PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
30612232-7	2019	Long-term follow-up found that all 12 patients received autologous stem cell transplant, melphalan-based therapy or lenalidomide/thalidomide-based therapy obtained clinical improvement, of which eight experienced decreased levels of VEGF by 50% or back to normal.	Melphalan	89-98	vascular endothelial growth factor A	Homo sapiens	233-237
30925767-9	2019	Interestingly, melphalan induced reactive oxygen species, a significant decrease in GSH concentration, protein and lipd oxydation together with NRF2 (NF-E2-related factor 2) pathway activation.	Melphalan	15-24	NFE2 like bZIP transcription factor 2	Homo sapiens	144-148
30925767-9	2019	Interestingly, melphalan induced reactive oxygen species, a significant decrease in GSH concentration, protein and lipd oxydation together with NRF2 (NF-E2-related factor 2) pathway activation.	Melphalan	15-24	NFE2 like bZIP transcription factor 2	Homo sapiens	150-172
29691234-2	2018	Herein, we demonstrated that doxorubicin- and melphalan-treated senescent cells display increased expression of IL15, a cytokine involved in NK cell activation, proliferation, and maturation.	Melphalan	46-55	interleukin 15	Homo sapiens	112-116
29501779-1	2018	We conducted a prospective phase 2 trial of gemcitabine, busulfan and melphalan (Gem/Bu/Mel) with autologous stem cell transplantation (ASCT) in patients with primary refractory or poor-risk relapsed Hodgkin lymphoma (HL) (ie, extranodal relapse or within 1 year of frontline therapy).	Melphalan	70-79	GTP binding protein overexpressed in skeletal muscle	Homo sapiens	81-84
30732646-8	2019	Finally, blockade of CSF1R substantially recovered the melphalan-induced cytotoxicity reduced by pre-ASCT M-MDSCs.	Melphalan	55-64	colony stimulating factor 1 receptor	Homo sapiens	21-26
30591441-2	2019	This study aimed to investigate the impact of a single nucleotide polymorphism (SNP) rs4240803 in SLC7A5 on the gene expression, ex vivo sensitivity to melphalan, and clinical outcomes in MM patients who were undergoing autologous stem cell transplantation with high-dose melphalan.	Melphalan	152-161	solute carrier family 7 member 5	Homo sapiens	98-104
30591441-6	2019	CONCLUSION: rs4240803 impacted the expression of SLC7A5, thus contributing to the clinical response of MM patients to melphalan therapy.	Melphalan	118-127	solute carrier family 7 member 5	Homo sapiens	49-55
30353128-6	2019	The combination of ERK1/2, Akt, and NF-kappaB inhibitors with melphalan reversed melphalan resistance via suppression of Survivin expression and enhanced Bim expression in melphalan-resistant cells.	Melphalan	62-71	BCL2 like 11	Homo sapiens	154-157
30353128-10	2019	Our findings suggest that HIF-1alpha, ERK1/2, Akt, and NF-kappaB inhibitors are potentially useful as anti-MDR agents for the treatment of melphalan-resistant MM.	Melphalan	139-148	hypoxia inducible factor 1 subunit alpha	Homo sapiens	26-36
30353128-10	2019	Our findings suggest that HIF-1alpha, ERK1/2, Akt, and NF-kappaB inhibitors are potentially useful as anti-MDR agents for the treatment of melphalan-resistant MM.	Melphalan	139-148	mitogen-activated protein kinase 3	Homo sapiens	38-44
30353128-10	2019	Our findings suggest that HIF-1alpha, ERK1/2, Akt, and NF-kappaB inhibitors are potentially useful as anti-MDR agents for the treatment of melphalan-resistant MM.	Melphalan	139-148	AKT serine/threonine kinase 1	Homo sapiens	46-49
