule-associated protein 2	Rattus norvegicus	145-150
33576458-7	2021	CY administration also deactivated the cortex NF-kappaB/NLR family pyrin domain containing 3 inflammasome signaling pathway, and decreased serum TNF-alpha, IL-1beta and IL-6 concentrations.	Cyclophosphamide	0-2	NLR family, pyrin domain containing 3	Rattus norvegicus	56-92
33576458-7	2021	CY administration also deactivated the cortex NF-kappaB/NLR family pyrin domain containing 3 inflammasome signaling pathway, and decreased serum TNF-alpha, IL-1beta and IL-6 concentrations.	Cyclophosphamide	0-2	tumor necrosis factor	Rattus norvegicus	145-154
33576458-7	2021	CY administration also deactivated the cortex NF-kappaB/NLR family pyrin domain containing 3 inflammasome signaling pathway, and decreased serum TNF-alpha, IL-1beta and IL-6 concentrations.	Cyclophosphamide	0-2	interleukin 1 alpha	Rattus norvegicus	156-164
33385344-0	2021	Loss of fibroblast growth factor receptor 2 (FGFR2) leads to defective bladder urothelial regeneration after Cyclophosphamide injury.	Cyclophosphamide	109-125	fibroblast growth factor receptor 2	Mus musculus	45-50
33576458-7	2021	CY administration also deactivated the cortex NF-kappaB/NLR family pyrin domain containing 3 inflammasome signaling pathway, and decreased serum TNF-alpha, IL-1beta and IL-6 concentrations.	Cyclophosphamide	0-2	interleukin 6	Rattus norvegicus	169-173
33385344-3	2021	We assessed actions of fibroblast growth factor receptor 2 (FGFR2) in urothelium after Cyclophosphamide.	Cyclophosphamide	87-103	fibroblast growth factor receptor 2	Mus musculus	23-58
33576458-8	2021	Moreover, CY treatment inhibited Fe2+ and reactive oxygen species accumulation, and reversed acyl-CoA synthetase long-chain family member 4, transferrin receptor 1, glutathione peroxidase 4 and ferritin heavy chain 1 protein expression levels in the brain.	Cyclophosphamide	10-12	acyl-CoA synthetase long-chain family member 4	Rattus norvegicus	93-139
33385344-3	2021	We assessed actions of fibroblast growth factor receptor 2 (FGFR2) in urothelium after Cyclophosphamide.	Cyclophosphamide	87-103	fibroblast growth factor receptor 2	Mus musculus	60-65
33576458-8	2021	Moreover, CY treatment inhibited Fe2+ and reactive oxygen species accumulation, and reversed acyl-CoA synthetase long-chain family member 4, transferrin receptor 1, glutathione peroxidase 4 and ferritin heavy chain 1 protein expression levels in the brain.	Cyclophosphamide	10-12	glutathione peroxidase 4	Rattus norvegicus	165-189
32496149-3	2021	One hundred fifteen premenopausal women with newly diagnosed breast cancer were genotyped for single nucleotide polymorphisms (SNPs) in genes involved in cyclophosphamide activation (CYP3A4 and CYP2C19) and detoxification (GSTP1 and GSTA1).	Cyclophosphamide	154-170	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	183-189
33576458-8	2021	Moreover, CY treatment inhibited Fe2+ and reactive oxygen species accumulation, and reversed acyl-CoA synthetase long-chain family member 4, transferrin receptor 1, glutathione peroxidase 4 and ferritin heavy chain 1 protein expression levels in the brain.	Cyclophosphamide	10-12	ferritin heavy chain 1	Rattus norvegicus	194-216
32496149-9	2021	In younger breast cancer survivors undergoing cyclophosphamide-based chemotherapy, genetic variation in CYP2C19 and GSTA1 merits further study to determine its relationship with CROF.IMPACT STATEMENTWhat is already known on this subject?	Cyclophosphamide	46-62	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	104-111
32496149-9	2021	In younger breast cancer survivors undergoing cyclophosphamide-based chemotherapy, genetic variation in CYP2C19 and GSTA1 merits further study to determine its relationship with CROF.IMPACT STATEMENTWhat is already known on this subject?	Cyclophosphamide	46-62	glutathione S-transferase alpha 1	Homo sapiens	116-121
32496149-13	2021	Studies have shown genetic variation in p450 enzymes is associated with differential clinical outcomes after cyclophosphamide treatment: breast cancer patients homozygous for GSTA1 minor allele had improved overall survival; lupus patients homozygous for CYP2C19 minor allele had increased risk for CROF; and CYP3A4*1B I was associated with decreased risk for CROF.What do the results of this study add?	Cyclophosphamide	109-125	glutathione S-transferase alpha 1	Homo sapiens	175-180
32496149-13	2021	Studies have shown genetic variation in p450 enzymes is associated with differential clinical outcomes after cyclophosphamide treatment: breast cancer patients homozygous for GSTA1 minor allele had improved overall survival; lupus patients homozygous for CYP2C19 minor allele had increased risk for CROF; and CYP3A4*1B I was associated with decreased risk for CROF.What do the results of this study add?	Cyclophosphamide	109-125	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	255-262
32496149-13	2021	Studies have shown genetic variation in p450 enzymes is associated with differential clinical outcomes after cyclophosphamide treatment: breast cancer patients homozygous for GSTA1 minor allele had improved overall survival; lupus patients homozygous for CYP2C19 minor allele had increased risk for CROF; and CYP3A4*1B I was associated with decreased risk for CROF.What do the results of this study add?	Cyclophosphamide	109-125	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	309-315
33166580-7	2021	Anti-PLA2R titers showed a significant decrease in both groups but the proportion of anti-PLA2R-positive patients who achieved immunological response (depletion of anti-PLA2R antibodies) was significantly higher at three and six months in the corticosteroid-cyclophosphamide group (77% and 92%, respectively), as compared to the tacrolimus-rituximab group (45% and 70%, respectively).	Cyclophosphamide	258-274	phospholipase A2 receptor 1	Homo sapiens	90-95
33166580-7	2021	Anti-PLA2R titers showed a significant decrease in both groups but the proportion of anti-PLA2R-positive patients who achieved immunological response (depletion of anti-PLA2R antibodies) was significantly higher at three and six months in the corticosteroid-cyclophosphamide group (77% and 92%, respectively), as compared to the tacrolimus-rituximab group (45% and 70%, respectively).	Cyclophosphamide	258-274	phospholipase A2 receptor 1	Homo sapiens	90-95
33205491-3	2021	The immunomodulatory properties of RBP were investigated using human monocyte-derived dendritic cells (moDC) in vitro, and cyclophosphamide (CTX)-induced immunosuppressive mouse model.	Cyclophosphamide	123-139	retinol binding protein 4	Homo sapiens	35-38
33725933-0	2021	Evaluating the role of GSTP1 genetic polymorphism (rs1695, 313A>G) as a predictor in cyclophosphamide-induced toxicities.	Cyclophosphamide	85-101	glutathione S-transferase pi 1	Homo sapiens	23-28
33725933-1	2021	ABSTRACT: The association between Glutathione S-transferase Pi 1(GSTP1) genetic polymorphism (rs1695, 313A>G) and cyclophosphamide-induced toxicities has been widely investigated in previous studies, however, the results were inconsistent.	Cyclophosphamide	114-130	glutathione S-transferase pi 1	Homo sapiens	34-64
33725933-1	2021	ABSTRACT: The association between Glutathione S-transferase Pi 1(GSTP1) genetic polymorphism (rs1695, 313A>G) and cyclophosphamide-induced toxicities has been widely investigated in previous studies, however, the results were inconsistent.	Cyclophosphamide	114-130	glutathione S-transferase pi 1	Homo sapiens	65-70
33725933-3	2021	Risk ratios (RRs) and 95% confidence intervals (95% CIs) were used to estimate the association between GSTP1 rs1695 polymorphism and cyclophosphamide-induced hemotoxicity, gastrointestinal toxicity, infection, and neurotoxicity.A total of 13 studies were eventually included.	Cyclophosphamide	133-149	glutathione S-transferase pi 1	Homo sapiens	103-108
33725933-4	2021	Compared with the GSTP1 rs1695 AA genotype carriers, patients with AG and GG genotypes had an increased risk of cyclophosphamide-induced gastrointestinal toxicity (RR, 1.61; 95% CI, 1.18-2.19; P = .003) and infection (RR, 1.57; 95% CI, 1.00-2.48; P = .05) in the overall population.	Cyclophosphamide	112-128	glutathione S-transferase pi 1	Homo sapiens	18-23
33725933-5	2021	In the subgroup analyses, there were significant associations between GSTP1 rs1695 polymorphism and the risk of cyclophosphamide-induced myelosuppression (RR, 2.10; 95% CI, 1.60-2.76; P < .00001), gastrointestinal toxicity (RR, 1.77; 95%CI, 1.25-2.53; P = .001), and infection (RR, 2.01; 95% CI, 1.14-3.54; P = .02) in systemic lupus erythematosus (SLE) or lupus nephritis syndrome patients, but not in cancer patients.Our results confirmed an essential role for the GSTP1 rs1695 polymorphism in the prediction of cyclophosphamide-induced myelosuppression, gastrointestinal toxicity, and infection in SLE or lupus nephritis syndrome patients.	Cyclophosphamide	112-128	glutathione S-transferase pi 1	Homo sapiens	70-75
33725933-5	2021	In the subgroup analyses, there were significant associations between GSTP1 rs1695 polymorphism and the risk of cyclophosphamide-induced myelosuppression (RR, 2.10; 95% CI, 1.60-2.76; P < .00001), gastrointestinal toxicity (RR, 1.77; 95%CI, 1.25-2.53; P = .001), and infection (RR, 2.01; 95% CI, 1.14-3.54; P = .02) in systemic lupus erythematosus (SLE) or lupus nephritis syndrome patients, but not in cancer patients.Our results confirmed an essential role for the GSTP1 rs1695 polymorphism in the prediction of cyclophosphamide-induced myelosuppression, gastrointestinal toxicity, and infection in SLE or lupus nephritis syndrome patients.	Cyclophosphamide	112-128	glutathione S-transferase pi 1	Homo sapiens	467-472
33734921-1	2021	BACKGROUND: Treatment with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is standard of care first line treatment for diffuse large B-cell lymphoma (DLBCL), though outcomes remain suboptimal.	Cyclophosphamide	38-54	DNA damage inducible transcript 3	Homo sapiens	100-104
33796409-6	2021	With the addition of one-day prior cyclophosphamide (CY) lymphodepletion, anti-CEA CAR T cell treatment delayed the median survival of MC38/CEA and E0771/CEA tumor-bearing CEATg mice by ten and 3 days, respectively.	Cyclophosphamide	35-51	carcinoembryonic antigen gene family	Mus musculus	79-82
33796409-6	2021	With the addition of one-day prior cyclophosphamide (CY) lymphodepletion, anti-CEA CAR T cell treatment delayed the median survival of MC38/CEA and E0771/CEA tumor-bearing CEATg mice by ten and 3 days, respectively.	Cyclophosphamide	35-51	nuclear receptor subfamily 1, group I, member 3	Mus musculus	83-86
33796409-6	2021	With the addition of one-day prior cyclophosphamide (CY) lymphodepletion, anti-CEA CAR T cell treatment delayed the median survival of MC38/CEA and E0771/CEA tumor-bearing CEATg mice by ten and 3 days, respectively.	Cyclophosphamide	53-55	carcinoembryonic antigen gene family	Mus musculus	79-82
33796409-6	2021	With the addition of one-day prior cyclophosphamide (CY) lymphodepletion, anti-CEA CAR T cell treatment delayed the median survival of MC38/CEA and E0771/CEA tumor-bearing CEATg mice by ten and 3 days, respectively.	Cyclophosphamide	53-55	nuclear receptor subfamily 1, group I, member 3	Mus musculus	83-86
33796409-6	2021	With the addition of one-day prior cyclophosphamide (CY) lymphodepletion, anti-CEA CAR T cell treatment delayed the median survival of MC38/CEA and E0771/CEA tumor-bearing CEATg mice by ten and 3 days, respectively.	Cyclophosphamide	53-55	carcinoembryonic antigen gene family	Mus musculus	140-143
33658647-0	2021	Impact of infused CD34+ stem cell dosing for allogeneic peripheral blood stem cell transplantation with post-transplant cyclophosphamide.	Cyclophosphamide	120-136	CD34 molecule	Homo sapiens	18-22
33845140-5	2021	Cancer patients with high RGS18 expression were more sensitive to cyclophosphamide and nelarabine, whereas those with high RGS19 expression were more sensitive to cladribine and nelarabine.	Cyclophosphamide	66-82	regulator of G protein signaling 18	Homo sapiens	26-31
33688781-1	2021	Peripheral T-cell lymphoma (PTCL) is a group of aggressive lymphomas commonly treated with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP).	Cyclophosphamide	91-107	DNA damage inducible transcript 3	Homo sapiens	151-155
33534414-0	2021	Exceptional response to cyclophosphamide and dexamethasone in a patient with metastatic castrate-resistant prostate cancer and RB1 mutation.	Cyclophosphamide	24-40	RB transcriptional corepressor 1	Homo sapiens	127-130
33534414-4	2021	Here, we report on a patient with recurrent, metastatic castrate-resistant prostate cancer and identified RB1 mutation with progressive symptomatology, who was treated with cyclophosphamide and dexamethasone after other standard treatment regimens failed.	Cyclophosphamide	173-189	RB transcriptional corepressor 1	Homo sapiens	106-109
32779754-4	2021	Results obtained revealed that CYP-administered rats significantly (p < .05) had elevated activities of ChE, ecto-5"-nucleotidase and thiobarbituric acid reactive species (TBARS), and concomitantly decreased in the antioxidant indices.	Cyclophosphamide	31-34	5' nucleotidase, ecto	Rattus norvegicus	109-129
33483276-1	2021	BACKGROUND: The R-CHOP regimen (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone) is the standard therapy for patients with diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	43-59	DNA damage inducible transcript 3	Homo sapiens	18-22
33389495-0	2021	Effect of the drug cyclophosphamide on the activity of porcine kidney betaine aldehyde dehydrogenase.	Cyclophosphamide	19-35	aldehyde dehydrogenase 7 family member A1	Homo sapiens	70-100
33389495-4	2021	The antineoplastic and immuno-suppressant pre-drug cyclophosphamide (CTX), and its bioactivation products, have two highly oxidating chlorine atoms.	Cyclophosphamide	51-67	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	69-72
33599403-2	2021	Drugs metabolized mainly by CYP2B6 include artemisinin, bupropion, cyclophosphamide, efavirenz, ketamine, and methadone.	Cyclophosphamide	67-83	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	28-34
33647456-4	2021	We demonstrated that cyclophosphamide (Cy) pre-conditioning significantly modified the immunosuppressive TME and was required to uncover the efficacy of PSCA-CAR T cells in metastatic prostate and pancreas cancer models, with no observed toxicities in normal tissues with endogenous expression of PSCA.	Cyclophosphamide	21-37	prostate stem cell antigen	Mus musculus	153-157
33647456-4	2021	We demonstrated that cyclophosphamide (Cy) pre-conditioning significantly modified the immunosuppressive TME and was required to uncover the efficacy of PSCA-CAR T cells in metastatic prostate and pancreas cancer models, with no observed toxicities in normal tissues with endogenous expression of PSCA.	Cyclophosphamide	39-41	prostate stem cell antigen	Mus musculus	153-157
33663060-12	2021	The effect of Cyclophosphamide (CTX) +CS on crescent IgAN was better than that of other risk factors.	Cyclophosphamide	14-30	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	32-35
33625586-1	2021	BACKGROUND: A combination of rituximab with cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is the standard first-line therapy for diffuse large B cell lymphoma (DLBCL), the most common aggressive lymphoma in adults.	Cyclophosphamide	44-60	DNA damage inducible transcript 3	Homo sapiens	106-110
33594937-6	2021	AMH was lower in Cy group, whereas AMH levels were similar among other groups.	Cyclophosphamide	17-19	anti-Mullerian hormone	Rattus norvegicus	0-3
33594937-8	2021	The expressions of Sirt1, Foxo3a were up-regulated and p53, Caspase-3, and Bax were down-regulated in Res + Cy and Res groups (p < .05).	Cyclophosphamide	108-110	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	55-58
33594937-8	2021	The expressions of Sirt1, Foxo3a were up-regulated and p53, Caspase-3, and Bax were down-regulated in Res + Cy and Res groups (p < .05).	Cyclophosphamide	108-110	caspase 3	Rattus norvegicus	60-69
33594937-8	2021	The expressions of Sirt1, Foxo3a were up-regulated and p53, Caspase-3, and Bax were down-regulated in Res + Cy and Res groups (p < .05).	Cyclophosphamide	108-110	BCL2 associated X, apoptosis regulator	Rattus norvegicus	75-78
33573703-1	2021	BACKGROUND: Although R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) remains the standard chemotherapy regimen for diffuse large B cell lymphoma (DLBCL) patients, not all patients are responsive to the scheme, and there is no effective method to predict treatment response.	Cyclophosphamide	40-56	DNA damage inducible transcript 3	Homo sapiens	23-27
33592897-8	2021	INTERVENTIONS: The patient was first treated with the cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) regimen.	Cyclophosphamide	54-70	DNA damage inducible transcript 3	Homo sapiens	114-118
33539328-12	2021	In this report, we present the case of a young woman with FSGS recurrence after a kidney transplant, achieving remission successfully with cyclophosphamide.	Cyclophosphamide	139-155	actinin alpha 4	Homo sapiens	58-62
33539328-13	2021	Cyclophosphamide can be used a treatment of FSGS recurrence in a transplanted kidney when all other options have been exhausted.	Cyclophosphamide	0-16	actinin alpha 4	Homo sapiens	44-48
33613687-0	2021	Moxibustion against Cyclophosphamide-Induced Premature Ovarian Failure in Rats through Inhibiting NLRP3-/Caspase-1-/GSDMD-Dependent Pyroptosis.	Cyclophosphamide	20-36	NLR family, pyrin domain containing 3	Rattus norvegicus	98-103
33613687-0	2021	Moxibustion against Cyclophosphamide-Induced Premature Ovarian Failure in Rats through Inhibiting NLRP3-/Caspase-1-/GSDMD-Dependent Pyroptosis.	Cyclophosphamide	20-36	caspase 1	Rattus norvegicus	105-114
33613687-4	2021	The aim of the present study was to investigate the protective effect of moxibustion against cyclophosphamide- (CP-) induced POF and to determine the underlying mechanisms.	Cyclophosphamide	93-109	POF1B actin binding protein	Homo sapiens	125-128
33585350-0	2021	Clinical utilization of long-acting granulocyte colony-stimulating factor (pegfilgrastim) prophylaxis in breast cancer patients with adjuvant docetaxel-cyclophosphamide chemotherapy.	Cyclophosphamide	152-168	colony stimulating factor 3	Homo sapiens	36-73
33679728-0	2021	Elafin as a Predictive Biomarker of Acute Skin Graft-Versus-Host Disease After Haploidentical Stem Cell Transplantation Using Post-Transplant High-Dose Cyclophosphamide.	Cyclophosphamide	152-168	peptidase inhibitor 3	Homo sapiens	0-6
33592119-10	2021	Patients treated with cytarabine had the highest yield of CD34+ cells (median 7.5 x 106 /kg vs 5.8 and 2.4 for etoposide and cyclophosphamide, P = .001).	Cyclophosphamide	125-141	CD34 molecule	Homo sapiens	58-62
33592119-11	2021	Higher percentage of patients was able to collect >=2 x 106 CD34+ cells/kg during one leukapheresis after cytarabine (76% vs 21% for cyclophosphamide vs 36% for etoposide, P = .001).	Cyclophosphamide	133-149	CD34 molecule	Homo sapiens	60-64
33565424-0	2021	Protective effect of bone marrow mesenchymal stem cell-derived exosomes against the reproductive toxicity of cyclophosphamide is associated with the p38MAPK/ERK and AKT signaling pathways.	Cyclophosphamide	109-125	mitogen-activated protein kinase 14	Mus musculus	149-156
33565424-0	2021	Protective effect of bone marrow mesenchymal stem cell-derived exosomes against the reproductive toxicity of cyclophosphamide is associated with the p38MAPK/ERK and AKT signaling pathways.	Cyclophosphamide	109-125	mitogen-activated protein kinase 1	Mus musculus	157-160
33565424-0	2021	Protective effect of bone marrow mesenchymal stem cell-derived exosomes against the reproductive toxicity of cyclophosphamide is associated with the p38MAPK/ERK and AKT signaling pathways.	Cyclophosphamide	109-125	thymoma viral proto-oncogene 1	Mus musculus	165-168
33576399-9	2021	Half of the patients with anti-MDA5 antibodies received more than three medications including intravenous cyclophosphamide, especially patients with ILD.	Cyclophosphamide	106-122	interferon induced with helicase C domain 1	Homo sapiens	31-35
33576399-11	2021	CONCLUSION: Anti-MDA5 antibodies are the most common MSA type in Japan, and patients with this antibody are characterized by ILD at onset, multiple medications including intravenous cyclophosphamide, drug-free remission, and a lower frequency of relapse.	Cyclophosphamide	182-198	interferon induced with helicase C domain 1	Homo sapiens	17-21
33268528-0	2021	Cyclophosphamide and vinorelbine activate stem-like CD8+ T cells and improve anti-PD-1 efficacy in triple-negative breast cancer.	Cyclophosphamide	0-16	CD8a molecule	Homo sapiens	52-55
33268528-0	2021	Cyclophosphamide and vinorelbine activate stem-like CD8+ T cells and improve anti-PD-1 efficacy in triple-negative breast cancer.	Cyclophosphamide	0-16	programmed cell death 1	Homo sapiens	82-86
32661806-0	2021	Influence of glutathione S transferase A1 gene polymorphism (-69C > T, rs3957356) on intravenous cyclophosphamide efficacy and side effects: a case-control study in Egyptian patients with lupus nephritis.	Cyclophosphamide	97-113	glutathione S-transferase alpha 1	Homo sapiens	13-41
32661806-8	2021	The aim of this case-control study was to address the association between GSTA1 polymorphism (-69C > T, rs3957356), and the rate of response to and side effects of intravenous CYC in LN patients.	Cyclophosphamide	176-179	glutathione S-transferase alpha 1	Homo sapiens	74-79
33275987-0	2021	Cilostazol preconditioning alleviates cyclophosphamide-induced cardiotoxicity in male rats: Mechanistic insights into SIRT1 signaling pathway.	Cyclophosphamide	38-54	sirtuin 1	Rattus norvegicus	118-123
33275987-8	2021	KEY FINDINGS: CYP injection contributed to cardiac injury manifested as significant increases in plasma activities of heart enzymes and cardiac troponin I levels.	Cyclophosphamide	14-17	troponin I3, cardiac type	Rattus norvegicus	136-154
33275987-10	2021	Cilostazol induced 3 fold up-regulation of SIRT1 and promoted the antioxidant defense response through FoxO1-related mechanism in hearts of CYP-treated rats.	Cyclophosphamide	140-143	forkhead box O1	Rattus norvegicus	103-108
33275987-11	2021	Cilostazol suppressed the CYP-induced up-regulation of PARP1 and p53, and blocked the NF-kB p65-mediated inflammatory response in hearts of CYP-treated rats.	Cyclophosphamide	26-29	poly (ADP-ribose) polymerase 1	Rattus norvegicus	55-60
33275987-11	2021	Cilostazol suppressed the CYP-induced up-regulation of PARP1 and p53, and blocked the NF-kB p65-mediated inflammatory response in hearts of CYP-treated rats.	Cyclophosphamide	26-29	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	65-68
33275987-13	2021	SIGNIFICANCE: These data provided insights into the mechanism underlying the cardioprotective effect of cilostazol in CYP-treated rats through upregulation of SIRT1 signaling, suggesting that cilostazol might be a candidate modality for CYP-induced cardiotoxicity.	Cyclophosphamide	118-121	sirtuin 1	Rattus norvegicus	159-164
33275987-13	2021	SIGNIFICANCE: These data provided insights into the mechanism underlying the cardioprotective effect of cilostazol in CYP-treated rats through upregulation of SIRT1 signaling, suggesting that cilostazol might be a candidate modality for CYP-induced cardiotoxicity.	Cyclophosphamide	237-240	sirtuin 1	Rattus norvegicus	159-164
33333050-6	2021	In addition, CYP induced marked increases in the levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), interleukin-6 (IL-6), and nitric oxide (NO) confirmed by histological alterations.	Cyclophosphamide	13-16	interleukin 6	Rattus norvegicus	145-149
33333050-0	2021	Downregulation of redox imbalance and iNOS/NF-kB/caspase-3 signalling with zinc supplementation prevents urotoxicity of cyclophosphamide-induced hemorrhagic cystitis in rats.	Cyclophosphamide	120-136	nitric oxide synthase 2	Rattus norvegicus	38-42
33089597-2	2021	Here, we determined whether an inhibitor of EZH2 enhanced the effect of standard of care chemotherapeutic agents: irinotecan, vincristine, and cyclophosphamide.	Cyclophosphamide	143-159	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	44-48
33150486-6	2021	Results indicated that alkylating agents, cyclophosphamide and ifosfamide, but also the antimetabolite cytarabine and asparaginase were associated with a decreased percentage of positive tubules and a lower number of positive cells per tubule for the analyzed markers.	Cyclophosphamide	42-58	asparaginase	Homo sapiens	118-130
33572634-1	2021	BACKGROUND: The t (2; 5) chromosomal rearrangement of the ALK gene with nucleophosmin 1 gene (NPM1), resulting in an NPM1-ALK fusion, was first demonstrated in 1994 in anaplastic large cell lymphoma, (ALCL), a T-cell lymphoma responsive to cyclophosphamide, abriblastine, vincristine and prednisone in approximately 80% of cases; refractory cases usually respond favorably to brentuximab vedotin.	Cyclophosphamide	240-256	ALK receptor tyrosine kinase	Homo sapiens	58-61
33572634-1	2021	BACKGROUND: The t (2; 5) chromosomal rearrangement of the ALK gene with nucleophosmin 1 gene (NPM1), resulting in an NPM1-ALK fusion, was first demonstrated in 1994 in anaplastic large cell lymphoma, (ALCL), a T-cell lymphoma responsive to cyclophosphamide, abriblastine, vincristine and prednisone in approximately 80% of cases; refractory cases usually respond favorably to brentuximab vedotin.	Cyclophosphamide	240-256	nucleophosmin 1	Homo sapiens	94-98
33572634-1	2021	BACKGROUND: The t (2; 5) chromosomal rearrangement of the ALK gene with nucleophosmin 1 gene (NPM1), resulting in an NPM1-ALK fusion, was first demonstrated in 1994 in anaplastic large cell lymphoma, (ALCL), a T-cell lymphoma responsive to cyclophosphamide, abriblastine, vincristine and prednisone in approximately 80% of cases; refractory cases usually respond favorably to brentuximab vedotin.	Cyclophosphamide	240-256	nucleophosmin 1	Homo sapiens	117-121
33572634-1	2021	BACKGROUND: The t (2; 5) chromosomal rearrangement of the ALK gene with nucleophosmin 1 gene (NPM1), resulting in an NPM1-ALK fusion, was first demonstrated in 1994 in anaplastic large cell lymphoma, (ALCL), a T-cell lymphoma responsive to cyclophosphamide, abriblastine, vincristine and prednisone in approximately 80% of cases; refractory cases usually respond favorably to brentuximab vedotin.	Cyclophosphamide	240-256	ALK receptor tyrosine kinase	Homo sapiens	122-125
33536743-1	2021	Background: Cyclophosphamide (CP) is an anticancer alkylating group (nitrogen mustard) and a prodrug that will be metabolized to form its active metabolite, 4-hydroxycyclophosphamide (4-OHCP).	Cyclophosphamide	12-28	ceruloplasmin	Homo sapiens	30-32
33536743-8	2021	In majority of Malay cancer patients, cyclophosphamide would be bioactivated through 4-hydroxylation in hepar rapidly as indicated by the high value of the bioactivity ratio or the increased CP clearance and 4-OHCP level.	Cyclophosphamide	38-54	ceruloplasmin	Homo sapiens	191-193
33569051-1	2020	Cyclophosphamide (CTX) is a major component of the chemotherapy conditioning regimens used in the clinic to prepare cancer patients for hematopoietic stem cell transplantation or adoptive T cell therapy.	Cyclophosphamide	0-16	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	18-21
33552684-9	2021	CD64 expression on macrophages directly correlated with MM cell clearance and was essential to the observed synergy between cyclophosphamide and daratumumab, as tumor clearance was attenuated in the presence of a FcgammaRI/CD64 blocking agent.	Cyclophosphamide	124-140	Fc gamma receptor Ia	Homo sapiens	0-4
33552684-9	2021	CD64 expression on macrophages directly correlated with MM cell clearance and was essential to the observed synergy between cyclophosphamide and daratumumab, as tumor clearance was attenuated in the presence of a FcgammaRI/CD64 blocking agent.	Cyclophosphamide	124-140	Fc gamma receptor Ia	Homo sapiens	213-222
33552684-9	2021	CD64 expression on macrophages directly correlated with MM cell clearance and was essential to the observed synergy between cyclophosphamide and daratumumab, as tumor clearance was attenuated in the presence of a FcgammaRI/CD64 blocking agent.	Cyclophosphamide	124-140	Fc gamma receptor Ia	Homo sapiens	223-227
33333050-0	2021	Downregulation of redox imbalance and iNOS/NF-kB/caspase-3 signalling with zinc supplementation prevents urotoxicity of cyclophosphamide-induced hemorrhagic cystitis in rats.	Cyclophosphamide	120-136	nuclear factor kappa B subunit 1	Rattus norvegicus	43-48
33458904-9	2021	In cyclophosphamide-treated mice, PI3K/Akt/mTOR pathway inhibition with mTOR inhibitors and AS101 preserved the PF pool.	Cyclophosphamide	3-19	thymoma viral proto-oncogene 1	Mus musculus	39-42
33333050-0	2021	Downregulation of redox imbalance and iNOS/NF-kB/caspase-3 signalling with zinc supplementation prevents urotoxicity of cyclophosphamide-induced hemorrhagic cystitis in rats.	Cyclophosphamide	120-136	caspase 3	Rattus norvegicus	49-58
33333050-6	2021	In addition, CYP induced marked increases in the levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), interleukin-6 (IL-6), and nitric oxide (NO) confirmed by histological alterations.	Cyclophosphamide	13-16	tumor necrosis factor	Rattus norvegicus	59-86
33333050-6	2021	In addition, CYP induced marked increases in the levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), interleukin-6 (IL-6), and nitric oxide (NO) confirmed by histological alterations.	Cyclophosphamide	13-16	tumor necrosis factor	Rattus norvegicus	88-97
33333050-6	2021	In addition, CYP induced marked increases in the levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), interleukin-6 (IL-6), and nitric oxide (NO) confirmed by histological alterations.	Cyclophosphamide	13-16	interleukin 1 beta	Rattus norvegicus	100-117
33333050-6	2021	In addition, CYP induced marked increases in the levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), interleukin-6 (IL-6), and nitric oxide (NO) confirmed by histological alterations.	Cyclophosphamide	13-16	interleukin 1 alpha	Rattus norvegicus	119-127
33333050-6	2021	In addition, CYP induced marked increases in the levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), interleukin-6 (IL-6), and nitric oxide (NO) confirmed by histological alterations.	Cyclophosphamide	13-16	interleukin 6	Rattus norvegicus	130-143
33543290-1	2021	Cyclophosphamide (CP) could cause severe gonadotoxicity via imbalanced activation of primordial follicles through PI3K/AKT/mTOR activation.	Cyclophosphamide	0-16	thymoma viral proto-oncogene 1	Mus musculus	119-122
33543290-1	2021	Cyclophosphamide (CP) could cause severe gonadotoxicity via imbalanced activation of primordial follicles through PI3K/AKT/mTOR activation.	Cyclophosphamide	0-16	mechanistic target of rapamycin kinase	Mus musculus	123-127
33472956-5	2021	We identified 45 effective compounds from the screen and found that cell cycle checkpoint kinase (CHK1/2) inhibition synergistically enhanced the cytotoxic activity of clinically used chemotherapeutics cyclophosphamide, cisplatin, and gemcitabine.	Cyclophosphamide	202-218	checkpoint kinase 1	Homo sapiens	68-96
33472956-5	2021	We identified 45 effective compounds from the screen and found that cell cycle checkpoint kinase (CHK1/2) inhibition synergistically enhanced the cytotoxic activity of clinically used chemotherapeutics cyclophosphamide, cisplatin, and gemcitabine.	Cyclophosphamide	202-218	checkpoint kinase 1	Homo sapiens	98-104
33458904-9	2021	In cyclophosphamide-treated mice, PI3K/Akt/mTOR pathway inhibition with mTOR inhibitors and AS101 preserved the PF pool.	Cyclophosphamide	3-19	mechanistic target of rapamycin kinase	Mus musculus	43-47
33458904-9	2021	In cyclophosphamide-treated mice, PI3K/Akt/mTOR pathway inhibition with mTOR inhibitors and AS101 preserved the PF pool.	Cyclophosphamide	3-19	mechanistic target of rapamycin kinase	Mus musculus	72-76
32867615-2	2021	Although the triple combination therapy with high-dose glucocorticoids, cyclophosphamide, and a calcineurin inhibitor has been used to treat anti-MDA-5 antibody-positive rapidly progressive ILD, the prognosis of these patients remains poor despite this intensive therapy.	Cyclophosphamide	72-88	interferon induced with helicase C domain 1	Homo sapiens	146-151
33431979-5	2021	Ingenuity Pathway Analysis predicted a significant decrease in the expression of anti-apoptotic pro-Akt PECAM1 (p = 2.13E-09), IKBKE (p = 0.0001), and ANGPT1 (p = 0.003), and reduced activation of PI3K/PTEN/Akt after cyclophosphamide.	Cyclophosphamide	217-233	PROA	Homo sapiens	96-110
33431979-5	2021	Ingenuity Pathway Analysis predicted a significant decrease in the expression of anti-apoptotic pro-Akt PECAM1 (p = 2.13E-09), IKBKE (p = 0.0001), and ANGPT1 (p = 0.003), and reduced activation of PI3K/PTEN/Akt after cyclophosphamide.	Cyclophosphamide	217-233	AKT serine/threonine kinase 1	Homo sapiens	100-103
33422655-0	2021	Zihuai recipe alleviates cyclophosphamide-induced diminished ovarian reserve via suppressing PI3K/AKT-mediated apoptosis.	Cyclophosphamide	25-41	AKT serine/threonine kinase 1	Rattus norvegicus	98-101
33414495-12	2021	Baseline plasma Hsp90 predicts the 12-month change in DLCO in SSc-ILD patients treated with cyclophosphamide.	Cyclophosphamide	92-108	heat shock protein 90 alpha family class A member 1	Homo sapiens	16-21
33169683-0	2021	Nephroprotective effect of exogenous hydrogen sulfide donor against cyclophosphamide-induced toxicity is mediated by Nrf2/HO-1/NF-kappaB signaling pathway.	Cyclophosphamide	68-84	NFE2 like bZIP transcription factor 2	Rattus norvegicus	117-121
33169683-0	2021	Nephroprotective effect of exogenous hydrogen sulfide donor against cyclophosphamide-induced toxicity is mediated by Nrf2/HO-1/NF-kappaB signaling pathway.	Cyclophosphamide	68-84	heme oxygenase 1	Rattus norvegicus	122-126
33436910-2	2021	This study aimed to compare the area under the plasma concentration-time curves (AUCs) of vincristine (VCR), doxorubicin (DXR), and cyclophosphamide (CPA) between (R-)CHOP and (R-)miniCHOP regimens.	Cyclophosphamide	132-148	DNA damage inducible transcript 3	Homo sapiens	167-171
33436910-5	2021	The median AUCs of DXR and CPA were significantly smaller in the (R-)miniCHOP group than in the (R-)CHOP group (168.7 vs. 257.9 ng h/mL, P = 0.003, and 219.9 vs. 301.7 microg h/mL, P = 0.020, respectively).	Cyclophosphamide	27-30	DNA damage inducible transcript 3	Homo sapiens	73-77
33436910-7	2021	It is possible that the AUCs of VCR, DXR, and CPA in patients aged 80 years and older receiving (R-)miniCHOP therapy may be lower than those in patients 65-79 years old receiving (R-)CHOP therapy.	Cyclophosphamide	46-49	DNA damage inducible transcript 3	Homo sapiens	104-108
33505756-12	2021	After treatment with methylprednisolone and intravenous cyclophosphamide pulse therapies, renal function improved and MPO-ANCA levels decreased.	Cyclophosphamide	56-72	myeloperoxidase	Homo sapiens	118-121
33189675-0	2021	Suppression of adenosine A2a receptors alleviates bladder overactivity and hyperalgesia in cyclophosphamide-induced cystitis by inhibiting TRPV1.	Cyclophosphamide	91-107	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	139-144
33189675-13	2021	These results suggest that suppression of adenosine A2a receptors in bladder afferents alleviates bladder overactivity and hyperalgesia elicited by CYP-induced cystitis in rats by inhibiting TRPV1, indicating that the adenosine A2a receptor in bladder afferents is a potential therapeutic target for the treatment of IC/BPS.	Cyclophosphamide	148-151	adenosine A2a receptor	Rattus norvegicus	42-64
32687015-10	2021	TNF inhibitors should be discontinued in patients who develop rapidly progressive glomerulonephritis, and these patients should be treated with immunosuppressive drugs, such as massive corticosteroids and cyclophosphamide.	Cyclophosphamide	205-221	tumor necrosis factor	Homo sapiens	0-3
33342073-2	2021	However, women who have undergone cyclophosphamide (Cy) treatment have decreased AMH levels due to damaged GCs.	Cyclophosphamide	34-50	anti-Mullerian hormone	Homo sapiens	81-84
33039531-8	2020	Blood levels of complement C3, alpha-2-macroglobulin, ceruloplasmin and transferrin were modulated by treatment with CYP.	Cyclophosphamide	117-120	complement C3	Oreochromis niloticus	16-29
33039531-8	2020	Blood levels of complement C3, alpha-2-macroglobulin, ceruloplasmin and transferrin were modulated by treatment with CYP.	Cyclophosphamide	117-120	ceruloplasmin	Oreochromis niloticus	54-67
33039531-8	2020	Blood levels of complement C3, alpha-2-macroglobulin, ceruloplasmin and transferrin were modulated by treatment with CYP.	Cyclophosphamide	117-120	serotransferrin-like	Oreochromis niloticus	72-83
33256379-1	2020	Patients with MYC-rearrangement positive large B-cell lymphoma (MYC+ LBCL) have an inferior prognosis following standard first-line therapy with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP) as compared to patients without MYC rearrangement.	Cyclophosphamide	156-172	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	14-17
33256379-1	2020	Patients with MYC-rearrangement positive large B-cell lymphoma (MYC+ LBCL) have an inferior prognosis following standard first-line therapy with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP) as compared to patients without MYC rearrangement.	Cyclophosphamide	156-172	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	64-67
33256379-1	2020	Patients with MYC-rearrangement positive large B-cell lymphoma (MYC+ LBCL) have an inferior prognosis following standard first-line therapy with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP) as compared to patients without MYC rearrangement.	Cyclophosphamide	156-172	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	64-67
33374035-0	2021	Successful engraftment of haploidentical stem cell transplant with post-transplantation cyclophosphamide in a patient with adenosine deaminase deficiency.	Cyclophosphamide	88-104	adenosine deaminase	Homo sapiens	123-142
33342073-5	2021	Twenty-four hours post-Cy exposure, a decrease in serum AMH levels was seen due to a reduction in the number of follicle-stimulating hormone receptor (FSHR)+ AMH+ GCs and their ability to produce AMH.	Cyclophosphamide	23-25	anti-Mullerian hormone	Mus musculus	158-161
33342073-6	2021	However, 4 weeks after Cy treatment, serum AMH levels were still decreased due to the decreased number of FSHR+ AMH+ GCs, however, their AMH-producing ability was unaltered.	Cyclophosphamide	23-25	anti-Mullerian hormone	Mus musculus	43-46
33342073-6	2021	However, 4 weeks after Cy treatment, serum AMH levels were still decreased due to the decreased number of FSHR+ AMH+ GCs, however, their AMH-producing ability was unaltered.	Cyclophosphamide	23-25	follicle stimulating hormone receptor	Mus musculus	106-110
33342073-6	2021	However, 4 weeks after Cy treatment, serum AMH levels were still decreased due to the decreased number of FSHR+ AMH+ GCs, however, their AMH-producing ability was unaltered.	Cyclophosphamide	23-25	anti-Mullerian hormone	Mus musculus	112-115
33342073-6	2021	However, 4 weeks after Cy treatment, serum AMH levels were still decreased due to the decreased number of FSHR+ AMH+ GCs, however, their AMH-producing ability was unaltered.	Cyclophosphamide	23-25	anti-Mullerian hormone	Mus musculus	112-115
33342073-7	2021	Consistently, in vitro, Cy-induced low AMH production in FSHR+ AMH+ hGL5 cells (immortalized human GCs) was restored 24 h after Cy treatment, although their numbers remained decreased.	Cyclophosphamide	24-26	anti-Mullerian hormone	Homo sapiens	39-42
33342073-7	2021	Consistently, in vitro, Cy-induced low AMH production in FSHR+ AMH+ hGL5 cells (immortalized human GCs) was restored 24 h after Cy treatment, although their numbers remained decreased.	Cyclophosphamide	24-26	follicle stimulating hormone receptor	Homo sapiens	57-61
33342073-7	2021	Consistently, in vitro, Cy-induced low AMH production in FSHR+ AMH+ hGL5 cells (immortalized human GCs) was restored 24 h after Cy treatment, although their numbers remained decreased.	Cyclophosphamide	24-26	anti-Mullerian hormone	Homo sapiens	63-66
33342073-7	2021	Consistently, in vitro, Cy-induced low AMH production in FSHR+ AMH+ hGL5 cells (immortalized human GCs) was restored 24 h after Cy treatment, although their numbers remained decreased.	Cyclophosphamide	128-130	follicle stimulating hormone receptor	Homo sapiens	57-61
33342073-8	2021	Thus, the surviving GCs after Cy exposure had intact AMH-producing ability.	Cyclophosphamide	30-32	anti-Mullerian hormone	Homo sapiens	53-56