30353128-10	2019	Our findings suggest that HIF-1alpha, ERK1/2, Akt, and NF-kappaB inhibitors are potentially useful as anti-MDR agents for the treatment of melphalan-resistant MM.	Melphalan	139-148	nuclear factor kappa B subunit 1	Homo sapiens	55-64
30343510-4	2018	Granulocyte-colony stimulating factor (G-CSF) is given to stimulate neutrophil proliferation after melphalan administration.	Melphalan	99-108	colony stimulating factor 3	Homo sapiens	0-37
30343510-4	2018	Granulocyte-colony stimulating factor (G-CSF) is given to stimulate neutrophil proliferation after melphalan administration.	Melphalan	99-108	colony stimulating factor 3	Homo sapiens	39-44
29295500-0	2017	Decitabine and Melphalan Fail to Reactivate p73 in p53 Deficient Myeloma Cells.	Melphalan	15-24	tumor protein p73	Homo sapiens	44-47
29729664-0	2018	Complete response to orally administered melphalan in malignant pleural effusion from an occult female genital organ primary neoplasm with BRCA1/2 mutations: a case report.	Melphalan	41-50	BRCA1 DNA repair associated	Homo sapiens	139-146
29729664-5	2018	While a previous case report demonstrated a surprising cure of platinum-resistant ovarian cancer with BRCA2 mutation by orally administered melphalan.	Melphalan	140-149	BRCA2 DNA repair associated	Homo sapiens	102-107
29729664-11	2018	CONCLUSIONS: This is so far the second report of long-term remission of advanced female genital organ cancer with BRCA mutations achieved by orally administered melphalan.	Melphalan	161-170	BRCA1 DNA repair associated	Homo sapiens	114-118
29729664-12	2018	BRCA1/2 mutations and even all "BRCAness" of malignancy, at least ovarian cancer and ovarian-related cancers, probably not only correlate with high efficacy of poly(adenosine diphosphate-ribose) polymerase inhibitors but also lead to a high-potential cure by orally administered melphalan.	Melphalan	279-288	BRCA1 DNA repair associated	Homo sapiens	0-5
29057477-7	2018	These results indicate that MIP-1alpha neutralizing antibodies or MIP-1alpha siRNA enhance the cytotoxic effect of melphalan and bortezomib by suppressing the chemokine receptor/ERK and chemokine receptor/Akt/mTOR pathways.	Melphalan	115-124	C-C motif chemokine ligand 3	Homo sapiens	28-38
29057477-7	2018	These results indicate that MIP-1alpha neutralizing antibodies or MIP-1alpha siRNA enhance the cytotoxic effect of melphalan and bortezomib by suppressing the chemokine receptor/ERK and chemokine receptor/Akt/mTOR pathways.	Melphalan	115-124	C-C motif chemokine ligand 3	Homo sapiens	66-76
29057477-7	2018	These results indicate that MIP-1alpha neutralizing antibodies or MIP-1alpha siRNA enhance the cytotoxic effect of melphalan and bortezomib by suppressing the chemokine receptor/ERK and chemokine receptor/Akt/mTOR pathways.	Melphalan	115-124	C-X-C motif chemokine receptor 4	Homo sapiens	159-177
29057477-7	2018	These results indicate that MIP-1alpha neutralizing antibodies or MIP-1alpha siRNA enhance the cytotoxic effect of melphalan and bortezomib by suppressing the chemokine receptor/ERK and chemokine receptor/Akt/mTOR pathways.	Melphalan	115-124	mitogen-activated protein kinase 1	Homo sapiens	178-181
29057477-7	2018	These results indicate that MIP-1alpha neutralizing antibodies or MIP-1alpha siRNA enhance the cytotoxic effect of melphalan and bortezomib by suppressing the chemokine receptor/ERK and chemokine receptor/Akt/mTOR pathways.	Melphalan	115-124	C-X-C motif chemokine receptor 4	Homo sapiens	186-204