33317571-1	2020	As a widely recognized standard regimen, R-CHOP (rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone) is able to cure two-thirds patients with diffuse large B cell lymphoma (DLBCL), and the remaining patients suffer from refractory or relapsed disease due to resistance to R-CHOP and fare poorly.	Cyclophosphamide	64-80	DNA damage inducible transcript 3	Homo sapiens	43-47
33220676-3	2020	We aimed to detect the immunoenhancement effects of SF-2 in macrophages and cyclophosphamide (CYP)-induced immunosuppression mouse models.	Cyclophosphamide	76-92	serine and arginine-rich splicing factor 1	Mus musculus	52-56
33220676-3	2020	We aimed to detect the immunoenhancement effects of SF-2 in macrophages and cyclophosphamide (CYP)-induced immunosuppression mouse models.	Cyclophosphamide	94-97	serine and arginine-rich splicing factor 1	Mus musculus	52-56
33220676-7	2020	Furthermore, SF-2 significantly increased the body weight, spleen index, thymus index, and inflammatory cell counts in CYP-induced immunosuppression mouse models.	Cyclophosphamide	119-122	serine and arginine-rich splicing factor 1	Mus musculus	13-17
33277452-3	2020	Cyclophosphamide (CP) has been used in the treatment of SRNS, but its effectiveness has been questioned.	Cyclophosphamide	0-16	ceruloplasmin	Homo sapiens	18-20
33039509-13	2020	CONCLUSION: This study showed that both GnRH agonist and thiol preserved or improved structural changes in the hypothalamus caused by cyclophosphamide in mice, suggesting that using thiol and especially GnRH agonist along with chemotherapy drugs may have protective effects on fertility.	Cyclophosphamide	134-150	gonadotropin releasing hormone 1	Mus musculus	40-44
32447619-0	2020	Treatment for IgA nephropathy with stage 3 or 4 chronic kidney disease: low-dose corticosteroids combined with oral cyclophosphamide.	Cyclophosphamide	116-132	CD79a molecule	Homo sapiens	14-17
33342073-2	2021	However, women who have undergone cyclophosphamide (Cy) treatment have decreased AMH levels due to damaged GCs.	Cyclophosphamide	52-54	anti-Mullerian hormone	Homo sapiens	81-84
33342073-3	2021	This study establishes flow cytometry protocols for identification of GCs and investigates the cause of the Cy-induced AMH decrease by analyzing the number of GCs and their AMH production at the single cell level.	Cyclophosphamide	108-110	anti-Mullerian hormone	Homo sapiens	119-122
33342073-3	2021	This study establishes flow cytometry protocols for identification of GCs and investigates the cause of the Cy-induced AMH decrease by analyzing the number of GCs and their AMH production at the single cell level.	Cyclophosphamide	108-110	anti-Mullerian hormone	Homo sapiens	173-176
33342073-5	2021	Twenty-four hours post-Cy exposure, a decrease in serum AMH levels was seen due to a reduction in the number of follicle-stimulating hormone receptor (FSHR)+ AMH+ GCs and their ability to produce AMH.	Cyclophosphamide	23-25	anti-Mullerian hormone	Mus musculus	56-59
33342073-5	2021	Twenty-four hours post-Cy exposure, a decrease in serum AMH levels was seen due to a reduction in the number of follicle-stimulating hormone receptor (FSHR)+ AMH+ GCs and their ability to produce AMH.	Cyclophosphamide	23-25	follicle stimulating hormone receptor	Homo sapiens	112-149
33342073-5	2021	Twenty-four hours post-Cy exposure, a decrease in serum AMH levels was seen due to a reduction in the number of follicle-stimulating hormone receptor (FSHR)+ AMH+ GCs and their ability to produce AMH.	Cyclophosphamide	23-25	follicle stimulating hormone receptor	Mus musculus	151-155
33342073-5	2021	Twenty-four hours post-Cy exposure, a decrease in serum AMH levels was seen due to a reduction in the number of follicle-stimulating hormone receptor (FSHR)+ AMH+ GCs and their ability to produce AMH.	Cyclophosphamide	23-25	anti-Mullerian hormone	Mus musculus	158-161
33269174-3	2020	Recent studies have demonstrated a potential benefit with combination of dose-adjusted rituximab, etoposide, prednisone, vincristine, cyclophosphamide, and doxorubicin (DA-REPOCH) in comparison to standard combination chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) in ABC DLBCL patients.	Cyclophosphamide	134-150	DNA damage inducible transcript 3	Homo sapiens	296-300
33230132-2	2020	The standard treatment is the CHOP chemotherapy protocols that include cyclophosphamide, doxorubicin, vincristine and prednisone, where the majority of dogs achieve complete/partial response; however, it is very important to predict non-responsive cases to improve treatment and to develop new targeted therapies.	Cyclophosphamide	71-87	DNA damage inducible transcript 3	Homo sapiens	30-34
33238601-0	2020	Raspberry Ketones Attenuate Cyclophosphamide-Induced Pulmonary Toxicity in Mice through Inhibition of Oxidative Stress and NF-KappaB Pathway.	Cyclophosphamide	28-44	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	123-132
33175570-0	2021	Ethanol and cyclophosphamide induce similar nephrotoxic effects: possible role for Nox4 and superoxide.	Cyclophosphamide	12-28	NADPH oxidase 4	Mus musculus	83-87
33266362-5	2020	Oral administration of live K040706 prevented the CYP-induced decreases in body weight, thymus index, natural killer (NK) cell activity, T and B cell proliferation, and cytokine (interferon (IFN)-gamma, interleukin (IL)-2, and IL-12) production.	Cyclophosphamide	50-53	interferon gamma	Mus musculus	179-201
33266362-5	2020	Oral administration of live K040706 prevented the CYP-induced decreases in body weight, thymus index, natural killer (NK) cell activity, T and B cell proliferation, and cytokine (interferon (IFN)-gamma, interleukin (IL)-2, and IL-12) production.	Cyclophosphamide	50-53	interleukin 2	Mus musculus	203-221
33262946-16	2020	Lower FOXO1 expression was associated with prednisone and cyclophosphamide resistance.	Cyclophosphamide	58-74	forkhead box O1	Mus musculus	6-11
33175570-7	2021	Up-regulation of Nox4 and increased activity of superoxide dismutase (SOD) were detected in the renal cortex of mice treated with ethanol, CYP or the combination of these drugs.	Cyclophosphamide	139-142	NADPH oxidase 4	Mus musculus	17-21
33231808-4	2020	polysaccharides</compound-id> to C57BL/6 mice treated with cyclophosphamide can increase the number of hematopoietic stem cells (CD117+34+) in the bone marrow.	Cyclophosphamide	59-75	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	129-134
32945942-3	2020	The ICE (ifosfamide, cyclophosphamide, and etoposide) regimen is often used as salvage therapy for r/r DLBCL.	Cyclophosphamide	21-37	carboxylesterase 2	Homo sapiens	4-7
32906032-1	2020	OBJECTIVE: To investigate the prevalence of the MUC5B promoter variant rs35705950 in patients with systemic sclerosis-interstitial lung disease (SSc-ILD) and whether its presence predicts response to immunosuppression with cyclophosphamide (CYC) and mycophenolate (MMF).	Cyclophosphamide	223-239	mucin 5B, oligomeric mucus/gel-forming	Homo sapiens	48-53
32877739-0	2020	Investigating the Role of Missense SNPs on ALDH 1A1 mediated pharmacokinetic resistance to cyclophosphamide.	Cyclophosphamide	91-107	aldehyde dehydrogenase 1 family member A1	Homo sapiens	43-51
33044099-1	2020	OBJECTIVE: To establish a mouse model of bioluminescent Klebsiella pneumoniae-induced lung infection, under different infection states after pretreatment with various dosages of cyclophosphamide (CTX).	Cyclophosphamide	178-194	V-set and immunoglobulin domain containing 2	Mus musculus	196-199
32623836-6	2020	ABT-737 combined with a low dose of cyclophosphamide, a major component of the conventional CHOP chemotherapy regimen for BL patients, reduced tumor growth during treatment but failed to improve the overall survival of BL xenograft mice.	Cyclophosphamide	36-52	DNA damage inducible transcript 3	Homo sapiens	92-96
32945456-7	2020	In addition, CD9 knockdown could suppress cell proliferation, adhesion, migration and invasion, and promote apoptosis and the efficacy of chemotherapeutic drugs (such as vincristine, daunorubicin, cyclophosphamide and dexamethasone) and the tyrosine kinase inhibitor imatinib in SUP-B15 cells.	Cyclophosphamide	197-213	CD9 molecule	Homo sapiens	13-16
32042095-3	2020	In current study, we aimed to explore the association between gene networks and overall survival (OS) of DLBCL patients treated with CHOP-based chemotherapy (cyclophosphamide combination with doxorubicin, vincristine and prednisone).	Cyclophosphamide	158-174	DNA damage inducible transcript 3	Homo sapiens	133-137
33099125-3	2020	According to the finding of most studies conducted on patients affected by different forms of neoplastic diseases, there are strong enough evidence of a prominent role of some drug such as doxorubicin, cyclophosphamide, cytarabine, methotrexate, 5-fluorouracil and cisplatin in causing chemo-fog related neurological impairment.	Cyclophosphamide	202-218	zinc finger protein, FOG family member 1	Homo sapiens	292-295
33125206-5	2020	For preconditioning, splenectomy + cyclophosphamide (CP) was employed in the first series (group A; n = 9).	Cyclophosphamide	35-51	ceruloplasmin	Homo sapiens	53-55
33204611-1	2020	In CD34+ cells mobilization of patients with multiple myeloma (MM), the use of Cyclophosphamide (CTX) at a dose of 2 g/m2 has low efficacy although also lower toxicity.	Cyclophosphamide	79-95	CD34 molecule	Homo sapiens	3-7
33138211-7	2020	Cyclophosphamide (Cy) in the graft-versus-host disease (GvHD) prevention protocol downregulated KIR2DL1 to just 25% of the original donor value, and the FEAM (Fludarabine + Etoposid + Ara-C + Melphalan) conditioning protocol reduced KIR2DL3.	Cyclophosphamide	0-16	killer cell immunoglobulin like receptor, two Ig domains and long cytoplasmic tail 1	Homo sapiens	96-103
33138211-7	2020	Cyclophosphamide (Cy) in the graft-versus-host disease (GvHD) prevention protocol downregulated KIR2DL1 to just 25% of the original donor value, and the FEAM (Fludarabine + Etoposid + Ara-C + Melphalan) conditioning protocol reduced KIR2DL3.	Cyclophosphamide	0-16	killer cell immunoglobulin like receptor, two Ig domains and long cytoplasmic tail 3	Homo sapiens	233-240
33138211-7	2020	Cyclophosphamide (Cy) in the graft-versus-host disease (GvHD) prevention protocol downregulated KIR2DL1 to just 25% of the original donor value, and the FEAM (Fludarabine + Etoposid + Ara-C + Melphalan) conditioning protocol reduced KIR2DL3.	Cyclophosphamide	0-2	killer cell immunoglobulin like receptor, two Ig domains and long cytoplasmic tail 1	Homo sapiens	96-103
33138211-7	2020	Cyclophosphamide (Cy) in the graft-versus-host disease (GvHD) prevention protocol downregulated KIR2DL1 to just 25% of the original donor value, and the FEAM (Fludarabine + Etoposid + Ara-C + Melphalan) conditioning protocol reduced KIR2DL3.	Cyclophosphamide	0-2	killer cell immunoglobulin like receptor, two Ig domains and long cytoplasmic tail 3	Homo sapiens	233-240
33080006-0	2020	Allogeneic transplantation for Ph+ acute lymphoblastic leukemia with posttransplantation cyclophosphamide.	Cyclophosphamide	89-105	phenylalanine hydroxylase	Homo sapiens	31-33
33108457-0	2020	Class II HLA mismatch improves outcomes following haploidentical transplantation with posttransplant cyclophosphamide.	Cyclophosphamide	101-117	major histocompatibility complex, class II, DR beta 1	Homo sapiens	9-12
33120740-9	2020	OUTCOMES: After fludarabine and cyclophosphamide (FC) lymphodepletion chemotherapy, pre-existing CAR-T cells were revitalized and the patient developed grade 2 cytokine release syndrome (CRS) contributing to the regression of relapsed B-cell lymphoma.	Cyclophosphamide	32-48	CXADR pseudogene 1	Homo sapiens	97-100
33120841-4	2020	PATIENT CONCERNS: A 47-year-old Chinese man with membranous nephropathy presented recurrent edema and acute kidney injury after a 3-day course of low dose DAC infusion because of cyclophosphamide-relating thrombocytopenia.	Cyclophosphamide	179-195	arylacetamide deacetylase	Homo sapiens	155-158
33084015-9	2021	By light microscopy, CPH group showed degeneration and necrosis of hippocampal neurocytes, significantly reduced thickness of the neurocyte cell layers, increased expression of GFAB and caspase 3 immunostains and significantly elevated apoptotic index.	Cyclophosphamide	21-24	caspase 3	Rattus norvegicus	186-195
32738410-1	2020	The structure-specific ERCC1-XPF endonuclease is essential for repairing bulky DNA lesions and helix distortions induced by UV radiation, which forms cyclobutane pyrimidine dimers (CPDs), or chemicals that crosslink DNA strands such as cyclophosphamide and platinum-based chemotherapeutic agents.	Cyclophosphamide	236-252	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	23-28
32738410-1	2020	The structure-specific ERCC1-XPF endonuclease is essential for repairing bulky DNA lesions and helix distortions induced by UV radiation, which forms cyclobutane pyrimidine dimers (CPDs), or chemicals that crosslink DNA strands such as cyclophosphamide and platinum-based chemotherapeutic agents.	Cyclophosphamide	236-252	ERCC excision repair 4, endonuclease catalytic subunit	Homo sapiens	29-32
33028899-9	2020	Finally, TH-MYCN transgenic mice were administered cyclophosphamide alone or in combination with an anti-GD2 or anti-4-1BB monoclonal antibody, which resulted in increase in survival in both combination therapies.	Cyclophosphamide	51-67	tyrosine hydroxylase	Mus musculus	9-11
33116822-6	2020	Subsequently, the patient was treated by six cycles of CHOP (cyclophosphamide + doxorubicin + vincristine + hydroprednisone) regimens.	Cyclophosphamide	61-77	DNA damage inducible transcript 3	Homo sapiens	55-59
32653621-3	2020	The use of T-cell replete haploidentical HCT with post-transplant cyclophosphamide(Haplo-PTCy) in children with PID has been described in few case-series.	Cyclophosphamide	66-82	metastasis associated 1 family member 2	Homo sapiens	112-115
32777141-8	2020	When tested with standard-of-care cytotoxics at human Cmax -equivalent concentrations, MYCN-amplified and non-MYCN-amplified PDCs showed a differential response to cyclophosphamide and topotecan, which mirrored the corresponding patients" responses, and correlated with gene signatures of chemosensitivity.	Cyclophosphamide	164-180	MYCN proto-oncogene, bHLH transcription factor	Homo sapiens	87-91
32777141-8	2020	When tested with standard-of-care cytotoxics at human Cmax -equivalent concentrations, MYCN-amplified and non-MYCN-amplified PDCs showed a differential response to cyclophosphamide and topotecan, which mirrored the corresponding patients" responses, and correlated with gene signatures of chemosensitivity.	Cyclophosphamide	164-180	MYCN proto-oncogene, bHLH transcription factor	Homo sapiens	110-114
32906032-1	2020	OBJECTIVE: To investigate the prevalence of the MUC5B promoter variant rs35705950 in patients with systemic sclerosis-interstitial lung disease (SSc-ILD) and whether its presence predicts response to immunosuppression with cyclophosphamide (CYC) and mycophenolate (MMF).	Cyclophosphamide	241-244	mucin 5B, oligomeric mucus/gel-forming	Homo sapiens	48-53
32586769-2	2020	Although granulocyte colony-stimulating factor (G-CSF) supported cyclophosphamide (CY) is used as the pre-ASCT mobilization regimen, there is no consensus on the optimal dosage of CY.	Cyclophosphamide	65-81	colony stimulating factor 3	Homo sapiens	9-46
32586769-2	2020	Although granulocyte colony-stimulating factor (G-CSF) supported cyclophosphamide (CY) is used as the pre-ASCT mobilization regimen, there is no consensus on the optimal dosage of CY.	Cyclophosphamide	65-81	colony stimulating factor 3	Homo sapiens	48-53
32499108-7	2020	RESULTS: Mobilization with ID - cyclophosphamide and G-CSF resulted in a significantly higher CD34+ peak mean on day 1 yield (119 CD34+ muL vs 67.3; p = 0.06) and in total average CD34+ yield (mean collection 10.6 x 106/kg vs 5.8 x 106/kg; p = 0.004) compared to patients mobilized with G-CSF and plerixafor.	Cyclophosphamide	32-48	CD34 molecule	Homo sapiens	94-98
32994268-5	2020	PBL is an extremely aggressive lymphoma and is usually treated using a CHOP-like regimen (cyclophosphamide, doxorubicin, vincristine and prednisone/dexamethasone), but with poor outcome.	Cyclophosphamide	90-106	DNA damage inducible transcript 3	Homo sapiens	71-75
32499108-7	2020	RESULTS: Mobilization with ID - cyclophosphamide and G-CSF resulted in a significantly higher CD34+ peak mean on day 1 yield (119 CD34+ muL vs 67.3; p = 0.06) and in total average CD34+ yield (mean collection 10.6 x 106/kg vs 5.8 x 106/kg; p = 0.004) compared to patients mobilized with G-CSF and plerixafor.	Cyclophosphamide	32-48	CD34 molecule	Homo sapiens	130-134
32499108-7	2020	RESULTS: Mobilization with ID - cyclophosphamide and G-CSF resulted in a significantly higher CD34+ peak mean on day 1 yield (119 CD34+ muL vs 67.3; p = 0.06) and in total average CD34+ yield (mean collection 10.6 x 106/kg vs 5.8 x 106/kg; p = 0.004) compared to patients mobilized with G-CSF and plerixafor.	Cyclophosphamide	32-48	CD34 molecule	Homo sapiens	130-134
32499108-7	2020	RESULTS: Mobilization with ID - cyclophosphamide and G-CSF resulted in a significantly higher CD34+ peak mean on day 1 yield (119 CD34+ muL vs 67.3; p = 0.06) and in total average CD34+ yield (mean collection 10.6 x 106/kg vs 5.8 x 106/kg; p = 0.004) compared to patients mobilized with G-CSF and plerixafor.	Cyclophosphamide	32-48	colony stimulating factor 3	Homo sapiens	287-292
33083373-5	2020	To investigate the protective effect of EAP against CPA-induced genotoxicity, human peripheral lymphocyte cultures were used.	Cyclophosphamide	52-55	glutamyl aminopeptidase	Homo sapiens	40-43
32915975-2	2020	Exposure to R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone) is likely to increase the risk of fracture, but evidence is lacking to define fracture incidence in this group.	Cyclophosphamide	31-47	DNA damage inducible transcript 3	Homo sapiens	14-18
32619674-11	2020	Cyclophosphamide administration significantly induced histopathological damages and increased MDA, p-p38/p38, p-STAT3/STAT3, and PARP levels compared with the saline group.	Cyclophosphamide	0-16	mitogen activated protein kinase 14	Rattus norvegicus	101-104
32619674-11	2020	Cyclophosphamide administration significantly induced histopathological damages and increased MDA, p-p38/p38, p-STAT3/STAT3, and PARP levels compared with the saline group.	Cyclophosphamide	0-16	mitogen activated protein kinase 14	Rattus norvegicus	105-108
32619674-11	2020	Cyclophosphamide administration significantly induced histopathological damages and increased MDA, p-p38/p38, p-STAT3/STAT3, and PARP levels compared with the saline group.	Cyclophosphamide	0-16	signal transducer and activator of transcription 3	Rattus norvegicus	112-117
32619674-11	2020	Cyclophosphamide administration significantly induced histopathological damages and increased MDA, p-p38/p38, p-STAT3/STAT3, and PARP levels compared with the saline group.	Cyclophosphamide	0-16	signal transducer and activator of transcription 3	Rattus norvegicus	118-123
32931951-4	2021	Multiple therapeutic strategies are currently investigated in order to increase response rates to anti-PD1/PD-L1 through adding chemotherapy, anti-angiogenic agents, DNA damage (PARP inhibitors, cyclophosphamide and/or radiotherapy) or other immune checkpoint inhibitors (CTLA-4, etc..).	Cyclophosphamide	195-211	CD274 molecule	Felis catus	107-112
32615180-1	2020	The goal of our study was to determine whether GPR55 agonists, O-1602, could reverse the cyclophosphamide (CYP)-induced changes in cystometric and inflammatory parameters, indicative of the development of bladder inflammation and overactivity.	Cyclophosphamide	89-105	G protein-coupled receptor 55	Rattus norvegicus	47-52
32982414-6	2020	Furthermore, 72 Balb/c nude mice with breast cancer were randomly assigned to three groups that received different doses of cyclophosphamide (CTX) (control, 100 mg/kg, and 200 mg/kg), and the alterations in serum AMH levels and ovarian follicles were recorded and analyzed.	Cyclophosphamide	124-140	V-set and immunoglobulin domain containing 2	Mus musculus	142-145
32901060-2	2020	A reduced phytoplasma titre found in infected defective-mutant Atseor1ko plants in previous work raised the speculation that non-conjugated SEOR2 is involved in the phytohormone-mediated suppression of Chrysanthemum Yellows (CY)-phytoplasma infection transmitted by Euscelidius variegatus (Ev).	Cyclophosphamide	225-227	sieve element occlusion protein	Arabidopsis thaliana	140-145
32615180-2	2020	If confirmed, the stimulation of novel cannabinoid receptor - GPR55, could be a reasonable strategy as a treatment of CYP-induced haemorrhagic cystitis.	Cyclophosphamide	118-121	G protein-coupled receptor 55	Rattus norvegicus	62-67
32615180-7	2020	Intravenous administration of the GPR55 agonist to animals that received CYP significantly decreased Evans Blue extravasation and increased urothelium thickness.	Cyclophosphamide	73-76	G protein-coupled receptor 55	Rattus norvegicus	34-39
33499894-10	2020	CONCLUSION: These observations in 72 BCP-ALL cell lines suggested that the risk allele of the relapse-linked SNPs of ARID5B may be involved in a higher relapse rate because of resistance to chemotherapeutic agents such as VCR, CY, and AraC.	Cyclophosphamide	227-229	AT-rich interaction domain 5B	Homo sapiens	117-123
31734911-14	2020	On the other hand, in the boron+cyclophosphamide group pretreatment with boron protected, the bladder tissue and the number of bcl-2-positive cells increased, and bax and caspase-3-positive cells decreased, showing antiapoptotic effects of boron against cyclophosphamide-induced toxicity.	Cyclophosphamide	32-48	BCL2, apoptosis regulator	Rattus norvegicus	127-132
31734911-14	2020	On the other hand, in the boron+cyclophosphamide group pretreatment with boron protected, the bladder tissue and the number of bcl-2-positive cells increased, and bax and caspase-3-positive cells decreased, showing antiapoptotic effects of boron against cyclophosphamide-induced toxicity.	Cyclophosphamide	32-48	BCL2 associated X, apoptosis regulator	Rattus norvegicus	163-166
31734911-14	2020	On the other hand, in the boron+cyclophosphamide group pretreatment with boron protected, the bladder tissue and the number of bcl-2-positive cells increased, and bax and caspase-3-positive cells decreased, showing antiapoptotic effects of boron against cyclophosphamide-induced toxicity.	Cyclophosphamide	32-48	caspase 3	Rattus norvegicus	171-180
32717620-0	2020	Review of conditioning regimens for haplo-identical donor transplants using post-transplant cyclophosphamide in recipients of G-CSF mobilised peripheral stem cell.	Cyclophosphamide	92-108	colony stimulating factor 3	Homo sapiens	126-131
32615180-1	2020	The goal of our study was to determine whether GPR55 agonists, O-1602, could reverse the cyclophosphamide (CYP)-induced changes in cystometric and inflammatory parameters, indicative of the development of bladder inflammation and overactivity.	Cyclophosphamide	107-110	G protein-coupled receptor 55	Rattus norvegicus	47-52
32504759-0	2020	Ameliorate effect of pyrroloquinoline quinone against cyclophosphamide-induced nephrotoxicity by activating the Nrf2 pathway and inhibiting the NLRP3 pathway.	Cyclophosphamide	54-70	nuclear factor, erythroid derived 2, like 2	Mus musculus	112-116
32869669-0	2022	Alogliptin attenuates cyclophosphamide-induced nephrotoxicity: a novel therapeutic approach through modulating MAP3K/JNK/SMAD3 signaling cascade.	Cyclophosphamide	22-38	mitogen-activated protein kinase 8	Rattus norvegicus	117-120
32869669-0	2022	Alogliptin attenuates cyclophosphamide-induced nephrotoxicity: a novel therapeutic approach through modulating MAP3K/JNK/SMAD3 signaling cascade.	Cyclophosphamide	22-38	SMAD family member 3	Rattus norvegicus	121-126
32449206-0	2020	Phospholipase-A2 receptor antibody, 24 hours proteinuria, and serum albumin as indicators of cyclophosphamide efficacy in idiopathic membranous nephropathy.	Cyclophosphamide	93-109	phospholipase A2 group IB	Homo sapiens	0-16
32504759-0	2020	Ameliorate effect of pyrroloquinoline quinone against cyclophosphamide-induced nephrotoxicity by activating the Nrf2 pathway and inhibiting the NLRP3 pathway.	Cyclophosphamide	54-70	NLR family, pyrin domain containing 3	Mus musculus	144-149
32504759-1	2020	AIMS: Cyclophosphamide (CTX) is an effective anti-tumor and immunosuppressive agent, but it induces nephrotoxicity in clinical applications.	Cyclophosphamide	6-22	V-set and immunoglobulin domain containing 2	Mus musculus	24-27
32982732-0	2020	Jian-Pi-Bu-Xue-Formula Alleviates Cyclophosphamide-Induced Myelosuppression via Up-Regulating NRF2/HO1/NQO1 Signaling.	Cyclophosphamide	34-50	NFE2 like bZIP transcription factor 2	Homo sapiens	94-98
32400945-9	2020	IgAN-C were also more likely to receive immunosuppressants (66% vs 43%, P = 0.01) such as prednisolone (63% vs 38%, P = 0.006) and cyclophosphamide (12% vs 2%, P = 0.03).	Cyclophosphamide	131-147	IGAN1	Homo sapiens	0-4
33377708-8	2020	CONCLUSIONS: Bushen Huoxue Recipe can reduce cyclophosphamide-induced apoptosis of testicular spermatogenic cells in mice, which may be associated with its ability of regulating the expressions of Bax and Bcl-2 mRNA and proteins in the testis tissue.	Cyclophosphamide	45-61	BCL2-associated X protein	Mus musculus	197-200
33377708-8	2020	CONCLUSIONS: Bushen Huoxue Recipe can reduce cyclophosphamide-induced apoptosis of testicular spermatogenic cells in mice, which may be associated with its ability of regulating the expressions of Bax and Bcl-2 mRNA and proteins in the testis tissue.	Cyclophosphamide	45-61	B cell leukemia/lymphoma 2	Mus musculus	205-210
32982732-0	2020	Jian-Pi-Bu-Xue-Formula Alleviates Cyclophosphamide-Induced Myelosuppression via Up-Regulating NRF2/HO1/NQO1 Signaling.	Cyclophosphamide	34-50	heme oxygenase 1	Homo sapiens	99-102
32982732-0	2020	Jian-Pi-Bu-Xue-Formula Alleviates Cyclophosphamide-Induced Myelosuppression via Up-Regulating NRF2/HO1/NQO1 Signaling.	Cyclophosphamide	34-50	NAD(P)H quinone dehydrogenase 1	Homo sapiens	103-107
32908623-0	2020	Polysaccharides from Hemp Seed Protect against Cyclophosphamide-Induced Intestinal Oxidative Damage via Nrf2-Keap1 Signaling Pathway in Mice.	Cyclophosphamide	47-63	nuclear factor, erythroid derived 2, like 2	Mus musculus	104-108
32908623-0	2020	Polysaccharides from Hemp Seed Protect against Cyclophosphamide-Induced Intestinal Oxidative Damage via Nrf2-Keap1 Signaling Pathway in Mice.	Cyclophosphamide	47-63	kelch-like ECH-associated protein 1	Mus musculus	109-114
32908623-7	2020	Collectively, our findings indicated that HSP had protective effects on intestinal oxidative damage induced by Cy in mice, and its mechanism might be related to the activation of Nrf2-Keap1 signaling pathway.	Cyclophosphamide	111-113	nuclear factor, erythroid derived 2, like 2	Mus musculus	179-183
32908623-7	2020	Collectively, our findings indicated that HSP had protective effects on intestinal oxidative damage induced by Cy in mice, and its mechanism might be related to the activation of Nrf2-Keap1 signaling pathway.	Cyclophosphamide	111-113	kelch-like ECH-associated protein 1	Mus musculus	184-189
32905193-0	2020	Alogliptin: a novel approach against cyclophosphamide-induced hepatic injury via modulating SIRT1/FoxO1 pathway.	Cyclophosphamide	37-53	sirtuin 1	Rattus norvegicus	92-97
32905193-0	2020	Alogliptin: a novel approach against cyclophosphamide-induced hepatic injury via modulating SIRT1/FoxO1 pathway.	Cyclophosphamide	37-53	forkhead box O1	Rattus norvegicus	98-103
31749145-0	2020	Metronomic cyclophosphamide induces regulatory T cells depletion and PSA specific T cells reactivation in patients with biochemical recurrent prostate cancer.	Cyclophosphamide	11-27	aminopeptidase puromycin sensitive	Homo sapiens	69-72
32752195-5	2020	A 24-h CY prediction formula was developed with data from IF1, IF2 and IF3 trials (calibration) and successively validated by applying it to 12 PR trials made with IF milk in six different cheese factories (external validation).	Cyclophosphamide	7-9	ATP synthase inhibitory factor subunit 1	Bos taurus	58-61
32799907-11	2020	Serum FSH levels increased (p = 0.03), while AMH (p = 0.002) and inhibin B (p < 0.001) levels decreased significantly with 6 months of CYC therapy.	Cyclophosphamide	135-138	anti-Mullerian hormone	Homo sapiens	45-48
32823691-0	2020	Protective Effect of Low Molecular Weight Peptides from Solenocera crassicornis Head against Cyclophosphamide-Induced Nephrotoxicity in Mice via the Keap1/Nrf2 Pathway.	Cyclophosphamide	93-109	kelch-like ECH-associated protein 1	Mus musculus	149-154
32823691-0	2020	Protective Effect of Low Molecular Weight Peptides from Solenocera crassicornis Head against Cyclophosphamide-Induced Nephrotoxicity in Mice via the Keap1/Nrf2 Pathway.	Cyclophosphamide	93-109	nuclear factor, erythroid derived 2, like 2	Mus musculus	155-159
33093947-3	2020	R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisolone) is accepted as the international standard first-line regimen, but improvement in first line treatment is needed.	Cyclophosphamide	19-35	DNA damage inducible transcript 3	Homo sapiens	2-6
32707767-6	2020	The CPA-induced CSE upregulation, as well as bladder pain was prevented by HMGB1 inactivation, inhibition of HMGB1 release from macrophages, antagonists of RAGE or P2X4/P2X7 receptors, and N-acetylcysteine, an antioxidant.	Cyclophosphamide	4-7	high mobility group box 1	Mus musculus	75-80
32298020-6	2020	RESULTS: The mean peak of CD34+ cells/ul in peripheral blood was 132 (range, 84-202) in Ara-C and 51 (range, 29-69) in Cy cohort (p < 0.001).	Cyclophosphamide	119-121	CD34 molecule	Homo sapiens	26-30
32707767-1	2020	Cystitis-related bladder pain involves RAGE activation by HMGB1, and increased Cav3.2 T-type Ca2+ channel activity by H2S, generated by upregulated cystathionine-gamma-lyase (CSE) in mice treated with cyclophosphamide (CPA).	Cyclophosphamide	201-217	cystathionase (cystathionine gamma-lyase)	Mus musculus	148-173
32707767-1	2020	Cystitis-related bladder pain involves RAGE activation by HMGB1, and increased Cav3.2 T-type Ca2+ channel activity by H2S, generated by upregulated cystathionine-gamma-lyase (CSE) in mice treated with cyclophosphamide (CPA).	Cyclophosphamide	201-217	cystathionase (cystathionine gamma-lyase)	Mus musculus	175-178
32707767-1	2020	Cystitis-related bladder pain involves RAGE activation by HMGB1, and increased Cav3.2 T-type Ca2+ channel activity by H2S, generated by upregulated cystathionine-gamma-lyase (CSE) in mice treated with cyclophosphamide (CPA).	Cyclophosphamide	219-222	cystathionase (cystathionine gamma-lyase)	Mus musculus	175-178
32707767-3	2020	Bladder pain (nociceptive behavior/referred hyperalgesia) and immuno-reactive CSE expression in the bladder were determined in CPA-treated female mice.	Cyclophosphamide	127-130	cystathionase (cystathionine gamma-lyase)	Mus musculus	78-81
32707767-5	2020	The CPA-induced bladder pain was abolished by pharmacological inhibition of T-type Ca2+ channels or CSE, and genetic deletion of Cav3.2.	Cyclophosphamide	4-7	cystathionase (cystathionine gamma-lyase)	Mus musculus	100-103
32707767-5	2020	The CPA-induced bladder pain was abolished by pharmacological inhibition of T-type Ca2+ channels or CSE, and genetic deletion of Cav3.2.	Cyclophosphamide	4-7	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	129-135
32707767-6	2020	The CPA-induced CSE upregulation, as well as bladder pain was prevented by HMGB1 inactivation, inhibition of HMGB1 release from macrophages, antagonists of RAGE or P2X4/P2X7 receptors, and N-acetylcysteine, an antioxidant.	Cyclophosphamide	4-7	cystathionase (cystathionine gamma-lyase)	Mus musculus	16-19
32707767-6	2020	The CPA-induced CSE upregulation, as well as bladder pain was prevented by HMGB1 inactivation, inhibition of HMGB1 release from macrophages, antagonists of RAGE or P2X4/P2X7 receptors, and N-acetylcysteine, an antioxidant.	Cyclophosphamide	4-7	high mobility group box 1	Mus musculus	109-114
32707767-6	2020	The CPA-induced CSE upregulation, as well as bladder pain was prevented by HMGB1 inactivation, inhibition of HMGB1 release from macrophages, antagonists of RAGE or P2X4/P2X7 receptors, and N-acetylcysteine, an antioxidant.	Cyclophosphamide	4-7	MOK protein kinase	Mus musculus	156-160
32707767-6	2020	The CPA-induced CSE upregulation, as well as bladder pain was prevented by HMGB1 inactivation, inhibition of HMGB1 release from macrophages, antagonists of RAGE or P2X4/P2X7 receptors, and N-acetylcysteine, an antioxidant.	Cyclophosphamide	4-7	purinergic receptor P2X, ligand-gated ion channel 4	Mus musculus	164-168
32707767-6	2020	The CPA-induced CSE upregulation, as well as bladder pain was prevented by HMGB1 inactivation, inhibition of HMGB1 release from macrophages, antagonists of RAGE or P2X4/P2X7 receptors, and N-acetylcysteine, an antioxidant.	Cyclophosphamide	4-7	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	169-173
32707767-9	2020	Together, our data suggest that CPA, once metabolized to acrolein, causes urothelial ATP-mediated, redox-dependent HMGB1 release from macrophages, which in turn causes RAGE-mediated CSE upregulation and subsequent H2S-targeted Cav3.2-dependent nociceptor excitation, resulting in bladder pain.	Cyclophosphamide	32-35	high mobility group box 1	Mus musculus	115-120
32707767-9	2020	Together, our data suggest that CPA, once metabolized to acrolein, causes urothelial ATP-mediated, redox-dependent HMGB1 release from macrophages, which in turn causes RAGE-mediated CSE upregulation and subsequent H2S-targeted Cav3.2-dependent nociceptor excitation, resulting in bladder pain.	Cyclophosphamide	32-35	MOK protein kinase	Mus musculus	168-172
32707767-9	2020	Together, our data suggest that CPA, once metabolized to acrolein, causes urothelial ATP-mediated, redox-dependent HMGB1 release from macrophages, which in turn causes RAGE-mediated CSE upregulation and subsequent H2S-targeted Cav3.2-dependent nociceptor excitation, resulting in bladder pain.	Cyclophosphamide	32-35	cystathionase (cystathionine gamma-lyase)	Mus musculus	182-185
32707767-9	2020	Together, our data suggest that CPA, once metabolized to acrolein, causes urothelial ATP-mediated, redox-dependent HMGB1 release from macrophages, which in turn causes RAGE-mediated CSE upregulation and subsequent H2S-targeted Cav3.2-dependent nociceptor excitation, resulting in bladder pain.	Cyclophosphamide	32-35	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	227-233
32685149-8	2020	Doxorubicin and cyclophosphamide (CP), which are included in the current treatment regimen for MCL, enhance the NF-kappaB activity and increase CD83 expression on MCL cell lines.	Cyclophosphamide	16-32	nuclear factor kappa B subunit 1	Homo sapiens	112-121
32685149-8	2020	Doxorubicin and cyclophosphamide (CP), which are included in the current treatment regimen for MCL, enhance the NF-kappaB activity and increase CD83 expression on MCL cell lines.	Cyclophosphamide	16-32	CD83 antigen	Mus musculus	144-148
32651830-4	2020	Enhanced relative expression of the GCLM gene was found in all studied drug-resistant strains; the expression of the GSR and GPX1 genes was increased only in cells of the cyclophosphamide-resistant strain.	Cyclophosphamide	171-187	gutter shaped root	Mus musculus	117-120
32521683-10	2020	Additionally, the expression of ZO-2 was increased and IL-6 was decreased in the CYP plus intravesical instillation with PRP group compared with the CYP-induced acute IC/PBS group.	Cyclophosphamide	81-84	tight junction protein 2	Rattus norvegicus	32-36
32521683-10	2020	Additionally, the expression of ZO-2 was increased and IL-6 was decreased in the CYP plus intravesical instillation with PRP group compared with the CYP-induced acute IC/PBS group.	Cyclophosphamide	81-84	interleukin 6	Rattus norvegicus	55-59
32521683-11	2020	CONCLUSION: These findings suggest that PRP modulate urothelial repair, which ameliorate the increase in urination frequency in rats treated with CYP.	Cyclophosphamide	146-149	proline rich protein 2-like 1	Rattus norvegicus	40-43
32171146-3	2020	Through the analysis of body weight, spleen and thymus indexes, peripheral blood routine and pathological section of femur, it was obviously that DBD could significantly improve acetylphenylhydrazine (APH) + cyclophosphamide (CTX) induced anemia mice in the present work.	Cyclophosphamide	208-224	V-set and immunoglobulin domain containing 2	Mus musculus	226-229
32172064-8	2020	Doxorubicin/cyclophosphamide + IMMUNEPOTENT CRP decreased tumor volume, prolonged survival, increased infiltrating and systemic CD8+ T cells and decreased tumor suppressor molecules (such as PD-L1, Gal-3, and IL-10 among others).	Cyclophosphamide	12-28	CD274 antigen	Mus musculus	191-196
32172064-8	2020	Doxorubicin/cyclophosphamide + IMMUNEPOTENT CRP decreased tumor volume, prolonged survival, increased infiltrating and systemic CD8+ T cells and decreased tumor suppressor molecules (such as PD-L1, Gal-3, and IL-10 among others).	Cyclophosphamide	12-28	lectin, galactose binding, soluble 3	Mus musculus	198-203
32615949-10	2020	CONCLUSION: Collectively, the unique mechanism of etoposide with G-CSF-induced mobilization is associated with IL-8 secretion from the BMSCs, which is responsible for the enhanced proliferation and mobilization of HSCs in the bone marrow; this was not observed with mobilization using cyclophosphamide with G-CSF or G-CSF alone.	Cyclophosphamide	285-301	colony stimulating factor 3	Homo sapiens	65-70
32615949-10	2020	CONCLUSION: Collectively, the unique mechanism of etoposide with G-CSF-induced mobilization is associated with IL-8 secretion from the BMSCs, which is responsible for the enhanced proliferation and mobilization of HSCs in the bone marrow; this was not observed with mobilization using cyclophosphamide with G-CSF or G-CSF alone.	Cyclophosphamide	285-301	C-X-C motif chemokine ligand 8	Homo sapiens	111-115
32417940-2	2020	Progression or relapse of FL within 2 years (so-called POD24) after diagnosis is associated with a poor outcome for patients treated with R-CHOP (rituximab plus cyclophosphamide, doxorubicin, vincristine, prednisone) in clinical trials.	Cyclophosphamide	161-177	DNA damage inducible transcript 3	Homo sapiens	140-144
32648457-1	2020	BACKGROUND: The CHOP regimen comprising cyclophosphamide, doxorubicin, vincristine, and prednisone is a basic chemotherapeutic regimen for diffuse large B cell lymphoma (DLBCL).	Cyclophosphamide	40-56	DNA damage inducible transcript 3	Homo sapiens	16-20
32122920-7	2020	DNAJB7-specific T cells were capable of killing colorectal tumor lines in vitro, and the IFN-g+ response was markedly magnified by control of immunosuppression with cyclophosphamide in cancer patients.	Cyclophosphamide	165-181	DnaJ heat shock protein family (Hsp40) member B7	Homo sapiens	0-6
32122920-7	2020	DNAJB7-specific T cells were capable of killing colorectal tumor lines in vitro, and the IFN-g+ response was markedly magnified by control of immunosuppression with cyclophosphamide in cancer patients.	Cyclophosphamide	165-181	interferon gamma	Homo sapiens	89-94
32173650-3	2020	EXPERIMENTAL DESIGN: Therefore, we conducted a neoadjuvant, randomized study to quantify the immunologic effects of a granulocyte-macrophage colony-stimulating factor (GM-CSF)-secreting allogeneic cellular vaccine in combination with low-dose cyclophosphamide (Cy/GVAX) followed by degarelix versus degarelix alone in patients with high-risk localized prostate adenocarcinoma who were planned for radical prostatectomy.	Cyclophosphamide	243-259	colony stimulating factor 2	Homo sapiens	168-174
32279153-12	2020	ZO-2 expression in the bladder was increased in the CYP + pentosan polysulfate and frankincense + myrrha groups compared with the CYP-induced acute IC/PBS group (P<0.05).	Cyclophosphamide	52-55	tight junction protein 2	Rattus norvegicus	0-4
32279153-12	2020	ZO-2 expression in the bladder was increased in the CYP + pentosan polysulfate and frankincense + myrrha groups compared with the CYP-induced acute IC/PBS group (P<0.05).	Cyclophosphamide	130-133	tight junction protein 2	Rattus norvegicus	0-4
32129080-1	2020	OBJECTIVE: Oxidative stress is one of the major mechanisms of cyclophosphamide (CPX)-induced toxicities.	Cyclophosphamide	62-78	coproporphyrinogen oxidase	Mus musculus	80-83
33680016-0	2020	Naringenin Enhances the Anti-Cancer Effect of Cyclophosphamide against MDA-MB-231 Breast Cancer Cells Via Targeting the STAT3 Signaling Pathway.	Cyclophosphamide	46-62	signal transducer and activator of transcription 3	Homo sapiens	120-125
33680016-11	2020	Caspases 3 and 9 were activated by Naringenin, an influence, which was augmented via cyclophosphamide.	Cyclophosphamide	85-101	caspase 3	Homo sapiens	0-16
32537703-0	2020	Metformin and/or low dose radiation reduces cardiotoxicity and apoptosis induced by cyclophosphamide through SIRT-1/SOD and BAX/Bcl-2 pathways in rats.	Cyclophosphamide	84-100	sirtuin 1	Rattus norvegicus	109-115
32537703-0	2020	Metformin and/or low dose radiation reduces cardiotoxicity and apoptosis induced by cyclophosphamide through SIRT-1/SOD and BAX/Bcl-2 pathways in rats.	Cyclophosphamide	84-100	BCL2 associated X, apoptosis regulator	Rattus norvegicus	124-127
32537703-0	2020	Metformin and/or low dose radiation reduces cardiotoxicity and apoptosis induced by cyclophosphamide through SIRT-1/SOD and BAX/Bcl-2 pathways in rats.	Cyclophosphamide	84-100	BCL2, apoptosis regulator	Rattus norvegicus	128-133
33377721-9	2020	CONCLUSIONS: Cuscuta chinensis flavonoids can significantly down-regulate the expression of GM-CSF in the testis of the rats with cyclophosphamide-induced oligozoospermia.	Cyclophosphamide	130-146	colony stimulating factor 2	Rattus norvegicus	92-98
32606309-4	2020	BCL2 expression of 332 patients (221 patients for the training set and 111 patients for the validation set) with newly diagnosed DLBCL who received R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) were analyzed using the tumor-specific automated quantitative analysis (AQUA) scoring method based on multiplex immunofluorescence.	Cyclophosphamide	167-183	BCL2 apoptosis regulator	Homo sapiens	0-4
32605327-2	2020	The aim of this study was to detect the immunomodulatory effects of EP2 on RAW 264.7 macrophages and cyclophosphamide (CYP)-induced immunosuppression mouse models.	Cyclophosphamide	101-117	prostaglandin E receptor 2 (subtype EP2)	Mus musculus	68-71
32605327-6	2020	Moreover, EP2 significantly increased the body weight, spleen index, thymus index, inflammatory cell counts, and the levels of IL-1beta, IL-6, and TNF-alpha in CYP-induced immunosuppression mouse models.	Cyclophosphamide	160-163	prostaglandin E receptor 2 (subtype EP2)	Mus musculus	10-13
32923145-7	2020	tSNE analysis of the flow data revealed a resident phenotype of CD8+ T cells (PD-1+TIM-3+CTLA-4+) within untreated tumors, whereas DPX/CPA treatment induced recruitment of a novel population of CD8+ T cells (PD-1+TIM-3+CTLA-4-) within tumors.	Cyclophosphamide	135-138	programmed cell death 1	Mus musculus	208-212
32923145-7	2020	tSNE analysis of the flow data revealed a resident phenotype of CD8+ T cells (PD-1+TIM-3+CTLA-4+) within untreated tumors, whereas DPX/CPA treatment induced recruitment of a novel population of CD8+ T cells (PD-1+TIM-3+CTLA-4-) within tumors.	Cyclophosphamide	135-138	hepatitis A virus cellular receptor 2	Mus musculus	213-218
32923145-7	2020	tSNE analysis of the flow data revealed a resident phenotype of CD8+ T cells (PD-1+TIM-3+CTLA-4+) within untreated tumors, whereas DPX/CPA treatment induced recruitment of a novel population of CD8+ T cells (PD-1+TIM-3+CTLA-4-) within tumors.	Cyclophosphamide	135-138	cytotoxic T-lymphocyte-associated protein 4	Mus musculus	219-225
32619893-4	2020	CASE PRESENTATION: We present the case report of a patient with pseudo-tumoral lesion and myelitis refractory to steroids and cyclophosphamide who successfully showed remission after treatment with an anti-CD20 therapy.	Cyclophosphamide	126-142	keratin 20	Homo sapiens	206-210
32578533-5	2020	Tyrosinase-crosslinked alginate sulfate tyramine (ASTA) hydrogels showed strong adhesion to native cartilage tissue with higher bond strength compared to alginate tyramine (AlgTA).	Cyclophosphamide	50-54	tyrosinase	Homo sapiens	0-10
32578533-6	2020	Both ASTA and AlgTA hydrogels supported the viability of encapsulated bovine chondrocytes and induced a strong increase in the expression of chondrogenic genes such as collagen 2, aggrecan and Sox9.	Cyclophosphamide	5-9	SRY-box transcription factor 9	Bos taurus	193-197
32578533-7	2020	Aggrecan and Sox9 gene expression of chondrocytes in ASTA hydrogels were significantly higher than those in AlgTA.	Cyclophosphamide	53-57	SRY-box transcription factor 9	Bos taurus	13-17
31429907-10	2020	Overall, anti-IFN-gamma autoantibody levels decreased over time in Thailand (P&lt;0.001) and the US (P=0.017), as well as with cyclophosphamide (P=0.01) and rituximab therapy (P=0.001).	Cyclophosphamide	127-143	interferon gamma	Homo sapiens	14-23
32651830-4	2020	Enhanced relative expression of the GCLM gene was found in all studied drug-resistant strains; the expression of the GSR and GPX1 genes was increased only in cells of the cyclophosphamide-resistant strain.	Cyclophosphamide	171-187	glutathione peroxidase 1	Mus musculus	125-129
32443586-7	2020	We have found that cyclophosphamide significantly decreased the expression of T cell genes, such as CD3 (cluster of differentiation 3) and CD4, and reduced their infiltration into mouse lung tissues.	Cyclophosphamide	19-35	CD3 antigen, epsilon polypeptide	Mus musculus	100-103
32558438-0	2020	Treatment with Gonadotropin Releasing Hormone Agonists in Systemic Lupus Erythematosus Patients Receiving Cyclophosphamide: A Long-term Follow-up Study.	Cyclophosphamide	106-122	gonadotropin releasing hormone 1	Homo sapiens	15-45
32558438-10	2020	Premature ovarian failure (POF) prevalence was significantly lower in SLE women treated by cyclophosphamide plus triptorelin compared to controls (11.1% vs. 33.3%, P = 0.0002).	Cyclophosphamide	91-107	POF1B actin binding protein	Homo sapiens	27-30
32558438-11	2020	The occurrence of POF was significantly associated with higher age at the time of cyclophosphamide treatment (P = 0.008).	Cyclophosphamide	82-98	POF1B actin binding protein	Homo sapiens	18-21
32558438-13	2020	CONCLUSIONS: The study provides information about the efficacy of co-treatment with GnRH-a in SLE women receiving cyclophosphamide, as demonstrated by the lower POF incidence compared to untreated subjects, based on long-term follow-up.	Cyclophosphamide	114-130	gonadotropin releasing hormone 1	Homo sapiens	84-88
32558438-13	2020	CONCLUSIONS: The study provides information about the efficacy of co-treatment with GnRH-a in SLE women receiving cyclophosphamide, as demonstrated by the lower POF incidence compared to untreated subjects, based on long-term follow-up.	Cyclophosphamide	114-130	POF1B actin binding protein	Homo sapiens	161-164
32443586-7	2020	We have found that cyclophosphamide significantly decreased the expression of T cell genes, such as CD3 (cluster of differentiation 3) and CD4, and reduced their infiltration into mouse lung tissues.	Cyclophosphamide	19-35	CD4 antigen	Mus musculus	139-142
32443586-9	2020	Correspondingly, the expression of the human CFTR transgene has been significantly improved with cyclophosphamide administration compared to the group with no treatment.	Cyclophosphamide	97-113	CF transmembrane conductance regulator	Homo sapiens	45-49
32187361-11	2020	The identification of both good and poor risk subtypes in patients treated with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) clearly show the clinical value of the approach, confirming the need for a consensus classification.	Cyclophosphamide	99-115	DNA damage inducible transcript 3	Homo sapiens	82-86
31776320-0	2020	Neoadjuvant chemotherapy of capecitabine + epirubicin + cyclophosphamide combination therapy ( "CEX" therapy) for HER-2 negative breast cancer, as retrospective study in our institute.	Cyclophosphamide	56-72	erb-b2 receptor tyrosine kinase 2	Homo sapiens	114-119
31776320-1	2020	BACKGROUND: We have modified and performed neoadjuvant chemotherapy (NAC) using capecitabine + epirubicin + cyclophosphamide combination therapy ( "CEX" ) for HER-2 negative breast cancer.	Cyclophosphamide	108-124	erb-b2 receptor tyrosine kinase 2	Homo sapiens	159-164
31869443-0	2020	Digital ulcerations in anti-MDA5 dermatomyositis: Complete resolution following treatment with cyclophosphamide.	Cyclophosphamide	95-111	interferon induced with helicase C domain 1	Homo sapiens	28-32
32577494-5	2020	Continuous oral administration of low-dose CPA (20 mg/kg/day) prevented atherosclerosis in apolipoprotein E-deficient (apoE-/-) mice fed with a high fat diet.	Cyclophosphamide	43-46	apolipoprotein E	Mus musculus	119-123
32577494-11	2020	Conclusions: The results demonstrate that oral treatment with CPA inhibits initiation and progression of atherosclerosis in the apoE-/- mouse model through immunomodulatory effects on lymphoid and inflammatory cells.	Cyclophosphamide	62-65	apolipoprotein E	Mus musculus	128-132
32461977-2	2020	This study is aimed at evaluating the efficacy of epirubicin/cyclophosphamide with weekly paclitaxel-trastuzumab as neoadjuvant chemotherapies in HER2+ BC patients.	Cyclophosphamide	61-77	erb-b2 receptor tyrosine kinase 2	Homo sapiens	146-150
32083540-6	2020	POF was significantly associated with anti-Sm (p=0.0004), anti-RNP (p=0.02), anti-cardiolipin (p=0.0008), lupus anticoagulant (p=0.0002), treatment with cyclophosphamide (p=0.0001), azathioprine (p=0.0001), mycophenolate mofetil (p=0.0001), cyclosporine A (p=0.007).	Cyclophosphamide	153-169	POF1B actin binding protein	Homo sapiens	0-3
31883395-7	2020	Adriyamicin/cyclophosphamide and Paclitaxel resistant MDA-MB-231 cells activated NRP-1/TNC/Integrin beta3/FAK/NF-kappaBp65 axis and displayed a decrease in breast cancer resistant protein (BCRP/ABCB2).	Cyclophosphamide	12-28	neuropilin 1	Homo sapiens	81-86
31883395-7	2020	Adriyamicin/cyclophosphamide and Paclitaxel resistant MDA-MB-231 cells activated NRP-1/TNC/Integrin beta3/FAK/NF-kappaBp65 axis and displayed a decrease in breast cancer resistant protein (BCRP/ABCB2).	Cyclophosphamide	12-28	tenascin C	Homo sapiens	87-90
31883395-7	2020	Adriyamicin/cyclophosphamide and Paclitaxel resistant MDA-MB-231 cells activated NRP-1/TNC/Integrin beta3/FAK/NF-kappaBp65 axis and displayed a decrease in breast cancer resistant protein (BCRP/ABCB2).	Cyclophosphamide	12-28	integrin subunit beta 3	Homo sapiens	91-105
31883395-7	2020	Adriyamicin/cyclophosphamide and Paclitaxel resistant MDA-MB-231 cells activated NRP-1/TNC/Integrin beta3/FAK/NF-kappaBp65 axis and displayed a decrease in breast cancer resistant protein (BCRP/ABCB2).	Cyclophosphamide	12-28	protein tyrosine kinase 2	Homo sapiens	106-109
31883395-7	2020	Adriyamicin/cyclophosphamide and Paclitaxel resistant MDA-MB-231 cells activated NRP-1/TNC/Integrin beta3/FAK/NF-kappaBp65 axis and displayed a decrease in breast cancer resistant protein (BCRP/ABCB2).	Cyclophosphamide	12-28	RELA proto-oncogene, NF-kB subunit	Homo sapiens	110-122
31883395-7	2020	Adriyamicin/cyclophosphamide and Paclitaxel resistant MDA-MB-231 cells activated NRP-1/TNC/Integrin beta3/FAK/NF-kappaBp65 axis and displayed a decrease in breast cancer resistant protein (BCRP/ABCB2).	Cyclophosphamide	12-28	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	189-193
31883395-7	2020	Adriyamicin/cyclophosphamide and Paclitaxel resistant MDA-MB-231 cells activated NRP-1/TNC/Integrin beta3/FAK/NF-kappaBp65 axis and displayed a decrease in breast cancer resistant protein (BCRP/ABCB2).	Cyclophosphamide	12-28	transporter 1, ATP binding cassette subfamily B member	Homo sapiens	194-199
31883395-8	2020	In turn, resistant MCF7 cells to Adriamycin/cyclophosphamide (4xAC), induced HER2 expression which converted MCF7 subtype from being a luminal A to luminal B-HER2 type, upregulated NRP-1, ER-alpha, and EGFR and activated PI3K/AKT/NF-kappaBp65 axis.	Cyclophosphamide	44-60	erb-b2 receptor tyrosine kinase 2	Homo sapiens	77-81
31883395-8	2020	In turn, resistant MCF7 cells to Adriamycin/cyclophosphamide (4xAC), induced HER2 expression which converted MCF7 subtype from being a luminal A to luminal B-HER2 type, upregulated NRP-1, ER-alpha, and EGFR and activated PI3K/AKT/NF-kappaBp65 axis.	Cyclophosphamide	44-60	erb-b2 receptor tyrosine kinase 2	Homo sapiens	158-162
31883395-8	2020	In turn, resistant MCF7 cells to Adriamycin/cyclophosphamide (4xAC), induced HER2 expression which converted MCF7 subtype from being a luminal A to luminal B-HER2 type, upregulated NRP-1, ER-alpha, and EGFR and activated PI3K/AKT/NF-kappaBp65 axis.	Cyclophosphamide	44-60	neuropilin 1	Homo sapiens	181-186
31883395-8	2020	In turn, resistant MCF7 cells to Adriamycin/cyclophosphamide (4xAC), induced HER2 expression which converted MCF7 subtype from being a luminal A to luminal B-HER2 type, upregulated NRP-1, ER-alpha, and EGFR and activated PI3K/AKT/NF-kappaBp65 axis.	Cyclophosphamide	44-60	estrogen receptor 1	Homo sapiens	188-196
31883395-8	2020	In turn, resistant MCF7 cells to Adriamycin/cyclophosphamide (4xAC), induced HER2 expression which converted MCF7 subtype from being a luminal A to luminal B-HER2 type, upregulated NRP-1, ER-alpha, and EGFR and activated PI3K/AKT/NF-kappaBp65 axis.	Cyclophosphamide	44-60	epidermal growth factor receptor	Homo sapiens	202-206
31883395-8	2020	In turn, resistant MCF7 cells to Adriamycin/cyclophosphamide (4xAC), induced HER2 expression which converted MCF7 subtype from being a luminal A to luminal B-HER2 type, upregulated NRP-1, ER-alpha, and EGFR and activated PI3K/AKT/NF-kappaBp65 axis.	Cyclophosphamide	44-60	AKT serine/threonine kinase 1	Homo sapiens	226-229
31883395-8	2020	In turn, resistant MCF7 cells to Adriamycin/cyclophosphamide (4xAC), induced HER2 expression which converted MCF7 subtype from being a luminal A to luminal B-HER2 type, upregulated NRP-1, ER-alpha, and EGFR and activated PI3K/AKT/NF-kappaBp65 axis.	Cyclophosphamide	44-60	RELA proto-oncogene, NF-kB subunit	Homo sapiens	230-242
32083540-8	2020	POF is associated with specific SLE-related autoantibodies and the use of immunosuppressant drugs, in particular cyclophosphamide.	Cyclophosphamide	113-129	POF1B actin binding protein	Homo sapiens	0-3
32250167-1	2020	While combination of rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) cures most patients with diffuse large B-cell lymphoma (DLBCL), those with high-risk international prognostic index disease have inferior survival.	Cyclophosphamide	32-48	DNA damage inducible transcript 3	Homo sapiens	93-97
32568258-6	2020	N-acetylcysteine increased the number of immune cells and decreased TNF-alpha production after cyclophosphamide injection and decreased TNF-alpha, IFN-gamma, NF-kappaB, and IL-8 expression and increased IL-10 expression in peripheral blood mononuclear cells.	Cyclophosphamide	95-111	tumor necrosis factor	Sus scrofa	68-77
32010961-5	2020	This association is highly drug-specific for subgroups treated with the MRP1 substrates cyclophosphamide (log-rank p = 0.0011) and doxorubicin (log-rank p = 0.0088) independent of age and tumor stage, whereas no association was found in individuals treated with tamoxifen (log-rank p = 0.13).	Cyclophosphamide	88-104	ATP binding cassette subfamily C member 1	Homo sapiens	72-76
32953676-7	2020	Conclusion: The combination of cyclophosphamide, prednisolone, and Qing Shen Fang improves conditions of patients with LN and significantly reduces their IFN-gamma and IL-4 levels in serum.	Cyclophosphamide	31-47	interferon gamma	Homo sapiens	154-163
32953676-7	2020	Conclusion: The combination of cyclophosphamide, prednisolone, and Qing Shen Fang improves conditions of patients with LN and significantly reduces their IFN-gamma and IL-4 levels in serum.	Cyclophosphamide	31-47	interleukin 4	Homo sapiens	168-172
32343796-12	2020	Similar results were seen in 10 SAA patients who received the identical nonmyeloablative regimen with posttransplant cyclophosphamide but matched donor transplants.	Cyclophosphamide	117-133	serum amyloid A1 cluster	Homo sapiens	32-35
32462961-6	2020	She was treated with glucocorticoids and cyclophosphamide (CTX) for six months at which time her kidney function had improved and she avoided the need for dialysis.	Cyclophosphamide	41-57	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	59-62
32044694-0	2020	Anti-CV2/CRMP5 antibody-associated hemorrhagic leukoencephalomyelitis treated with steroids, intravenous immunoglobulin, plasmapheresis, and cyclophosphamide.	Cyclophosphamide	141-157	BMP binding endothelial regulator	Homo sapiens	5-8
32044694-0	2020	Anti-CV2/CRMP5 antibody-associated hemorrhagic leukoencephalomyelitis treated with steroids, intravenous immunoglobulin, plasmapheresis, and cyclophosphamide.	Cyclophosphamide	141-157	dihydropyrimidinase like 5	Homo sapiens	9-14
32105755-7	2020	Moreover, cyclophosphamide-induced pain behaviors and referred mechanical hyperalgesia were dose-dependently reduced by sigma1-R antagonists (BD-1063, NE-100 and S1RA) in WT but not in sigma1-KO mice.	Cyclophosphamide	10-26	sigma non-opioid intracellular receptor 1	Mus musculus	120-128
32105755-9	2020	Together these findings suggest that sigma1-R plays a functional role in the mechanisms underlying cyclophosphamide-induced cystitis, and modulates morphine analgesia against urological pain.	Cyclophosphamide	99-115	sigma non-opioid intracellular receptor 1	Mus musculus	37-45
32349779-1	2020	BACKGROUND: Cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP)/CHOP-like chemotherapy is widely used in peripheral T cell lymphoma (PTCL).	Cyclophosphamide	12-28	DNA damage inducible transcript 3	Homo sapiens	74-78
32365611-0	2020	Lipocalin2 Induced by Bacterial Flagellin Protects Mice against Cyclophosphamide Mediated Neutropenic Sepsis.	Cyclophosphamide	64-80	lipocalin 2	Mus musculus	0-10
32365611-4	2020	The TLR5 agonist bacterial flagellin derived from Vibrio vulnificus extended the survival of cyclophosphamide-treated mice by reducing the bacterial load in internal organs.	Cyclophosphamide	93-109	toll-like receptor 5	Mus musculus	4-8
32343796-13	2020	Haplo BMT with posttransplant cyclophosphamide represents a potential cure in SAA, with all 20 R/R currently alive, disease-free, and with no evidence of active GVHD.	Cyclophosphamide	30-46	serum amyloid A1 cluster	Homo sapiens	78-81
32306006-11	2020	Further molecular biological detections found that the lowest lactate level and regulatory T cells ratio were found in Fei-Liu-Ping ointment + cyclophosphamide group and these expressions of GLUT4, HK1, GRP78, CA-IX were suppressed.	Cyclophosphamide	143-159	solute carrier family 2 (facilitated glucose transporter), member 4	Mus musculus	191-196
32175574-0	2020	Corrigendum: G-CSF-mobilized peripheral blood mononuclear cells combined with platelet-rich plasma accelerate restoration of ovarian function in cyclophosphamide-induced POI rats .	Cyclophosphamide	145-161	colony stimulating factor 3	Rattus norvegicus	13-18
32390827-12	2020	CYP2C9 *2 or *3 carriers were associated with increased clearance of CPA.	Cyclophosphamide	69-72	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
32390827-18	2020	CYP3A5 and CYP2C9 genotypes, BSA, BMI, and CPA dosage regimen influence PK of CPA.	Cyclophosphamide	43-46	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
32390827-18	2020	CYP3A5 and CYP2C9 genotypes, BSA, BMI, and CPA dosage regimen influence PK of CPA.	Cyclophosphamide	78-81	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	0-6
32390827-18	2020	CYP3A5 and CYP2C9 genotypes, BSA, BMI, and CPA dosage regimen influence PK of CPA.	Cyclophosphamide	78-81	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	11-17
32306006-11	2020	Further molecular biological detections found that the lowest lactate level and regulatory T cells ratio were found in Fei-Liu-Ping ointment + cyclophosphamide group and these expressions of GLUT4, HK1, GRP78, CA-IX were suppressed.	Cyclophosphamide	143-159	heat shock protein 5	Mus musculus	203-208
32306006-11	2020	Further molecular biological detections found that the lowest lactate level and regulatory T cells ratio were found in Fei-Liu-Ping ointment + cyclophosphamide group and these expressions of GLUT4, HK1, GRP78, CA-IX were suppressed.	Cyclophosphamide	143-159	carbonic anhydrase 9	Mus musculus	210-215
32306006-13	2020	In addition, the Fei-Liu-Ping ointment + cyclophosphamide group"s cell apoptosis increased significantly compared with saline group and there were significant differences on expressions of HIF-1alpha, Bcl-2, Bax, Caspase-3, IL-2 for this group compared with saline group.	Cyclophosphamide	41-57	hypoxia inducible factor 1, alpha subunit	Mus musculus	189-199
32306006-13	2020	In addition, the Fei-Liu-Ping ointment + cyclophosphamide group"s cell apoptosis increased significantly compared with saline group and there were significant differences on expressions of HIF-1alpha, Bcl-2, Bax, Caspase-3, IL-2 for this group compared with saline group.	Cyclophosphamide	41-57	B cell leukemia/lymphoma 2	Mus musculus	201-206
32306006-13	2020	In addition, the Fei-Liu-Ping ointment + cyclophosphamide group"s cell apoptosis increased significantly compared with saline group and there were significant differences on expressions of HIF-1alpha, Bcl-2, Bax, Caspase-3, IL-2 for this group compared with saline group.	Cyclophosphamide	41-57	BCL2-associated X protein	Mus musculus	208-211
32306006-13	2020	In addition, the Fei-Liu-Ping ointment + cyclophosphamide group"s cell apoptosis increased significantly compared with saline group and there were significant differences on expressions of HIF-1alpha, Bcl-2, Bax, Caspase-3, IL-2 for this group compared with saline group.	Cyclophosphamide	41-57	caspase 3	Mus musculus	213-222
32306006-13	2020	In addition, the Fei-Liu-Ping ointment + cyclophosphamide group"s cell apoptosis increased significantly compared with saline group and there were significant differences on expressions of HIF-1alpha, Bcl-2, Bax, Caspase-3, IL-2 for this group compared with saline group.	Cyclophosphamide	41-57	interleukin 2	Mus musculus	224-228
32241292-0	2020	Normalization of magnesium deficiency attenuated mechanical allodynia, depressive-like behaviors, and memory deficits associated with cyclophosphamide-induced cystitis by inhibiting TNF-alpha/NF-kappaB signaling in female rats.	Cyclophosphamide	134-150	tumor necrosis factor	Rattus norvegicus	182-191
32112707-5	2020	In a small sample size, etoposide, prednisone, vincristine, cyclophosphamide, doxorubicin, and rituximab (EPOCH-R) achieved better outcomes than a regimen of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP).	Cyclophosphamide	60-76	DNA damage inducible transcript 3	Homo sapiens	231-235
32097092-0	2020	TBCRC 031: Randomized Phase II Study of Neoadjuvant Cisplatin Versus Doxorubicin-Cyclophosphamide in Germline BRCA Carriers With HER2-Negative Breast Cancer (the INFORM trial).	Cyclophosphamide	81-97	BRCA1 DNA repair associated	Homo sapiens	110-114
32308430-8	2020	The rate of cleaved Caspase-3 expression in the testosterone plus cyclophosphamide group was lower than that in the cyclophosphamide alone group (28.4% vs 48.6%, p=0.03).	Cyclophosphamide	66-82	caspase 3	Homo sapiens	20-29
32308430-8	2020	The rate of cleaved Caspase-3 expression in the testosterone plus cyclophosphamide group was lower than that in the cyclophosphamide alone group (28.4% vs 48.6%, p=0.03).	Cyclophosphamide	116-132	caspase 3	Homo sapiens	20-29
31866283-0	2020	Ovarian protection with gonadotropin-releasing hormone agonists during cyclophosphamide therapy in systemic lupus erythematosus.	Cyclophosphamide	71-87	gonadotropin releasing hormone 1	Homo sapiens	24-54
31899360-0	2020	Donor KIR2DS1-mediated Decreased Relapse and Improved Survival, Depending on Remission Status at HLA-Haploidentical Transplantation with Post-transplantation Cyclophosphamide.	Cyclophosphamide	158-174	killer cell immunoglobulin like receptor, two Ig domains and short cytoplasmic tail 1	Homo sapiens	6-13
32066295-7	2020	Furthermore; histological changes, tumor necrosis factor (TNF) and caspase-3 immuno-expressions were evaluated.Results: CYC group showed hepatotoxic effect in the form of a significant increase in ALT, AST, MDA, NOx, IL-1beta levels; TNF and caspase-3 immuno-expression.	Cyclophosphamide	120-123	tumor necrosis factor-like	Rattus norvegicus	35-56
32066295-7	2020	Furthermore; histological changes, tumor necrosis factor (TNF) and caspase-3 immuno-expressions were evaluated.Results: CYC group showed hepatotoxic effect in the form of a significant increase in ALT, AST, MDA, NOx, IL-1beta levels; TNF and caspase-3 immuno-expression.	Cyclophosphamide	120-123	tumor necrosis factor-like	Rattus norvegicus	58-61
32066295-7	2020	Furthermore; histological changes, tumor necrosis factor (TNF) and caspase-3 immuno-expressions were evaluated.Results: CYC group showed hepatotoxic effect in the form of a significant increase in ALT, AST, MDA, NOx, IL-1beta levels; TNF and caspase-3 immuno-expression.	Cyclophosphamide	120-123	caspase 3	Rattus norvegicus	67-76
32066295-7	2020	Furthermore; histological changes, tumor necrosis factor (TNF) and caspase-3 immuno-expressions were evaluated.Results: CYC group showed hepatotoxic effect in the form of a significant increase in ALT, AST, MDA, NOx, IL-1beta levels; TNF and caspase-3 immuno-expression.	Cyclophosphamide	120-123	interleukin 1 alpha	Rattus norvegicus	217-225
32066295-7	2020	Furthermore; histological changes, tumor necrosis factor (TNF) and caspase-3 immuno-expressions were evaluated.Results: CYC group showed hepatotoxic effect in the form of a significant increase in ALT, AST, MDA, NOx, IL-1beta levels; TNF and caspase-3 immuno-expression.	Cyclophosphamide	120-123	tumor necrosis factor-like	Rattus norvegicus	234-237
32066295-7	2020	Furthermore; histological changes, tumor necrosis factor (TNF) and caspase-3 immuno-expressions were evaluated.Results: CYC group showed hepatotoxic effect in the form of a significant increase in ALT, AST, MDA, NOx, IL-1beta levels; TNF and caspase-3 immuno-expression.	Cyclophosphamide	120-123	caspase 3	Rattus norvegicus	242-251
32066295-9	2020	Ketotifen showed a significant improvement in all parameters.Conclusion: Mast cell stabilizer, ketotifen possesses potent ameliorative effects against the hepatotoxic effect of CYC by reducing oxidative stress, inflammatory process, and apoptosis through regulation of Sirt1/Nrf2/TNF pathway.	Cyclophosphamide	177-180	sirtuin 1	Rattus norvegicus	269-274
32066295-9	2020	Ketotifen showed a significant improvement in all parameters.Conclusion: Mast cell stabilizer, ketotifen possesses potent ameliorative effects against the hepatotoxic effect of CYC by reducing oxidative stress, inflammatory process, and apoptosis through regulation of Sirt1/Nrf2/TNF pathway.	Cyclophosphamide	177-180	NFE2 like bZIP transcription factor 2	Rattus norvegicus	275-279
32066295-9	2020	Ketotifen showed a significant improvement in all parameters.Conclusion: Mast cell stabilizer, ketotifen possesses potent ameliorative effects against the hepatotoxic effect of CYC by reducing oxidative stress, inflammatory process, and apoptosis through regulation of Sirt1/Nrf2/TNF pathway.	Cyclophosphamide	177-180	tumor necrosis factor-like	Rattus norvegicus	280-283
32020412-10	2020	CONCLUSION: Our study may provide evidence that PRP could protect ovarian function against ovarian damage induced by Cy.	Cyclophosphamide	117-119	proline rich protein 2-like 1	Rattus norvegicus	48-51
32566462-8	2020	In addition, circulating concentrations of VEGF are reduced by cyclophosphamide administered at continuous low doses, which might underpin some of the observed vascular toxicity, such as stroke, as seen in patients treated with VEGF inhibitors.	Cyclophosphamide	63-79	vascular endothelial growth factor A	Homo sapiens	43-47
32566462-8	2020	In addition, circulating concentrations of VEGF are reduced by cyclophosphamide administered at continuous low doses, which might underpin some of the observed vascular toxicity, such as stroke, as seen in patients treated with VEGF inhibitors.	Cyclophosphamide	63-79	vascular endothelial growth factor A	Homo sapiens	228-232
32269142-5	2020	CASE PRESENTATION: We launched a phase I trial incorporating four weekly doses of IFN-gamma in an ACT regimen of high-dose cyclophosphamide (HD Cy), NY-ESO-1-specific T cells, and postinfusion low-dose interleukin (IL)-2.	Cyclophosphamide	123-139	interferon gamma	Homo sapiens	82-91
32079091-6	2020	For the current study, the coding regions of KRAS were deep-sequenced in 80 newly diagnosed MM patients, uniformely treated with three cycles of bortezomib plus dexamethasone and cyclophosphamide (VCD)-induction, followed by high-dose chemotherapy and autologous stem cell transplantation.	Cyclophosphamide	179-195	KRAS proto-oncogene, GTPase	Homo sapiens	45-49
32172395-0	2020	Characterization of a Long-Acting Site-Specific PEGylated Murine GM-CSF Analog and Analysis of Its Hematopoietic Properties in Normal and Cyclophosphamide-Treated Neutropenic Rats.	Cyclophosphamide	138-154	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	65-71
32164276-11	2020	In fact, patients carrying mutated IGHV genes in the absence of TP53 disruption experience a long-lasting and durable response to chemoimmunotherapy after fludarabine, cyclophosphamide, and rituximab (FCR) treatment with a survival superimposable to that of a matched general population.	Cyclophosphamide	168-184	immunoglobulin heavy variable 3-69-1 (pseudogene)	Homo sapiens	35-39
31524333-0	2020	A Multicenter Prospective Study of the Efficacy and Safety of Combined Immunosuppressive Therapy with High-Dose Glucocorticoid, Tacrolimus, and Cyclophosphamide in Interstitial Lung Diseases Accompanied by Anti-Melanoma Differentiation-Associated Gene 5-Positive Dermatomyositis.	Cyclophosphamide	144-160	interferon induced with helicase C domain 1	Homo sapiens	206-253
31089272-0	2020	CTLA4Ig-based T-cell costimulation blockade is associated with reduction of adenovirus viremia following post-transplantation cyclophosphamide-based haploidentical transplantation.	Cyclophosphamide	126-142	cytotoxic T-lymphocyte associated protein 4	Homo sapiens	0-5
32057615-0	2020	Mobilization kinetics of CD34+ hematopoietic stem cells stimulated by G-CSF and cyclophosphamide in patients with multiple sclerosis who receive an autotransplant.	Cyclophosphamide	80-96	CD34 molecule	Homo sapiens	25-29
32057615-13	2020	CONCLUSIONS: Mobilization with G-CSF and Cy in MS patients resulted in effective CD34+ hematoprogenitors release from the bone marrow and in intra-apheresis recruitment.	Cyclophosphamide	41-43	CD34 molecule	Homo sapiens	81-85
32231196-6	2020	RESULTS: The high CD5 expression level was linked to better bendamustine (BEN) and cyclophosphamide (CP) CLL B cells response in contrast to B cells with low CD5 expression.	Cyclophosphamide	83-99	CD5 molecule	Homo sapiens	18-21
31620822-7	2020	It was found that CH could ameliorate CYP-induced elevations of ALT, ALP, AST, urea, creatinine, MDA, and hepatorenal deterioration, and enhance antioxidant enzymes" activities such as SOD, CAT, and GPx, and GSH"s level.	Cyclophosphamide	38-41	PDZ and LIM domain 3	Rattus norvegicus	69-72
32093742-2	2020	Immunosuppressive therapy with cyclophosphamide (CTX) is often successful in reducing proteinuria, but its use is associated with severe side effects.	Cyclophosphamide	31-47	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	49-52
32290265-4	2020	In the present study, we show that combined anti-PDL1 and anti-PDL2 antibodies optimally synergize with cyclophosphamide but not with cisplatin, and that the magnitude and duration of the therapeutic response is dependent on the immunogenic potential of the drug and of the tumor itself.	Cyclophosphamide	104-120	CD274 molecule	Homo sapiens	49-53
32290265-4	2020	In the present study, we show that combined anti-PDL1 and anti-PDL2 antibodies optimally synergize with cyclophosphamide but not with cisplatin, and that the magnitude and duration of the therapeutic response is dependent on the immunogenic potential of the drug and of the tumor itself.	Cyclophosphamide	104-120	programmed cell death 1 ligand 2	Homo sapiens	63-67
30778771-0	2020	Association of SLC28A3 Gene Expression and CYP2B6*6 Allele with the Response to Fludarabine Plus Cyclophosphamide in Chronic Lymphocytic Leukemia Patients.	Cyclophosphamide	97-113	solute carrier family 28 member 3	Homo sapiens	15-22
30778771-0	2020	Association of SLC28A3 Gene Expression and CYP2B6*6 Allele with the Response to Fludarabine Plus Cyclophosphamide in Chronic Lymphocytic Leukemia Patients.	Cyclophosphamide	97-113	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	43-49
32231024-0	2020	Genetic Polymorphism of GSTP-1 Affects Cyclophosphamide Treatment of Autoimmune Diseases.	Cyclophosphamide	39-55	glutathione S-transferase pi 1	Homo sapiens	24-30
32231024-6	2020	It was found that the GSTP1 I105V allelic variation significantly associated with the cyclophosphamide treatment-dependent disease-remissions.	Cyclophosphamide	86-102	glutathione S-transferase pi 1	Homo sapiens	22-27
32231024-9	2020	Since this variant of GSTP1 can be characterized by lower conjugation capacity that results in an elongated and higher therapeutic dose of cyclophosphamide, our data suggest that the decreased activity of this variant of GSTP1 can be in the background of the more effective disease treatment.	Cyclophosphamide	139-155	glutathione S-transferase pi 1	Homo sapiens	22-27
32231024-9	2020	Since this variant of GSTP1 can be characterized by lower conjugation capacity that results in an elongated and higher therapeutic dose of cyclophosphamide, our data suggest that the decreased activity of this variant of GSTP1 can be in the background of the more effective disease treatment.	Cyclophosphamide	139-155	glutathione S-transferase pi 1	Homo sapiens	221-226
32175536-0	2020	Longan pulp polysaccharide protects against cyclophosphamide-induced immunosuppression in mice by promoting intestinal secretory IgA synthesis.	Cyclophosphamide	44-60	immunoglobulin heavy constant alpha	Mus musculus	129-132
32175536-3	2020	Results showed that LP increased the thymus index, spleen index, and serum IgA level in cyclophosphamide (CTX)-treated mice.	Cyclophosphamide	88-104	immunoglobulin heavy constant alpha	Mus musculus	75-78
32269999-0	2020	A Qualitative Transcriptional Signature for Predicting Extreme Resistance of ER-Negative Breast Cancer to Paclitaxel, Doxorubicin, and Cyclophosphamide Neoadjuvant Chemotherapy.	Cyclophosphamide	135-151	estrogen receptor 1	Homo sapiens	77-79
32231196-10	2020	The CD180 expression was detected in CLL B cells which were more susceptible to fludarabine and cyclophosphamide (FC) combinatory action.	Cyclophosphamide	96-112	CD180 molecule	Homo sapiens	4-9
31707050-12	2020	The effect of SF-PQR on reversing immunosuppression induced by cyclophosphamide was significantly reduced (P < 0.05) evidenced by the inhibition of net growth rate of body weight, immune organ index, IL-6 level and SOD activity.	Cyclophosphamide	63-79	interleukin 6	Mus musculus	200-204
31537899-5	2020	Furthermore, we demonstrate that BMSC-derived exosomes prevent ovarian follicular atresia in cyclophosphamide (CTX)-treated rats via the delivery of miR-144-5p, which can be transferred to cocultured CTX-damaged granulosa cells (GCs) to decrease GC apoptosis.	Cyclophosphamide	93-109	microRNA 144	Rattus norvegicus	149-156
31900967-3	2020	In addition, there was a paucity of studies investigating the difference of therapeutic effects between Cyclophosphamide and Cyclosporin A in PLA2R-associated IMN.	Cyclophosphamide	104-120	phospholipase A2 receptor 1	Homo sapiens	142-147
31900967-10	2020	In PLA2R-associated IMN, patients receiving cyclophosphamide had a higher probability to achieve remission compared with those receiving cyclosporin A (Log-rank test, P = 0.018) while there was no difference in renal survival.	Cyclophosphamide	44-60	phospholipase A2 receptor 1	Homo sapiens	3-8
31900967-13	2020	Compared with cyclosporin A, cyclophosphamide exerted better therapeutic effects in remission of proteinuria and may be the preferred immunosuppressant for PLA2R-associated IMN.	Cyclophosphamide	29-45	phospholipase A2 receptor 1	Homo sapiens	156-161
31025241-2	2020	The commonly used chemotherapy drug, cyclophosphamide (CTX), induces liver injury by increasing the reactive oxygen species (ROS) level.	Cyclophosphamide	37-53	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	55-58
32135634-0	2020	[The effects of cyclophosphamide binding mesenchymal stem cells on IFN-gamma induced 32D cells apoptosis and its mechanism].	Cyclophosphamide	16-32	interferon gamma	Mus musculus	67-76
31821109-6	2020	CRx was either docetaxel plus cyclophosphamide or doxorubicin and cyclophosphamide followed by weekly paclitaxel for 12 weeks.	Cyclophosphamide	66-82	cone-rod homeobox	Homo sapiens	0-3
32033362-6	2020	Cyclophosphamide-intoxicated mice showed significant increases (p &lt; 0.05) in the serum levels of liver enzymes, pancreatic amylase and tissue levels of malondialdehyde, and TNF-alpha, as well as a significant decrease (p &lt; 0.05) in the serum insulin level.	Cyclophosphamide	0-16	tumor necrosis factor	Mus musculus	176-185
31812447-12	2020	It was also observed that, while p27 immunoreactivity significantly increased in the nuclei of granulosa and theca cells in the CYP group; MgSO4 treatment significantly reduced these immunoreactivities.	Cyclophosphamide	128-131	cyclin-dependent kinase inhibitor 1B	Rattus norvegicus	33-36
31869244-0	2020	Cyclophosphamide-induced cystitis results in NLRP3-mediated inflammation in the hippocampus and symptoms of depression in rats.	Cyclophosphamide	0-16	NLR family, pyrin domain containing 3	Rattus norvegicus	45-50
31765733-4	2020	Antibody against the type-I interferon receptor IFNAR1 blocked the cyclophosphamide-stimulated induction of these genes in both cultured glioma cells and implanted gliomas.	Cyclophosphamide	67-83	interferon alpha and beta receptor subunit 1	Homo sapiens	48-54
31765733-5	2020	Furthermore, IFNAR1 antibody strongly inhibited the MEDIC cyclophosphamide-stimulated increases in tumor cell infiltration of macrophages, dendritic cells, B-cells, as well as natural killer cells and cytotoxic T-cells and their cytotoxic effectors.	Cyclophosphamide	58-74	interferon alpha and beta receptor subunit 1	Homo sapiens	13-19
31902733-4	2020	Our findings demonstrate good outcomes following induction treatment with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone), suggesting that these cases can be treated as DLBCL rather than primary central nervous system lymphoma, obviating the need for more aggressive and toxic approaches.	Cyclophosphamide	93-109	DNA damage inducible transcript 3	Homo sapiens	76-80
31734373-6	2020	In this study, a purified polysaccharide was primarily extracted from the flowers of Apios americana Medik (AAM), which can improve the immunosuppression induced by cyclophosphamide (CTX).	Cyclophosphamide	165-181	V-set and immunoglobulin domain containing 2	Mus musculus	183-186
32211111-1	2020	This study aimed to determine the correlation of human epidermal growth factor receptor 2 (HER2) codon 655 A>G polymorphism with cardiotoxicity risk in HER2-positive breast cancer patients undergoing epirubicin/cyclophosphamide followed by docetaxel plus trastuzumab (EC-D-T) adjuvant chemotherapy.	Cyclophosphamide	211-227	erb-b2 receptor tyrosine kinase 2	Homo sapiens	55-89
32211111-1	2020	This study aimed to determine the correlation of human epidermal growth factor receptor 2 (HER2) codon 655 A>G polymorphism with cardiotoxicity risk in HER2-positive breast cancer patients undergoing epirubicin/cyclophosphamide followed by docetaxel plus trastuzumab (EC-D-T) adjuvant chemotherapy.	Cyclophosphamide	211-227	erb-b2 receptor tyrosine kinase 2	Homo sapiens	91-95
32028388-7	2020	INTERVENTIONS: The patient was successfully treated by Poly-chemotherapy with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vindesine and prednisolone).	Cyclophosphamide	97-113	DNA damage inducible transcript 3	Homo sapiens	80-84
31631445-11	2020	Mobilization after <=3 chemotherapy cycles and cycles including cyclophosphamide resulted in a significantly higher yield of CD34+ cells.	Cyclophosphamide	64-80	CD34 molecule	Homo sapiens	125-129
32027281-1	2020	OBJECTIVE: To analyze the clinical efficacy and side effects of reduced-dose of cyclophosphamide combined cyclosporine A for severe aplastic anemia(SAA) children.	Cyclophosphamide	80-96	serum amyloid A1 cluster	Homo sapiens	148-151
31880407-3	2020	Herein, we report a 14-year-old girl of Haitian descent with sickle beta zero thalassemia on chronic hydroxyurea therapy who developed FMS-like tyrosine kinase 3 (FLT3)-mutated acute myeloid leukemia and underwent a complete disease remission following a combination chemotherapy with sorafenib and was subsequently treated using a T cell replete unmanipulated haploidentical bone marrow transplantation followed by post-transplant cyclophosphamide.	Cyclophosphamide	432-448	fms related receptor tyrosine kinase 3	Homo sapiens	135-161