29057477-7	2018	These results indicate that MIP-1alpha neutralizing antibodies or MIP-1alpha siRNA enhance the cytotoxic effect of melphalan and bortezomib by suppressing the chemokine receptor/ERK and chemokine receptor/Akt/mTOR pathways.	Melphalan	115-124	AKT serine/threonine kinase 1	Homo sapiens	205-208
29057477-7	2018	These results indicate that MIP-1alpha neutralizing antibodies or MIP-1alpha siRNA enhance the cytotoxic effect of melphalan and bortezomib by suppressing the chemokine receptor/ERK and chemokine receptor/Akt/mTOR pathways.	Melphalan	115-124	mechanistic target of rapamycin kinase	Homo sapiens	209-213
29217776-0	2018	Melphalan 140 mg/m2 or 200 mg/m2 for autologous transplantation in myeloma: results from the Collaboration to Collect Autologous Transplant Outcomes in Lymphoma and Myeloma (CALM) study.	Melphalan	0-9	synaptosome associated protein 91	Homo sapiens	174-178
28626216-6	2018	Furthermore, the combination of CSF1R blockade and chemotherapy such as bortezomib or melphalan displayed an additive therapeutic efficacy against established myeloma.	Melphalan	86-95	colony stimulating factor 1 receptor	Homo sapiens	32-37
29057477-3	2018	In the present study, an MIP-1alpha neutralizing antibody suppressed cell proliferation and enhanced the cytotoxic effect of melphalan or bortezomib on MM cells.	Melphalan	125-134	C-C motif chemokine ligand 3	Homo sapiens	25-35
29057477-5	2018	Moreover, combination treatment with MIP-1alpha neutralizing antibody and melphalan or bortezomib inhibited extracellular signal regulated kinase 1/2 (ERK1/2), Akt, and mammalian target of rapamycin (mTOR) activation, Bcl-2, Bcl-xL, and Survivin expression, and upregulated the expression of Bim and cleaved Poly (ADP-ribose) polymerase (PARP).	Melphalan	74-83	mitogen-activated protein kinase 1	Homo sapiens	108-149
29057477-5	2018	Moreover, combination treatment with MIP-1alpha neutralizing antibody and melphalan or bortezomib inhibited extracellular signal regulated kinase 1/2 (ERK1/2), Akt, and mammalian target of rapamycin (mTOR) activation, Bcl-2, Bcl-xL, and Survivin expression, and upregulated the expression of Bim and cleaved Poly (ADP-ribose) polymerase (PARP).	Melphalan	74-83	mitogen-activated protein kinase 3	Homo sapiens	151-157
29057477-5	2018	Moreover, combination treatment with MIP-1alpha neutralizing antibody and melphalan or bortezomib inhibited extracellular signal regulated kinase 1/2 (ERK1/2), Akt, and mammalian target of rapamycin (mTOR) activation, Bcl-2, Bcl-xL, and Survivin expression, and upregulated the expression of Bim and cleaved Poly (ADP-ribose) polymerase (PARP).	Melphalan	74-83	AKT serine/threonine kinase 1	Homo sapiens	160-163
29057477-5	2018	Moreover, combination treatment with MIP-1alpha neutralizing antibody and melphalan or bortezomib inhibited extracellular signal regulated kinase 1/2 (ERK1/2), Akt, and mammalian target of rapamycin (mTOR) activation, Bcl-2, Bcl-xL, and Survivin expression, and upregulated the expression of Bim and cleaved Poly (ADP-ribose) polymerase (PARP).	Melphalan	74-83	mechanistic target of rapamycin kinase	Homo sapiens	169-198
29057477-5	2018	Moreover, combination treatment with MIP-1alpha neutralizing antibody and melphalan or bortezomib inhibited extracellular signal regulated kinase 1/2 (ERK1/2), Akt, and mammalian target of rapamycin (mTOR) activation, Bcl-2, Bcl-xL, and Survivin expression, and upregulated the expression of Bim and cleaved Poly (ADP-ribose) polymerase (PARP).	Melphalan	74-83	mechanistic target of rapamycin kinase	Homo sapiens	200-204