31880407-3	2020	Herein, we report a 14-year-old girl of Haitian descent with sickle beta zero thalassemia on chronic hydroxyurea therapy who developed FMS-like tyrosine kinase 3 (FLT3)-mutated acute myeloid leukemia and underwent a complete disease remission following a combination chemotherapy with sorafenib and was subsequently treated using a T cell replete unmanipulated haploidentical bone marrow transplantation followed by post-transplant cyclophosphamide.	Cyclophosphamide	432-448	fms related receptor tyrosine kinase 3	Homo sapiens	163-167
32055439-4	2020	We report a patient with anti-MDA5 Ab-positive RP-ILD who was refractory to intensive therapies including steroids, cyclosporine, and intravenous cyclophosphamide, and then treated by PE to prevent the progression of RP-ILD.	Cyclophosphamide	146-162	interferon induced with helicase C domain 1	Homo sapiens	30-34
32027281-8	2020	CONCLUSION: The results show that reduced-dose cyclophosphamide (30 mg/kg d for 4 consecutive days) combinated with CsA (initial dose 4 mg/kg d, and drugvallery concentration >150 ng/ml) can make 7 of 10 children with severe aplastic anemia achieve complete response or partial response, and this regimen may be the second line regimen selected for some SAA children.	Cyclophosphamide	47-63	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	116-119
32027281-8	2020	CONCLUSION: The results show that reduced-dose cyclophosphamide (30 mg/kg d for 4 consecutive days) combinated with CsA (initial dose 4 mg/kg d, and drugvallery concentration >150 ng/ml) can make 7 of 10 children with severe aplastic anemia achieve complete response or partial response, and this regimen may be the second line regimen selected for some SAA children.	Cyclophosphamide	47-63	serum amyloid A1 cluster	Homo sapiens	354-357
32023984-0	2020	Low Dose Cyclophosphamide Modulates Tumor Microenvironment by TGF-beta Signaling Pathway.	Cyclophosphamide	9-25	transforming growth factor alpha	Mus musculus	62-70
33346421-0	2020	[Regulatory effect of Jinkui Shenqi Pills on the gene expression of the Nrf2 signaling pathway in cyclophosphamide-induced testis injury in mice].	Cyclophosphamide	98-114	nuclear factor, erythroid derived 2, like 2	Mus musculus	72-76
33346421-9	2020	CONCLUSIONS: Jinkui Shenqi Pills can effectively inhibit cyclophosphamide-induced testis injury, which may be related to its effect of regulating the gene expression of the Nrf2 signaling pathway and enhancing the activity of antioxidant enzymes.	Cyclophosphamide	57-73	nuclear factor, erythroid derived 2, like 2	Mus musculus	173-177
31821506-13	2020	Docetaxel, cyclophosphamide and trastuzumab might be an option for primary systemic therapy in human epidermal growth factor receptor-2-positive early breast cancer.	Cyclophosphamide	11-27	erb-b2 receptor tyrosine kinase 2	Homo sapiens	101-135
31672491-6	2020	In addition, the combination significantly enhanced inhibition on tumor cell proliferation by standard EwS chemotherapy drugs, including cyclophosphamide and ifosfamide.	Cyclophosphamide	137-153	EWS RNA binding protein 1	Homo sapiens	103-106
31931832-3	2020	Moreover, it has been shown that brain-derived neurotrophic factor (BDNF) participates in the regulation of neuroinflammation and pathological pain through BDNF-TrkB signaling; however, whether it plays a role in cyclophosphamide (CYP)-induced cystitis remains unclear.	Cyclophosphamide	231-234	brain derived neurotrophic factor	Homo sapiens	68-72
32010435-3	2020	Here, we investigated the combination of the WEE1 inhibitor, AZD1775, with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) and radiation therapy (RT), with the aim of improving first-line treatment.	Cyclophosphamide	75-91	WEE1 G2 checkpoint kinase	Sus scrofa	45-49
31931832-0	2020	BDNF promotes activation of astrocytes and microglia contributing to neuroinflammation and mechanical allodynia in cyclophosphamide-induced cystitis.	Cyclophosphamide	115-131	brain derived neurotrophic factor	Homo sapiens	0-4
31915006-6	2020	The serum KL-6 level of 32 patients from the CTD-ILD group who received cyclophosphamide (CTX) pulse therapy were sampled and measured, by enzyme linked immunosorbent assay (ELISA), at three time points: before treatment, 3 months after treatment and 6 months after treatment.	Cyclophosphamide	72-88	mucin 1, cell surface associated	Homo sapiens	10-14
31654636-0	2020	Keratinocyte growth factor reduces injury and leads to early recovery from cyclophosphamide bladder injury.	Cyclophosphamide	75-91	fibroblast growth factor 7	Mus musculus	0-26
31654636-1	2020	Keratinocyte growth factor (KGF) improves outcomes after cyclophosphamide-induced bladder injury.	Cyclophosphamide	57-73	fibroblast growth factor 7	Mus musculus	0-26
31654636-1	2020	Keratinocyte growth factor (KGF) improves outcomes after cyclophosphamide-induced bladder injury.	Cyclophosphamide	57-73	fibroblast growth factor 7	Mus musculus	28-31
31654636-5	2020	Six and 24 hours post-cyclophosphamide treatment, KGF-pretreated mice also had apparent pERK-driven proliferation of mostly keratin 5 (KRT5)+/KRT14- intermediate cells.	Cyclophosphamide	22-38	fibroblast growth factor 7	Mus musculus	50-53
31654636-5	2020	Six and 24 hours post-cyclophosphamide treatment, KGF-pretreated mice also had apparent pERK-driven proliferation of mostly keratin 5 (KRT5)+/KRT14- intermediate cells.	Cyclophosphamide	22-38	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	88-92
31654636-8	2020	Ten and 28 days post cyclophosphamide treatment, KGF-pretreated mice had little proliferation and marked restoration of urothelial layers, whereas the PBS-group had ongoing regeneration.	Cyclophosphamide	21-37	fibroblast growth factor 7	Mus musculus	49-52
31654636-10	2020	KGF-pretreatment blocks cyclophosphamide-induced intermediate and basal cell apoptosis likely by pAKT and drives pERK-mediated KRT5+/KRT14- cell proliferation, leading to early urothelial regeneration.	Cyclophosphamide	24-40	fibroblast growth factor 7	Mus musculus	0-3
32475918-7	2020	PSP elevated the CD4+/CD8+ ratio is a dose-dependent manner and increased the levels of interleukin-2 (IL-2) and tumor necrosis factor-alpha (TNF-alpha) in the sera of Cy-treated mice.	Cyclophosphamide	168-170	CD4 antigen	Mus musculus	17-20
32475918-7	2020	PSP elevated the CD4+/CD8+ ratio is a dose-dependent manner and increased the levels of interleukin-2 (IL-2) and tumor necrosis factor-alpha (TNF-alpha) in the sera of Cy-treated mice.	Cyclophosphamide	168-170	interleukin 2	Mus musculus	88-101
32475918-7	2020	PSP elevated the CD4+/CD8+ ratio is a dose-dependent manner and increased the levels of interleukin-2 (IL-2) and tumor necrosis factor-alpha (TNF-alpha) in the sera of Cy-treated mice.	Cyclophosphamide	168-170	interleukin 2	Mus musculus	103-107
32475918-7	2020	PSP elevated the CD4+/CD8+ ratio is a dose-dependent manner and increased the levels of interleukin-2 (IL-2) and tumor necrosis factor-alpha (TNF-alpha) in the sera of Cy-treated mice.	Cyclophosphamide	168-170	tumor necrosis factor	Mus musculus	113-140
32475918-7	2020	PSP elevated the CD4+/CD8+ ratio is a dose-dependent manner and increased the levels of interleukin-2 (IL-2) and tumor necrosis factor-alpha (TNF-alpha) in the sera of Cy-treated mice.	Cyclophosphamide	168-170	tumor necrosis factor	Mus musculus	142-151
32356430-0	2020	LLLT enhance cyclophosphamide induced TRPM2 channel activation in human colon cancer cells.	Cyclophosphamide	13-29	transient receptor potential cation channel subfamily M member 2	Homo sapiens	38-43
32356430-2	2020	We aimed to reveal the effects of (LLLT) on apoptosis of colon cancer and on the efficacy of cyclophosphamide via Transient receptor potential melastatin 2 (TRPM2) channels.	Cyclophosphamide	93-109	transient receptor potential cation channel subfamily M member 2	Homo sapiens	114-155
32356430-2	2020	We aimed to reveal the effects of (LLLT) on apoptosis of colon cancer and on the efficacy of cyclophosphamide via Transient receptor potential melastatin 2 (TRPM2) channels.	Cyclophosphamide	93-109	transient receptor potential cation channel subfamily M member 2	Homo sapiens	157-162
32356430-7	2020	TRPM2 channel stimulator administration resulted in significantly increased apoptosis levels compared to the control group, in cyclophosphamide + low level laser group the apoptosis level was significantly increased compared to the cyclophosphamide-only group.	Cyclophosphamide	127-143	transient receptor potential cation channel subfamily M member 2	Homo sapiens	0-5
32356430-7	2020	TRPM2 channel stimulator administration resulted in significantly increased apoptosis levels compared to the control group, in cyclophosphamide + low level laser group the apoptosis level was significantly increased compared to the cyclophosphamide-only group.	Cyclophosphamide	232-248	transient receptor potential cation channel subfamily M member 2	Homo sapiens	0-5
32356430-8	2020	CONCLUSIONS: It has been shown that apoptotic effects of cyclophosphamide on colon cancer cells were directly related to TRPM2 channels, low level laser increased apoptosis in colon cancer cells through TRPM2 channels and induced apoptotic effect of cyclophosphamide (Fig.	Cyclophosphamide	57-73	transient receptor potential cation channel subfamily M member 2	Homo sapiens	121-126
32356430-8	2020	CONCLUSIONS: It has been shown that apoptotic effects of cyclophosphamide on colon cancer cells were directly related to TRPM2 channels, low level laser increased apoptosis in colon cancer cells through TRPM2 channels and induced apoptotic effect of cyclophosphamide (Fig.	Cyclophosphamide	57-73	transient receptor potential cation channel subfamily M member 2	Homo sapiens	203-208
32356430-8	2020	CONCLUSIONS: It has been shown that apoptotic effects of cyclophosphamide on colon cancer cells were directly related to TRPM2 channels, low level laser increased apoptosis in colon cancer cells through TRPM2 channels and induced apoptotic effect of cyclophosphamide (Fig.	Cyclophosphamide	250-266	transient receptor potential cation channel subfamily M member 2	Homo sapiens	121-126
32356430-8	2020	CONCLUSIONS: It has been shown that apoptotic effects of cyclophosphamide on colon cancer cells were directly related to TRPM2 channels, low level laser increased apoptosis in colon cancer cells through TRPM2 channels and induced apoptotic effect of cyclophosphamide (Fig.	Cyclophosphamide	250-266	transient receptor potential cation channel subfamily M member 2	Homo sapiens	203-208
31702882-0	2020	Pretransplant active disease status and HLA class II mismatching are associated with increased incidence and severity of cytokine release syndrome after haploidentical transplantation with posttransplant cyclophosphamide.	Cyclophosphamide	204-220	major histocompatibility complex, class II, DR beta 1	Homo sapiens	40-43
31702882-1	2020	Cytokine release syndrome (CRS) represents a life-threatening side effect after haploidentical stem cell transplantation (Haplo-SCT) with posttransplant cyclophosphamide (PT-Cy).	Cyclophosphamide	153-169	twist family bHLH transcription factor 1	Homo sapiens	27-30
31555969-0	2020	Analysis of glutathione S-transferase and cytochrome P450 gene polymorphism in recipients of dose-adjusted busulfan-cyclophosphamide conditioning.	Cyclophosphamide	107-132	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	42-57
31773494-0	2020	Correction to: Analysis of glutathione S-transferase and cytochrome P450 gene polymorphism in recipients of dose-adjusted busulfan-cyclophosphamide conditioning.	Cyclophosphamide	122-147	glutathione S-transferase kappa 1	Homo sapiens	27-52
31773494-0	2020	Correction to: Analysis of glutathione S-transferase and cytochrome P450 gene polymorphism in recipients of dose-adjusted busulfan-cyclophosphamide conditioning.	Cyclophosphamide	122-147	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	57-72
32922496-0	2020	STAT3-mediated Apoptotic-enhancing Function of Sclareol Against Breast Cancer Cells and Cell Sensitization to Cyclophosphamide.	Cyclophosphamide	110-126	signal transducer and activator of transcription 3	Homo sapiens	0-5
31931832-4	2020	This study aimed to confirm whether BDNF-TrkB signaling modulates neuroinflammation and mechanical allodynia in CYP-induced cystitis and determine how it occurs.	Cyclophosphamide	112-115	brain derived neurotrophic factor	Homo sapiens	36-40
31931832-4	2020	This study aimed to confirm whether BDNF-TrkB signaling modulates neuroinflammation and mechanical allodynia in CYP-induced cystitis and determine how it occurs.	Cyclophosphamide	112-115	neurotrophic receptor tyrosine kinase 2	Homo sapiens	41-45
31931832-9	2020	RESULTS: BDNF-TrkB signaling was upregulated significantly in the SDH after CYP was injected.	Cyclophosphamide	76-79	brain derived neurotrophic factor	Homo sapiens	9-13
31931832-9	2020	RESULTS: BDNF-TrkB signaling was upregulated significantly in the SDH after CYP was injected.	Cyclophosphamide	76-79	neurotrophic receptor tyrosine kinase 2	Homo sapiens	14-18
31931832-12	2020	Besides, the intrathecal injection of exogenous BDNF further decreased the mechanical withdrawal threshold, promoted activation of astrocytes and microglia, and increased the release of TNF-alpha and IL-1beta in the SDH of our CYP-induced cystitis model.	Cyclophosphamide	227-230	brain derived neurotrophic factor	Homo sapiens	48-52
31931832-12	2020	Besides, the intrathecal injection of exogenous BDNF further decreased the mechanical withdrawal threshold, promoted activation of astrocytes and microglia, and increased the release of TNF-alpha and IL-1beta in the SDH of our CYP-induced cystitis model.	Cyclophosphamide	227-230	tumor necrosis factor	Homo sapiens	186-195
31931832-12	2020	Besides, the intrathecal injection of exogenous BDNF further decreased the mechanical withdrawal threshold, promoted activation of astrocytes and microglia, and increased the release of TNF-alpha and IL-1beta in the SDH of our CYP-induced cystitis model.	Cyclophosphamide	227-230	interleukin 1 beta	Homo sapiens	200-208
31931832-13	2020	CONCLUSIONS: In our CYP-induced cystitis model, BDNF promoted the activation of astrocytes and microglia to release TNF-alpha and IL-1beta, aggravating neuroinflammation and leading to mechanical allodynia through BDNF-TrkB-p38/JNK signaling.	Cyclophosphamide	20-23	brain derived neurotrophic factor	Homo sapiens	48-52
31931832-13	2020	CONCLUSIONS: In our CYP-induced cystitis model, BDNF promoted the activation of astrocytes and microglia to release TNF-alpha and IL-1beta, aggravating neuroinflammation and leading to mechanical allodynia through BDNF-TrkB-p38/JNK signaling.	Cyclophosphamide	20-23	tumor necrosis factor	Homo sapiens	116-125
31931832-13	2020	CONCLUSIONS: In our CYP-induced cystitis model, BDNF promoted the activation of astrocytes and microglia to release TNF-alpha and IL-1beta, aggravating neuroinflammation and leading to mechanical allodynia through BDNF-TrkB-p38/JNK signaling.	Cyclophosphamide	20-23	interleukin 1 beta	Homo sapiens	130-138
31709586-4	2020	In addition, followed by the preservation of histo-architectures of the epididymis, testes, and brain in the rats treated with CPA, curcumin helped in increasing the sperm quality and quantity and suppressing both the inflammatory indices and the activities of caspase-3, while pretreatment with curcumin gave a better result than posttreatment with curcumin.	Cyclophosphamide	127-130	caspase 3	Rattus norvegicus	261-270
31570787-5	2020	We exposed preneoplastic, hTERT-immortalized Barrett"s cell, CP-C and CP-A, to the oncogenic bile acid, deoxycholic acid (DCA), for 1 year.	Cyclophosphamide	61-65	telomerase reverse transcriptase	Homo sapiens	26-31
31729056-0	2020	Cannabinoid receptor 2 activation decreases severity of cyclophosphamide-induced cystitis via regulating autophagy.	Cyclophosphamide	56-72	cannabinoid receptor 2 (macrophage)	Mus musculus	0-22
31729056-2	2020	The objective of this study was to determine efficacy and mechanism of CB2 activation on cyclophosphamide (CYP)-induced cystitis in vivo.	Cyclophosphamide	89-105	cannabinoid receptor 2 (macrophage)	Mus musculus	71-74
31729056-2	2020	The objective of this study was to determine efficacy and mechanism of CB2 activation on cyclophosphamide (CYP)-induced cystitis in vivo.	Cyclophosphamide	107-110	cannabinoid receptor 2 (macrophage)	Mus musculus	71-74
31729056-8	2020	The expression of CB2 in bladder was significantly increased in CYP-treated mice.	Cyclophosphamide	64-67	cannabinoid receptor 2 (macrophage)	Mus musculus	18-21
31729056-11	2020	Activating CB2 with JWH-133 significantly alleviated bladder tissue inflammatory responses and oxidative stress induced by CYP.	Cyclophosphamide	123-126	cannabinoid receptor 2 (macrophage)	Mus musculus	11-14
31729056-15	2020	CONCLUSIONS: Activation of CB2 decreased severity of CYP-induced cystitis and ameliorated bladder inflammation.	Cyclophosphamide	53-56	cannabinoid receptor 2 (macrophage)	Mus musculus	27-30
31921384-0	2019	Low-dose metronomic cyclophosphamide complements the actions of an intratumoral C-class CpG TLR9 agonist to potentiate innate immunity and drive potent T cell-mediated anti-tumor responses.	Cyclophosphamide	20-36	toll-like receptor 9	Mus musculus	92-96
31889842-1	2020	In order to research the role of soybean oligosaccharides (SBOSs) on improvements in the microenvironment of intestinal flora and immune function of cyclophosphamide (CTX) immunosuppressive mice.	Cyclophosphamide	149-165	V-set and immunoglobulin domain containing 2	Mus musculus	167-170
31777548-0	2019	Effects of cyclophosphamide combined with prednisone on TNF-alpha expression in treatment of patients with interstitial lung disease.	Cyclophosphamide	11-27	tumor necrosis factor	Homo sapiens	56-65
31868632-1	2019	BACKGROUND: Six cycles of R-CHOP (rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone) are the standard treatment for aggressive B-cell non-Hodgkin lymphoma.	Cyclophosphamide	49-65	DNA damage inducible transcript 3	Homo sapiens	28-32
32175521-11	2020	Conclusions: BRCA1 promoter methylation is predictive of improved disease outcome in patients receiving cyclophosphamide, methotrexate, and fluorouracil drug treatment.	Cyclophosphamide	104-120	BRCA1 DNA repair associated	Homo sapiens	13-18
32104586-0	2020	Antitumor immunity of low-dose cyclophosphamide: changes in T cells and cytokines TGF-beta and IL-10 in mice with colon-cancer liver metastasis.	Cyclophosphamide	31-47	transforming growth factor alpha	Mus musculus	82-90
32104586-0	2020	Antitumor immunity of low-dose cyclophosphamide: changes in T cells and cytokines TGF-beta and IL-10 in mice with colon-cancer liver metastasis.	Cyclophosphamide	31-47	interleukin 10	Mus musculus	95-100
31404943-11	2019	Furthermore, Clock ablation sensitized mice to coumarin toxicity by downregulating CYP2A4/5-mediated metabolism (a detoxification pathway), and to cyclophosphamide toxicity by upregulating CYP2B10-mediated metabolism (generating the toxic metabolite 4-hydroxycyclophosphamide).	Cyclophosphamide	147-163	circadian locomotor output cycles kaput	Mus musculus	13-18
31777548-1	2019	Effects of cyclophosphamide combined with prednisone on TNF-alpha expression in the treatment of patients with interstitial lung disease (ILD), and its clinical significance were investigated.	Cyclophosphamide	11-27	tumor necrosis factor	Homo sapiens	56-65
31777548-10	2019	In conclusion, cyclophosphamide combined with prednisone is effective and safe in the treatment of ILD without severe adverse reactions, reducing TNF-alpha expression level, and therefore is worthy of clinical application.	Cyclophosphamide	15-31	tumor necrosis factor	Homo sapiens	146-155
32186620-2	2019	Since 2013, the treatment of these patients in the public system is based on CTD (cyclophosphamide, thalidomide, and dexamethasone).	Cyclophosphamide	82-98	CTD	Homo sapiens	77-80
30101679-1	2019	OBJECTIVES: Chemoimmunotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisolone combined with rituximab (R-CHOP) is currently the first-line therapy for diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	36-52	DNA damage inducible transcript 3	Homo sapiens	124-128
31185769-2	2019	Among 65% of patients receiving treatment after diagnosis, R-CHOP (Rituximab, Cyclophosphamide, Doxorubicin, Vincristine, Prednisone) was the most common frontline therapy, increasing with more recent treatment year: 51% (2001-2003) vs. 69% (2010-2014).	Cyclophosphamide	78-94	DNA damage inducible transcript 3	Homo sapiens	61-65
31852157-11	2019	INTERVENTIONS: The current first-line treatment for diffuse large B-cell lymphoma is the cyclophosphamide, adriamycin, vincristine, prednisone (CHOP) protocol.	Cyclophosphamide	89-105	DNA damage inducible transcript 3	Homo sapiens	144-148
31818187-8	2020	AMD3100 and Cy treatment significantly blocked this differentiation process of MSCs by suppressing CXCR4 expression and TGF-beta1 secretion.	Cyclophosphamide	12-14	C-X-C motif chemokine receptor 4	Homo sapiens	99-104
31818187-8	2020	AMD3100 and Cy treatment significantly blocked this differentiation process of MSCs by suppressing CXCR4 expression and TGF-beta1 secretion.	Cyclophosphamide	12-14	transforming growth factor beta 1	Homo sapiens	120-129
31825725-6	2020	The involvement of CXCR4 and TGF-beta1 was verified with addition of CXCR4 inhibitor AMD3100 and TGF-beta1 inhibitor cyclophosphamide (Cy) both in vitro and in vivo.Results: There were more CXCR4-positive cells at the liver metastatic tissues compared to the primary sites.	Cyclophosphamide	135-137	C-X-C motif chemokine receptor 4	Homo sapiens	19-24
31825725-6	2020	The involvement of CXCR4 and TGF-beta1 was verified with addition of CXCR4 inhibitor AMD3100 and TGF-beta1 inhibitor cyclophosphamide (Cy) both in vitro and in vivo.Results: There were more CXCR4-positive cells at the liver metastatic tissues compared to the primary sites.	Cyclophosphamide	135-137	transforming growth factor beta 1	Homo sapiens	29-38
31825725-10	2020	In a mouse hepatic metastasis model, treated with AMD3100 or Cy blocked the metastatic potential of HCT116 cells and the hepatic CAFs differentiation.Conclusions: These results indicated that CXCR4/TGF-beta1 axis plays an important role in CRC liver metastasis through mediating HSCs differentiation into CAFs, providing preclinical evidences that blockade of the axis might be beneficial for anti-metastasis therapy in CRC.	Cyclophosphamide	61-63	C-X-C motif chemokine receptor 4	Homo sapiens	192-197
31825725-10	2020	In a mouse hepatic metastasis model, treated with AMD3100 or Cy blocked the metastatic potential of HCT116 cells and the hepatic CAFs differentiation.Conclusions: These results indicated that CXCR4/TGF-beta1 axis plays an important role in CRC liver metastasis through mediating HSCs differentiation into CAFs, providing preclinical evidences that blockade of the axis might be beneficial for anti-metastasis therapy in CRC.	Cyclophosphamide	61-63	transforming growth factor beta 1	Homo sapiens	198-207
31801245-8	2019	RESULTS: Cyclophosphamide triggered activation of the extrinsic pathway of apoptosis mediated by BAX in CC.	Cyclophosphamide	9-25	BCL2 associated X, apoptosis regulator	Homo sapiens	97-100
31801186-1	2019	Expression of the anti-apoptotic B-cell lymphoma 2 (BCL-2) protein in patients with diffuse large B-cell lymphoma (DLBCL) strongly correlates with resistance to standard therapy with cyclophosphamide, vincristine, doxorubicin, prednisolone, and rituximab (R-CHOP).	Cyclophosphamide	183-199	BCL2 apoptosis regulator	Homo sapiens	33-50
31832222-1	2019	Background: Cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) regimen includes a high dose of prednisolone (100 mg/body), which exhibits an anticancer and antiemetic effect.	Cyclophosphamide	12-28	DNA damage inducible transcript 3	Homo sapiens	74-78
31801186-1	2019	Expression of the anti-apoptotic B-cell lymphoma 2 (BCL-2) protein in patients with diffuse large B-cell lymphoma (DLBCL) strongly correlates with resistance to standard therapy with cyclophosphamide, vincristine, doxorubicin, prednisolone, and rituximab (R-CHOP).	Cyclophosphamide	183-199	BCL2 apoptosis regulator	Homo sapiens	52-57
31195139-0	2019	Clinical Impacts of Using Serum IL-6 Level as an Indicator of Cytokine Release Syndrome after HLA-Haploidentical Transplantation with Post-Transplantation Cyclophosphamide.	Cyclophosphamide	155-171	interleukin 6	Homo sapiens	32-36
31719636-3	2019	The study aimed to elucidate the effects of insulin (INS), an inexpensive drug with a convincing safety profile, on the susceptibility of colon cancer to chemotherapeutic agents: 5-fluorouracil (FU), oxaliplatin (OXA), irinotecan (IRI), cyclophosphamide (CPA) and docetaxel (DOC).	Cyclophosphamide	237-253	insulin	Homo sapiens	44-51
31719636-3	2019	The study aimed to elucidate the effects of insulin (INS), an inexpensive drug with a convincing safety profile, on the susceptibility of colon cancer to chemotherapeutic agents: 5-fluorouracil (FU), oxaliplatin (OXA), irinotecan (IRI), cyclophosphamide (CPA) and docetaxel (DOC).	Cyclophosphamide	255-258	insulin	Homo sapiens	44-51
31502114-0	2019	Prophylactic administration of granulocyte colony-stimulating factor in epirubicin and cyclophosphamide chemotherapy for Japanese breast cancer patients: a retrospective study.	Cyclophosphamide	87-103	colony stimulating factor 3	Homo sapiens	31-68
31314918-1	2019	OBJECTIVES: R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone) is the standard therapy for patients with previously untreated diffuse large B-cell lymphomas (DLBCL).	Cyclophosphamide	31-47	DNA damage inducible transcript 3	Homo sapiens	14-18
31557371-0	2019	Upregulation of FSHR and PCNA by administration of coenzyme Q10 on cyclophosphamide-induced premature ovarian failure in a mouse model.	Cyclophosphamide	67-83	follicle stimulating hormone receptor	Mus musculus	16-20
31557371-0	2019	Upregulation of FSHR and PCNA by administration of coenzyme Q10 on cyclophosphamide-induced premature ovarian failure in a mouse model.	Cyclophosphamide	67-83	proliferating cell nuclear antigen	Mus musculus	25-29
31686598-0	2019	Severe and prolonged cyclophosphamide-induced hepatotoxicity in a breast cancer patient carrying a CYP2B6*7 variant.	Cyclophosphamide	21-37	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	99-105
31686598-7	2019	CYP2B6 and ALDH3A1 genotyping may play a role in guiding cyclophosphamide therapy.	Cyclophosphamide	57-73	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	0-6
31686598-7	2019	CYP2B6 and ALDH3A1 genotyping may play a role in guiding cyclophosphamide therapy.	Cyclophosphamide	57-73	aldehyde dehydrogenase 3 family member A1	Homo sapiens	11-18
30808504-8	2019	As for therapeutic strategy, moderate dose prednisone (15-40mg/d) and cyclophosphamide (CTX) are mainly different between two subgroups.	Cyclophosphamide	70-86	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	88-91
31646979-6	2019	In comparing CsA vs. cyclophosphamide (CYC), the results indicated that the CsA group had higher TR than the CYC group.	Cyclophosphamide	21-37	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	76-79
31646979-6	2019	In comparing CsA vs. cyclophosphamide (CYC), the results indicated that the CsA group had higher TR than the CYC group.	Cyclophosphamide	39-42	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	76-79
31646979-6	2019	In comparing CsA vs. cyclophosphamide (CYC), the results indicated that the CsA group had higher TR than the CYC group.	Cyclophosphamide	109-112	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	13-16
31222719-1	2019	Central nervous system (CNS) relapse following R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisolone) occurs in 2-5% of patents with diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	66-82	DNA damage inducible transcript 3	Homo sapiens	49-53
30890769-0	2019	Donor-derived CD4+/CCR7+ T-cell impact on acute GVHD incidence following haplo-HCT after reduced intensity conditioning and posttransplant cyclophosphamide.	Cyclophosphamide	139-155	CD4 molecule	Homo sapiens	14-17
30890769-0	2019	Donor-derived CD4+/CCR7+ T-cell impact on acute GVHD incidence following haplo-HCT after reduced intensity conditioning and posttransplant cyclophosphamide.	Cyclophosphamide	139-155	C-C motif chemokine receptor 7	Homo sapiens	19-23
31632401-0	2019	Interleukin-6 as Biomarker for Acute GvHD and Survival After Allogeneic Transplant With Post-transplant Cyclophosphamide.	Cyclophosphamide	104-120	interleukin 6	Homo sapiens	0-13
31247375-0	2019	Human constitutive androstane receptor agonist DL5016: A novel sensitizer for cyclophosphamide-based chemotherapies.	Cyclophosphamide	78-94	nuclear receptor subfamily 1 group I member 3	Homo sapiens	6-38
31247375-2	2019	As a prodrug, CPA is activated by cytochrome P450 2B6 (CYP2B6), which is transcriptionally regulated by the human constitutive androstane receptor (hCAR).	Cyclophosphamide	14-17	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	34-53
31247375-2	2019	As a prodrug, CPA is activated by cytochrome P450 2B6 (CYP2B6), which is transcriptionally regulated by the human constitutive androstane receptor (hCAR).	Cyclophosphamide	14-17	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	55-61
31247375-2	2019	As a prodrug, CPA is activated by cytochrome P450 2B6 (CYP2B6), which is transcriptionally regulated by the human constitutive androstane receptor (hCAR).	Cyclophosphamide	14-17	nuclear receptor subfamily 1 group I member 3	Homo sapiens	114-146
31247375-2	2019	As a prodrug, CPA is activated by cytochrome P450 2B6 (CYP2B6), which is transcriptionally regulated by the human constitutive androstane receptor (hCAR).	Cyclophosphamide	14-17	CXADR Ig-like cell adhesion molecule	Homo sapiens	148-152
31247375-3	2019	Therefore, hCAR agonists represent novel sensitizers for CPA-based therapies.	Cyclophosphamide	57-60	CXADR Ig-like cell adhesion molecule	Homo sapiens	11-15
31562295-6	2019	Cyclophosphamide exposure induced the activation of both DNAPK-gammaH2AX-checkpoint kinase 2 (CHK2)-p53/TAp63alpha isoform and protein kinase B (AKT)-forkhead box O3 (FOXO3a) signaling axes in the nucleus of oocytes.	Cyclophosphamide	0-16	checkpoint kinase 2	Mus musculus	57-92
31562295-6	2019	Cyclophosphamide exposure induced the activation of both DNAPK-gammaH2AX-checkpoint kinase 2 (CHK2)-p53/TAp63alpha isoform and protein kinase B (AKT)-forkhead box O3 (FOXO3a) signaling axes in the nucleus of oocytes.	Cyclophosphamide	0-16	checkpoint kinase 2	Mus musculus	94-98
31562295-6	2019	Cyclophosphamide exposure induced the activation of both DNAPK-gammaH2AX-checkpoint kinase 2 (CHK2)-p53/TAp63alpha isoform and protein kinase B (AKT)-forkhead box O3 (FOXO3a) signaling axes in the nucleus of oocytes.	Cyclophosphamide	0-16	transformation related protein 53, pseudogene	Mus musculus	100-103
31562295-6	2019	Cyclophosphamide exposure induced the activation of both DNAPK-gammaH2AX-checkpoint kinase 2 (CHK2)-p53/TAp63alpha isoform and protein kinase B (AKT)-forkhead box O3 (FOXO3a) signaling axes in the nucleus of oocytes.	Cyclophosphamide	0-16	thymoma viral proto-oncogene 1	Mus musculus	145-148
31562295-6	2019	Cyclophosphamide exposure induced the activation of both DNAPK-gammaH2AX-checkpoint kinase 2 (CHK2)-p53/TAp63alpha isoform and protein kinase B (AKT)-forkhead box O3 (FOXO3a) signaling axes in the nucleus of oocytes.	Cyclophosphamide	0-16	forkhead box O3	Mus musculus	150-165
31562295-6	2019	Cyclophosphamide exposure induced the activation of both DNAPK-gammaH2AX-checkpoint kinase 2 (CHK2)-p53/TAp63alpha isoform and protein kinase B (AKT)-forkhead box O3 (FOXO3a) signaling axes in the nucleus of oocytes.	Cyclophosphamide	0-16	forkhead box O3	Mus musculus	167-173
31562295-9	2019	On the contrary, the administration of an allosteric ABL activator enhanced the lethal effects of cyclophosphamide while shortening mouse fertility.	Cyclophosphamide	98-114	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	53-56
31302713-1	2019	PURPOSE: These studies determined whether the acetylcholinesterase inhibitors, donepezil and galantamine, both of which are approved for the treatment of cognitive deficits in Alzheimer"s disease, can prevent or reverse spatial memory deficits in mice induced by cyclophosphamide and doxorubicin, cytotoxic agents commonly used to treat breast cancer.	Cyclophosphamide	263-279	acetylcholinesterase	Mus musculus	46-66
31536574-1	2019	Metronomic chemotherapy using the 5-FU prodrug uracil-tegafur (UFT) and cyclophosphamide (CTX) was previously shown to only modestly delay primary tumor growth, but nevertheless markedly suppressed the development of micro-metastasis in an orthotopic breast cancer xenograft model, using the metastatic variant of the MDA-MB-231 cell line, 231/LM2-4.	Cyclophosphamide	72-88	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	90-93
31369707-3	2019	Inhibition of ERCC1-XPF has been shown to potentiate cytotoxicity of platinum-based drugs and cyclophosphamide in cancer cells.	Cyclophosphamide	94-110	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	14-19
31369707-3	2019	Inhibition of ERCC1-XPF has been shown to potentiate cytotoxicity of platinum-based drugs and cyclophosphamide in cancer cells.	Cyclophosphamide	94-110	ERCC excision repair 4, endonuclease catalytic subunit	Homo sapiens	20-23
31514476-7	2019	The results showed that the plasma levels of TIMP-1 in the group of patients receiving HT were significantly lower than those levels found in the control group after the epirubicin-cyclophosphamide chemotherapy.	Cyclophosphamide	181-197	TIMP metallopeptidase inhibitor 1	Homo sapiens	45-51
31102789-3	2019	Jmjd3 and Col1/3 expression was detected in a cystitis mouse model that was developed by intraperitoneal injection of cyclophosphamide (CYP).	Cyclophosphamide	118-134	KDM1 lysine (K)-specific demethylase 6B	Mus musculus	0-5
31102789-3	2019	Jmjd3 and Col1/3 expression was detected in a cystitis mouse model that was developed by intraperitoneal injection of cyclophosphamide (CYP).	Cyclophosphamide	136-139	KDM1 lysine (K)-specific demethylase 6B	Mus musculus	0-5
31102789-6	2019	CYP induced cystitis significantly increased Jmjd3, Col1 and Col3 expression in the bladder muscle cells.	Cyclophosphamide	0-3	lysine demethylase 6B	Homo sapiens	45-50
31218720-0	2019	The importance of both CYP2C19 and CYP2B6 germline variations in cyclophosphamide pharmacokinetics and clinical outcomes.	Cyclophosphamide	65-81	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	35-41
31410111-1	2019	Cyclophosphamide (CTX) as an alkylating agent is used for treating a range of tumor types and allergic diseases.	Cyclophosphamide	0-16	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	18-21
31642426-1	2019	OBJECTIVE: To study the clinical effect and safety of double filtration plasmapheresis (DFPP) combined with double pulse therapy with methylprednisolone (MP) and cyclophosphamide (CTX) in the treatment of children with severe Henoch-Schonlein purpura nephritis (HSPN).	Cyclophosphamide	162-178	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	180-183
31310795-2	2019	Here, we found that cyclophosphamide induced significantly decrease in alpha-Klotho (Kl) expression in mouse ovarian granulosa cells (mOGCs), suggesting that cyclophosphamide inhibited Kl expression.	Cyclophosphamide	20-36	klotho	Mus musculus	77-83
31310795-2	2019	Here, we found that cyclophosphamide induced significantly decrease in alpha-Klotho (Kl) expression in mouse ovarian granulosa cells (mOGCs), suggesting that cyclophosphamide inhibited Kl expression.	Cyclophosphamide	158-174	klotho	Mus musculus	77-83
31310795-7	2019	Finally, we found that cyclophosphamide attenuated the autophagy function of mOGCs via upregulating microRNA-15b expression, which silenced the endogenous Kl mRNA expression and stimulated the activity of the downstream TGFbeta1/Smad pathway.	Cyclophosphamide	23-39	microRNA 15b	Mus musculus	100-112
31310795-7	2019	Finally, we found that cyclophosphamide attenuated the autophagy function of mOGCs via upregulating microRNA-15b expression, which silenced the endogenous Kl mRNA expression and stimulated the activity of the downstream TGFbeta1/Smad pathway.	Cyclophosphamide	23-39	transforming growth factor, beta 1	Mus musculus	220-228
31310795-9	2019	It elucidated the underlying epigenetic regulatory mechanism, whereby cyclophosphamide-dependent microRNA-15b inhibited Kl expression, leading to the reduced ability of mOGCs to induce autophagy and ROS scavenging, ultimately causing POF.	Cyclophosphamide	70-86	microRNA 15b	Mus musculus	97-109
31136760-4	2019	Liver sinusoidal endothelial injury induced by CPA (20, 40 mg/kg) in mice was evidenced by the elevated hepatic metalloproteinase-9 (MMP-9) expression, and the results from liver histological evaluation and scanning electron microscope observation.	Cyclophosphamide	47-50	matrix metallopeptidase 9	Mus musculus	133-138
31250176-4	2019	Interference of rAMH with Cy chemotoxicity was assessed on a human breast cancer cell line and an in vivo mouse model of human leukaemia.	Cyclophosphamide	26-28	anti-Mullerian hormone	Rattus norvegicus	16-20
31356540-10	2019	Eliminating ROS with N-acetylcysteine or preinject CY into rat jugular vein reduces the expression of IL-6, TNF-a, and, especially, IL-1b in an in vivo I/R model.	Cyclophosphamide	51-53	interleukin 6	Rattus norvegicus	102-106
31356540-10	2019	Eliminating ROS with N-acetylcysteine or preinject CY into rat jugular vein reduces the expression of IL-6, TNF-a, and, especially, IL-1b in an in vivo I/R model.	Cyclophosphamide	51-53	tumor necrosis factor	Rattus norvegicus	108-113
31356540-10	2019	Eliminating ROS with N-acetylcysteine or preinject CY into rat jugular vein reduces the expression of IL-6, TNF-a, and, especially, IL-1b in an in vivo I/R model.	Cyclophosphamide	51-53	interleukin 1 beta	Rattus norvegicus	132-137
31356540-11	2019	Also, CY pretreatment strongly reduces ischemia/reperfusion-induced NLRP3 up-expression and caspase-1 activation.	Cyclophosphamide	6-8	NLR family, pyrin domain containing 3	Rattus norvegicus	68-73
31356540-11	2019	Also, CY pretreatment strongly reduces ischemia/reperfusion-induced NLRP3 up-expression and caspase-1 activation.	Cyclophosphamide	6-8	caspase 1	Rattus norvegicus	92-101
31136760-5	2019	CPA increased hepatic infiltration of neutrophils, liver myeloperoxidase (MPO) activity, serum interleukin-6 (IL-6) content, hepatic IL-6 mRNA expression, toll-like receptor-4 (TLR4) expression and nuclear factor kappaB (NFkappaB) activation in mice.	Cyclophosphamide	0-3	myeloperoxidase	Mus musculus	57-72
31136760-5	2019	CPA increased hepatic infiltration of neutrophils, liver myeloperoxidase (MPO) activity, serum interleukin-6 (IL-6) content, hepatic IL-6 mRNA expression, toll-like receptor-4 (TLR4) expression and nuclear factor kappaB (NFkappaB) activation in mice.	Cyclophosphamide	0-3	myeloperoxidase	Mus musculus	74-77
31136760-5	2019	CPA increased hepatic infiltration of neutrophils, liver myeloperoxidase (MPO) activity, serum interleukin-6 (IL-6) content, hepatic IL-6 mRNA expression, toll-like receptor-4 (TLR4) expression and nuclear factor kappaB (NFkappaB) activation in mice.	Cyclophosphamide	0-3	interleukin 6	Mus musculus	95-108
31136760-5	2019	CPA increased hepatic infiltration of neutrophils, liver myeloperoxidase (MPO) activity, serum interleukin-6 (IL-6) content, hepatic IL-6 mRNA expression, toll-like receptor-4 (TLR4) expression and nuclear factor kappaB (NFkappaB) activation in mice.	Cyclophosphamide	0-3	interleukin 6	Mus musculus	110-114
31136760-5	2019	CPA increased hepatic infiltration of neutrophils, liver myeloperoxidase (MPO) activity, serum interleukin-6 (IL-6) content, hepatic IL-6 mRNA expression, toll-like receptor-4 (TLR4) expression and nuclear factor kappaB (NFkappaB) activation in mice.	Cyclophosphamide	0-3	interleukin 6	Mus musculus	133-137
31136760-5	2019	CPA increased hepatic infiltration of neutrophils, liver myeloperoxidase (MPO) activity, serum interleukin-6 (IL-6) content, hepatic IL-6 mRNA expression, toll-like receptor-4 (TLR4) expression and nuclear factor kappaB (NFkappaB) activation in mice.	Cyclophosphamide	0-3	toll-like receptor 4	Mus musculus	155-175
31136760-5	2019	CPA increased hepatic infiltration of neutrophils, liver myeloperoxidase (MPO) activity, serum interleukin-6 (IL-6) content, hepatic IL-6 mRNA expression, toll-like receptor-4 (TLR4) expression and nuclear factor kappaB (NFkappaB) activation in mice.	Cyclophosphamide	0-3	toll-like receptor 4	Mus musculus	177-181
31136760-5	2019	CPA increased hepatic infiltration of neutrophils, liver myeloperoxidase (MPO) activity, serum interleukin-6 (IL-6) content, hepatic IL-6 mRNA expression, toll-like receptor-4 (TLR4) expression and nuclear factor kappaB (NFkappaB) activation in mice.	Cyclophosphamide	0-3	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	221-229