29057477-5	2018	Moreover, combination treatment with MIP-1alpha neutralizing antibody and melphalan or bortezomib inhibited extracellular signal regulated kinase 1/2 (ERK1/2), Akt, and mammalian target of rapamycin (mTOR) activation, Bcl-2, Bcl-xL, and Survivin expression, and upregulated the expression of Bim and cleaved Poly (ADP-ribose) polymerase (PARP).	Melphalan	74-83	BCL2 apoptosis regulator	Homo sapiens	218-223
29057477-5	2018	Moreover, combination treatment with MIP-1alpha neutralizing antibody and melphalan or bortezomib inhibited extracellular signal regulated kinase 1/2 (ERK1/2), Akt, and mammalian target of rapamycin (mTOR) activation, Bcl-2, Bcl-xL, and Survivin expression, and upregulated the expression of Bim and cleaved Poly (ADP-ribose) polymerase (PARP).	Melphalan	74-83	BCL2 like 1	Homo sapiens	225-231
29057477-5	2018	Moreover, combination treatment with MIP-1alpha neutralizing antibody and melphalan or bortezomib inhibited extracellular signal regulated kinase 1/2 (ERK1/2), Akt, and mammalian target of rapamycin (mTOR) activation, Bcl-2, Bcl-xL, and Survivin expression, and upregulated the expression of Bim and cleaved Poly (ADP-ribose) polymerase (PARP).	Melphalan	74-83	BCL2 like 11	Homo sapiens	292-295
29057477-5	2018	Moreover, combination treatment with MIP-1alpha neutralizing antibody and melphalan or bortezomib inhibited extracellular signal regulated kinase 1/2 (ERK1/2), Akt, and mammalian target of rapamycin (mTOR) activation, Bcl-2, Bcl-xL, and Survivin expression, and upregulated the expression of Bim and cleaved Poly (ADP-ribose) polymerase (PARP).	Melphalan	74-83	poly(ADP-ribose) polymerase 1	Homo sapiens	308-336
29057477-5	2018	Moreover, combination treatment with MIP-1alpha neutralizing antibody and melphalan or bortezomib inhibited extracellular signal regulated kinase 1/2 (ERK1/2), Akt, and mammalian target of rapamycin (mTOR) activation, Bcl-2, Bcl-xL, and Survivin expression, and upregulated the expression of Bim and cleaved Poly (ADP-ribose) polymerase (PARP).	Melphalan	74-83	poly(ADP-ribose) polymerase 1	Homo sapiens	338-342
29057477-6	2018	Treatment of IM9 cells with MIP-1alpha siRNA suppressed the activation of ERK1/2, Akt, and mTOR, and enhanced the cytotoxic effect of melphalan and bortezomib.	Melphalan	134-143	C-C motif chemokine ligand 3	Homo sapiens	28-38
29463311-4	2018	CASE PRESENTATION: A 60-year-old man with a history of plasma cell myeloma with IGH-MAF gene rearrangement and RAS/RAF mutations developed multiple soft tissue lesions one year following melphalan-based chemotherapy and autologous stem cell transplant.	Melphalan	187-196	immunoglobulin heavy locus	Homo sapiens	80-83
29463311-4	2018	CASE PRESENTATION: A 60-year-old man with a history of plasma cell myeloma with IGH-MAF gene rearrangement and RAS/RAF mutations developed multiple soft tissue lesions one year following melphalan-based chemotherapy and autologous stem cell transplant.	Melphalan	187-196	MAF bZIP transcription factor	Homo sapiens	84-87
29463311-4	2018	CASE PRESENTATION: A 60-year-old man with a history of plasma cell myeloma with IGH-MAF gene rearrangement and RAS/RAF mutations developed multiple soft tissue lesions one year following melphalan-based chemotherapy and autologous stem cell transplant.	Melphalan	187-196	zinc fingers and homeoboxes 2	Homo sapiens	115-118
30121664-2	2018	METHODS: Plasmids that could interfere with the expression of linc00515 and ATG14 were loaded into myeloma cells, which were cultured with melphalan.	Melphalan	139-148	long intergenic non-protein coding RNA 515	Homo sapiens	62-71
30121664-2	2018	METHODS: Plasmids that could interfere with the expression of linc00515 and ATG14 were loaded into myeloma cells, which were cultured with melphalan.	Melphalan	139-148	autophagy related 14	Homo sapiens	76-81
29295500-0	2017	Decitabine and Melphalan Fail to Reactivate p73 in p53 Deficient Myeloma Cells.	Melphalan	15-24	tumor protein p53	Homo sapiens	51-54
28969419-7	2017	Moreover, in vivo antitumor efficacy was further significantly increased by combination treatment with the chemotherapeutic drug, melphalan, suggesting a synergistic effect attributable to enhanced drug uptake into the tumor as a result of TNFalpha-mediated enhanced vascular permeability.	Melphalan	130-139	tumor necrosis factor	Mus musculus	240-248
29022281-10	2017	Similar unadjusted ORRs were noted in the melphalan treatment groups with and without TNFalpha (72.0 and 67.0%, respectively; p = 0.27).	Melphalan	42-51	tumor necrosis factor	Homo sapiens	86-94
28906482-2	2017	Currently, VMP (bortezomib, melphalan, prednisone) is one of the standard regimens recommended as the first-line therapy for patients with MM ineligible for high-dose chemotherapy (HDT) with autologous stem-cell transplantation (auto-SCT).	Melphalan	28-37	neurensin 1	Homo sapiens	11-14
28394191-0	2017	The PARP inhibitor olaparib enhances the cytotoxicity of combined gemcitabine, busulfan and melphalan in lymphoma cells.	Melphalan	92-101	poly(ADP-ribose) polymerase 1	Homo sapiens	4-8
26527748-5	2016	Inhibition of miR-221/222 overcame melphalan resistance and triggered apoptosis of multiple myeloma cells in vitro, in the presence or absence of human bone marrow (BM) stromal cells.	Melphalan	35-44	microRNA 221	Homo sapiens	14-21
28486243-3	2017	Because methylation of MGMT promoter increases the efficacy of alkylating agents, studies on melanoma outcome of patients treated with melphalan regional chemotherapy should consider this epigenetic change.	Melphalan	135-144	O-6-methylguanine-DNA methyltransferase	Homo sapiens	23-27
28486243-4	2017	This study aims to evaluate whether the survival of stage III melanoma patients treated with melphalan regional chemotherapy may be correlated with MGMT methylation status.	Melphalan	93-102	O-6-methylguanine-DNA methyltransferase	Homo sapiens	148-152
28486243-12	2017	Our data suggest that MGMT promoter methylation could be an important factor in determining which melanoma patients should receive melphalan regional chemotherapy, but its prognostic significance in the routine clinical setting needs to be clarified in a larger study.	Melphalan	131-140	O-6-methylguanine-DNA methyltransferase	Homo sapiens	22-26
28150872-6	2017	Here we investigated select ANRIL SNPs in DNA from patient-derived peripheral blood mononuclear cells obtained from 108 MM patients treated with high-dose melphalan followed by HSCT.	Melphalan	155-164	CDKN2B antisense RNA 1	Homo sapiens	28-33
28150872-8	2017	Our results indicate that ANRIL may be involved in melphalan-mediated apoptosis via down-regulating p14ARF and subsequent p53, and that the rs2151280 polymorphism may be a potential prognostic biomarker for relapse in melphalan-treated MM patients.	Melphalan	51-60	CDKN2B antisense RNA 1	Homo sapiens	26-31
28150872-8	2017	Our results indicate that ANRIL may be involved in melphalan-mediated apoptosis via down-regulating p14ARF and subsequent p53, and that the rs2151280 polymorphism may be a potential prognostic biomarker for relapse in melphalan-treated MM patients.	Melphalan	218-227	CDKN2B antisense RNA 1	Homo sapiens	26-31