31136760-6	2019	Elevated serum contents of damage associated molecular patterns (DAMPs) including high mobility group box 1 (HMGB1), heat shock protein 60 (HSP60) and glucose-regulated protein 94 (Grp94) were found in mice treated with CPA.	Cyclophosphamide	220-223	high mobility group box 1	Mus musculus	82-107
31136760-6	2019	Elevated serum contents of damage associated molecular patterns (DAMPs) including high mobility group box 1 (HMGB1), heat shock protein 60 (HSP60) and glucose-regulated protein 94 (Grp94) were found in mice treated with CPA.	Cyclophosphamide	220-223	high mobility group box 1	Mus musculus	109-114
31136760-6	2019	Elevated serum contents of damage associated molecular patterns (DAMPs) including high mobility group box 1 (HMGB1), heat shock protein 60 (HSP60) and glucose-regulated protein 94 (Grp94) were found in mice treated with CPA.	Cyclophosphamide	220-223	heat shock protein 1 (chaperonin)	Mus musculus	117-138
31136760-6	2019	Elevated serum contents of damage associated molecular patterns (DAMPs) including high mobility group box 1 (HMGB1), heat shock protein 60 (HSP60) and glucose-regulated protein 94 (Grp94) were found in mice treated with CPA.	Cyclophosphamide	220-223	heat shock protein 1 (chaperonin)	Mus musculus	140-145
31136760-6	2019	Elevated serum contents of damage associated molecular patterns (DAMPs) including high mobility group box 1 (HMGB1), heat shock protein 60 (HSP60) and glucose-regulated protein 94 (Grp94) were found in mice treated with CPA.	Cyclophosphamide	220-223	heat shock protein 90, beta (Grp94), member 1	Mus musculus	151-179
31136760-6	2019	Elevated serum contents of damage associated molecular patterns (DAMPs) including high mobility group box 1 (HMGB1), heat shock protein 60 (HSP60) and glucose-regulated protein 94 (Grp94) were found in mice treated with CPA.	Cyclophosphamide	220-223	heat shock protein 90, beta (Grp94), member 1	Mus musculus	181-186
31136760-7	2019	Liver sinusoidal endothelial injury and inflammation induced by CPA were diminished in TLR4 knock-out mice.	Cyclophosphamide	64-67	toll-like receptor 4	Mus musculus	87-91
31136760-9	2019	In summary, these results indicate that TLR4-NFkappaB-mediated inflammatory injury initiated by DAMPs was critically involved in CPA-induced hepatotoxicity.	Cyclophosphamide	129-132	toll-like receptor 4	Mus musculus	40-44
31136760-9	2019	In summary, these results indicate that TLR4-NFkappaB-mediated inflammatory injury initiated by DAMPs was critically involved in CPA-induced hepatotoxicity.	Cyclophosphamide	129-132	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	45-53
31048086-10	2019	pGI reduced early mortality associated with CRGNB in colonized patients undergoing post-transplant cyclophosphamide-based haploidentical HCT.	Cyclophosphamide	99-115	glucose-6-phosphate isomerase	Homo sapiens	0-3
31472897-3	2019	In cyclophosphamide-induced immunosuppressed mice, DSP increased serum levels of TNF-alpha, IL-6 and IFN-gamma (enzyme-linked immunosorbent assay, ELISA), and ameliorated the imbalance of the community of gut microbiota as detected by 16S ribosomal RNA gene sequencing.	Cyclophosphamide	3-19	tumor necrosis factor	Mus musculus	81-90
31472897-3	2019	In cyclophosphamide-induced immunosuppressed mice, DSP increased serum levels of TNF-alpha, IL-6 and IFN-gamma (enzyme-linked immunosorbent assay, ELISA), and ameliorated the imbalance of the community of gut microbiota as detected by 16S ribosomal RNA gene sequencing.	Cyclophosphamide	3-19	interleukin 6	Mus musculus	92-96
31472897-3	2019	In cyclophosphamide-induced immunosuppressed mice, DSP increased serum levels of TNF-alpha, IL-6 and IFN-gamma (enzyme-linked immunosorbent assay, ELISA), and ameliorated the imbalance of the community of gut microbiota as detected by 16S ribosomal RNA gene sequencing.	Cyclophosphamide	3-19	interferon gamma	Mus musculus	101-110
31202006-8	2019	Firstly, CY down-regulated the expression of CD86 on THP-1 cells while DNCB up-regulated its expression.	Cyclophosphamide	9-11	CD86 molecule	Homo sapiens	45-49
31202006-11	2019	Finally, only CY could lead to an increase in heme oxygenase 1 (HMOX1) expression.	Cyclophosphamide	14-16	heme oxygenase 1	Homo sapiens	46-62
31202006-11	2019	Finally, only CY could lead to an increase in heme oxygenase 1 (HMOX1) expression.	Cyclophosphamide	14-16	heme oxygenase 1	Homo sapiens	64-69
31124308-9	2019	Patients who received steroids or cyclophosphamide showed a significant reduction in CCN2 levels.	Cyclophosphamide	34-50	cellular communication network factor 2	Homo sapiens	85-89
31355400-0	2019	Water-soluble polysaccharides from Grifola Frondosa fruiting bodies protect against immunosuppression in cyclophosphamide-induced mice via JAK2/STAT3/SOCS signal transduction pathways.	Cyclophosphamide	105-121	Janus kinase 2	Mus musculus	139-143
31355400-0	2019	Water-soluble polysaccharides from Grifola Frondosa fruiting bodies protect against immunosuppression in cyclophosphamide-induced mice via JAK2/STAT3/SOCS signal transduction pathways.	Cyclophosphamide	105-121	signal transducer and activator of transcription 3	Mus musculus	144-149
31355400-0	2019	Water-soluble polysaccharides from Grifola Frondosa fruiting bodies protect against immunosuppression in cyclophosphamide-induced mice via JAK2/STAT3/SOCS signal transduction pathways.	Cyclophosphamide	105-121	cytokine inducible SH2-containing protein	Mus musculus	150-154
31208944-1	2019	BACKGROUND: Fludarabine, cyclophosphamide, and rituximab (FCR) can improve disease-free survival for younger (age <=65 years) fit patients with chronic lymphocytic leukaemia with mutated IGHV.	Cyclophosphamide	25-41	immunoglobulin heavy variable 3-69-1 (pseudogene)	Homo sapiens	187-191
31079239-6	2019	The increased levels of the protein p-53 and the reduced levels of the proteins c-Jun and c-Fos at higher concentrations of ASTA, as well as, suggest the pro-apoptotic and anti-cancerous effects that this extract has on hepatocellular carcinomas, confirmed also by caspase-3 activation.	Cyclophosphamide	124-128	caspase 3	Homo sapiens	265-274
31079239-6	2019	The increased levels of the protein p-53 and the reduced levels of the proteins c-Jun and c-Fos at higher concentrations of ASTA, as well as, suggest the pro-apoptotic and anti-cancerous effects that this extract has on hepatocellular carcinomas, confirmed also by caspase-3 activation.	Cyclophosphamide	124-128	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	80-85
31079239-6	2019	The increased levels of the protein p-53 and the reduced levels of the proteins c-Jun and c-Fos at higher concentrations of ASTA, as well as, suggest the pro-apoptotic and anti-cancerous effects that this extract has on hepatocellular carcinomas, confirmed also by caspase-3 activation.	Cyclophosphamide	124-128	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	90-95
31281657-0	2019	Adjuvant recombinant thrombomodulin therapy for hepatopathy induced by vincristine, actinomycin D, and cyclophosphamide in pediatric rhabdomyosarcoma: A case report.	Cyclophosphamide	103-119	thrombomodulin	Homo sapiens	21-35
31340918-9	2019	CONCLUSIONS: LIPUS can alleviate the hematopoietic damage after combined chemotherapy with doxorubicin with cyclophosphamide probably by increasing the expressions of ICAM- 1, VCAM-1, IL- 3, and GM-CSF.	Cyclophosphamide	108-124	intercellular adhesion molecule 1	Rattus norvegicus	167-174
31340918-9	2019	CONCLUSIONS: LIPUS can alleviate the hematopoietic damage after combined chemotherapy with doxorubicin with cyclophosphamide probably by increasing the expressions of ICAM- 1, VCAM-1, IL- 3, and GM-CSF.	Cyclophosphamide	108-124	vascular cell adhesion molecule 1	Rattus norvegicus	176-182
31340918-9	2019	CONCLUSIONS: LIPUS can alleviate the hematopoietic damage after combined chemotherapy with doxorubicin with cyclophosphamide probably by increasing the expressions of ICAM- 1, VCAM-1, IL- 3, and GM-CSF.	Cyclophosphamide	108-124	colony stimulating factor 2	Rattus norvegicus	195-201
31277751-3	2019	Cyclophosphamide (CYC) was the first drug demonstrated to afford successful treatment and improvement in AAV.	Cyclophosphamide	0-16	adeno-associated virus integration site 1	Homo sapiens	105-108
31277751-3	2019	Cyclophosphamide (CYC) was the first drug demonstrated to afford successful treatment and improvement in AAV.	Cyclophosphamide	18-21	adeno-associated virus integration site 1	Homo sapiens	105-108
31467580-0	2019	C-Phycocyanin Alleviates Bladder Inflammation and Dysfunction in Cyclophosphamide-Induced Cystitis in a Mouse Model by Inhibiting COX-2 and EP4.	Cyclophosphamide	65-81	prostaglandin E receptor 4 (subtype EP4)	Mus musculus	140-143
31467580-1	2019	Objective: To explore the effect of C-phycocyanin (C-PC) on voiding behavior and histological changes in cyclophosphamide- (CYP-) induced cystitis in mice.	Cyclophosphamide	105-121	peptidyl-prolyl isomerase G (cyclophilin G)	Mus musculus	124-127
31118164-2	2019	The use of R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) could overcome these difficulties, but blood-brain barrier (BBB) penetration of related drugs is poor.	Cyclophosphamide	30-46	DNA damage inducible transcript 3	Homo sapiens	13-17
31360632-1	2019	Patients of clinically amyopathic dermatomyositis associated with rapidly progressive interstitial pneumonia (CADM-RFIP) with positive anti-MDA5 antibody usually presents rapid deterioration and traditional therapy such as cyclophosphamide combined with high-dose prednisone pulse therapy shows no clear benefit at whiles.	Cyclophosphamide	223-239	interferon induced with helicase C domain 1	Homo sapiens	140-144
31040105-5	2019	Cyclophosphamide induced endoplasmic reticulum (ER) stress in BM-resident lymphoma cells in vivo that resulted in ATF4-mediated paracrine secretion of VEGFA, massive macrophage infiltration, and clearance of alemtuzumab-opsonized cells.	Cyclophosphamide	0-16	activating transcription factor 4	Homo sapiens	114-118
30995112-0	2019	Functional effects of blocking VEGF/VEGFR2 signaling in the rat urinary bladder in acute and chronic CYP-induced cystitis.	Cyclophosphamide	101-104	vascular endothelial growth factor A	Rattus norvegicus	31-35
30995112-0	2019	Functional effects of blocking VEGF/VEGFR2 signaling in the rat urinary bladder in acute and chronic CYP-induced cystitis.	Cyclophosphamide	101-104	kinase insert domain receptor	Rattus norvegicus	36-42
30995112-4	2019	In the present study, we quantified VEGF alternative splice variant expression in lower urinary tract tissues under control conditions and with cyclophosphamide (CYP)-induced cystitis.	Cyclophosphamide	144-160	vascular endothelial growth factor A	Homo sapiens	36-40
30995112-4	2019	In the present study, we quantified VEGF alternative splice variant expression in lower urinary tract tissues under control conditions and with cyclophosphamide (CYP)-induced cystitis.	Cyclophosphamide	162-165	vascular endothelial growth factor A	Homo sapiens	36-40
30995112-6	2019	With VEGFR2 blockade, bladder capacity increased (P <= 0.01) in male and female control rats as well as in male and female rats with acute (P <= 0.05) or chronic (P <= 0.01 or P <= 0.05, respectively) CYP-induced cystitis.	Cyclophosphamide	201-204	kinase insert domain receptor	Rattus norvegicus	5-11
31034039-0	2019	G-CSF-mobilized peripheral blood mononuclear cells combined with platelet-rich plasma accelerate restoration of ovarian function in cyclophosphamide-induced POI rats .	Cyclophosphamide	132-148	colony stimulating factor 3	Rattus norvegicus	0-5
31040105-5	2019	Cyclophosphamide induced endoplasmic reticulum (ER) stress in BM-resident lymphoma cells in vivo that resulted in ATF4-mediated paracrine secretion of VEGFA, massive macrophage infiltration, and clearance of alemtuzumab-opsonized cells.	Cyclophosphamide	0-16	vascular endothelial growth factor A	Homo sapiens	151-156
31040105-6	2019	BM macrophages isolated after cyclophosphamide treatment had increased phagocytic capacity that was reversed by VEGFA blockade or SYK inhibition.	Cyclophosphamide	30-46	vascular endothelial growth factor A	Homo sapiens	112-117
31346878-2	2019	Intraperitoneal injections of cyclophosphamide in a dose of 100 mg/kg on days 1, 3, 5, and 7 of the experiment reduced leukocyte count and the relative number of CD4+ T cells in the blood, and also depleted the cellular composition of splenic white pulp on day 10.	Cyclophosphamide	30-46	CD4 antigen	Mus musculus	162-165
31040105-6	2019	BM macrophages isolated after cyclophosphamide treatment had increased phagocytic capacity that was reversed by VEGFA blockade or SYK inhibition.	Cyclophosphamide	30-46	spleen associated tyrosine kinase	Homo sapiens	130-133
31316467-0	2019	Cyclophosphamide Regulates N6-Methyladenosine and m6A RNA Enzyme Levels in Human Granulosa Cells and in Ovaries of a Premature Ovarian Aging Mouse Model.	Cyclophosphamide	0-16	glycoprotein M6A	Homo sapiens	50-53
30719970-10	2019	Intravenous cyclophosphamide pulse therapy decreased FcgammaRIIB expression levels on memory B cell subsets.	Cyclophosphamide	12-28	Fc gamma receptor IIb	Homo sapiens	53-64
31516154-4	2019	He was managed by the oncologist with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) regimen which alleviated his symptoms considerably after completion of three cycles and was under follow-up.	Cyclophosphamide	57-73	DNA damage inducible transcript 3	Homo sapiens	40-44
31087594-7	2019	cyclophosphamide pulse significantly increased serum CXCL14 levels as compared with the baseline in SSc patients with interstitial lung disease successfully treated with this therapy.	Cyclophosphamide	0-16	C-X-C motif chemokine ligand 14	Homo sapiens	53-59
29151283-1	2019	BACKGROUND/AIMS: This study was to evaluate the clinical significance of infusion-related reaction (IRR) of rituximab in diffuse large B-cell lymphoma (DLBCL) patients who received R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone) as a first-line chemotherapy.	Cyclophosphamide	200-216	insulin receptor related receptor	Homo sapiens	100-103
31185690-0	2019	Drop of Butyrylcholinesterase Activity after Cyclophosphamide Conditioning as a Predictive Marker of Liver Transplant-Related Complications and Its Correlation with Transplant-Related Mortality in Pediatric Hematopoietic Stem Cell Recipients.	Cyclophosphamide	45-61	butyrylcholinesterase	Homo sapiens	8-29
31089650-0	2019	Protective effects of polysaccharides from Cordyceps gunnii mycelia against cyclophosphamide-induced immunosuppression to TLR4/TRAF6/NF-kappaB signalling in BALB/c mice.	Cyclophosphamide	76-92	toll-like receptor 4	Mus musculus	122-126
31089650-0	2019	Protective effects of polysaccharides from Cordyceps gunnii mycelia against cyclophosphamide-induced immunosuppression to TLR4/TRAF6/NF-kappaB signalling in BALB/c mice.	Cyclophosphamide	76-92	TNF receptor-associated factor 6	Mus musculus	127-132
31089650-0	2019	Protective effects of polysaccharides from Cordyceps gunnii mycelia against cyclophosphamide-induced immunosuppression to TLR4/TRAF6/NF-kappaB signalling in BALB/c mice.	Cyclophosphamide	76-92	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	133-142
31089650-2	2019	In this study, the aim was to investigate the effect of polysaccharides from Cordyceps gunnii mycelia (PPS) in cyclophosphamide (CTX)-induced immunodeficient mice.	Cyclophosphamide	111-127	V-set and immunoglobulin domain containing 2	Mus musculus	129-132
31185690-3	2019	We have observed a variable reduction in serum butyrylcholinesterase (BChE) activity after a cyclophosphamide-containing conditioning regimen.	Cyclophosphamide	93-109	butyrylcholinesterase	Homo sapiens	47-68
31185690-3	2019	We have observed a variable reduction in serum butyrylcholinesterase (BChE) activity after a cyclophosphamide-containing conditioning regimen.	Cyclophosphamide	93-109	butyrylcholinesterase	Homo sapiens	70-74
31124322-8	2019	Corresponding with the reduction in autoantibodies, data suggest that CYC treatment lowered circulating CD45R+ B cells.	Cyclophosphamide	70-73	protein tyrosine phosphatase, receptor type, C	Mus musculus	104-109
30939201-8	2019	Taken together, these observations suggest that a short exposure to rhFSH induces chemoresistance to DOX and CPA in human breast cancer cells via HIF-1alpha activation.	Cyclophosphamide	109-112	hypoxia inducible factor 1 subunit alpha	Homo sapiens	146-156
30989724-0	2019	Neuregulin-1-ErbB signaling promotes microglia activation contributing to mechanical allodynia of cyclophosphamide-induced cystitis.	Cyclophosphamide	98-114	neuregulin 1	Rattus norvegicus	0-12
30756132-0	2019	Metronomic cyclophosphamide attenuates mTOR-mediated expansion of regulatory T cells, but does not impact clinical outcome in patients with metastatic renal cell cancer treated with everolimus.	Cyclophosphamide	11-27	mechanistic target of rapamycin kinase	Homo sapiens	39-43
30756132-5	2019	MATERIALS AND METHODS: In a multicenter phase 2 study, performed in patients with mRCC not amenable to or progressive on a vascular endothelial growth factor (VEGF)-receptor tyrosine kinase inhibitor (TKI) containing treatment regimen, we assessed whether the addition of this metronomic dosing schedule of cyclophosphamide to therapy with everolimus could result in an improvement of progression-free survival (PFS) after 4 months of treatment.	Cyclophosphamide	307-323	vascular endothelial growth factor A	Homo sapiens	159-163
30545921-3	2019	The AALL1131 trial was designed to determine, in a randomized fashion, whether substitution with cyclophosphamide/etoposide (experimental arm 1) would improve the 4-year disease-free survival of children, adolescents, and young adults with very high-risk B-cell acute lymphoblastic leukemia compared to a modified Berlin-Frankfurt-Munster regimen (control arm).	Cyclophosphamide	97-113	kallikrein related peptidase 4	Homo sapiens	138-143
30633472-10	2019	Bax protein expression was reduced in the cyclophosphamide (20%) and cyclophosphamide+N-acetylcysteine (20%) groups when compared with the Control (50%) and N-acetylcysteine (50%) groups.	Cyclophosphamide	42-58	BCL2 associated X, apoptosis regulator	Rattus norvegicus	0-3
30633472-10	2019	Bax protein expression was reduced in the cyclophosphamide (20%) and cyclophosphamide+N-acetylcysteine (20%) groups when compared with the Control (50%) and N-acetylcysteine (50%) groups.	Cyclophosphamide	69-85	BCL2 associated X, apoptosis regulator	Rattus norvegicus	0-3
31106153-7	2019	In vitro validation of the former result showed an increase in the secreted and cellular NRP-1 levels in resistant MDA-MB-231 cells to the most common NAC regimen Adriyamicin/cyclophosphamide+Paclitaxel (AC+PAC).	Cyclophosphamide	175-191	neuropilin 1	Homo sapiens	89-94
30986272-0	2019	Correction: The role of AKT and FOXO3 in preventing ovarian toxicity induced by cyclophosphamide.	Cyclophosphamide	80-96	AKT serine/threonine kinase 1	Homo sapiens	24-27
30986272-0	2019	Correction: The role of AKT and FOXO3 in preventing ovarian toxicity induced by cyclophosphamide.	Cyclophosphamide	80-96	forkhead box O3	Homo sapiens	32-37
31031723-1	2019	Cyclophosphamide (CTX), a clinically important antineoplastic drug, also leads to some side effects such as nausea, vomiting and diarrhea in the consumer.	Cyclophosphamide	0-16	V-set and immunoglobulin domain containing 2	Mus musculus	18-21
31143518-6	2019	Moreover, a combination of the anti-ICOS mAb with cyclophosphamide reduced tumor growth, and that was associated with an improved CD8 to Treg ratio.	Cyclophosphamide	50-66	inducible T cell costimulator	Homo sapiens	36-40
31143518-6	2019	Moreover, a combination of the anti-ICOS mAb with cyclophosphamide reduced tumor growth, and that was associated with an improved CD8 to Treg ratio.	Cyclophosphamide	50-66	CD8a molecule	Homo sapiens	130-133
32775480-8	2019	The results from studies in animals including cyclophosphamide-induced hemorrhagic cystitis strongly support the role of P2X7 receptors in inflammation.	Cyclophosphamide	46-62	purinergic receptor P2X 7	Homo sapiens	121-125
30952749-0	2019	Neoadjuvant Chemotherapy With Nab-paclitaxel Plus Trastuzumab Followed by 5-Fluorouracil/Epirubicin/Cyclophosphamide for HER2-positive Operable Breast Cancer: A Multicenter Phase II Trial.	Cyclophosphamide	100-116	erb-b2 receptor tyrosine kinase 2	Homo sapiens	121-125
30508546-3	2019	Biweekly cyclophosphamide injection improved vascular permeability and structural abnormalities of endothelial cell-specific Fli1 knockout mice in 2 weeks and in 3 months, respectively.	Cyclophosphamide	9-25	Friend leukemia integration 1	Mus musculus	125-129
30664262-6	2019	ELISA revealed an elevation in the levels of IL-6 and a reduction in IFN-gamma levels with CPA treatment.	Cyclophosphamide	91-94	interferon gamma	Mus musculus	69-78
30508546-4	2019	In endothelial cell-specific Fli1 knockout mice, a single dose of cyclophosphamide was sufficient to normalize the decreased expression of alpha-smooth muscle actin in dermal blood vessels and improve the impaired neovascularization in skin-embedded Matrigel plug.	Cyclophosphamide	66-82	Friend leukemia integration 1	Mus musculus	29-33
30508546-6	2019	In SSc patients, serum CCN1 levels were significantly increased after intravenous cyclophosphamide pulse.	Cyclophosphamide	82-98	cellular communication network factor 1	Mus musculus	23-27
30508546-7	2019	Taken together, these results indicate that cyclophosphamide improves Fli1 deficiency-dependent vascular changes by normalizing the expression of angiogenesis- and vasculogenesis-related molecules and endothelial Fli1, which may help to explain the beneficial effect of cyclophosphamide on SSc vasculopathy.	Cyclophosphamide	44-60	Friend leukemia integration 1	Mus musculus	70-74
30508546-7	2019	Taken together, these results indicate that cyclophosphamide improves Fli1 deficiency-dependent vascular changes by normalizing the expression of angiogenesis- and vasculogenesis-related molecules and endothelial Fli1, which may help to explain the beneficial effect of cyclophosphamide on SSc vasculopathy.	Cyclophosphamide	44-60	Friend leukemia integration 1	Mus musculus	213-217
30508546-7	2019	Taken together, these results indicate that cyclophosphamide improves Fli1 deficiency-dependent vascular changes by normalizing the expression of angiogenesis- and vasculogenesis-related molecules and endothelial Fli1, which may help to explain the beneficial effect of cyclophosphamide on SSc vasculopathy.	Cyclophosphamide	270-286	Friend leukemia integration 1	Mus musculus	70-74
30887825-1	2019	AIM: To evaluate activity of metronomic cyclophosphamide (mCTX) in heavily pretreated metastatic castration-resistant prostate cancer (mCRPC) patients.	Cyclophosphamide	40-56	V-set and immunoglobulin domain containing 2	Mus musculus	58-62
30506662-1	2019	This study clarified the protective effect of ganoderic acid A (GAA) on cyclophosphamide (CP)-induced hepatotoxicity in mice.	Cyclophosphamide	72-88	glucosidase, alpha, acid	Mus musculus	64-67
30785826-0	2019	West German Study PlanB Trial: Adjuvant Four Cycles of Epirubicin and Cyclophosphamide Plus Docetaxel Versus Six Cycles of Docetaxel and Cyclophosphamide in HER2-Negative Early Breast Cancer.	Cyclophosphamide	137-153	erb-b2 receptor tyrosine kinase 2	Homo sapiens	157-161
30689002-0	2019	Cyclophosphamide dose adjustment based on body weight and albuminemia in elderly patients treated with R-mini-CHOP.	Cyclophosphamide	0-16	DNA damage inducible transcript 3	Homo sapiens	110-114
30787107-0	2019	Impact of KIR/HLA Incompatibilities on NK Cell Reconstitution and Clinical Outcome after T Cell-Replete Haploidentical Hematopoietic Stem Cell Transplantation with Posttransplant Cyclophosphamide.	Cyclophosphamide	179-195	killer cell immunoglobulin like receptor, two Ig domains and long cytoplasmic tail 4	Homo sapiens	10-13
30862756-1	2019	Cyclophosphamide (CTX) is widely used in cancer chemotherapy, but it often induces mucositis, in which the disruption of the gut microbiota might play a pivotal role.	Cyclophosphamide	0-16	V-set and immunoglobulin domain containing 2	Mus musculus	18-21
30652208-4	2019	Since metronomic cyclophosphamide (CTX) was shown to selectively deplete Tregs, a phase 1 clinical trial was conducted to comprehensively investigate the immune-modulating effects of several dosages and schedules of CTX in combination with the standard dose of everolimus, with the explicit aim to achieve selective Treg depletion.	Cyclophosphamide	17-33	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	35-38
30867701-7	2019	Also, after rituximab treatment, the expression levels of CD20 and PA IgG in lymphocytes were significantly lower than those in cyclophosphamide group (P&lt;0.05), and platelet count was higher than that in cyclophosphamide group (P&lt;0.05).	Cyclophosphamide	207-223	keratin 20	Homo sapiens	58-62
30262565-5	2019	When comparing the influence of anti-T-cell therapy, a delay in the reconstitution of the naive CD8+ T-cell repertoire was observed in patients who received in vivo T-cell depletion using antithymocyte globulin or post-transplantation cyclophosphamide in case of haploidentical transplantation.	Cyclophosphamide	235-251	CD8a molecule	Homo sapiens	96-99
30936600-2	2019	The aim of the present study was to investigate the effects of the coadministration of BMSCs and the G-CSF on damaged ovaries after creating a chemotherapy model with cyclophosphamide (CTX) in rats.	Cyclophosphamide	167-183	colony stimulating factor 3	Rattus norvegicus	101-106
30724726-4	2019	METHODOLOGY: We assessed whether hLp-nF1 could elevate the activation of NK cells and macrophages using cyclophosphamide (CP)-induced immunosuppressed BALB/c mice and RAW 264.7 macrophages.	Cyclophosphamide	104-120	HLP	Homo sapiens	33-36
30724726-4	2019	METHODOLOGY: We assessed whether hLp-nF1 could elevate the activation of NK cells and macrophages using cyclophosphamide (CP)-induced immunosuppressed BALB/c mice and RAW 264.7 macrophages.	Cyclophosphamide	104-120	neurofibromin 1	Mus musculus	37-40
29907903-8	2019	Leukocyte depletion experiments performed with cyclophosphamide, anti-Ly6G, or anti-CD3 antibodies indicated that the antinociceptive effect evoked by CCL4 depends on circulating T lymphocytes.	Cyclophosphamide	47-63	chemokine (C-C motif) ligand 4	Mus musculus	151-155
30307363-5	2019	She was treated with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) chemotherapy which was complicated by prolonged pancytopenia, without response.	Cyclophosphamide	21-37	DNA damage inducible transcript 3	Homo sapiens	80-84
30629411-3	2019	In this study, we first investigated the effects of CK on myelosuppression in mice induced by cyclophosphamide (CTX).	Cyclophosphamide	94-110	V-set and immunoglobulin domain containing 2	Mus musculus	112-115
30655615-0	2019	Phase 1 trial of olaparib and oral cyclophosphamide in BRCA breast cancer, recurrent BRCA ovarian cancer, non-BRCA triple-negative breast cancer, and non-BRCA ovarian cancer.	Cyclophosphamide	35-51	BRCA1 DNA repair associated	Homo sapiens	55-59
30406375-1	2019	The oncofoetal antigen 5T4 is a promising T cell target in the context of colorectal cancer, as demonstrated by a recent clinical study where 5T4-specific T cell responses, induced by vaccination or cyclophosphamide, were associated with a significantly prolonged survival of patients with metastatic disease.	Cyclophosphamide	199-215	trophoblast glycoprotein	Homo sapiens	23-26
30406375-1	2019	The oncofoetal antigen 5T4 is a promising T cell target in the context of colorectal cancer, as demonstrated by a recent clinical study where 5T4-specific T cell responses, induced by vaccination or cyclophosphamide, were associated with a significantly prolonged survival of patients with metastatic disease.	Cyclophosphamide	199-215	trophoblast glycoprotein	Homo sapiens	142-145
30530902-7	2019	We demonstrated that phospho-AKT (p-AKT) and cleaved PARP (cPARP) are present in primordial oocytes 3 days after CPA injection, consistent with the role of these markers as part of the apoptotic cascade.	Cyclophosphamide	113-116	collagen type XI alpha 2 chain	Homo sapiens	53-57
30111844-3	2019	We identified microRNA (miRNA) miR-34a as the most prominently upregulated miRNA during DDR in CLL cells in vitro and in vivo during FCR therapy (fludarabine, cyclophosphamide, rituximab).	Cyclophosphamide	159-175	microRNA 34a	Homo sapiens	31-38
30670057-17	2019	Use of CD34-selected auto-HSCT with high-dose cyclophosphamide monotherapy as a conditioning regimen may offer an excellent benefit-to-risk balance.	Cyclophosphamide	46-62	CD34 molecule	Homo sapiens	7-11
30500380-5	2019	In addition, we were interested to analyze acute cytotoxicity of the model drug cyclophosphamide (CPA) metabolized by HepG2-2C19 C1 and by a previously generated CYP3A4-overexpressing HepG2 cell clone.	Cyclophosphamide	80-96	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	162-168
30500380-5	2019	In addition, we were interested to analyze acute cytotoxicity of the model drug cyclophosphamide (CPA) metabolized by HepG2-2C19 C1 and by a previously generated CYP3A4-overexpressing HepG2 cell clone.	Cyclophosphamide	98-101	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	162-168
30500380-6	2019	Upon 10 mM CPA exposure, we were able to detect its metabolites 4-hydroxy-cyclophosphamide and acrolein in CYP3A4- and CYP2C19-expressing cell clones, but not in parental HepG2 cell line.	Cyclophosphamide	11-14	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	107-113
30500380-6	2019	Upon 10 mM CPA exposure, we were able to detect its metabolites 4-hydroxy-cyclophosphamide and acrolein in CYP3A4- and CYP2C19-expressing cell clones, but not in parental HepG2 cell line.	Cyclophosphamide	11-14	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	119-126
30669758-1	2019	Objective: Serum anti Mullerian hormone (AMH) was used to evaluate the effect of cyclophosphamide (CTX) on ovarian function in female patients with systemic lupus erythematosus (SLE).	Cyclophosphamide	81-97	anti-Mullerian hormone	Homo sapiens	41-44
30268651-10	2019	Moreover, XMT-WE promoted the secretion of interleukin-2 (IL-2) and interferon-gamma (IFN-gamma) in cyclophosphamide (CTX)-induced immunosuppressive mice.	Cyclophosphamide	100-116	interleukin 2	Mus musculus	58-62
30268651-10	2019	Moreover, XMT-WE promoted the secretion of interleukin-2 (IL-2) and interferon-gamma (IFN-gamma) in cyclophosphamide (CTX)-induced immunosuppressive mice.	Cyclophosphamide	100-116	interferon gamma	Mus musculus	68-84
30268651-10	2019	Moreover, XMT-WE promoted the secretion of interleukin-2 (IL-2) and interferon-gamma (IFN-gamma) in cyclophosphamide (CTX)-induced immunosuppressive mice.	Cyclophosphamide	100-116	interferon gamma	Mus musculus	86-95
30760223-4	2019	METHODS: In the present study, we investigated the potential role of a multi-target iron chelator, M30 in protecting against cyclophosphamide-induced alopecia in C57BL/6 mice implanted with an osmotic pump.	Cyclophosphamide	125-141	olfactory receptor family 10 subfamily N member 1	Mus musculus	99-102
30760223-5	2019	M30 enhanced hair growth and prevented cyclophosphamide-induced abnormal hair in the mice.	Cyclophosphamide	39-55	olfactory receptor family 10 subfamily N member 1	Mus musculus	0-3
30760223-6	2019	Furthermore, we examined the gene expression profiles derived from skin biopsy specimens of normal mice, cyclophosphamide-treated mice, and cyclophosphamide treated mice with M30 supplement.	Cyclophosphamide	140-156	olfactory receptor family 10 subfamily N member 1	Mus musculus	175-178
30760223-9	2019	CONCLUSION: Our study demonstrates that M30 treatment is a promising therapy for cyclophosphamide-induced alopecia and suggests that the top five genes have unique preventive effects in cyclophosphamide-induced transformation.	Cyclophosphamide	81-97	olfactory receptor family 10 subfamily N member 1	Mus musculus	40-43
30760223-9	2019	CONCLUSION: Our study demonstrates that M30 treatment is a promising therapy for cyclophosphamide-induced alopecia and suggests that the top five genes have unique preventive effects in cyclophosphamide-induced transformation.	Cyclophosphamide	186-202	olfactory receptor family 10 subfamily N member 1	Mus musculus	40-43
30472434-0	2019	Addendum to: Haploidentical Related Donor Hematopoietic Stem Cell Transplantation for DOCK8 Deficiency Using Post-Transplantation Cyclophosphamide.	Cyclophosphamide	130-146	dedicator of cytokinesis 8	Homo sapiens	86-91
30579147-0	2019	Corrigendum to "Aldehyde dehydrogenase 2 activation ameliorates cyclophosphamide-induced acute cardiotoxicity via detoxification of toxic aldehydes and suppression of cardiac cell death" [Journal of Molecular and Cellular Cardiology (JMCC) volume 121 (2018) 134-144].	Cyclophosphamide	64-80	aldehyde dehydrogenase 2 family member	Homo sapiens	16-40
31482020-0	2019	Effects of intravesical administration of sensory neuron-specific receptor agonist on voiding function in rats with cyclophosphamide-induced cystitis.	Cyclophosphamide	116-132	MAS-related G-protein coupled receptor, member C	Rattus norvegicus	42-74
31279962-3	2019	METHODS: We conducted a randomized phase II clinical trial to evaluate the therapeutic benefit of oral metronomic cyclophosphamide (CTX) alone and with the anti-angiogenic drug celecoxib in patients with gynecological malignancies.	Cyclophosphamide	114-130	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	132-135
31482020-11	2019	Conclusions: The current results indicate that intravesical administration of a selective rat sensory neuron-specific receptor 1 agonist can inhibit the micturition reflex and can ameliorate cyclophosphamide-induced bladder overactivity in rats.	Cyclophosphamide	191-207	MAS-related G-protein coupled receptor, member C	Rattus norvegicus	94-126
29958796-0	2019	Cyclophosphamide with or without fluorouracil followed by subcutaneous or intravenous interleukin-2 use in solid tumors: A feasibility off-label experience.	Cyclophosphamide	0-16	interleukin 2	Homo sapiens	86-99
31057112-7	2019	RESULTS: Our data showed that CPA significantly elevated brain AChE activity in the hippocampal region.	Cyclophosphamide	30-33	acetylcholinesterase	Rattus norvegicus	63-67
31057112-8	2019	A decrease in the total antioxidant capacity and a reduction in the CAT, SOD, and GPX activity occurred in the brains of the rats exposed to CPA.	Cyclophosphamide	141-144	catalase	Rattus norvegicus	68-71
30765674-5	2019	Neoadjuvant chemotherapy was chosen, and then combined treatment with epirubicin(EPI)and cyclophosphamide(CPA) was started.	Cyclophosphamide	89-105	carboxypeptidase A1	Homo sapiens	106-109
30113879-0	2019	AMH prevents primordial ovarian follicle loss and fertility alteration in cyclophosphamide-treated mice.	Cyclophosphamide	74-90	anti-Mullerian hormone	Mus musculus	0-3
30113879-7	2019	The aim of the present study was to evaluate, in a model of Cy-treated pubertal mice, whether AMH administration might restrain PMF depletion.	Cyclophosphamide	60-62	anti-Mullerian hormone	Mus musculus	94-97
30113879-8	2019	The counting of the total PMF number within mouse ovaries showed that recombinant AMH prevented Cy-induced PMF loss.	Cyclophosphamide	96-98	anti-Mullerian hormone	Mus musculus	82-85
30113879-11	2019	Taken together, these results support a protective role of AMH against Cy-induced follicular loss.	Cyclophosphamide	71-73	anti-Mullerian hormone	Mus musculus	59-62
30113879-13	2019	Therefore, concomitant recombinant AMH administration during chemotherapy might offer a new option for preserving young patients" fertility.-Sonigo, C., Beau, I., Grynberg, M., Binart, N. AMH prevents primordial ovarian follicle loss and fertility alteration in cyclophosphamide-treated mice.	Cyclophosphamide	262-278	anti-Mullerian hormone	Homo sapiens	35-38
30113879-13	2019	Therefore, concomitant recombinant AMH administration during chemotherapy might offer a new option for preserving young patients" fertility.-Sonigo, C., Beau, I., Grynberg, M., Binart, N. AMH prevents primordial ovarian follicle loss and fertility alteration in cyclophosphamide-treated mice.	Cyclophosphamide	262-278	anti-Mullerian hormone	Mus musculus	188-191
31685786-0	2019	Treatment with Methotrexate and Intravenous Cyclophosphamide Pulse Therapy Regulates the P-gp+CD4+ Cell-related Pathogenesis in a Representative Patient with Refractory Proliferative Lupus Nephritis.	Cyclophosphamide	44-60	ATP binding cassette subfamily B member 1	Homo sapiens	89-93
30168260-6	2019	While cyclophosphamide has revolutionized the management of AAV, increasing use of rituximab as an alternative induction regimen, as well as use of novel approaches involving reduced or no corticosteroid use for AAV and alternative agents such as avacopan (a complement 5a receptor antagonist) hold promise for lesser toxic induction regimens in the future.	Cyclophosphamide	6-22	adeno-associated virus integration site 1	Homo sapiens	60-63
29907809-0	2019	Killer cell immunoglobulin-like receptor ligand mismatching and outcome after haploidentical transplantation with post-transplant cyclophosphamide.	Cyclophosphamide	130-146	killer cell immunoglobulin like receptor, three Ig domains and long cytoplasmic tail 2	Homo sapiens	0-40
30320358-8	2019	These responses were dependent on hypoxia-induced HIF-1alpha activation, as evidenced by chemical inhibition of its transcriptional activity with 2-methoxyestradiol (2-ME), which enhanced the cytotoxic activity of CPA and IFA and increased apoptosis.	Cyclophosphamide	214-217	hypoxia inducible factor 1 subunit alpha	Homo sapiens	50-60
30320358-9	2019	Our results indicate that by stimulating HIF-1alpha activity, hypoxia downregulates the expression of CYP2B6, CYP3A4 and CYP3A5, that in turn leads to decreased conversion of CPA and IFA into their active forms and thus to diminished cytotoxicity.	Cyclophosphamide	175-178	hypoxia inducible factor 1 subunit alpha	Homo sapiens	41-51
30320358-9	2019	Our results indicate that by stimulating HIF-1alpha activity, hypoxia downregulates the expression of CYP2B6, CYP3A4 and CYP3A5, that in turn leads to decreased conversion of CPA and IFA into their active forms and thus to diminished cytotoxicity.	Cyclophosphamide	175-178	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	102-108
30320358-9	2019	Our results indicate that by stimulating HIF-1alpha activity, hypoxia downregulates the expression of CYP2B6, CYP3A4 and CYP3A5, that in turn leads to decreased conversion of CPA and IFA into their active forms and thus to diminished cytotoxicity.	Cyclophosphamide	175-178	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	110-116
30320358-9	2019	Our results indicate that by stimulating HIF-1alpha activity, hypoxia downregulates the expression of CYP2B6, CYP3A4 and CYP3A5, that in turn leads to decreased conversion of CPA and IFA into their active forms and thus to diminished cytotoxicity.	Cyclophosphamide	175-178	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	121-127
31597843-2	2019	R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) remains the standard treatment for diffuse large B-cell lymphoma (DLBCL) in line with the prior 2013 guidelines.	Cyclophosphamide	19-35	DNA damage inducible transcript 3	Homo sapiens	2-6
30580884-4	2019	In 1999, the patient developed FSGS 3 years after transplant, which was treated with plasmapheresis and cyclophosphamide.	Cyclophosphamide	104-120	actinin alpha 4	Homo sapiens	31-35
30554488-0	2019	Correlation of UGT2B7 Polymorphism with Cardiotoxicity in Breast Cancer Patients Undergoing Epirubicin/Cyclophosphamide-Docetaxel Adjuvant Chemotherapy.	Cyclophosphamide	103-119	UDP glucuronosyltransferase family 2 member B7	Homo sapiens	15-21
30554488-1	2019	PURPOSE: The present study aimed to investigate correlations between uridine glucuronosyltransferase 2B7 (UGT2B7) -161 single nucleotide polymorphism C to T (C&gt;T) and the occurrence of cardiotoxicity in Chinese breast cancer (BC) patients undergoing epirubicin/cyclophosphamide-docetaxel (EC-D) adjuvant chemotherapy.	Cyclophosphamide	264-280	UDP glucuronosyltransferase family 2 member B7	Homo sapiens	69-104
30554488-1	2019	PURPOSE: The present study aimed to investigate correlations between uridine glucuronosyltransferase 2B7 (UGT2B7) -161 single nucleotide polymorphism C to T (C&gt;T) and the occurrence of cardiotoxicity in Chinese breast cancer (BC) patients undergoing epirubicin/cyclophosphamide-docetaxel (EC-D) adjuvant chemotherapy.	Cyclophosphamide	264-280	UDP glucuronosyltransferase family 2 member B7	Homo sapiens	106-112
30687765-0	2018	Intravenous Cyclophosphamide Therapy for Anti-IFN-Gamma Autoantibody-Associated Mycobacterium abscessus Infection.	Cyclophosphamide	12-28	interferon gamma	Homo sapiens	46-55