27693638-0	2016	DNA-PKcs, a novel functional target of acriflavine, mediates acriflavine"s p53-dependent synergistic anti-tumor efficiency with melphalan.	Melphalan	128-137	protein kinase, DNA-activated, catalytic subunit	Homo sapiens	0-8
27693638-0	2016	DNA-PKcs, a novel functional target of acriflavine, mediates acriflavine"s p53-dependent synergistic anti-tumor efficiency with melphalan.	Melphalan	128-137	tumor protein p53	Homo sapiens	75-78
27685524-6	2016	MATERIALS AND METHODS: Melphalan (L-PAM) injected i.v.	Melphalan	23-32	peptidylglycine alpha-amidating monooxygenase	Rattus norvegicus	36-39
27091031-9	2016	Based on iron homeostasis disturbance, we postulated that prior induction of ferritin, through Nrf2 activation after oxidative stress, may be associated with the alteration of melphalan metabolism.	Melphalan	176-185	nuclear factor, erythroid derived 2, like 2	Mus musculus	95-99
26662105-12	2016	Five small molecules might be drug candidates to overcome the melphalan-induced vascular toxicity via targeting to MYC and JUN.	Melphalan	62-71	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	115-118
29207607-9	2017	Moreover, cyclin A2 depletion hypersensitized the cells to DNA damaging agents, such as cisplatin and melphalan.	Melphalan	102-111	cyclin A2	Homo sapiens	10-19
27516004-9	2017	Twenty-eight months after melphalan therapy the M-protein reappeared in the serum, and 2 months later SPD reappeared with histopathologically proven skin lesions at predilection sites.	Melphalan	26-35	myomesin 2	Homo sapiens	48-57
28092395-5	2017	Mean IOP 1 to 30 seconds after intravitreal melphalan (first injection) was 45.4 +- 14.3 mm Hg.	Melphalan	44-53	cytosolic iron-sulfur assembly component 3	Homo sapiens	5-10
27243412-5	2016	As such, etoposide and melphalan (VP16/MEL) or busulfan, cyclophosphamide, and etoposide (BuCyE) are currently being used with limited success.	Melphalan	23-32	host cell factor C1	Homo sapiens	34-38
27853638-4	2016	Melphalan treatment was able to enhance the surface expression of the stress-induced NKG2D ligands RAE-1 and MULT-1, and of the DNAM-1 ligand PVR (CD155) on MM cells, leading to better tumor cell recognition and killing by NK cells, as highlighted by NK cell increased degranulation triggered by melphalan-treated tumor cells.	Melphalan	0-9	killer cell lectin like receptor K1	Homo sapiens	85-90
27853638-4	2016	Melphalan treatment was able to enhance the surface expression of the stress-induced NKG2D ligands RAE-1 and MULT-1, and of the DNAM-1 ligand PVR (CD155) on MM cells, leading to better tumor cell recognition and killing by NK cells, as highlighted by NK cell increased degranulation triggered by melphalan-treated tumor cells.	Melphalan	0-9	ribonucleic acid export 1	Homo sapiens	99-104
27853638-4	2016	Melphalan treatment was able to enhance the surface expression of the stress-induced NKG2D ligands RAE-1 and MULT-1, and of the DNAM-1 ligand PVR (CD155) on MM cells, leading to better tumor cell recognition and killing by NK cells, as highlighted by NK cell increased degranulation triggered by melphalan-treated tumor cells.	Melphalan	0-9	CD226 molecule	Homo sapiens	128-134
27853638-4	2016	Melphalan treatment was able to enhance the surface expression of the stress-induced NKG2D ligands RAE-1 and MULT-1, and of the DNAM-1 ligand PVR (CD155) on MM cells, leading to better tumor cell recognition and killing by NK cells, as highlighted by NK cell increased degranulation triggered by melphalan-treated tumor cells.	Melphalan	0-9	PVR cell adhesion molecule	Homo sapiens	142-145
27853638-4	2016	Melphalan treatment was able to enhance the surface expression of the stress-induced NKG2D ligands RAE-1 and MULT-1, and of the DNAM-1 ligand PVR (CD155) on MM cells, leading to better tumor cell recognition and killing by NK cells, as highlighted by NK cell increased degranulation triggered by melphalan-treated tumor cells.	Melphalan	0-9	PVR cell adhesion molecule	Homo sapiens	147-152
27853638-6	2016	Furthermore, we showed that low doses of melphalan fail to induce tumor cell apoptosis, but promote the in vivo establishment of a senescent tumor cell population, harboring high levels of the stress-induced ligands RAE-1 and PVR.	Melphalan	41-50	ribonucleic acid export 1	Homo sapiens	216-221
27853638-6	2016	Furthermore, we showed that low doses of melphalan fail to induce tumor cell apoptosis, but promote the in vivo establishment of a senescent tumor cell population, harboring high levels of the stress-induced ligands RAE-1 and PVR.	Melphalan	41-50	PVR cell adhesion molecule	Homo sapiens	226-229
26827254-7	2016	RESULTS: In J82, RT4, TCCsup and 5637 UC cells, mel-flufen amplified the intracellular loading of melphalan in part via aminopeptidase N (ANPEP), resulting in increased cytotoxicity compared to melphalan alone.	Melphalan	98-107	alanyl aminopeptidase, membrane	Homo sapiens	120-136
26827254-7	2016	RESULTS: In J82, RT4, TCCsup and 5637 UC cells, mel-flufen amplified the intracellular loading of melphalan in part via aminopeptidase N (ANPEP), resulting in increased cytotoxicity compared to melphalan alone.	Melphalan	98-107	alanyl aminopeptidase, membrane	Homo sapiens	138-143
26827254-7	2016	RESULTS: In J82, RT4, TCCsup and 5637 UC cells, mel-flufen amplified the intracellular loading of melphalan in part via aminopeptidase N (ANPEP), resulting in increased cytotoxicity compared to melphalan alone.	Melphalan	194-203	alanyl aminopeptidase, membrane	Homo sapiens	138-143
26314844-8	2015	In particular, the treatment with ABCG2 McAb plus PTX-NPs induced the strongest therapeutic response and had an efficacy even better than that of melphalan/prednisone, a conventional regimen for MM patients.	Melphalan	146-155	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	34-39
26467917-7	2016	HDC was carmustine, etoposide, cytarabine, and melphalan (BEAM).	Melphalan	47-56	histidine decarboxylase	Homo sapiens	0-3
27910767-4	2016	Emerging evidence indicates that melphalan can foster an immunogenic microenvironment by inducing immunogenic cell death (ICD) as characterized by membrane translocation of endoplasmic reticulum protein calreticulin (CRT) and by release of chromatin-binding protein high-mobility group box 1 (HMGB1).	Melphalan	33-42	calreticulin	Homo sapiens	203-215
27910767-4	2016	Emerging evidence indicates that melphalan can foster an immunogenic microenvironment by inducing immunogenic cell death (ICD) as characterized by membrane translocation of endoplasmic reticulum protein calreticulin (CRT) and by release of chromatin-binding protein high-mobility group box 1 (HMGB1).	Melphalan	33-42	calreticulin	Homo sapiens	217-220
27910767-4	2016	Emerging evidence indicates that melphalan can foster an immunogenic microenvironment by inducing immunogenic cell death (ICD) as characterized by membrane translocation of endoplasmic reticulum protein calreticulin (CRT) and by release of chromatin-binding protein high-mobility group box 1 (HMGB1).	Melphalan	33-42	high mobility group box 1	Homo sapiens	266-291