30687062-5	2018	Methods: We describe a patient with HER2+, hormone receptor-negative, inflammatory metastatic breast cancer who was previously treated with doxorubicin, cyclophosphamide, and zoledronic acid followed by paclitaxel and trastuzumab.	Cyclophosphamide	153-169	erb-b2 receptor tyrosine kinase 2	Homo sapiens	36-40
30171947-0	2018	Sarcodon imbricatus polysaccharides protect against cyclophosphamide-induced immunosuppression via regulating Nrf2-mediated oxidative stress.	Cyclophosphamide	52-68	nuclear factor, erythroid derived 2, like 2	Mus musculus	110-114
30101910-1	2018	Objective Although R-CHOP (rituximab, cyclophosphamide, vincristine, doxorubicin, and prednisone) is a standard therapy for diffuse large B-cell lymphoma (DLBCL), the optimal dose for elderly patients remains unclear.	Cyclophosphamide	38-54	DNA damage inducible transcript 3	Homo sapiens	21-25
30788202-10	2018	The patient was treated with six courses of CHOP-R (cyclophosphamide, doxorubicin, vincristine, prednisone, and rituximab).	Cyclophosphamide	52-68	DNA damage inducible transcript 3	Homo sapiens	44-48
30372898-0	2018	Combination of Ginsenoside H dripping pills and cyclophosphamide improve paraneoplastic syndrome and inhibit postoperative recurrence via the reversion of Th1/Th2 shift.	Cyclophosphamide	48-64	negative elongation factor complex member C/D	Homo sapiens	155-158
30114420-6	2018	Meanwhile, cyclophosphamide treatment induces activation of p38 MAPK, c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) to causes intestinal damage and blockage of p38 MAPK, JNK and ERK activation contributed to the effect of OVT on the repair of intestinal damage.	Cyclophosphamide	11-27	mitogen-activated protein kinase 14	Mus musculus	60-68
30114420-6	2018	Meanwhile, cyclophosphamide treatment induces activation of p38 MAPK, c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) to causes intestinal damage and blockage of p38 MAPK, JNK and ERK activation contributed to the effect of OVT on the repair of intestinal damage.	Cyclophosphamide	11-27	mitogen-activated protein kinase 8	Mus musculus	70-93
30114420-6	2018	Meanwhile, cyclophosphamide treatment induces activation of p38 MAPK, c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) to causes intestinal damage and blockage of p38 MAPK, JNK and ERK activation contributed to the effect of OVT on the repair of intestinal damage.	Cyclophosphamide	11-27	mitogen-activated protein kinase 8	Mus musculus	95-98
30114420-6	2018	Meanwhile, cyclophosphamide treatment induces activation of p38 MAPK, c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) to causes intestinal damage and blockage of p38 MAPK, JNK and ERK activation contributed to the effect of OVT on the repair of intestinal damage.	Cyclophosphamide	11-27	mitogen-activated protein kinase 1	Mus musculus	104-141
30114420-6	2018	Meanwhile, cyclophosphamide treatment induces activation of p38 MAPK, c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) to causes intestinal damage and blockage of p38 MAPK, JNK and ERK activation contributed to the effect of OVT on the repair of intestinal damage.	Cyclophosphamide	11-27	mitogen-activated protein kinase 1	Mus musculus	143-146
30114420-6	2018	Meanwhile, cyclophosphamide treatment induces activation of p38 MAPK, c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) to causes intestinal damage and blockage of p38 MAPK, JNK and ERK activation contributed to the effect of OVT on the repair of intestinal damage.	Cyclophosphamide	11-27	mitogen-activated protein kinase 14	Mus musculus	60-63
30114420-6	2018	Meanwhile, cyclophosphamide treatment induces activation of p38 MAPK, c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) to causes intestinal damage and blockage of p38 MAPK, JNK and ERK activation contributed to the effect of OVT on the repair of intestinal damage.	Cyclophosphamide	11-27	mitogen-activated protein kinase 1	Mus musculus	64-68
30114420-6	2018	Meanwhile, cyclophosphamide treatment induces activation of p38 MAPK, c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) to causes intestinal damage and blockage of p38 MAPK, JNK and ERK activation contributed to the effect of OVT on the repair of intestinal damage.	Cyclophosphamide	11-27	mitogen-activated protein kinase 8	Mus musculus	202-205
30114420-6	2018	Meanwhile, cyclophosphamide treatment induces activation of p38 MAPK, c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) to causes intestinal damage and blockage of p38 MAPK, JNK and ERK activation contributed to the effect of OVT on the repair of intestinal damage.	Cyclophosphamide	11-27	mitogen-activated protein kinase 1	Mus musculus	210-213
30501868-2	2018	Multiple retrospective studies of R-CHOP (rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone or prednisolone) have shown a worse outcome in patients with MYC rearrangement (alone or with rearrangement of BCL2 or BCL6, or both) than in patients without MYC rearrangement, and suggest improved outcomes after more intensive treatment.	Cyclophosphamide	57-73	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	177-180
30289572-10	2018	Furthermore, our time-course analyses revealed a transient increase in serum KL-6 levels with a peak at 3 months after the first infusion of cyclophosphamide, which showed no relation to therapeutic efficacy.	Cyclophosphamide	141-157	mucin 1, cell surface associated	Homo sapiens	77-81
30340554-1	2018	BACKGROUND: Rituximab plus combination chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is broadly accepted as standard for the treatment of diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	57-73	DNA damage inducible transcript 3	Homo sapiens	119-123
30048737-6	2018	IL-2 production was reduced in response to treatment with well-known immunotoxicants cyclosporin A (CYA), dexamethasone (DEX), azathioprine (AZPR), methotrexate (MOT) and benzo(a)pyrene (BAP) but was not affected by treatment with cyclophosphamide (CYPH).	Cyclophosphamide	231-247	interleukin 2	Homo sapiens	0-4
30048737-6	2018	IL-2 production was reduced in response to treatment with well-known immunotoxicants cyclosporin A (CYA), dexamethasone (DEX), azathioprine (AZPR), methotrexate (MOT) and benzo(a)pyrene (BAP) but was not affected by treatment with cyclophosphamide (CYPH).	Cyclophosphamide	249-253	interleukin 2	Homo sapiens	0-4
30504317-3	2018	Fludarabine, cyclophosphamide, rituximab chemotherapy remains the standard frontline therapy for young fit patients with CLL, especially if IGHV mutated.	Cyclophosphamide	13-29	immunoglobulin heavy variable 3-69-1 (pseudogene)	Homo sapiens	140-144
30482157-4	2018	Following stimulation with cyclophosphamide, the inhibition of the elevated levels of TAK1/NF-kappaB and phospho-TAK1/NF-kappaB by ESWT and GPR120 agonists in RT4 cells was associated with a suppression of NF-kappaB translocation from the cytosol to the nucleus.	Cyclophosphamide	27-43	mitogen-activated protein kinase kinase kinase 7	Homo sapiens	86-90
30482157-4	2018	Following stimulation with cyclophosphamide, the inhibition of the elevated levels of TAK1/NF-kappaB and phospho-TAK1/NF-kappaB by ESWT and GPR120 agonists in RT4 cells was associated with a suppression of NF-kappaB translocation from the cytosol to the nucleus.	Cyclophosphamide	27-43	nuclear factor kappa B subunit 1	Homo sapiens	91-100
30482157-4	2018	Following stimulation with cyclophosphamide, the inhibition of the elevated levels of TAK1/NF-kappaB and phospho-TAK1/NF-kappaB by ESWT and GPR120 agonists in RT4 cells was associated with a suppression of NF-kappaB translocation from the cytosol to the nucleus.	Cyclophosphamide	27-43	mitogen-activated protein kinase kinase kinase 7	Homo sapiens	113-117
30482157-4	2018	Following stimulation with cyclophosphamide, the inhibition of the elevated levels of TAK1/NF-kappaB and phospho-TAK1/NF-kappaB by ESWT and GPR120 agonists in RT4 cells was associated with a suppression of NF-kappaB translocation from the cytosol to the nucleus.	Cyclophosphamide	27-43	nuclear factor kappa B subunit 1	Homo sapiens	118-127
30482157-4	2018	Following stimulation with cyclophosphamide, the inhibition of the elevated levels of TAK1/NF-kappaB and phospho-TAK1/NF-kappaB by ESWT and GPR120 agonists in RT4 cells was associated with a suppression of NF-kappaB translocation from the cytosol to the nucleus.	Cyclophosphamide	27-43	free fatty acid receptor 4	Homo sapiens	140-146
30482157-4	2018	Following stimulation with cyclophosphamide, the inhibition of the elevated levels of TAK1/NF-kappaB and phospho-TAK1/NF-kappaB by ESWT and GPR120 agonists in RT4 cells was associated with a suppression of NF-kappaB translocation from the cytosol to the nucleus.	Cyclophosphamide	27-43	nuclear factor kappa B subunit 1	Homo sapiens	118-127
29968488-0	2018	Effect of platelet-rich plasma (PRP) on ovarian structures in cyclophosphamide-induced ovarian failure in female rats: a stereological study.	Cyclophosphamide	62-78	proline rich protein 2-like 1	Rattus norvegicus	32-35
29968488-3	2018	OBJECTIVE: This study evaluates the effect of PRP on ovarian structures and function in cyclophosphamide (Cy)-induced ovarian failure in female rats by a stereological method.	Cyclophosphamide	88-104	proline rich protein 2-like 1	Rattus norvegicus	46-49
29968488-3	2018	OBJECTIVE: This study evaluates the effect of PRP on ovarian structures and function in cyclophosphamide (Cy)-induced ovarian failure in female rats by a stereological method.	Cyclophosphamide	106-108	proline rich protein 2-like 1	Rattus norvegicus	46-49
29802527-6	2018	Allograft biopsy revealed recurrent IgAN with crescents, which was successfully treated with pulse intravenous steroids and six monthly doses of intravenous cyclophosphamide.	Cyclophosphamide	157-173	IGAN1	Homo sapiens	36-40
29802527-8	2018	Although it is not an established treatment as in native kidneys, intravenous cyclophosphamide should probably be considered in kidney transplants with potentially reversible recurrent crescentic IgAN.	Cyclophosphamide	78-94	IGAN1	Homo sapiens	196-200
30360947-0	2018	Involvement of 5-HT2A receptor hyperfunction in the anxiety-like behavior induced by doxorubicin and cyclophosphamide combination treatment in rats.	Cyclophosphamide	101-117	5-hydroxytryptamine receptor 2A	Canis lupus familiaris	15-30
30360947-6	2018	Combination treatment with doxorubicin and cyclophosphamide significantly increased (+-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane, (a 5-HT2A receptor agonist)-induced wet-dog shake activity.	Cyclophosphamide	43-59	5-hydroxytryptamine receptor 2A	Canis lupus familiaris	139-154
30360947-8	2018	The anxiety-like behavior induced by doxorubicin and cyclophosphamide combination treatment is mediated by hyperfunctioning of the 5-HT2A receptor.	Cyclophosphamide	53-69	5-hydroxytryptamine receptor 2A	Canis lupus familiaris	131-146
30431571-4	2018	INTERVENTIONS AND OUTCOMES: Fortunately, the patient"s skin lesions subsided gradually after 3 cycles of cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) regimen.	Cyclophosphamide	105-121	DNA damage inducible transcript 3	Homo sapiens	167-171
30344717-9	2018	Furthermore, it was revealed that PARP-3 overexpression was associated with shorter survival time in patients with cyclophosphamide/doxorubicin or epirubicin/5-fluorouracil (CAF/CEF) chemotherapy compared with low PARP-3 expression, but not in patients with CAF/CEF + docetaxel chemotherapy.	Cyclophosphamide	115-131	poly(ADP-ribose) polymerase family member 3	Homo sapiens	34-40
30336565-9	2018	Finally, bergenin also reversed the Cy-induced decrease in the total antioxidant capacity including activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px).	Cyclophosphamide	36-38	catalase	Mus musculus	142-150
30336565-9	2018	Finally, bergenin also reversed the Cy-induced decrease in the total antioxidant capacity including activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px).	Cyclophosphamide	36-38	catalase	Mus musculus	152-155
30201214-1	2018	Genetic variations within cytochrome P450 2B6 (CYP2B6) contribute to inter-individual variation in the metabolism of clinically important drugs, including cyclophosphamide, bupropion, methadone and efavirenz (EFZ).	Cyclophosphamide	155-171	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	26-45
29780145-4	2018	Based on her cognitive impairment, muscle rigidity, and high levels of interleukin-6 in the cerebrospinal fluid, we believed she had developed a complication of a neuropsychiatric disease and administered corticosteroids and intravenous cyclophosphamide therapy.	Cyclophosphamide	237-253	interleukin 6	Homo sapiens	71-84
30201214-1	2018	Genetic variations within cytochrome P450 2B6 (CYP2B6) contribute to inter-individual variation in the metabolism of clinically important drugs, including cyclophosphamide, bupropion, methadone and efavirenz (EFZ).	Cyclophosphamide	155-171	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	47-53
29966970-1	2018	BACKGROUND: Aberrant microRNA (miRNAs) have recently been proposed as important regulators in acquiring resistance to cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) in diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	118-134	DNA-damage inducible transcript 3	Mus musculus	178-182
30190020-4	2018	Rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is a highly effective but potentially neurotoxic regimen.	Cyclophosphamide	11-27	DNA damage inducible transcript 3	Homo sapiens	73-77
30313105-6	2018	The patient was treated with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP).Neurological symptoms improved with R-CHOP.	Cyclophosphamide	40-56	DNA damage inducible transcript 3	Homo sapiens	146-150
30453718-4	2018	The expression of AKT protein was significantly inhibited in the celecoxib (CLB) group, the Feiliuping Gao (FLP) combination with cyclophosphamide (FLP+CTX) group, and the Feiliuping Gao combination with celecoxib (FLP+CLB) group (P&lt;0.05).	Cyclophosphamide	130-146	thymoma viral proto-oncogene 1	Mus musculus	18-21
30338042-0	2018	Lenalidomide combined with low-dose cyclophosphamide and prednisone modulates Ikaros and Aiolos in lymphocytes, resulting in immunostimulatory effects in lenalidomide-refractory multiple myeloma patients.	Cyclophosphamide	36-52	IKAROS family zinc finger 3	Homo sapiens	89-95
31949844-0	2018	Expression of hypoxia-inducible factor-1a predicts benefit from rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone in diffuse large B-cell lymphoma.	Cyclophosphamide	79-95	hypoxia inducible factor 1 subunit alpha	Homo sapiens	14-41
30063143-6	2018	Furthermore, when a low dose of cyclophosphamide (CP) was loaded into PD-1-expressing platelets to deplete regulatory T cells (Tregs), an increased frequency of reinvigorated CD8+ lymphocyte cells was observed within the postsurgery tumor microenvironment, directly preventing tumor relapse.	Cyclophosphamide	32-48	programmed cell death 1	Homo sapiens	70-74
30063143-6	2018	Furthermore, when a low dose of cyclophosphamide (CP) was loaded into PD-1-expressing platelets to deplete regulatory T cells (Tregs), an increased frequency of reinvigorated CD8+ lymphocyte cells was observed within the postsurgery tumor microenvironment, directly preventing tumor relapse.	Cyclophosphamide	32-48	CD8a molecule	Homo sapiens	175-178
29717937-0	2018	Deletion or pharmacological blockade of TLR4 confers protection against cyclophosphamide-induced mouse cystitis.	Cyclophosphamide	72-88	toll-like receptor 4	Mus musculus	40-44
29717937-2	2018	We investigate the role of toll-like receptor 4 (TLR4) on voiding dysfunction and inflammation in the cyclophosphamide (CYP)-induced mouse cystitis.	Cyclophosphamide	102-118	toll-like receptor 4	Mus musculus	27-47
29717937-2	2018	We investigate the role of toll-like receptor 4 (TLR4) on voiding dysfunction and inflammation in the cyclophosphamide (CYP)-induced mouse cystitis.	Cyclophosphamide	102-118	toll-like receptor 4	Mus musculus	49-53
29730008-0	2018	Ameliorative effects of Antrodia cinnamomea polysaccharides against cyclophosphamide-induced immunosuppression related to Nrf2/HO-1 signaling in BALB/c mice.	Cyclophosphamide	68-84	nuclear factor, erythroid derived 2, like 2	Mus musculus	122-126
29730008-0	2018	Ameliorative effects of Antrodia cinnamomea polysaccharides against cyclophosphamide-induced immunosuppression related to Nrf2/HO-1 signaling in BALB/c mice.	Cyclophosphamide	68-84	heme oxygenase 1	Mus musculus	127-131
31949844-2	2018	However, HIF-1alpha was suggested to predict improved survival in Western patients with diffuse large B-cell lymphoma (DLBCL) under rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) treatment.	Cyclophosphamide	147-163	hypoxia inducible factor 1 subunit alpha	Homo sapiens	9-19
30570890-0	2018	Adding anthracycline plus cyclophosphamide to adjuvant paclitaxel plus trastuzumab might be more reasonable in stage I hormone receptor negative HER-2 positive breast cancer patients.	Cyclophosphamide	26-42	erb-b2 receptor tyrosine kinase 2	Homo sapiens	145-150
30172345-1	2018	BACKGROUND: Immunochemotherapy with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is a standard front-line treatment for follicular lymphoma.	Cyclophosphamide	47-63	DNA damage inducible transcript 3	Homo sapiens	109-113
30235659-10	2018	When the first-line therapy of cyclophosphamide combined with prednisone is not enough to eradicate the inhibitor, especially for a higher inhibitor titer, anti-CD20 monoclonal antibody could play an important role.	Cyclophosphamide	31-47	keratin 20	Homo sapiens	161-165
30071053-0	2018	The role of AKT and FOXO3 in preventing ovarian toxicity induced by cyclophosphamide.	Cyclophosphamide	68-84	thymoma viral proto-oncogene 1	Mus musculus	12-15
30071053-0	2018	The role of AKT and FOXO3 in preventing ovarian toxicity induced by cyclophosphamide.	Cyclophosphamide	68-84	forkhead box O3	Mus musculus	20-25
30319329-3	2018	Methods: Patients with MBC were included when LDMC with oral cyclophosphamide (CTX) and methotrexate (MTX) was administered between 2009 and 2015.	Cyclophosphamide	61-77	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	79-82
29800788-0	2018	The effect of natural antioxidants in cyclophosphamide-induced hepatotoxicity: Role of Nrf2/HO-1 pathway.	Cyclophosphamide	38-54	NFE2 like bZIP transcription factor 2	Rattus norvegicus	87-91
29800788-0	2018	The effect of natural antioxidants in cyclophosphamide-induced hepatotoxicity: Role of Nrf2/HO-1 pathway.	Cyclophosphamide	38-54	heme oxygenase 1	Rattus norvegicus	92-96
29800788-6	2018	Injection of Cyclo showed marked increase in serum transaminases and alkaline phosphatase, hepatic malondialdehyde (MDA) and tumor necrosis factor-alpha (TNF- ) levels along with significant reduction in hepatic reduced glutathione (GSH), superoxide dismutase (SOD), and catalase levels in addition to downregulation of hepatic Nrf2 and HO-1 expressions and reduction in hepatic nuclear Nrf2 binding activity when compared with normal group.	Cyclophosphamide	13-18	tumor necrosis factor	Rattus norvegicus	125-152
29800788-6	2018	Injection of Cyclo showed marked increase in serum transaminases and alkaline phosphatase, hepatic malondialdehyde (MDA) and tumor necrosis factor-alpha (TNF- ) levels along with significant reduction in hepatic reduced glutathione (GSH), superoxide dismutase (SOD), and catalase levels in addition to downregulation of hepatic Nrf2 and HO-1 expressions and reduction in hepatic nuclear Nrf2 binding activity when compared with normal group.	Cyclophosphamide	13-18	tumor necrosis factor	Rattus norvegicus	154-158
29800788-6	2018	Injection of Cyclo showed marked increase in serum transaminases and alkaline phosphatase, hepatic malondialdehyde (MDA) and tumor necrosis factor-alpha (TNF- ) levels along with significant reduction in hepatic reduced glutathione (GSH), superoxide dismutase (SOD), and catalase levels in addition to downregulation of hepatic Nrf2 and HO-1 expressions and reduction in hepatic nuclear Nrf2 binding activity when compared with normal group.	Cyclophosphamide	13-18	catalase	Rattus norvegicus	271-279
29800788-6	2018	Injection of Cyclo showed marked increase in serum transaminases and alkaline phosphatase, hepatic malondialdehyde (MDA) and tumor necrosis factor-alpha (TNF- ) levels along with significant reduction in hepatic reduced glutathione (GSH), superoxide dismutase (SOD), and catalase levels in addition to downregulation of hepatic Nrf2 and HO-1 expressions and reduction in hepatic nuclear Nrf2 binding activity when compared with normal group.	Cyclophosphamide	13-18	NFE2 like bZIP transcription factor 2	Rattus norvegicus	328-332
29800788-6	2018	Injection of Cyclo showed marked increase in serum transaminases and alkaline phosphatase, hepatic malondialdehyde (MDA) and tumor necrosis factor-alpha (TNF- ) levels along with significant reduction in hepatic reduced glutathione (GSH), superoxide dismutase (SOD), and catalase levels in addition to downregulation of hepatic Nrf2 and HO-1 expressions and reduction in hepatic nuclear Nrf2 binding activity when compared with normal group.	Cyclophosphamide	13-18	heme oxygenase 1	Rattus norvegicus	337-341
29800788-6	2018	Injection of Cyclo showed marked increase in serum transaminases and alkaline phosphatase, hepatic malondialdehyde (MDA) and tumor necrosis factor-alpha (TNF- ) levels along with significant reduction in hepatic reduced glutathione (GSH), superoxide dismutase (SOD), and catalase levels in addition to downregulation of hepatic Nrf2 and HO-1 expressions and reduction in hepatic nuclear Nrf2 binding activity when compared with normal group.	Cyclophosphamide	13-18	NFE2 like bZIP transcription factor 2	Rattus norvegicus	387-391
29981795-0	2018	Aldehyde dehydrogenase 2 activation ameliorates cyclophosphamide-induced acute cardiotoxicity via detoxification of toxic aldehydes and suppression of cardiac cell death.	Cyclophosphamide	48-64	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	0-24
29981795-4	2018	We aimed to investigate the effects of aldehyde dehydrogenase 2 (ALDH2), an important endogenous cardioprotective enzyme, on CY-induced acute cardiotoxicity and the underlying mechanisms.	Cyclophosphamide	125-127	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	39-63
29981795-4	2018	We aimed to investigate the effects of aldehyde dehydrogenase 2 (ALDH2), an important endogenous cardioprotective enzyme, on CY-induced acute cardiotoxicity and the underlying mechanisms.	Cyclophosphamide	125-127	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	65-70
29981795-5	2018	It was found that ALDH2 knockout (KO) mice were more sensitive to CY-induced acute cardiotoxicity, presenting as higher serum levels of creatine kinase-MB isoform and lactate dehydrogenase, and significantly reduced myocardial contractility compared with C57BL/6 (WT) mice.	Cyclophosphamide	66-68	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	18-23
29981795-6	2018	In addition, cardiac cell death, especially necrosis, was obviously increased in ALDH2 KO mice compared with WT mice after CY treatment.	Cyclophosphamide	123-125	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	81-86
29981795-7	2018	Furthermore, accumulation of toxic aldehydes such as acrolein and 4-HNE and reactive oxygen species (ROS) in the myocardium were significantly elevated after CY in ALDH2 KO mice.	Cyclophosphamide	158-160	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	164-169
29981795-8	2018	Importantly, ALDH2 activation by Alda-1 pretreatment markedly attenuated CY-induced accumulation of toxic aldehydes, cardiac cell death and cardiac dysfunction, without affecting CY"s anti-tumor efficacy.	Cyclophosphamide	73-75	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	13-18
29981795-9	2018	In conclusion, the cardioprotective effects of ALDH2 activation against CY-induced acute cardiotoxicity are exerted via reducing toxic aldehydes accumulation and potentially interrupting the acrolein-ROS-aldehydes vicious circles, and thus alleviates myocardial cell death, without antagonizing the anti-tumor efficacy of CY.	Cyclophosphamide	72-74	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	47-52
29981795-9	2018	In conclusion, the cardioprotective effects of ALDH2 activation against CY-induced acute cardiotoxicity are exerted via reducing toxic aldehydes accumulation and potentially interrupting the acrolein-ROS-aldehydes vicious circles, and thus alleviates myocardial cell death, without antagonizing the anti-tumor efficacy of CY.	Cyclophosphamide	322-324	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	47-52
29981795-10	2018	Therefore, ALDH2 might be a promising prevention and treatment target for CY-induced acute cardiotoxicity.	Cyclophosphamide	74-76	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	11-16
30143021-11	2018	More importantly, they were resistant to cisplatin, oxaliplatin and cyclophosphamide exhibiting high cross-resistance along with alterations in expression of cancer-stem cell markers such as CD133, CD166, CD24, CD26, CXCR4, CD271 and CD274.	Cyclophosphamide	68-84	activated leukocyte cell adhesion molecule	Mus musculus	198-203
30143021-11	2018	More importantly, they were resistant to cisplatin, oxaliplatin and cyclophosphamide exhibiting high cross-resistance along with alterations in expression of cancer-stem cell markers such as CD133, CD166, CD24, CD26, CXCR4, CD271 and CD274.	Cyclophosphamide	68-84	CD24a antigen	Mus musculus	205-209
30143021-11	2018	More importantly, they were resistant to cisplatin, oxaliplatin and cyclophosphamide exhibiting high cross-resistance along with alterations in expression of cancer-stem cell markers such as CD133, CD166, CD24, CD26, CXCR4, CD271 and CD274.	Cyclophosphamide	68-84	chemokine (C-X-C motif) receptor 4	Mus musculus	217-222
30143021-11	2018	More importantly, they were resistant to cisplatin, oxaliplatin and cyclophosphamide exhibiting high cross-resistance along with alterations in expression of cancer-stem cell markers such as CD133, CD166, CD24, CD26, CXCR4, CD271 and CD274.	Cyclophosphamide	68-84	CD274 antigen	Mus musculus	234-239
30701926-1	2018	Nodal anaplastic ALK-negative large cell lymphoma (nALCL, ALK-) is a T-cell lymphoma that is characterized by aggressive clinical course and low sensitivity to SNOR (cyclophosphamide, doxorubicin, vincristine, prednisolone) and other chemotherapy regimen.	Cyclophosphamide	166-182	ALK receptor tyrosine kinase	Homo sapiens	17-20
30701926-1	2018	Nodal anaplastic ALK-negative large cell lymphoma (nALCL, ALK-) is a T-cell lymphoma that is characterized by aggressive clinical course and low sensitivity to SNOR (cyclophosphamide, doxorubicin, vincristine, prednisolone) and other chemotherapy regimen.	Cyclophosphamide	166-182	ALK receptor tyrosine kinase	Homo sapiens	58-61
30186977-4	2018	Discussion: The treatment protocol aims to reverse immune evasion of the tumor through a radiotherapy-induced self-vaccination effect, suppression of CD4+ CD25+ FoxP3+ regulatory T-cell function by metronomic cyclophosphamide, and effector T-cell reactivation owing to the inhibition of the PD-1-PD-L1 axis by avelumab.The immunologic interplay induced by the proposed combined treatment may theoretically improve the activity of avelumab without increasing its toxicity profile.Finally, an ancillary translational study will be extended to all the patients" population.	Cyclophosphamide	209-225	CD4 molecule	Homo sapiens	150-153
30186977-4	2018	Discussion: The treatment protocol aims to reverse immune evasion of the tumor through a radiotherapy-induced self-vaccination effect, suppression of CD4+ CD25+ FoxP3+ regulatory T-cell function by metronomic cyclophosphamide, and effector T-cell reactivation owing to the inhibition of the PD-1-PD-L1 axis by avelumab.The immunologic interplay induced by the proposed combined treatment may theoretically improve the activity of avelumab without increasing its toxicity profile.Finally, an ancillary translational study will be extended to all the patients" population.	Cyclophosphamide	209-225	interleukin 2 receptor subunit alpha	Homo sapiens	155-159
30186977-4	2018	Discussion: The treatment protocol aims to reverse immune evasion of the tumor through a radiotherapy-induced self-vaccination effect, suppression of CD4+ CD25+ FoxP3+ regulatory T-cell function by metronomic cyclophosphamide, and effector T-cell reactivation owing to the inhibition of the PD-1-PD-L1 axis by avelumab.The immunologic interplay induced by the proposed combined treatment may theoretically improve the activity of avelumab without increasing its toxicity profile.Finally, an ancillary translational study will be extended to all the patients" population.	Cyclophosphamide	209-225	forkhead box P3	Homo sapiens	161-166
29763643-11	2018	In addition, PRM3 obviously increased the levels of serum cytokines, markedly up-regulated the percentages of CD3+ and CD4+ T lymphocytes and the CD4+/CD8+ ratio of splenocytes, and effectively attenuated cyclophosphamide induced immunosuppression in mice.	Cyclophosphamide	205-221	protamine 3	Mus musculus	13-17
29763643-13	2018	GENERAL SIGNIFICANCE: This study reported a polysaccharide PRM3 from R. minima root exhibited potent immunoenhancing activity and significantly alleviated cyclophosphamide-induced immunosuppression through TLR4-NF-kappaB pathway.	Cyclophosphamide	155-171	protamine 3	Mus musculus	59-63
29199519-1	2018	High-grade B cell lymphoma with MYC and BCL2 rearrangements (double hit) has a poor prognosis with standard R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone).	Cyclophosphamide	127-143	BCL2 apoptosis regulator	Homo sapiens	40-44
29910179-3	2018	Here we report the use of CD19-targeted CAR T cells incorporating the intracellular signaling domain of CD28 (19-28z) as a consolidative therapy in 8 patients with residual CLL following first-line chemoimmunotherapy with pentostatin, cyclophosphamide, and rituximab.	Cyclophosphamide	235-251	CD19 molecule	Homo sapiens	26-30
29910179-3	2018	Here we report the use of CD19-targeted CAR T cells incorporating the intracellular signaling domain of CD28 (19-28z) as a consolidative therapy in 8 patients with residual CLL following first-line chemoimmunotherapy with pentostatin, cyclophosphamide, and rituximab.	Cyclophosphamide	235-251	CD28 molecule	Homo sapiens	104-108
29936365-0	2018	S-allyl cysteine ameliorates cyclophosphamide-induced downregulation of urothelial uroplakin IIIa with a concomitant effect on expression and release of CCL11and TNF-alpha in mice.	Cyclophosphamide	29-45	chemokine (C-C motif) ligand 11	Mus musculus	153-158
29957340-0	2018	Cyclophosphamide-modified murine peritoneal macrophages induce CD4+ T contrasuppressor cells that protect contact sensitivity T effector cells from suppression.	Cyclophosphamide	0-16	CD4 antigen	Mus musculus	63-66
29936365-0	2018	S-allyl cysteine ameliorates cyclophosphamide-induced downregulation of urothelial uroplakin IIIa with a concomitant effect on expression and release of CCL11and TNF-alpha in mice.	Cyclophosphamide	29-45	tumor necrosis factor	Mus musculus	162-171
29957340-12	2018	CONCLUSIONS: Our results show that in vivo treatment with CY influences mouse peritoneal Mf to induce CD4+ Tcs cells that protect CS-effector cells from suppressive signals of Ts cells.	Cyclophosphamide	58-60	CD4 antigen	Mus musculus	102-105
29936365-1	2018	BACKGROUND: The aim of this study was to evaluate the modulatory effect of S-allyl cysteine against cyclophosphamide-induced changes in uroplakin IIIa, CCL11 and TNF-alpha.	Cyclophosphamide	100-116	uroplakin 3A	Mus musculus	136-150
29936365-1	2018	BACKGROUND: The aim of this study was to evaluate the modulatory effect of S-allyl cysteine against cyclophosphamide-induced changes in uroplakin IIIa, CCL11 and TNF-alpha.	Cyclophosphamide	100-116	chemokine (C-C motif) ligand 11	Mus musculus	152-157
29936365-1	2018	BACKGROUND: The aim of this study was to evaluate the modulatory effect of S-allyl cysteine against cyclophosphamide-induced changes in uroplakin IIIa, CCL11 and TNF-alpha.	Cyclophosphamide	100-116	tumor necrosis factor	Mus musculus	162-171
29936365-5	2018	RESULTS: Cyclophosphamide caused hemorrhagic cystitis formation and downregulation of UPIIIa.	Cyclophosphamide	9-25	uroplakin 3A	Mus musculus	86-92
30524884-2	2018	Recently, the combination of autologous tumor lysate-pulsed dendritic cells (DC) and metronomic cyclophosphamide (mCTX) was reported as a feasible and well-tolerated treatment in malignant pleural mesothelioma patients and further as a method to reduce circulating Tregs.	Cyclophosphamide	96-112	V-set and immunoglobulin domain containing 2	Mus musculus	114-118
29984341-9	2018	Conclusions: Pioglitazone, a PPAR-gamma agonist, improved bladder function in cyclophosphamide-induced cystitis by both observed urinary frequency and measured cystometric capacity.	Cyclophosphamide	78-94	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	29-39
30105254-7	2018	In in vivo tests, EP4 was more effective at promoting the proliferation of lymphocytes and secretion of cytokines in mice immunosuppressed by cyclophosphamide than EP2 at the same concentration.	Cyclophosphamide	142-158	prostaglandin E receptor 4 (subtype EP4)	Mus musculus	18-21
30042281-4	2018	NAC with 5-fluorouracil, epirubicin, and cyclophosphamide(FEC)followed by docetaxel(DTX)was administered.	Cyclophosphamide	41-57	X-linked Kx blood group	Homo sapiens	0-3
29065744-1	2018	Activated B-cell-like (ABC) diffuse large B-cell lymphoma (DLBCL) is associated with worse survival after standard rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (RCHOP) chemoimmunotherapy compared to germinal center B-cell-like (GCB) subtype.	Cyclophosphamide	126-142	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	0-21
29976274-0	2018	Effects of Nesting Material on the Toxicologic Assessment of Cyclophosphamide in Crl:CD1(ICR) Mice.	Cyclophosphamide	61-77	CD1 antigen complex	Mus musculus	85-88
29065744-1	2018	Activated B-cell-like (ABC) diffuse large B-cell lymphoma (DLBCL) is associated with worse survival after standard rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (RCHOP) chemoimmunotherapy compared to germinal center B-cell-like (GCB) subtype.	Cyclophosphamide	126-142	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	23-26
29954431-2	2018	The main objective of our research was to improve the effectiveness of dendritic cell (DC)-based immunotherapy or chemoimmunotherapy composed of cyclophosphamide (CY) and DCs by application of lentivectors encoding shRNA specific to IL-10 (shIL10 LVs) in murine colon carcinoma MC38 model.	Cyclophosphamide	145-161	interleukin 10	Mus musculus	233-238
29749441-4	2018	The second aim was to evaluate the abilities of fludarabine (FDR) and mafosfamide (MFA; a metabolite of cyclophosphamide) to induce apoptosis of CD19-CAR-T cells via the use of Annexin V/propidium iodide double staining.	Cyclophosphamide	104-120	CD19 molecule	Homo sapiens	145-149
29749441-4	2018	The second aim was to evaluate the abilities of fludarabine (FDR) and mafosfamide (MFA; a metabolite of cyclophosphamide) to induce apoptosis of CD19-CAR-T cells via the use of Annexin V/propidium iodide double staining.	Cyclophosphamide	104-120	nuclear receptor subfamily 1 group I member 3	Homo sapiens	150-153
29417209-2	2018	We present a case of anti-MDA5 antibody-associated RP-ILD in a patient with arthritis but with no other clinical signs suggestive of DM or CADM successfully treated with a combination of cyclophosphamide, cyclosporine and corticoids.	Cyclophosphamide	187-203	interferon induced with helicase C domain 1	Homo sapiens	26-30
29954431-2	2018	The main objective of our research was to improve the effectiveness of dendritic cell (DC)-based immunotherapy or chemoimmunotherapy composed of cyclophosphamide (CY) and DCs by application of lentivectors encoding shRNA specific to IL-10 (shIL10 LVs) in murine colon carcinoma MC38 model.	Cyclophosphamide	163-165	interleukin 10	Mus musculus	233-238
29983710-8	2018	Results: Our results showed that body weight, histological injury, and AR expression in the testis were improved in the GnRHant + CPA group.	Cyclophosphamide	130-133	androgen receptor	Rattus norvegicus	71-73
29988729-9	2018	In clinical settings, IRX-2 is administered as part of a 21-day neoadjuvant regimen, which includes additional pharmacologic agents (low-dose cyclophosphamide, indomethacin, and zinc) to promote anticancer immunoresponses.	Cyclophosphamide	142-158	iroquois homeobox 2	Homo sapiens	22-27
29803913-3	2018	Preliminary studies have demonstrated the beneficial effects of a combination of cyclophosphamide (CTX) and methotrexate (MTX) in models of RA.	Cyclophosphamide	81-97	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	99-102
29905023-0	2018	Neoadjuvant endocrine therapy with exemestane followed by response-guided combination therapy with low-dose cyclophosphamide in postmenopausal patients with estrogen receptor-positive breast cancer: A multicenter, open-label, phase II study.	Cyclophosphamide	108-124	estrogen receptor 1	Homo sapiens	157-174
29971178-5	2018	All symptoms were ameliorated, and the serum level of PR3-ANCA declined following treatment with prednisolone and cyclophosphamide.	Cyclophosphamide	114-130	proteinase 3	Homo sapiens	54-57
29983710-10	2018	Conclusion: Our results indicate that the GnRHant administration before and after CPA in pubertal rats can protect long-term testicular injury induced by CPA via increased AR expression in the testes.	Cyclophosphamide	154-157	androgen receptor	Rattus norvegicus	172-174
29963517-2	2018	The R-CHOP therapy [rituximab (R), cyclophosphamide, hydroxy-doxorubicin, vincristine, and prednisone] is a popular and recommended regimen for primary therapy, prescribed by several treatment guidelines for WM.	Cyclophosphamide	35-51	DNA damage inducible transcript 3	Homo sapiens	6-10
31938438-3	2018	After treatment with seven cycles of CHOP (cyclophosphamide, doxorubicin, vincristine and prednisolone) like regimen, the patient developed to MPAL (B/myeloid) with del(7)(q22), t(6;9)(p23;q34), DEK/NUP214 fusion, as well as EZH2 and TET2 mutations.	Cyclophosphamide	37-41	DEK proto-oncogene	Homo sapiens	195-198
29733541-0	2018	A multicenter phase II trial of neoadjuvant letrozole plus low-dose cyclophosphamide in postmenopausal patients with estrogen receptor-positive breast cancer (JBCRG-07): therapeutic efficacy and clinical implications of circulating endothelial cells.	Cyclophosphamide	68-84	estrogen receptor 1	Homo sapiens	117-134
29733541-16	2018	In conclusion, neoadjuvant letrozole plus cyclophosphamide showed a good clinical response for postmenopausal patients with estrogen receptor-positive breast cancer.	Cyclophosphamide	42-58	estrogen receptor 1	Homo sapiens	124-141
31938438-3	2018	After treatment with seven cycles of CHOP (cyclophosphamide, doxorubicin, vincristine and prednisolone) like regimen, the patient developed to MPAL (B/myeloid) with del(7)(q22), t(6;9)(p23;q34), DEK/NUP214 fusion, as well as EZH2 and TET2 mutations.	Cyclophosphamide	43-59	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	225-229
29880173-0	2018	Downregulation of tight junction protein zonula occludens-2 and urothelium damage in a cyclophosphamide-induced mouse model of cystitis.	Cyclophosphamide	87-103	tight junction protein 2	Mus musculus	41-59
29784961-0	2018	Sarcodon imbricatus polysaccharides improve mouse hematopoietic function after cyclophosphamide-induced damage via G-CSF mediated JAK2/STAT3 pathway.	Cyclophosphamide	79-95	colony stimulating factor 3 (granulocyte)	Mus musculus	115-120
29784961-0	2018	Sarcodon imbricatus polysaccharides improve mouse hematopoietic function after cyclophosphamide-induced damage via G-CSF mediated JAK2/STAT3 pathway.	Cyclophosphamide	79-95	Janus kinase 2	Mus musculus	130-134
29784961-0	2018	Sarcodon imbricatus polysaccharides improve mouse hematopoietic function after cyclophosphamide-induced damage via G-CSF mediated JAK2/STAT3 pathway.	Cyclophosphamide	79-95	signal transducer and activator of transcription 3	Mus musculus	135-140
29598900-4	2018	In cells, one of the compound prevented recruitment of REV1 to PCNA foci on chromatin upon cisplatin treatment, delayed removal of UV-induced cyclopyrimidine dimers from nuclei, prevented UV-induced mutation of HPRT gene, and diminished clonogenic survival of cells that were challenged by cyclophosphamide or cisplatin.	Cyclophosphamide	290-306	REV1 DNA directed polymerase	Homo sapiens	55-59
29598900-4	2018	In cells, one of the compound prevented recruitment of REV1 to PCNA foci on chromatin upon cisplatin treatment, delayed removal of UV-induced cyclopyrimidine dimers from nuclei, prevented UV-induced mutation of HPRT gene, and diminished clonogenic survival of cells that were challenged by cyclophosphamide or cisplatin.	Cyclophosphamide	290-306	proliferating cell nuclear antigen	Homo sapiens	63-67
29598900-4	2018	In cells, one of the compound prevented recruitment of REV1 to PCNA foci on chromatin upon cisplatin treatment, delayed removal of UV-induced cyclopyrimidine dimers from nuclei, prevented UV-induced mutation of HPRT gene, and diminished clonogenic survival of cells that were challenged by cyclophosphamide or cisplatin.	Cyclophosphamide	290-306	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	211-215
29844872-2	2018	The aim of this study was to evaluate the influence of selected clinical and molecular factors including single nucleotide polymorphisms (SNPs) in CRBN gene on the efficacy of first line CTD (cyclophosphamide, thalidomide, dexamethasone) chemotherapy in patients with multiple myeloma.	Cyclophosphamide	192-208	cereblon	Homo sapiens	147-151
29735991-0	2018	Increased Piezo1 channel activity in interstitial Cajal-like cells induces bladder hyperactivity by functionally interacting with NCX1 in rats with cyclophosphamide-induced cystitis.	Cyclophosphamide	148-164	piezo-type mechanosensitive ion channel component 1	Rattus norvegicus	10-16
29735991-0	2018	Increased Piezo1 channel activity in interstitial Cajal-like cells induces bladder hyperactivity by functionally interacting with NCX1 in rats with cyclophosphamide-induced cystitis.	Cyclophosphamide	148-164	solute carrier family 8 member A1	Rattus norvegicus	130-134
29728077-11	2018	Consequently, sequential treatment with Adriamycin/Cyclophosphamide (AC) cytotoxic drugs to generate resistant cells indicated that BT-474 NRP-1 cells increased sensitivity to treatment by inactivating NRP-1/ITGB3/FAK/Akt/NF-kB p65 signaling compared to wild-type BT-474 resistant cells.	Cyclophosphamide	51-67	neuropilin 1	Homo sapiens	139-144
29728077-11	2018	Consequently, sequential treatment with Adriamycin/Cyclophosphamide (AC) cytotoxic drugs to generate resistant cells indicated that BT-474 NRP-1 cells increased sensitivity to treatment by inactivating NRP-1/ITGB3/FAK/Akt/NF-kB p65 signaling compared to wild-type BT-474 resistant cells.	Cyclophosphamide	51-67	neuropilin 1	Homo sapiens	202-207
29728077-11	2018	Consequently, sequential treatment with Adriamycin/Cyclophosphamide (AC) cytotoxic drugs to generate resistant cells indicated that BT-474 NRP-1 cells increased sensitivity to treatment by inactivating NRP-1/ITGB3/FAK/Akt/NF-kB p65 signaling compared to wild-type BT-474 resistant cells.	Cyclophosphamide	51-67	integrin subunit beta 3	Homo sapiens	208-213
29728077-12	2018	CONCLUSIONS: We thus report a novel mechanism correlating high baseline NRP-1 with upregulated TNC/ITGB3 signaling, but decreased ABCG2 expression, which sensitizes BT-474 NRP-1 cells to Adriamycin/Cyclophosphamide.	Cyclophosphamide	198-214	neuropilin 1	Homo sapiens	72-77
29719938-2	2018	METHODS: This analysis included 31 patients with RRMM treated with Rd who received cyclophosphamide (CRd) at biochemical relapse.	Cyclophosphamide	83-99	cone-rod homeobox	Homo sapiens	101-104
31938438-3	2018	After treatment with seven cycles of CHOP (cyclophosphamide, doxorubicin, vincristine and prednisolone) like regimen, the patient developed to MPAL (B/myeloid) with del(7)(q22), t(6;9)(p23;q34), DEK/NUP214 fusion, as well as EZH2 and TET2 mutations.	Cyclophosphamide	37-41	nucleoporin 214	Homo sapiens	199-205
31938438-3	2018	After treatment with seven cycles of CHOP (cyclophosphamide, doxorubicin, vincristine and prednisolone) like regimen, the patient developed to MPAL (B/myeloid) with del(7)(q22), t(6;9)(p23;q34), DEK/NUP214 fusion, as well as EZH2 and TET2 mutations.	Cyclophosphamide	37-41	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	225-229
31938438-3	2018	After treatment with seven cycles of CHOP (cyclophosphamide, doxorubicin, vincristine and prednisolone) like regimen, the patient developed to MPAL (B/myeloid) with del(7)(q22), t(6;9)(p23;q34), DEK/NUP214 fusion, as well as EZH2 and TET2 mutations.	Cyclophosphamide	37-41	tet methylcytosine dioxygenase 2	Homo sapiens	234-238
31938438-3	2018	After treatment with seven cycles of CHOP (cyclophosphamide, doxorubicin, vincristine and prednisolone) like regimen, the patient developed to MPAL (B/myeloid) with del(7)(q22), t(6;9)(p23;q34), DEK/NUP214 fusion, as well as EZH2 and TET2 mutations.	Cyclophosphamide	43-59	DEK proto-oncogene	Homo sapiens	195-198
31938438-3	2018	After treatment with seven cycles of CHOP (cyclophosphamide, doxorubicin, vincristine and prednisolone) like regimen, the patient developed to MPAL (B/myeloid) with del(7)(q22), t(6;9)(p23;q34), DEK/NUP214 fusion, as well as EZH2 and TET2 mutations.	Cyclophosphamide	43-59	nucleoporin 214	Homo sapiens	199-205
31938438-3	2018	After treatment with seven cycles of CHOP (cyclophosphamide, doxorubicin, vincristine and prednisolone) like regimen, the patient developed to MPAL (B/myeloid) with del(7)(q22), t(6;9)(p23;q34), DEK/NUP214 fusion, as well as EZH2 and TET2 mutations.	Cyclophosphamide	43-59	tet methylcytosine dioxygenase 2	Homo sapiens	234-238
29565454-7	2018	Oncomine analysis revealed that the expression levels of SIRT5 were higher in epirubicin/cyclophosphamide-docetaxel responders compared with non-responders.	Cyclophosphamide	89-105	sirtuin 5	Homo sapiens	57-62
29445054-8	2018	Finally, toxicogenomics analysis of HepG2 and HepaRG cells after exposure to AFB1 and CPA revealed that numerous p53-related genes were upregulated- and the expression of these genes was greater in HepaRG than in HepG2 cells.	Cyclophosphamide	86-89	tumor protein p53	Homo sapiens	113-116
29695766-0	2018	Vinorelbine, cyclophosphamide and 5-FU effects on the circulating and intratumoural landscape of immune cells improve anti-PD-L1 efficacy in preclinical models of breast cancer and lymphoma.	Cyclophosphamide	13-29	CD274 antigen	Mus musculus	123-128
29695766-7	2018	Vinorelbine, cyclophosphamide and 5-FU reduced circulating APCs.	Cyclophosphamide	13-29	amyloid P component, serum	Mus musculus	59-63
29695766-15	2018	CONCLUSIONS: Vinorelbine, cyclophosphamide and 5-FU have significant preclinical effects on circulating and tumour-infiltrating immune cells and can be used to obtain synergy with anti-PD-L1.	Cyclophosphamide	26-42	CD274 antigen	Mus musculus	185-190
29534229-14	2018	Cy affected AMH expression, while it was at least partially recovered when C1P is administered as well.	Cyclophosphamide	0-2	anti-Mullerian hormone	Mus musculus	12-15
29534229-17	2018	Cy increased the expression of BAX (P &lt; 0.01) and decreased the expression of BCLX-L compared to control ovaries (P &lt; 0.01).	Cyclophosphamide	0-2	BCL2-associated X protein	Mus musculus	31-34
29534229-17	2018	Cy increased the expression of BAX (P &lt; 0.01) and decreased the expression of BCLX-L compared to control ovaries (P &lt; 0.01).	Cyclophosphamide	0-2	BCL2-like 1	Mus musculus	81-87
29534229-18	2018	The ovarian BCLX-L:BAX ratio was also lower in Cy-treated mice (P &lt; 0.05).	Cyclophosphamide	47-49	BCL2-like 1	Mus musculus	12-18
29534229-18	2018	The ovarian BCLX-L:BAX ratio was also lower in Cy-treated mice (P &lt; 0.05).	Cyclophosphamide	47-49	BCL2-associated X protein	Mus musculus	19-22
29534229-20	2018	In addition, acid sphingomyelinase (A-SMase) expression was higher in Cy-treated ovaries, whilst remaining similar to the control in the Cy + C1P group.	Cyclophosphamide	70-72	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	13-34
29534229-20	2018	In addition, acid sphingomyelinase (A-SMase) expression was higher in Cy-treated ovaries, whilst remaining similar to the control in the Cy + C1P group.	Cyclophosphamide	70-72	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	36-43
29534229-20	2018	In addition, acid sphingomyelinase (A-SMase) expression was higher in Cy-treated ovaries, whilst remaining similar to the control in the Cy + C1P group.	Cyclophosphamide	137-139	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	13-34
29534229-20	2018	In addition, acid sphingomyelinase (A-SMase) expression was higher in Cy-treated ovaries, whilst remaining similar to the control in the Cy + C1P group.	Cyclophosphamide	137-139	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	36-43
29534229-26	2018	In Cy-treated ovaries alpha-SMA-positive cells showed a less uniform distribution around blood vessels.	Cyclophosphamide	3-5	actin alpha 2, smooth muscle, aorta	Mus musculus	22-31
29534229-27	2018	C1P coadministration partially prevented this Cy-induced effect, with a higher presence of alpha-SMA-positive cells surrounding vessels.	Cyclophosphamide	46-48	actin alpha 2, smooth muscle, aorta	Mus musculus	91-100
29914177-10	2018	Induction of the CYP2B6 in pediatric gliomas with lower expression of the enzyme, could be an alternative to improve the antitumoral effect of CPA treatment.	Cyclophosphamide	143-146	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	17-23
29407215-1	2018	Hydrogen sulfide (H2S) formed by cystathionine-gamma-lyase (CSE) enhances the activity of Cav3.2 T-type Ca2+ channels, contributing to the bladder pain accompanying hemorrhagic cystitis caused by systemic administration of cyclophosphamide (CPA) in mice.	Cyclophosphamide	223-239	cystathionase (cystathionine gamma-lyase)	Mus musculus	33-58
29407215-1	2018	Hydrogen sulfide (H2S) formed by cystathionine-gamma-lyase (CSE) enhances the activity of Cav3.2 T-type Ca2+ channels, contributing to the bladder pain accompanying hemorrhagic cystitis caused by systemic administration of cyclophosphamide (CPA) in mice.	Cyclophosphamide	223-239	cystathionase (cystathionine gamma-lyase)	Mus musculus	60-63
29407215-1	2018	Hydrogen sulfide (H2S) formed by cystathionine-gamma-lyase (CSE) enhances the activity of Cav3.2 T-type Ca2+ channels, contributing to the bladder pain accompanying hemorrhagic cystitis caused by systemic administration of cyclophosphamide (CPA) in mice.	Cyclophosphamide	223-239	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	90-96
29407215-1	2018	Hydrogen sulfide (H2S) formed by cystathionine-gamma-lyase (CSE) enhances the activity of Cav3.2 T-type Ca2+ channels, contributing to the bladder pain accompanying hemorrhagic cystitis caused by systemic administration of cyclophosphamide (CPA) in mice.	Cyclophosphamide	241-244	cystathionase (cystathionine gamma-lyase)	Mus musculus	33-58
29407215-1	2018	Hydrogen sulfide (H2S) formed by cystathionine-gamma-lyase (CSE) enhances the activity of Cav3.2 T-type Ca2+ channels, contributing to the bladder pain accompanying hemorrhagic cystitis caused by systemic administration of cyclophosphamide (CPA) in mice.	Cyclophosphamide	241-244	cystathionase (cystathionine gamma-lyase)	Mus musculus	60-63
29407215-1	2018	Hydrogen sulfide (H2S) formed by cystathionine-gamma-lyase (CSE) enhances the activity of Cav3.2 T-type Ca2+ channels, contributing to the bladder pain accompanying hemorrhagic cystitis caused by systemic administration of cyclophosphamide (CPA) in mice.	Cyclophosphamide	241-244	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	90-96
29407215-9	2018	The bladder pain and/or cystitis symptoms caused by substance P or CPA were prevented by the NK1 receptor antagonist.	Cyclophosphamide	67-70	tachykinin receptor 1	Mus musculus	93-105
29407215-10	2018	CSE in the bladder was upregulated by substance P or CPA, and the NK1 antagonist prevented the CPA-induced CSE upregulation.	Cyclophosphamide	53-56	cystathionase (cystathionine gamma-lyase)	Mus musculus	0-3
29407215-10	2018	CSE in the bladder was upregulated by substance P or CPA, and the NK1 antagonist prevented the CPA-induced CSE upregulation.	Cyclophosphamide	95-98	cystathionase (cystathionine gamma-lyase)	Mus musculus	0-3
29407215-10	2018	CSE in the bladder was upregulated by substance P or CPA, and the NK1 antagonist prevented the CPA-induced CSE upregulation.	Cyclophosphamide	95-98	tachykinin 1	Mus musculus	38-49
29407215-10	2018	CSE in the bladder was upregulated by substance P or CPA, and the NK1 antagonist prevented the CPA-induced CSE upregulation.	Cyclophosphamide	95-98	tachykinin 1	Mus musculus	66-69
29407215-10	2018	CSE in the bladder was upregulated by substance P or CPA, and the NK1 antagonist prevented the CPA-induced CSE upregulation.	Cyclophosphamide	95-98	cystathionase (cystathionine gamma-lyase)	Mus musculus	107-110
29674626-3	2018	We aimed to do a systematic review and meta-analysis on the relationships between overexpression MYC and/or BCL2 and DLBCLs treated with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP).	Cyclophosphamide	148-164	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	97-100
29524404-0	2018	Protective effect of ALDH2 against cyclophosphamide-induced acute hepatotoxicity via attenuating oxidative stress and reactive aldehydes.	Cyclophosphamide	35-51	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	21-26
29524404-3	2018	In this study, we determined the existence and extent of CY-induced acute hepatotoxicity and nephrotoxicity, and demonstrated the effect of ALDH2 on CY-induced acute tissue toxicity and related mechanisms.	Cyclophosphamide	149-151	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	140-145
29524404-5	2018	Biochemical analysis showed that plasma ALT was increased by 35.8% in KO + CY group and decreased by 21.1% in WT + CY + Alda-1 group compared to WT + CY group (P &lt; 0.05, respectively).	Cyclophosphamide	75-77	glutamic pyruvic transaminase, soluble	Mus musculus	40-43
29524404-5	2018	Biochemical analysis showed that plasma ALT was increased by 35.8% in KO + CY group and decreased by 21.1% in WT + CY + Alda-1 group compared to WT + CY group (P &lt; 0.05, respectively).	Cyclophosphamide	115-117	glutamic pyruvic transaminase, soluble	Mus musculus	40-43
29524404-5	2018	Biochemical analysis showed that plasma ALT was increased by 35.8% in KO + CY group and decreased by 21.1% in WT + CY + Alda-1 group compared to WT + CY group (P &lt; 0.05, respectively).	Cyclophosphamide	115-117	glutamic pyruvic transaminase, soluble	Mus musculus	40-43
29524404-8	2018	These findings demonstrate that CY could induce acute hepatotoxicity without nephrotoxicity, and ALDH2 plays a protective role in CY-induced acute hepatotoxicity.	Cyclophosphamide	130-132	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	97-102
29674626-3	2018	We aimed to do a systematic review and meta-analysis on the relationships between overexpression MYC and/or BCL2 and DLBCLs treated with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP).	Cyclophosphamide	148-164	BCL2 apoptosis regulator	Homo sapiens	108-112
29720885-2	2018	Cyclophosphamide-dacarbazine-vincristine (CVD) regimen is recommended as standard chemotherapy for advanced mPHEO/PGL.	Cyclophosphamide	0-16	pheomelanin	Mus musculus	108-117
29731965-10	2018	In this study, the presence of both TP53 mutation and 17p/TP53 deletion, but not the individual variants, was associated with poor prognosis in DLBCL patients after treatment with rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) or similar regimens.	Cyclophosphamide	191-207	tumor protein p53	Homo sapiens	36-40
29731965-10	2018	In this study, the presence of both TP53 mutation and 17p/TP53 deletion, but not the individual variants, was associated with poor prognosis in DLBCL patients after treatment with rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) or similar regimens.	Cyclophosphamide	191-207	tumor protein p53	Homo sapiens	58-62
29615109-3	2018	METHODS: We investigated the restorative effects of CP-MSCs on cyclophosphamide (CTX)-induced POF.	Cyclophosphamide	63-79	POF1B actin binding protein	Homo sapiens	94-97
29681802-0	2018	Expression and Function of Chemokines CXCL9-11 in Micturition Pathways in Cyclophosphamide (CYP)-Induced Cystitis and Somatic Sensitivity in Mice.	Cyclophosphamide	74-90	chemokine (C-X-C motif) ligand 9	Mus musculus	38-43
29681802-0	2018	Expression and Function of Chemokines CXCL9-11 in Micturition Pathways in Cyclophosphamide (CYP)-Induced Cystitis and Somatic Sensitivity in Mice.	Cyclophosphamide	92-95	chemokine (C-X-C motif) ligand 9	Mus musculus	38-43
29044685-2	2018	Bladder pain accompanying cyclophosphamide (CPA)-induced cystitis in mice has been shown to involve the functional upregulation of the CSE/H2 S/Cav 3.2 pathway.	Cyclophosphamide	26-42	cystathionase (cystathionine gamma-lyase)	Mus musculus	135-138
29044685-2	2018	Bladder pain accompanying cyclophosphamide (CPA)-induced cystitis in mice has been shown to involve the functional upregulation of the CSE/H2 S/Cav 3.2 pathway.	Cyclophosphamide	44-47	cystathionase (cystathionine gamma-lyase)	Mus musculus	135-138
29044685-7	2018	beta-Cyano-l-alanine, a reversible selective CSE inhibitor, prevented CPA-induced nociceptive behaviour, referred hyperalgesia, and, in part, increases in bladder weight.	Cyclophosphamide	70-73	cystathionase (cystathionine gamma-lyase)	Mus musculus	45-48
29044685-8	2018	CPA markedly increased phosphorylated NF-kappaB p65 levels in the bladder, an effect that was prevented by pyrrolidine dithiocarbamate (PDTC), an NF-kappaB inhibitor.	Cyclophosphamide	0-3	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	38-47
29044685-8	2018	CPA markedly increased phosphorylated NF-kappaB p65 levels in the bladder, an effect that was prevented by pyrrolidine dithiocarbamate (PDTC), an NF-kappaB inhibitor.	Cyclophosphamide	0-3	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	48-51
29044685-8	2018	CPA markedly increased phosphorylated NF-kappaB p65 levels in the bladder, an effect that was prevented by pyrrolidine dithiocarbamate (PDTC), an NF-kappaB inhibitor.	Cyclophosphamide	0-3	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	146-155
29044685-9	2018	PDTC and curcumin, which inhibits NF-kappaB signals, abolished CPA-induced nociceptive behaviour, referred hyperalgesia and, in part, increases in bladder weight.	Cyclophosphamide	63-66	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	34-43
29044685-10	2018	CPA caused the overexpression of CSE in the bladder, and this was prevented by PDTC or curcumin.	Cyclophosphamide	0-3	cystathionase (cystathionine gamma-lyase)	Mus musculus	33-36
29044685-11	2018	The CPA-induced activation of NF-kappaB signals appeared to cause CSE overexpression in the bladder, contributing to bladder pain and in part swelling, possibly through H2 S/Cav 3.2 signaling.	Cyclophosphamide	4-7	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	30-39
29044685-11	2018	The CPA-induced activation of NF-kappaB signals appeared to cause CSE overexpression in the bladder, contributing to bladder pain and in part swelling, possibly through H2 S/Cav 3.2 signaling.	Cyclophosphamide	4-7	cystathionase (cystathionine gamma-lyase)	Mus musculus	66-69
29367429-0	2018	Flt-3L Expansion of Recipient CD8alpha+ Dendritic Cells Deletes Alloreactive Donor T Cells and Represents an Alternative to Posttransplant Cyclophosphamide for the Prevention of GVHD.	Cyclophosphamide	139-155	fms related receptor tyrosine kinase 3 ligand	Homo sapiens	0-6
29893327-12	2018	Conclusion: We determined that uPAR and CAIX levels were higher in the fluorouracil, epirubicin, and cyclophosphamide (FEC) chemotherapy group than in the control group, but there was no difference between the FEC and epirubicin/adriamycin chemotherapy groups in terms of basal and postchemotherapy uPAR, CAIX levels.	Cyclophosphamide	101-117	plasminogen activator, urokinase receptor	Homo sapiens	31-35
29893327-12	2018	Conclusion: We determined that uPAR and CAIX levels were higher in the fluorouracil, epirubicin, and cyclophosphamide (FEC) chemotherapy group than in the control group, but there was no difference between the FEC and epirubicin/adriamycin chemotherapy groups in terms of basal and postchemotherapy uPAR, CAIX levels.	Cyclophosphamide	101-117	carbonic anhydrase 9	Homo sapiens	40-44
29050534-11	2018	Two copies of total C4 and homozygous deletion of C4A were associated with a disease course requiring cyclophosphamide therapy (OR = 4.044; p = 0.040 and OR = 5.798; p = 0.034, respectively).	Cyclophosphamide	102-118	complement C4A (Rodgers blood group)	Homo sapiens	50-53
28826042-1	2018	Oxidative DNA damage in bone marrow cells is the main side effect of chemotherapy drugs including cyclophosphamide (CTX).	Cyclophosphamide	98-114	V-set and immunoglobulin domain containing 2	Mus musculus	116-119
29438534-13	2018	MAIN RESULTS AND THE ROLE OF CHANCE: Cyclophosphamide induced a significant follicular loss of more than 50% in Fshb-/- mice regardless of previous treatment with gonadotropins and no difference was observed in cell proliferation or apoptosis.	Cyclophosphamide	37-53	follicle stimulating hormone beta	Mus musculus	112-116
30026678-8	2018	Conclusions: This study suggested that orally administered L.plantarum KLDS1.0318 may effectively accelerate the recovery of immunosuppressive mice caused by cyclophosphamide (CTX).	Cyclophosphamide	158-174	V-set and immunoglobulin domain containing 2	Mus musculus	176-179
29632537-3	2018	Recent studies also show that thalidomide analogs, cyclophosphamide, and other small molecules are able to act on TNFR2, resulting in the elimination of TNFR2-expressing Tregs.	Cyclophosphamide	51-67	TNF receptor superfamily member 1B	Homo sapiens	114-119
29632537-3	2018	Recent studies also show that thalidomide analogs, cyclophosphamide, and other small molecules are able to act on TNFR2, resulting in the elimination of TNFR2-expressing Tregs.	Cyclophosphamide	51-67	TNF receptor superfamily member 1B	Homo sapiens	153-158
29247781-0	2018	Killer Cell Immunoglobulin-Like Receptor-Ligand Mismatch in Donor versus Recipient Direction Provides Better Graft-versus-Tumor Effect in Patients with Hematologic Malignancies Undergoing Allogeneic T Cell-Replete Haploidentical Transplantation Followed by Post-Transplant Cyclophosphamide.	Cyclophosphamide	273-289	killer cell immunoglobulin like receptor, three Ig domains and long cytoplasmic tail 2	Homo sapiens	0-40
29504102-0	2018	Role of Matrix Metalloproteinase-2 in the Development of Cyclophosphamide-Induced Cardiomyopathy.	Cyclophosphamide	57-73	matrix metallopeptidase 2	Rattus norvegicus	8-34
29504102-1	2018	Immunohistochemical assay was employed to determine localization of MMP-2 in cardiomyocytes of WAG rats and changes in MMP-2 expression during modeled cardiomyopathy induced by single intraperitoneal injection of cyclophosphamide (125 mg/kg) alone or in combination with preventive intraperitoneal administration of an equal dose of asparcam-L (potassium-magnesium asparaginate) 30 min prior to the cytostatic.	Cyclophosphamide	213-229	matrix metallopeptidase 2	Rattus norvegicus	119-124
29504102-3	2018	During the development of cyclophosphamide-induced cardiomyopathy (in 3 days after injection), the index of MMP-2-positive cardiomyocyte nuclei increased by 76%.	Cyclophosphamide	26-42	matrix metallopeptidase 2	Rattus norvegicus	108-113
29504102-5	2018	Preventive injection of asparcam-L moderated the cardiotoxic effect of cyclophosphamide, which manifested in less pronounced increase in the volume density of cardiomyocytes with lytic changes (by 42%) and index of MMP-2+ cardiomyocyte nuclei (by 23%) in comparison with the rats exposed to cyclophosphamide alone.	Cyclophosphamide	71-87	matrix metallopeptidase 2	Rattus norvegicus	215-220
29433963-20	2018	INTERPRETATION: Addition of metronomic oral cyclophosphamide to trastuzumab plus pertuzumab in older and frail patients with HER2-positive metastatic breast cancer increased median progression-free survival by 7 months compared with dual HER2 blockade alone, with an acceptable safety profile.	Cyclophosphamide	44-60	erb-b2 receptor tyrosine kinase 2	Homo sapiens	125-129
28975621-0	2018	Role of interferon regulatory factor 1 in governing Treg depletion, Th1 polarization, inflammasome activation and antitumor efficacy of cyclophosphamide.	Cyclophosphamide	136-152	interferon regulatory factor 1	Mus musculus	8-38
28975621-1	2018	The antitumor effectiveness of cyclophosphamide (CTX) and other chemotherapeutics was shown to rely not only on direct cytotoxicity but also on immunogenic tumor cell death and systemic immunomodulatory mechanisms, including regulatory T cell (Treg) depletion, Th1 cell polarization, type I interferon (IFN) and proinflammatory cytokine production.	Cyclophosphamide	31-47	negative elongation factor complex member C/D, Th1l	Mus musculus	261-264
29433963-20	2018	INTERPRETATION: Addition of metronomic oral cyclophosphamide to trastuzumab plus pertuzumab in older and frail patients with HER2-positive metastatic breast cancer increased median progression-free survival by 7 months compared with dual HER2 blockade alone, with an acceptable safety profile.	Cyclophosphamide	44-60	erb-b2 receptor tyrosine kinase 2	Homo sapiens	238-242
30526892-1	2018	Survival following a diagnosis of anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) has improved since the introduction of cyclophosphamide-based immunosuppressive regimens and is now almost 80% at 5 years.	Cyclophosphamide	145-161	adeno-associated virus integration site 1	Homo sapiens	101-104
29467881-1	2018	Treatment with rituximab plus a regimen of cyclophosphamide, doxorubicin, vincristine and prednisolone (CHOP) for patients with diffuse large B-cell lymphoma (DLBCL) has proven efficacy in clinical trials.	Cyclophosphamide	43-59	DNA damage inducible transcript 3	Homo sapiens	104-108
29141128-0	2018	Immune-Enhancing Effect of Nanometric Lactobacillus plantarum nF1 (nLp-nF1) in a Mouse Model of Cyclophosphamide-Induced Immunosuppression.	Cyclophosphamide	96-112	neurofibromin 1	Mus musculus	62-65
29141128-0	2018	Immune-Enhancing Effect of Nanometric Lactobacillus plantarum nF1 (nLp-nF1) in a Mouse Model of Cyclophosphamide-Induced Immunosuppression.	Cyclophosphamide	96-112	neurofibromin 1	Mus musculus	71-74
28935542-2	2018	Poly-ADP-ribose-polymerase inhibition sensitizes tumor cells to cytotoxic agents, which induce DNA damage, including cyclophosphamide (C), and metronomic dosing of C may optimize potential for synergy.	Cyclophosphamide	117-133	poly(ADP-ribose) polymerase 1	Homo sapiens	0-26
29124456-0	2018	Serial immunological parameters in a phase II trial of exemestane and low-dose oral cyclophosphamide in advanced hormone receptor-positive breast cancer.	Cyclophosphamide	84-100	nuclear receptor subfamily 4 group A member 1	Homo sapiens	113-129
28939510-6	2018	In addition, PSP treatment restored the levels of IL-2, TNF-alpha, IL-8 and IL-10 in the serum of the Cy-treated mice in a dose-dependent manner.	Cyclophosphamide	102-104	interleukin 2	Mus musculus	50-54
29434755-12	2018	Serum interleukin (IL)-2 and IL-12 levels were significantly increased in S180 solid tumour-bearing mice treated with 200 or 100 mg/kg ASPS compared with mice in the normal, control and model groups (P&lt;0.05), whereas serum IL-2 and IL-12 levels were significantly decreased in the cyclophosphamide treatment group compared with the normal, control and model groups (P&lt;0.05).	Cyclophosphamide	284-300	alveolar soft part sarcoma chromosome region, candidate 1 (human)	Mus musculus	135-139
28939510-6	2018	In addition, PSP treatment restored the levels of IL-2, TNF-alpha, IL-8 and IL-10 in the serum of the Cy-treated mice in a dose-dependent manner.	Cyclophosphamide	102-104	interleukin 10	Mus musculus	76-81
28939510-6	2018	In addition, PSP treatment restored the levels of IL-2, TNF-alpha, IL-8 and IL-10 in the serum of the Cy-treated mice in a dose-dependent manner.	Cyclophosphamide	102-104	tumor necrosis factor	Mus musculus	56-65
28939510-6	2018	In addition, PSP treatment restored the levels of IL-2, TNF-alpha, IL-8 and IL-10 in the serum of the Cy-treated mice in a dose-dependent manner.	Cyclophosphamide	102-104	chemokine (C-X-C motif) ligand 15	Mus musculus	67-71
28785984-4	2018	Moreover, patients with proteinase 3 (PR3)-AAV may respond better to rituximab than cyclophosphamide.	Cyclophosphamide	84-100	proteinase 3	Homo sapiens	24-36
28785984-4	2018	Moreover, patients with proteinase 3 (PR3)-AAV may respond better to rituximab than cyclophosphamide.	Cyclophosphamide	84-100	proteinase 3	Homo sapiens	38-41
29079319-7	2018	Knocking down of PINCH-1 led to a significant (p-value&lt;0.05) enhancement in apoptosis in T47D cells in response to 4/6 (cyclophosphamide, celecoxib, paclitaxel, doxorubicin) drugs.	Cyclophosphamide	123-139	LIM zinc finger domain containing 1	Homo sapiens	17-24
29410666-2	2018	However, this model involves animals with high tumor burden, whereas in the clinics B-NHL patients are usually treated with chemotherapy (CHOP: cyclophosphamide, doxorubicin, vincristine, and prednisone) as first-line therapy prior to immunotherapy.	Cyclophosphamide	144-160	DNA damage inducible transcript 3	Homo sapiens	138-142
29403563-1	2018	The aim of this study was to analyze the prevalence and prognostic value of myeloid differentiation factor 88 (MYD88) L265P in diffuse large B-cell lymphoma (DLBCL) patients treated with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP).	Cyclophosphamide	202-218	MYD88 innate immune signal transduction adaptor	Homo sapiens	76-109
29403563-1	2018	The aim of this study was to analyze the prevalence and prognostic value of myeloid differentiation factor 88 (MYD88) L265P in diffuse large B-cell lymphoma (DLBCL) patients treated with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP).	Cyclophosphamide	202-218	MYD88 innate immune signal transduction adaptor	Homo sapiens	111-116
29397839-1	2018	OBJECTIVE: To study the value of absolute lymphocyte count/absolute monocyte count (ALC/AMC) and its effect on prognosis in patients with primary follicular lymphoma treated with rituximab combined with cyclophosphamide + doxorubicin + vincristine + prednisone (R-CHOP) chemotherapy.	Cyclophosphamide	203-219	allantoicase	Homo sapiens	84-87
29307711-2	2018	We report that dFB neurons communicate via inhibitory transmitters, including allatostatin-A (AstA), with interneurons connecting the superior arch with the ellipsoid body of the central complex.	Cyclophosphamide	94-98	Allatostatin A	Drosophila melanogaster	78-92
29129814-3	2018	The enhanced Cav3.2 activity by H2S formed by the upregulated cystathionine-gamma-lyase (CSE) is involved in the cyclophosphamide (CPA)-induced cystitis-related bladder pain in mice.	Cyclophosphamide	113-129	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	13-19
29129814-3	2018	The enhanced Cav3.2 activity by H2S formed by the upregulated cystathionine-gamma-lyase (CSE) is involved in the cyclophosphamide (CPA)-induced cystitis-related bladder pain in mice.	Cyclophosphamide	113-129	cystathionase (cystathionine gamma-lyase)	Mus musculus	89-92
29129814-3	2018	The enhanced Cav3.2 activity by H2S formed by the upregulated cystathionine-gamma-lyase (CSE) is involved in the cyclophosphamide (CPA)-induced cystitis-related bladder pain in mice.	Cyclophosphamide	131-134	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	13-19
29129814-3	2018	The enhanced Cav3.2 activity by H2S formed by the upregulated cystathionine-gamma-lyase (CSE) is involved in the cyclophosphamide (CPA)-induced cystitis-related bladder pain in mice.	Cyclophosphamide	131-134	cystathionase (cystathionine gamma-lyase)	Mus musculus	62-87
29129814-3	2018	The enhanced Cav3.2 activity by H2S formed by the upregulated cystathionine-gamma-lyase (CSE) is involved in the cyclophosphamide (CPA)-induced cystitis-related bladder pain in mice.	Cyclophosphamide	131-134	cystathionase (cystathionine gamma-lyase)	Mus musculus	89-92
29129814-6	2018	Acute zinc deficiency caused by systemic N,N,N",N"-tetrakis-(2-pyridylmethyl)-ethylendiamine (TPEN), a zinc chelator, mimicked the dietary zinc deficiency-induced Cav3.2-dependent promotion of BP/RH following CPA at 200mg/kg.	Cyclophosphamide	209-212	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	163-169
29129814-7	2018	CPA at 400mg/kg alone or TPEN plus CPA at 200mg/kg caused Cav3.2 overexpression accompanied by upregulation of Egr-1 and USP5, known to promote transcriptional expression and reduce proteasomal degradation of Cav3.2, respectively, in the dorsal root ganglia (DRG).	Cyclophosphamide	0-3	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	58-64
29129814-7	2018	CPA at 400mg/kg alone or TPEN plus CPA at 200mg/kg caused Cav3.2 overexpression accompanied by upregulation of Egr-1 and USP5, known to promote transcriptional expression and reduce proteasomal degradation of Cav3.2, respectively, in the dorsal root ganglia (DRG).	Cyclophosphamide	0-3	early growth response 1	Mus musculus	111-116
29129814-7	2018	CPA at 400mg/kg alone or TPEN plus CPA at 200mg/kg caused Cav3.2 overexpression accompanied by upregulation of Egr-1 and USP5, known to promote transcriptional expression and reduce proteasomal degradation of Cav3.2, respectively, in the dorsal root ganglia (DRG).	Cyclophosphamide	0-3	ubiquitin specific peptidase 5 (isopeptidase T)	Mus musculus	121-125
29129814-7	2018	CPA at 400mg/kg alone or TPEN plus CPA at 200mg/kg caused Cav3.2 overexpression accompanied by upregulation of Egr-1 and USP5, known to promote transcriptional expression and reduce proteasomal degradation of Cav3.2, respectively, in the dorsal root ganglia (DRG).	Cyclophosphamide	0-3	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	209-215
29129814-7	2018	CPA at 400mg/kg alone or TPEN plus CPA at 200mg/kg caused Cav3.2 overexpression accompanied by upregulation of Egr-1 and USP5, known to promote transcriptional expression and reduce proteasomal degradation of Cav3.2, respectively, in the dorsal root ganglia (DRG).	Cyclophosphamide	35-38	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	58-64
29129814-7	2018	CPA at 400mg/kg alone or TPEN plus CPA at 200mg/kg caused Cav3.2 overexpression accompanied by upregulation of Egr-1 and USP5, known to promote transcriptional expression and reduce proteasomal degradation of Cav3.2, respectively, in the dorsal root ganglia (DRG).	Cyclophosphamide	35-38	early growth response 1	Mus musculus	111-116
29129814-7	2018	CPA at 400mg/kg alone or TPEN plus CPA at 200mg/kg caused Cav3.2 overexpression accompanied by upregulation of Egr-1 and USP5, known to promote transcriptional expression and reduce proteasomal degradation of Cav3.2, respectively, in the dorsal root ganglia (DRG).	Cyclophosphamide	35-38	ubiquitin specific peptidase 5 (isopeptidase T)	Mus musculus	121-125
29129814-7	2018	CPA at 400mg/kg alone or TPEN plus CPA at 200mg/kg caused Cav3.2 overexpression accompanied by upregulation of Egr-1 and USP5, known to promote transcriptional expression and reduce proteasomal degradation of Cav3.2, respectively, in the dorsal root ganglia (DRG).	Cyclophosphamide	35-38	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	209-215
29129814-8	2018	The CSE inhibitor, beta-cyano-l-alanine, prevented the BP/RH and upregulation of Cav3.2, Egr-1 and USP5 in DRG following TPEN plus CPA at 200mg/kg.	Cyclophosphamide	131-134	cystathionase (cystathionine gamma-lyase)	Mus musculus	4-7
29129814-8	2018	The CSE inhibitor, beta-cyano-l-alanine, prevented the BP/RH and upregulation of Cav3.2, Egr-1 and USP5 in DRG following TPEN plus CPA at 200mg/kg.	Cyclophosphamide	131-134	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	81-87
29129814-8	2018	The CSE inhibitor, beta-cyano-l-alanine, prevented the BP/RH and upregulation of Cav3.2, Egr-1 and USP5 in DRG following TPEN plus CPA at 200mg/kg.	Cyclophosphamide	131-134	ubiquitin specific peptidase 5 (isopeptidase T)	Mus musculus	99-103
29129814-9	2018	Together, zinc deficiency promotes bladder pain accompanying CPA-induced cystitis by enhancing function and expression of Cav3.2 in nociceptors, suggesting a novel therapeutic avenue for treatment of bladder pain, such as zinc supplementation.	Cyclophosphamide	61-64	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	122-128
29293510-12	2018	We successfully showed that the combination of immune cell therapy and CPA was safe, might induce tumor-specific immune responses and clinical efficacy, and was accompanied by a decreased ratio of Tregs in patients with RNF43-positive advanced solid tumors.	Cyclophosphamide	71-74	ring finger protein 43	Homo sapiens	220-225
29156526-1	2018	BACKGROUND: Cyclophosphamide (CTX) is a widely used antitumor drug that can suppress the immune system.	Cyclophosphamide	12-28	V-set and immunoglobulin domain containing 2	Mus musculus	30-33
29164608-0	2018	The absolute percent deviation of IGHV mutation rather than a 98% cut-off predicts survival of chronic lymphocytic leukaemia patients treated with fludarabine, cyclophosphamide and rituximab.	Cyclophosphamide	160-176	immunoglobulin heavy variable 3-69-1 (pseudogene)	Homo sapiens	34-38
29205267-0	2018	The absolute percent deviation of IGHV mutation rather than a 98% cut-off predicts survival of chronic lymphocytic leukaemia patients treated with fludarabine, cyclophosphamide and rituximab.	Cyclophosphamide	160-176	immunoglobulin heavy variable 3-69-1 (pseudogene)	Homo sapiens	34-38
28947136-2	2018	Here, we report that BH3 mimetics selectively targeting BCL-xL, BCL-2 or MCL-1 (i.e. A-1331852, ABT-199, A-1210477) act in concert with multiple chemotherapeutic agents (i.e. vincristine (VCR), etoposide (ETO), doxorubicin, actinomycin D and cyclophosphamide) to induce apoptosis in rhabdomyosarcoma (RMS) cells.	Cyclophosphamide	242-258	BCL2 like 1	Homo sapiens	56-62
28947136-2	2018	Here, we report that BH3 mimetics selectively targeting BCL-xL, BCL-2 or MCL-1 (i.e. A-1331852, ABT-199, A-1210477) act in concert with multiple chemotherapeutic agents (i.e. vincristine (VCR), etoposide (ETO), doxorubicin, actinomycin D and cyclophosphamide) to induce apoptosis in rhabdomyosarcoma (RMS) cells.	Cyclophosphamide	242-258	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	73-78
30423551-9	2018	Moreover, mice engrafted with cells overexpressing COP1 showed a shortened survival, increased tumor cells burden in spleen and bone marrow (BM), and reduced tumor cell apoptosis even when fludarabine combined cyclophosphamide (F+C) therapy was administered.	Cyclophosphamide	210-226	COP1, E3 ubiquitin ligase	Mus musculus	51-55
29078731-3	2018	In the present study, the immune regulatory effect of LP was investigated in normal mice and Lewis lung carcinoma (LLC)-bearing mice treated with cyclophosphamide (CTX).	Cyclophosphamide	146-162	V-set and immunoglobulin domain containing 2	Mus musculus	164-167
30147102-13	2018	The median PSA progression-free survival with cyclophosphamide was 4.7 months (range: 0.9-13.5 months).	Cyclophosphamide	46-62	kallikrein related peptidase 3	Homo sapiens	11-14
30147102-17	2018	In few patients, cyclophosphamide induced durable PSA response.	Cyclophosphamide	17-33	kallikrein related peptidase 3	Homo sapiens	50-53
29515301-1	2018	Calcineurin inhibitors (CNIs) are the preferred drugs for treatment of childhood steroid-resistant nephrotic syndrome (SRNS) who are also resistant to cyclophosphamide (CYC).	Cyclophosphamide	151-167	cytochrome c, somatic	Homo sapiens	169-172
29136560-3	2018	As a result, cyclophosphamide-induced cystitis in mice showed an increased LD level in serum, and the contents of cytokines (IL-6, TNF-alpha) were elevated.	Cyclophosphamide	13-29	interleukin 6	Mus musculus	125-129
29136560-3	2018	As a result, cyclophosphamide-induced cystitis in mice showed an increased LD level in serum, and the contents of cytokines (IL-6, TNF-alpha) were elevated.	Cyclophosphamide	13-29	tumor necrosis factor	Mus musculus	131-140
29348080-3	2018	Data indicated that cyclophosphamide caused obvious changes in mice such as significant reduction (P&lt;0.01) of glutathione reductase activity (GR), vitamin C (Vc) content and total antioxidant capacity (T-AOC) in the testes, as well as elevation (P&lt;0.01) of abnormal rates of sperm and fetus, and a decrease in the total fetal count and average fetal count (P&lt;0.01), were totally alleviated by SIP.	Cyclophosphamide	20-36	glutathione reductase	Mus musculus	113-134
29737107-7	2018	R-CHOP (rituximab,cyclophosphamide,epirubicin,vindesine,prednisone) or CHOP regimen chemotherapy significantly improved the survival of the patients (P=0.000 2).	Cyclophosphamide	18-34	DNA damage inducible transcript 3	Homo sapiens	2-6
29129814-3	2018	The enhanced Cav3.2 activity by H2S formed by the upregulated cystathionine-gamma-lyase (CSE) is involved in the cyclophosphamide (CPA)-induced cystitis-related bladder pain in mice.	Cyclophosphamide	113-129	cystathionase (cystathionine gamma-lyase)	Mus musculus	62-87
29270058-7	2017	Cyclophosphamide produced a significant dose-dependent reduction in amh (p &lt; 0.001); trastuzumab was associated with increased amh in survivors with normal cycles.	Cyclophosphamide	0-16	anti-Mullerian hormone	Homo sapiens	68-71
29222275-8	2017	The mutation status of IGHV genes represents a predictive biomarker for identifying patients that may benefit the most from chemoimmunotherapy with fludarabine, cyclophosphamide, and rituximab.	Cyclophosphamide	161-177	immunoglobulin heavy variable 3-69-1 (pseudogene)	Homo sapiens	23-27
28847710-2	2017	Specifically, the nongerminal center B cell-like (non-GCB) subtype, composed predominantly of the activated B cell-like (ABC) molecular subtype, has been shown to portend poor prognosis because of its more aggressive nature and resistance to standard cyclophosphamide, hydroxydaunorubicin, oncovin, prednisone (CHOP)-like chemotherapy compared with the GCB subtype.	Cyclophosphamide	251-267	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	121-124
29333403-1	2017	Background: While cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) is the most commonly used chemotherapeutic regimen for patients with peripheral T-cell lymphomas (PTCLs), elderly patients are more vulnerable to associated toxicities.	Cyclophosphamide	18-34	DNA damage inducible transcript 3	Homo sapiens	80-84
29054890-4	2017	Gemcitabine and cyclophosphamide analogues enhanced the potential immunogenicity of 4T1 mammary carcinoma cells by increasing the expression of antigen-presenting molecules (MHC-I, MHC-II, and CD1d) and promoting exposure or release of immunogenic cell death markers (calreticulin, HMGB1, and ATP).	Cyclophosphamide	16-32	histocompatibility-2, MHC	Mus musculus	181-187
29054890-4	2017	Gemcitabine and cyclophosphamide analogues enhanced the potential immunogenicity of 4T1 mammary carcinoma cells by increasing the expression of antigen-presenting molecules (MHC-I, MHC-II, and CD1d) and promoting exposure or release of immunogenic cell death markers (calreticulin, HMGB1, and ATP).	Cyclophosphamide	16-32	CD1d1 antigen	Mus musculus	193-197
29054890-4	2017	Gemcitabine and cyclophosphamide analogues enhanced the potential immunogenicity of 4T1 mammary carcinoma cells by increasing the expression of antigen-presenting molecules (MHC-I, MHC-II, and CD1d) and promoting exposure or release of immunogenic cell death markers (calreticulin, HMGB1, and ATP).	Cyclophosphamide	16-32	calreticulin	Mus musculus	268-280
29054890-4	2017	Gemcitabine and cyclophosphamide analogues enhanced the potential immunogenicity of 4T1 mammary carcinoma cells by increasing the expression of antigen-presenting molecules (MHC-I, MHC-II, and CD1d) and promoting exposure or release of immunogenic cell death markers (calreticulin, HMGB1, and ATP).	Cyclophosphamide	16-32	high mobility group box 1	Mus musculus	282-287
29390559-1	2017	OBJECTIVE: This study systemically evaluated the efficacy and safety of intermittent intravenous pulse therapy with different doses of cyclophosphamide (CTX) for the treatment of lupus nephritis (LN).	Cyclophosphamide	135-151	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	153-156
29308284-5	2017	She commenced adjuvant trastuzumab and letrozole therapy, and following the sixth injection of trastuzumab, she was admitted with clinical features consistent with a flare of ASS, which included swinging fever, interstitial lung disease, myositis, and possible subclinical myocarditis, despite recent treatment with cyclophosphamide.	Cyclophosphamide	316-332	argininosuccinate synthase 1	Homo sapiens	175-178
29390394-0	2017	Recombinant human thrombopoietin improves the efficacy of intermediate-dose cyclophosphamide plus granulocyte colony-stimulating factor in mobilizing peripheral blood stem cells in patients with multiple myeloma: A cohort study.	Cyclophosphamide	76-92	thrombopoietin	Homo sapiens	18-32
28140733-5	2017	BD model mice were established by injecting N-acetylphenylhydrazine (APH) and cyclophosphamide (CTX) (ip).	Cyclophosphamide	78-94	V-set and immunoglobulin domain containing 2	Mus musculus	96-99
29157803-0	2017	Iridoid glycosides fraction from Picrorhiza kurroa attenuates cyclophosphamide-induced renal toxicity and peripheral neuropathy via PPAR-gamma mediated inhibition of inflammation and apoptosis.	Cyclophosphamide	62-78	peroxisome proliferator activated receptor gamma	Mus musculus	132-142
29184078-6	2017	The permeability of FD-4 and expression of ZO-1 and OCLN in cyclophosphamide-treated IPEC-J2 cells were reduced by capric acid.	Cyclophosphamide	60-76	zonula occludens 1	Sus scrofa	43-47
29184078-6	2017	The permeability of FD-4 and expression of ZO-1 and OCLN in cyclophosphamide-treated IPEC-J2 cells were reduced by capric acid.	Cyclophosphamide	60-76	occludin	Sus scrofa	52-56
29184078-7	2017	Dietary capric acid reduced TNF-alpha, IL-6, and MDA levels and increased SOD, GPx, and the expression of genes related to pro-inflammatory, oxidative stress, and intestinal barrier functions in cyclophosphamide-treated miniature pigs.	Cyclophosphamide	195-211	tumor necrosis factor	Sus scrofa	28-37
29025740-1	2017	In chronic lymphocytic leukemia (CLL) patients with mutated IGHV, 3 recent studies have demonstrated prolonged progression-free survival (PFS) after treatment with fludarabine-cyclophosphamide-rituximab (FCR) chemoimmunotherapy.	Cyclophosphamide	176-192	immunoglobulin heavy variable 3-69-1 (pseudogene)	Homo sapiens	60-64
28855352-8	2017	Cyclophosphamide-treated patients demonstrating the most enhanced IFNgamma+ tumor-specific T-cell responses exhibited a significant delay in tumor progression [HR = 0.29; 95% confidence interval (CI), 0.12-0.69; P = 0.0047), compared with nonresponders and no-treatment controls.Conclusions: Cyclophosphamide-induced Treg depletion is mirrored by a striking boost in antitumor immunity.	Cyclophosphamide	0-16	interferon gamma	Homo sapiens	66-74
28855352-8	2017	Cyclophosphamide-treated patients demonstrating the most enhanced IFNgamma+ tumor-specific T-cell responses exhibited a significant delay in tumor progression [HR = 0.29; 95% confidence interval (CI), 0.12-0.69; P = 0.0047), compared with nonresponders and no-treatment controls.Conclusions: Cyclophosphamide-induced Treg depletion is mirrored by a striking boost in antitumor immunity.	Cyclophosphamide	292-308	interferon gamma	Homo sapiens	66-74
28922724-0	2017	Oyster (Ostrea plicatula Gmelin) polysaccharides intervention ameliorates cyclophosphamide-Induced genotoxicity and hepatotoxicity in mice via the Nrf2-ARE pathway.	Cyclophosphamide	74-90	nuclear factor, erythroid derived 2, like 2	Mus musculus	147-151
28346662-3	2017	Here, we report three cases of anti-MDA5 antibody-associated DM with RP-ILD in which the patients were treated with combined-modality therapy, including high-dose prednisolone, tacrolimus, intravenous cyclophosphamide and intravenous immunoglobulin (IVIG).	Cyclophosphamide	201-217	interferon induced with helicase C domain 1	Homo sapiens	36-40
28815584-3	2017	Fifty percent of CD8+ memory T lymphocytes in the spleen are eliminated by cyclophosphamide within 14 days, indicating that numbers of at least 50% of splenic CD8+ memory T lymphocytes are maintained by proliferation.	Cyclophosphamide	75-91	CD8a molecule	Homo sapiens	17-20
29114880-7	2017	47: 1900-1905) argue against this dogma, as they provide evidence that CD8 memory T cells in murine bone marrow are not proliferating, but largely quiescent, which protects them from elimination by the cytostatic drug Cyclophosphamide.	Cyclophosphamide	218-234	CD8a molecule	Homo sapiens	71-74
28663002-11	2017	There is evidence of a differential treatment approach and patients with anti-TIF1gamma autoantibodies are significantly more likely to receive aggressive treatment with IV cyclophosphamide and/or biologic drugs, clear trends are also visible in other autoantibody subgroups.	Cyclophosphamide	173-189	tripartite motif containing 33	Homo sapiens	78-87
28463080-16	2017	In the induction phase, cyclophosphamide (CTX) and mycophenolate mofetil (MMF) were equally effective in the patients with the same pathological type.	Cyclophosphamide	24-40	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	42-45
28956128-7	2017	Glucocorticoid and cyclophosphamide therapies remain the mainstay for treating AAV.	Cyclophosphamide	19-35	adeno-associated virus integration site 1	Homo sapiens	79-82
29296861-2	2017	Despite producing somewhat less-than-satisfactory results, the combination of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) remains the de facto standard in PTCL treatment.	Cyclophosphamide	78-94	DNA damage inducible transcript 3	Homo sapiens	138-142
29079801-3	2017	Intratumoral delivery of HMGN1 with low dose of Cytoxan cured mice bearing small (    0.5 cm), but not large (    1.0 cm) CT26 tumors.	Cyclophosphamide	48-55	high mobility group nucleosomal binding domain 1	Mus musculus	25-30
29070044-0	2017	Neoadjuvant everolimus plus letrozole versus fluorouracil, epirubicin and cyclophosphamide for ER-positive, HER2-negative breast cancer: study protocol for a randomized pilot trial.	Cyclophosphamide	74-90	estrogen receptor 1	Homo sapiens	95-97
28549771-0	2017	Calcineurin and mTOR Inhibitor-Free Post-Transplantation Cyclophosphamide and Bortezomib Combination for Graft-versus-Host Disease Prevention after Peripheral Blood Allogeneic Hematopoietic Stem Cell Transplantation: A Phase I/II Study.	Cyclophosphamide	57-73	mechanistic target of rapamycin kinase	Homo sapiens	16-20
28581681-0	2017	Anti-vascular endothelial growth factor treatment decreases bladder pain in cyclophosphamide cystitis: a Multidisciplinary Approach to the Study of Chronic Pelvic Pain (MAPP) Research Network animal model study.	Cyclophosphamide	76-92	vascular endothelial growth factor A	Mus musculus	0-39
28787548-0	2017	Contrasting effects of cyclophosphamide on anti-CTL-associated protein 4 blockade therapy in two mouse tumor models.	Cyclophosphamide	23-39	cytotoxic T-lymphocyte-associated protein 4	Mus musculus	43-72
29077150-1	2017	OBJECTIVE: To investigate the therapeutic effect of drug therapy with cyclophosphamide and leflunomide on the joint function damage of patients with systemic lupus erythematosus (SLE) and its regulatory effects on expression levels of programmed death receptor 1, Notch signaling pathway genes and interferon-inducible protein 10 in peripheral blood mononuclear cells.	Cyclophosphamide	70-86	notch receptor 1	Homo sapiens	264-269
29077150-8	2017	The positive expression rate of peripheral blood mononuclear cell Notch1 in leflunomide group after treatment was significantly decreased, and the curative effect was superior to that in cyclophosphamide group (p&lt;0.05).	Cyclophosphamide	187-203	notch receptor 1	Homo sapiens	66-72
29077150-10	2017	The comparison of positive expression rate of nuclear factor-kappaB (NF-kappaB) in peripheral blood mononuclear cells between the two groups after treatment showed that the curative effect in leflunomide group was superior to that in cyclophosphamide group (p&lt;0.05).	Cyclophosphamide	234-250	nuclear factor kappa B subunit 1	Homo sapiens	46-67
29077150-10	2017	The comparison of positive expression rate of nuclear factor-kappaB (NF-kappaB) in peripheral blood mononuclear cells between the two groups after treatment showed that the curative effect in leflunomide group was superior to that in cyclophosphamide group (p&lt;0.05).	Cyclophosphamide	234-250	nuclear factor kappa B subunit 1	Homo sapiens	69-78
29237963-7	2017	RESULTS: On univariate analysis, cyclophosphamide with total-body irradiation (TBI) based conditioning regimen and lower body mass index (BMI) were associated with lower CsA-1, while use of fludarabine and higher BMI were associated with higher CsA-1.	Cyclophosphamide	33-49	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	170-173
29237963-7	2017	RESULTS: On univariate analysis, cyclophosphamide with total-body irradiation (TBI) based conditioning regimen and lower body mass index (BMI) were associated with lower CsA-1, while use of fludarabine and higher BMI were associated with higher CsA-1.	Cyclophosphamide	33-49	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	245-248
32300400-5	2017	Patients with MLL- and CDKN2A-positive DLBCL may benefit from therapy with a dose-adjusted regimen of rituximab, etoposide, prednisone, vincristine, cyclophosphamide, and doxorubicin (DA-R-EPOCH) compared to traditional rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone (R-CHOP).	Cyclophosphamide	149-165	lysine methyltransferase 2A	Homo sapiens	14-17
32300400-5	2017	Patients with MLL- and CDKN2A-positive DLBCL may benefit from therapy with a dose-adjusted regimen of rituximab, etoposide, prednisone, vincristine, cyclophosphamide, and doxorubicin (DA-R-EPOCH) compared to traditional rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone (R-CHOP).	Cyclophosphamide	231-247	lysine methyltransferase 2A	Homo sapiens	14-17
32300400-5	2017	Patients with MLL- and CDKN2A-positive DLBCL may benefit from therapy with a dose-adjusted regimen of rituximab, etoposide, prednisone, vincristine, cyclophosphamide, and doxorubicin (DA-R-EPOCH) compared to traditional rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone (R-CHOP).	Cyclophosphamide	231-247	cyclin dependent kinase inhibitor 2A	Homo sapiens	23-29
28791403-10	2017	Among DLBCL cases, the TP53 mutations shortened both OS and PFS of patients treated with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone) and decreased both OS and PFS of patients with secondary DLBCL disease.	Cyclophosphamide	108-124	tumor protein p53	Homo sapiens	23-27
28791403-10	2017	Among DLBCL cases, the TP53 mutations shortened both OS and PFS of patients treated with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone) and decreased both OS and PFS of patients with secondary DLBCL disease.	Cyclophosphamide	108-124	DNA damage inducible transcript 3	Homo sapiens	91-95
28752532-4	2017	In MDA-MB-231 cells, 20 muM rutin enhanced cytotoxicity related to cyclophosphamide and methotrexate.	Cyclophosphamide	67-83	latexin	Homo sapiens	24-27
28976264-0	2017	Epistatic interactions among CYP2C19*2, CYP3A4 and GSTP1 on the cyclophosphamide therapy in lupus nephritis patients.	Cyclophosphamide	64-80	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	29-36
28976264-0	2017	Epistatic interactions among CYP2C19*2, CYP3A4 and GSTP1 on the cyclophosphamide therapy in lupus nephritis patients.	Cyclophosphamide	64-80	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	40-46
28976264-0	2017	Epistatic interactions among CYP2C19*2, CYP3A4 and GSTP1 on the cyclophosphamide therapy in lupus nephritis patients.	Cyclophosphamide	64-80	glutathione S-transferase pi 1	Homo sapiens	51-56
28976264-1	2017	AIM: To investigate the impact of genetic variants in CYP2C9, CYP2C19, CYP3A4, GSTT1, GSTM1 and GSTP1 on the efficacy of cyclophosphamide (CYC) therapy in patients with lupus nephritis.	Cyclophosphamide	121-137	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	62-69
28976264-1	2017	AIM: To investigate the impact of genetic variants in CYP2C9, CYP2C19, CYP3A4, GSTT1, GSTM1 and GSTP1 on the efficacy of cyclophosphamide (CYC) therapy in patients with lupus nephritis.	Cyclophosphamide	121-137	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	71-77
28976264-1	2017	AIM: To investigate the impact of genetic variants in CYP2C9, CYP2C19, CYP3A4, GSTT1, GSTM1 and GSTP1 on the efficacy of cyclophosphamide (CYC) therapy in patients with lupus nephritis.	Cyclophosphamide	121-137	glutathione S-transferase theta 1	Homo sapiens	79-84
28976264-1	2017	AIM: To investigate the impact of genetic variants in CYP2C9, CYP2C19, CYP3A4, GSTT1, GSTM1 and GSTP1 on the efficacy of cyclophosphamide (CYC) therapy in patients with lupus nephritis.	Cyclophosphamide	121-137	glutathione S-transferase mu 1	Homo sapiens	86-91
28976264-1	2017	AIM: To investigate the impact of genetic variants in CYP2C9, CYP2C19, CYP3A4, GSTT1, GSTM1 and GSTP1 on the efficacy of cyclophosphamide (CYC) therapy in patients with lupus nephritis.	Cyclophosphamide	121-137	glutathione S-transferase pi 1	Homo sapiens	96-101
28976264-1	2017	AIM: To investigate the impact of genetic variants in CYP2C9, CYP2C19, CYP3A4, GSTT1, GSTM1 and GSTP1 on the efficacy of cyclophosphamide (CYC) therapy in patients with lupus nephritis.	Cyclophosphamide	139-142	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	71-77
28976264-1	2017	AIM: To investigate the impact of genetic variants in CYP2C9, CYP2C19, CYP3A4, GSTT1, GSTM1 and GSTP1 on the efficacy of cyclophosphamide (CYC) therapy in patients with lupus nephritis.	Cyclophosphamide	139-142	glutathione S-transferase theta 1	Homo sapiens	79-84
28976264-1	2017	AIM: To investigate the impact of genetic variants in CYP2C9, CYP2C19, CYP3A4, GSTT1, GSTM1 and GSTP1 on the efficacy of cyclophosphamide (CYC) therapy in patients with lupus nephritis.	Cyclophosphamide	139-142	glutathione S-transferase mu 1	Homo sapiens	86-91
28976264-1	2017	AIM: To investigate the impact of genetic variants in CYP2C9, CYP2C19, CYP3A4, GSTT1, GSTM1 and GSTP1 on the efficacy of cyclophosphamide (CYC) therapy in patients with lupus nephritis.	Cyclophosphamide	139-142	glutathione S-transferase pi 1	Homo sapiens	96-101
28973980-4	2017	Both tested polysaccharides PS-Fuc and PS-FCS have a similar activity to r G-CSF, causing pronounced neutropoiesis stimulation in animals with myelosuppression induced by cyclophosphamide (CPh).	Cyclophosphamide	171-187	colony stimulating factor 3 (granulocyte)	Mus musculus	75-80
29147612-0	2017	Low-dose post-transplant cyclophosphamide can mitigate GVHD and enhance the G-CSF/ATG induced GVHD protective activity and improve haploidentical transplant outcomes.	Cyclophosphamide	25-41	colony stimulating factor 3 (granulocyte)	Mus musculus	76-81
28711021-9	2017	Further studies revealed that VC-IV sensitized tumor cells to cyclophosphamide therapy by down-regulating the anti-apoptotic protein Bcl-2 and by up-regulating molecules like p53, Bax, cytochrome c, caspases, which led to PARP cleavage and apoptosis.	Cyclophosphamide	62-78	B cell leukemia/lymphoma 2	Mus musculus	133-138
28827748-0	2017	Calf Spleen Extractive Injection protects mice against cyclophosphamide-induced hematopoietic injury through G-CSF-mediated JAK2/STAT3 signaling.	Cyclophosphamide	55-71	peripheral blood stem cell response to granulocyte colony stimulating factor 1	Mus musculus	109-114
28499912-1	2017	Cyclophosphamide (CTX) is a chemotherapeutic agent widely used to treat ovarian, breast, and hematological cancers as well as autoimmune disorders.	Cyclophosphamide	0-16	V-set and immunoglobulin domain containing 2	Mus musculus	18-21
28636891-2	2017	Thalidomide or bortezomib may be combined with cyclophosphamide and dexamethasone, in what are known as the CTD and VCD protocols, respectively.	Cyclophosphamide	47-63	CTD	Homo sapiens	108-111
28827748-0	2017	Calf Spleen Extractive Injection protects mice against cyclophosphamide-induced hematopoietic injury through G-CSF-mediated JAK2/STAT3 signaling.	Cyclophosphamide	55-71	Janus kinase 2	Mus musculus	124-128
28827748-0	2017	Calf Spleen Extractive Injection protects mice against cyclophosphamide-induced hematopoietic injury through G-CSF-mediated JAK2/STAT3 signaling.	Cyclophosphamide	55-71	signal transducer and activator of transcription 3	Mus musculus	129-134
28814333-0	2017	Rapamycin Prevents cyclophosphamide-induced Over-activation of Primordial Follicle pool through PI3K/Akt/mTOR Signaling Pathway in vivo.	Cyclophosphamide	19-35	thymoma viral proto-oncogene 1	Mus musculus	101-104
28814333-0	2017	Rapamycin Prevents cyclophosphamide-induced Over-activation of Primordial Follicle pool through PI3K/Akt/mTOR Signaling Pathway in vivo.	Cyclophosphamide	19-35	mechanistic target of rapamycin kinase	Mus musculus	105-109
28814333-5	2017	RESULTS: Cyclophosphamide depleted the follicular reserve and induced the phosphorylation of the key proteins of PI3K/Akt/mTOR pathway in mice in a dose-dependent manner.	Cyclophosphamide	9-25	thymoma viral proto-oncogene 1	Mus musculus	118-121
28814333-5	2017	RESULTS: Cyclophosphamide depleted the follicular reserve and induced the phosphorylation of the key proteins of PI3K/Akt/mTOR pathway in mice in a dose-dependent manner.	Cyclophosphamide	9-25	mechanistic target of rapamycin kinase	Mus musculus	122-126
28814333-9	2017	Compared to p-Akt/Akt and p-mtor/mtor, p-rps6/rps6 was significantly decreased in rapamycin + cyclophosphamide group (P &lt; 0.05), indicating that rapamycin attenuated the increased level of phosphorylation of rpS6 after cyclophosphamide treatment.	Cyclophosphamide	94-110	thymoma viral proto-oncogene 1	Mus musculus	14-17
28814333-9	2017	Compared to p-Akt/Akt and p-mtor/mtor, p-rps6/rps6 was significantly decreased in rapamycin + cyclophosphamide group (P &lt; 0.05), indicating that rapamycin attenuated the increased level of phosphorylation of rpS6 after cyclophosphamide treatment.	Cyclophosphamide	94-110	mechanistic target of rapamycin kinase	Mus musculus	28-32
28814333-9	2017	Compared to p-Akt/Akt and p-mtor/mtor, p-rps6/rps6 was significantly decreased in rapamycin + cyclophosphamide group (P &lt; 0.05), indicating that rapamycin attenuated the increased level of phosphorylation of rpS6 after cyclophosphamide treatment.	Cyclophosphamide	94-110	mechanistic target of rapamycin kinase	Mus musculus	33-37
28814333-9	2017	Compared to p-Akt/Akt and p-mtor/mtor, p-rps6/rps6 was significantly decreased in rapamycin + cyclophosphamide group (P &lt; 0.05), indicating that rapamycin attenuated the increased level of phosphorylation of rpS6 after cyclophosphamide treatment.	Cyclophosphamide	94-110	ribosomal protein S6	Mus musculus	41-45
28814333-9	2017	Compared to p-Akt/Akt and p-mtor/mtor, p-rps6/rps6 was significantly decreased in rapamycin + cyclophosphamide group (P &lt; 0.05), indicating that rapamycin attenuated the increased level of phosphorylation of rpS6 after cyclophosphamide treatment.	Cyclophosphamide	94-110	ribosomal protein S6	Mus musculus	46-50
28814333-9	2017	Compared to p-Akt/Akt and p-mtor/mtor, p-rps6/rps6 was significantly decreased in rapamycin + cyclophosphamide group (P &lt; 0.05), indicating that rapamycin attenuated the increased level of phosphorylation of rpS6 after cyclophosphamide treatment.	Cyclophosphamide	94-110	ribosomal protein S6	Mus musculus	211-215
28814333-9	2017	Compared to p-Akt/Akt and p-mtor/mtor, p-rps6/rps6 was significantly decreased in rapamycin + cyclophosphamide group (P &lt; 0.05), indicating that rapamycin attenuated the increased level of phosphorylation of rpS6 after cyclophosphamide treatment.	Cyclophosphamide	222-238	ribosomal protein S6	Mus musculus	41-45
28814333-10	2017	CONCLUSIONS: Rapamycin can prevent the primordial follicle activation induced by cyclophosphamide through PI3K/Akt/mTOR signaling pathway and thus plays a role in preserving the follicle pool.	Cyclophosphamide	81-97	thymoma viral proto-oncogene 1	Mus musculus	111-114
28814333-10	2017	CONCLUSIONS: Rapamycin can prevent the primordial follicle activation induced by cyclophosphamide through PI3K/Akt/mTOR signaling pathway and thus plays a role in preserving the follicle pool.	Cyclophosphamide	81-97	mechanistic target of rapamycin kinase	Mus musculus	115-119
28807003-11	2017	The chemotherapy-induced POF model was built into rats by intraperitoneal cyclophosphamide injection.	Cyclophosphamide	74-90	POF1B actin binding protein	Homo sapiens	25-28
28807058-16	2017	CONCLUSIONS: Increased ROS generation and decreased ALDH activity confirmed that CY metabolites HCY and acrolein are strongly implicated in cardiotoxicity.	Cyclophosphamide	81-83	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	52-56
28605593-4	2017	Cotreatment with previously identified ellipticine and pregnanol derivatives that recognize the MYC G-quadruplex and BCL2 i-motif promoter DNA structures lowered mRNA levels and subsequently enhanced sensitivity to a standard chemotherapy drug, cyclophosphamide, in DLBCL cell lines.	Cyclophosphamide	245-261	myelocytomatosis oncogene	Mus musculus	96-99
28605593-4	2017	Cotreatment with previously identified ellipticine and pregnanol derivatives that recognize the MYC G-quadruplex and BCL2 i-motif promoter DNA structures lowered mRNA levels and subsequently enhanced sensitivity to a standard chemotherapy drug, cyclophosphamide, in DLBCL cell lines.	Cyclophosphamide	245-261	B cell leukemia/lymphoma 2	Mus musculus	117-121
28786954-2	2017	Cyclophosphamide (CTX), in spite advances in chemotherapy and immunosuppressive regimes, is prone to cause severe toxicity due to its chloroacetaldehyde (CAA) metabolite produced by CYP3A.	Cyclophosphamide	0-16	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	182-187
28666424-8	2017	Significant improvement was noticed after three cycles of chemotherapy of THP-COP (pirarubicin, cyclophosphamide, vincristine, and prednisolone).	Cyclophosphamide	96-112	caspase recruitment domain family member 16	Homo sapiens	78-81
25503432-0	2017	Phase I Study of Amrubicin and Cyclophosphamide in Patients With Advanced Solid Organ Malignancies: HOG LUN 07-130.	Cyclophosphamide	31-47	TOP1 binding arginine/serine rich protein, E3 ubiquitin ligase	Homo sapiens	104-107
28575809-0	2017	Lutein mitigates cyclophosphamide induced lung and liver injury via NF-kappaB/MAPK dependent mechanism.	Cyclophosphamide	17-33	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	68-77
28575809-0	2017	Lutein mitigates cyclophosphamide induced lung and liver injury via NF-kappaB/MAPK dependent mechanism.	Cyclophosphamide	17-33	mitogen-activated protein kinase 14	Mus musculus	78-82
28860445-3	2017	She was treated with NAC of docetaxel, doxorubicin, and cyclophosphamide(TAC)using pegfilgrastim.	Cyclophosphamide	56-72	synuclein alpha	Homo sapiens	21-24
28463035-0	2017	Inhibition of NF-kappaB/TNF-alpha pathway may be involved in the protective effect of resveratrol against cyclophosphamide-induced multi-organ toxicity.	Cyclophosphamide	106-122	nuclear factor kappa B subunit 1	Homo sapiens	14-23
28463035-0	2017	Inhibition of NF-kappaB/TNF-alpha pathway may be involved in the protective effect of resveratrol against cyclophosphamide-induced multi-organ toxicity.	Cyclophosphamide	106-122	tumor necrosis factor	Homo sapiens	24-33
28751718-7	2017	We employed these models in conjunction with transcriptome analyses following cyclophosphamide treatment to reveal that Atm deficiency is associated with an exquisite and genotype-specific sensitivity against PARP inhibition.	Cyclophosphamide	78-94	poly (ADP-ribose) polymerase family, member 1	Mus musculus	209-213
28494646-8	2017	In conclusion, a high-dose fludarabine (Flu), busulfan (Bu), cyclophosphamide (CTX)-based conditioning regimen was well tolerated and significantly speeded hematopoietic recovery.	Cyclophosphamide	61-77	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	79-82
28522441-2	2017	We hypothesized that rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) could decrease rates of relapse and transformation.	Cyclophosphamide	36-52	DNA damage inducible transcript 3	Homo sapiens	98-102
28725161-1	2017	BACKGROUND: Rituximab combined with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) is used as standard frontline regimen for diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	36-52	DNA damage inducible transcript 3	Homo sapiens	95-99
28744217-14	2017	Article summary: (1) Children carrying functional alleles in GSTM1 and CYP2C9 are at high risk for developing hemorrhagic cystitis following treatment with busulfan and cyclophosphamide based conditioning regimen.	Cyclophosphamide	169-185	glutathione S-transferase mu 1	Homo sapiens	61-66
28744217-14	2017	Article summary: (1) Children carrying functional alleles in GSTM1 and CYP2C9 are at high risk for developing hemorrhagic cystitis following treatment with busulfan and cyclophosphamide based conditioning regimen.	Cyclophosphamide	169-185	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	71-77
28527347-2	2017	Plumieride restores the suppressed cell mediated, humoral immune response and also enhances the release of TNF- alpha, IFN-gamma, and IL-2 (Th-1) in immune compromised cyclosporine and cyclophosphamide treated balb/c mice.	Cyclophosphamide	185-201	tumor necrosis factor	Mus musculus	107-117
28527347-2	2017	Plumieride restores the suppressed cell mediated, humoral immune response and also enhances the release of TNF- alpha, IFN-gamma, and IL-2 (Th-1) in immune compromised cyclosporine and cyclophosphamide treated balb/c mice.	Cyclophosphamide	185-201	negative elongation factor complex member C/D, Th1l	Mus musculus	140-144
27206429-3	2017	To address this issue, we investigated the expression and inducibility of CYP2C8 and CYP3A4 and their responsiveness against cyclophosphamide (CPA) and organophosphorus pesticide monocrotophos (MCP), a known developmental neurotoxicant in human neural (SH-SY5Y) and glial (U373-MG) cell lines.	Cyclophosphamide	125-141	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	74-80
28977934-8	2017	Shuanghuang Shengbai completely reversed the cyclophosphamide-induced decreases in white blood cells, proliferation index of bone marrow cells, and the ratio of CD34+SCA1+ bone marrow hematopoietic stem cells (P&lt;0.05).	Cyclophosphamide	45-61	CD34 antigen	Mus musculus	161-165
28084020-0	2017	Successful treatment of type B insulin resistance with mixed connective tissue disease by pulse glucocorticoids and cyclophosphamide.	Cyclophosphamide	116-132	insulin	Homo sapiens	31-38
28084020-2	2017	We report the successful treatment of a patient with refractory type B insulin resistance with pulse glucocorticoids and cyclophosphamide.	Cyclophosphamide	121-137	insulin	Homo sapiens	71-78
27206429-3	2017	To address this issue, we investigated the expression and inducibility of CYP2C8 and CYP3A4 and their responsiveness against cyclophosphamide (CPA) and organophosphorus pesticide monocrotophos (MCP), a known developmental neurotoxicant in human neural (SH-SY5Y) and glial (U373-MG) cell lines.	Cyclophosphamide	125-141	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	85-91
27206429-3	2017	To address this issue, we investigated the expression and inducibility of CYP2C8 and CYP3A4 and their responsiveness against cyclophosphamide (CPA) and organophosphorus pesticide monocrotophos (MCP), a known developmental neurotoxicant in human neural (SH-SY5Y) and glial (U373-MG) cell lines.	Cyclophosphamide	143-146	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	74-80
27206429-3	2017	To address this issue, we investigated the expression and inducibility of CYP2C8 and CYP3A4 and their responsiveness against cyclophosphamide (CPA) and organophosphorus pesticide monocrotophos (MCP), a known developmental neurotoxicant in human neural (SH-SY5Y) and glial (U373-MG) cell lines.	Cyclophosphamide	143-146	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	85-91
27206429-4	2017	CPA induced significant expression of CYP2C8 and CYP3A4 in both types of cells in a time-dependent manner.	Cyclophosphamide	0-3	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	38-44
27206429-4	2017	CPA induced significant expression of CYP2C8 and CYP3A4 in both types of cells in a time-dependent manner.	Cyclophosphamide	0-3	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	49-55
27206429-10	2017	Similarly, the known CYP inducer CPA has also shown significant high docking scores with the two studied CYP regulators.	Cyclophosphamide	33-36	peptidylprolyl isomerase G	Homo sapiens	21-24
27206429-10	2017	Similarly, the known CYP inducer CPA has also shown significant high docking scores with the two studied CYP regulators.	Cyclophosphamide	33-36	peptidylprolyl isomerase G	Homo sapiens	105-108
28560425-9	2017	Signal transducer and activator of transcription 5A (STAT5A), FYN proto-oncogene, Src family tyrosine kinase and spleen associated tyrosine kinase were revealed to be the hub genes in multiple enriched biological processes and signaling pathways, indicating that these were involved in mediating cyclophosphamide sensitivity in CML cells.	Cyclophosphamide	296-312	signal transducer and activator of transcription 5A	Homo sapiens	0-51
28560425-9	2017	Signal transducer and activator of transcription 5A (STAT5A), FYN proto-oncogene, Src family tyrosine kinase and spleen associated tyrosine kinase were revealed to be the hub genes in multiple enriched biological processes and signaling pathways, indicating that these were involved in mediating cyclophosphamide sensitivity in CML cells.	Cyclophosphamide	296-312	signal transducer and activator of transcription 5A	Homo sapiens	53-59
28560425-9	2017	Signal transducer and activator of transcription 5A (STAT5A), FYN proto-oncogene, Src family tyrosine kinase and spleen associated tyrosine kinase were revealed to be the hub genes in multiple enriched biological processes and signaling pathways, indicating that these were involved in mediating cyclophosphamide sensitivity in CML cells.	Cyclophosphamide	296-312	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	82-85
28560425-11	2017	Furthermore, selective knockdown of STAT5A and S100 calcium binding protein A4 (S100A4) recovered cyclophosphamide sensitivity in K-562 cells, suggesting their involvement in drug resistance.	Cyclophosphamide	98-114	signal transducer and activator of transcription 5A	Homo sapiens	36-42
28560425-11	2017	Furthermore, selective knockdown of STAT5A and S100 calcium binding protein A4 (S100A4) recovered cyclophosphamide sensitivity in K-562 cells, suggesting their involvement in drug resistance.	Cyclophosphamide	98-114	S100 calcium binding protein A4	Homo sapiens	47-78
28560425-11	2017	Furthermore, selective knockdown of STAT5A and S100 calcium binding protein A4 (S100A4) recovered cyclophosphamide sensitivity in K-562 cells, suggesting their involvement in drug resistance.	Cyclophosphamide	98-114	S100 calcium binding protein A4	Homo sapiens	80-86
28560425-12	2017	The present study identified several potential genes and pathways contributing to cyclophosphamide resistance, and confirmed the involvement of STAT5A and S100A4 in drug resistance.	Cyclophosphamide	82-98	signal transducer and activator of transcription 5A	Homo sapiens	144-150
28560425-12	2017	The present study identified several potential genes and pathways contributing to cyclophosphamide resistance, and confirmed the involvement of STAT5A and S100A4 in drug resistance.	Cyclophosphamide	82-98	S100 calcium binding protein A4	Homo sapiens	155-161
28713366-0	2017	Intratumoral Lentivector-Mediated TGF-beta1 Gene Downregulation As a Potent Strategy for Enhancing the Antitumor Effect of Therapy Composed of Cyclophosphamide and Dendritic Cells.	Cyclophosphamide	143-159	transforming growth factor, beta 1	Mus musculus	34-43
28713366-3	2017	The main purpose of the study was to improve the effectiveness of DC-based immunotherapy or chemoimmunotherapy composed of cyclophosphamide (CY) and DCs by application of lentivectors (LVs)-encoding short hairpin RNA specific for TGF-beta1 (shTGFbeta1 LVs).	Cyclophosphamide	123-139	transforming growth factor, beta 1	Mus musculus	230-239
28713366-7	2017	However, when the proposed scheme was complemented by pretreatment with a low dose of CY, we noticed high MC38 TGI together with decreased number of MDSCs in tumor and induction of Th1-type response.	Cyclophosphamide	86-88	negative elongation factor complex member C/D, Th1l	Mus musculus	181-184
28713366-10	2017	However, simultaneous reduction of TGF-beta1 in tumor microenvironment and its remodeling by pretreatment with a low dose of CY facilitates the settlement of peritumorally inoculated DCs and supports them in restoration and activation of a potent antitumor response.	Cyclophosphamide	125-127	transforming growth factor, beta 1	Mus musculus	35-44
28619061-5	2017	Following trials in scleroderma-ILD, cyclophosphamide is the accepted standard of care for individuals with severe or progressive CTD-related ILD.	Cyclophosphamide	37-53	CTD	Homo sapiens	130-133
30108864-5	2017	The results indicated that AOS can restore cyclophosphamide-induced immunosuppression by stimulating the secretion of GM-CSF, which promoted the differentiation of progenitor cells after proliferation.	Cyclophosphamide	43-59	colony stimulating factor 2	Homo sapiens	118-124
28327893-1	2017	Background: Our aim was to evaluate whether the cell of origin (COO) as defined by the Hans algorithm and MYC/BCL2 coexpression, which are the two main biological risk factors in elderly patients treated with rituximab, cyclophosphamide, doxorubicin hydrochloride, vincristine, and prednisolone (R-CHOP), maintain their prognostic value in a large prospective clinical trial.	Cyclophosphamide	220-236	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	106-109
28126501-6	2017	The administration of 30ng of CCL5 also induced hyperalgesia in mice with reduced number of circulating white blood cells in response to cyclophosphamide or with selective neutrophil depletion induced by an anti-Ly6G antibody.	Cyclophosphamide	137-153	chemokine (C-C motif) ligand 5	Mus musculus	30-34
28188670-8	2017	These results suggested that combined treatment with low dose CPA could provide clinical benefits in aBTC patients under PPV, possibly through prevention of IL-6-mediated immune suppression.	Cyclophosphamide	62-65	interleukin 6	Homo sapiens	157-161
28361910-10	2017	miR-9 targeted the Her-2 messenger RNA and increased responsiveness of BC cells to docetaxel (DOC) or cyclophosphamide treatment.	Cyclophosphamide	102-118	erb-b2 receptor tyrosine kinase 2	Homo sapiens	19-24
28154089-0	2017	Genetic polymorphism at BCL2 as a predictor for rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone efficacy in patients with diffuse large B-cell lymphoma.	Cyclophosphamide	59-75	BCL2 apoptosis regulator	Homo sapiens	24-28
28288951-0	2017	Haploidentical Related Donor Hematopoietic Stem Cell Transplantation for Dedicator-of-Cytokinesis 8 Deficiency Using Post-Transplantation Cyclophosphamide.	Cyclophosphamide	138-154	dedicator of cytokinesis 8	Homo sapiens	73-99
28280079-5	2017	Using a murine xenotransplant model to emulate a clinical treatment strategy, established ALDH1A1- leukemias were also sensitive to in vivo treatment with cyclophosphamide combined with arsenic trioxide.	Cyclophosphamide	155-171	aldehyde dehydrogenase family 1, subfamily A1	Mus musculus	90-97
28280079-6	2017	These results demonstrate that targeting ALDH1A1- leukemic cells with toxic ALDH1A1 substrates such as arsenic and cyclophosphamide may be a novel targeted therapeutic strategy for this subset of acute myeloid leukemias.	Cyclophosphamide	115-131	aldehyde dehydrogenase family 1, subfamily A1	Mus musculus	41-48
28280079-6	2017	These results demonstrate that targeting ALDH1A1- leukemic cells with toxic ALDH1A1 substrates such as arsenic and cyclophosphamide may be a novel targeted therapeutic strategy for this subset of acute myeloid leukemias.	Cyclophosphamide	115-131	aldehyde dehydrogenase family 1, subfamily A1	Mus musculus	76-83
26449182-1	2017	The CHOP regimen consisting of cyclophosphamide, doxorubicin (DOX), vincristine and prednisolone has been the most used regimen for peripheral T-cell lymphoma, not otherwise specified (PTCL-NOS).	Cyclophosphamide	31-47	DNA damage inducible transcript 3	Homo sapiens	4-8
28028749-0	2017	Oral cyclophosphamide was effective for Coombs-negative autoimmune hemolytic anemia in CD16+CD56- chronic lymphoproliferative disorder of NK-cells.	Cyclophosphamide	5-21	Fc gamma receptor IIIa	Homo sapiens	87-91
28028749-0	2017	Oral cyclophosphamide was effective for Coombs-negative autoimmune hemolytic anemia in CD16+CD56- chronic lymphoproliferative disorder of NK-cells.	Cyclophosphamide	5-21	neural cell adhesion molecule 1	Homo sapiens	92-96
28508578-1	2017	The murine mouse lymphoblastic lymphoma cell line (EL4) tumor model is an established in vivo apoptosis model for the investigation of novel cancer imaging agents and immunological treatments due to the rapid and significant response of the EL4 tumors to cyclophosphamide and etoposide combination chemotherapy.	Cyclophosphamide	255-271	epilepsy 4	Mus musculus	51-54
28508578-1	2017	The murine mouse lymphoblastic lymphoma cell line (EL4) tumor model is an established in vivo apoptosis model for the investigation of novel cancer imaging agents and immunological treatments due to the rapid and significant response of the EL4 tumors to cyclophosphamide and etoposide combination chemotherapy.	Cyclophosphamide	255-271	epilepsy 4	Mus musculus	241-244
28631569-0	2017	Insulin-induced enhancement of MCF-7 breast cancer cell response to 5-fluorouracil and cyclophosphamide.	Cyclophosphamide	87-103	insulin	Homo sapiens	0-7
28631569-2	2017	Insulin-induced sensitivity of MCF-7 breast cancer cells to chemotherapeutic agents 5-fluorouracil and cyclophosphamide was evaluated.	Cyclophosphamide	103-119	insulin	Homo sapiens	0-7