27910767-4	2016	Emerging evidence indicates that melphalan can foster an immunogenic microenvironment by inducing immunogenic cell death (ICD) as characterized by membrane translocation of endoplasmic reticulum protein calreticulin (CRT) and by release of chromatin-binding protein high-mobility group box 1 (HMGB1).	Melphalan	33-42	high mobility group box 1	Homo sapiens	293-298
26414189-0	2016	Single nucleotide polymorphisms in TP53 but not KRAS or MDM2 are predictive of clinical outcome in multiple myeloma treated with high-dose melphalan and autologous stem cell support.	Melphalan	139-148	tumor protein p53	Homo sapiens	35-39
26378741-1	2015	IMPORTANCE: Intravitreous injections of melphalan hydrochloride are increasingly used in the treatment of vitreous seeding of retinoblastoma.	Melphalan	40-63	RB transcriptional corepressor 1	Homo sapiens	126-140
26622581-0	2015	Leukemia cells are sensitized to temozolomide, carmustine and melphalan by the inhibition of O6-methylguanine-DNA methyltransferase.	Melphalan	62-71	O-6-methylguanine-DNA methyltransferase	Homo sapiens	93-131
26622581-8	2015	Treatment of the cells with TMZ, BCNU or MEL in combination with O6-benzylguanine, an MGMT inhibitor, was demonstrated to sensitize the two cell lines to these agents.	Melphalan	41-44	O-6-methylguanine-DNA methyltransferase	Homo sapiens	86-90
26112942-5	2015	AIM: To study the influence of combination of enterosorption and pharmaceutical analogue of naturally occurring G-CSF (filgrastim) on bone marrow protection and the growth of grafted tumor in a case of injection of melphalan (Mel).	Melphalan	215-224	colony stimulating factor 3	Rattus norvegicus	112-117
25762540-0	2015	Antitumor immunity triggered by melphalan is potentiated by melanoma cell surface-associated calreticulin.	Melphalan	32-41	calreticulin	Homo sapiens	93-105
25762540-6	2015	Our results illustrate how melphalan triggers inflammatory cell death that can be leveraged by immunomodulators such as the danger signal calreticulin.	Melphalan	27-36	calreticulin	Homo sapiens	138-150
25621797-2	2015	Here, we report on 41 HL patients with active disease after salvage therapy and who received high-dose melphalan (HD-PAM) and auto-SCT as a bridge to a second autologous or an allogeneic transplantation between 2002 and 2013 at our center.	Melphalan	103-112	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	117-120
25477469-4	2015	We examined the effects of structural analogs of p-aminohippurate (PAH), melphalan, chlorambucil, and bendamustine, on OAT1-mediated [(3)H]PAH uptake and OAT3- and OAT4-mediated [(3)H]estrone sulfate (ES) uptake in stably transfected human embryonic kidney-293 cells.	Melphalan	73-82	solute carrier family 22 member 6	Homo sapiens	119-123
25560408-0	2015	Alkylating agent melphalan augments the efficacy of adoptive immunotherapy using tumor-specific CD4+ T cells.	Melphalan	17-26	CD4 antigen	Mus musculus	96-99
25395420-8	2015	Interestingly, RSK2 inhibition also sensitized MM cells to bortezomib, melphalan, and dexamethasone, but did not downregulate Ikaros or influence lenalidomide-mediated downregulation of tumor necrosis factor-alpha or increase lenalidomide-induced IL-2 upregulation.	Melphalan	71-80	ribosomal protein S6 kinase A3	Homo sapiens	15-19
24646553-10	2015	ADH-1 increased vascular permeability without effecting tumor interstitial fluid pressure, leading to increased delivery of LPAM but not TMZ.	Melphalan	124-128	alcohol dehydrogenase 1C (class I), gamma polypeptide	Rattus norvegicus	0-5
24385553-11	2014	CONCLUSIONS: Ophthalmic arterial melphalan infusion is a safe and effective means to treat RB.	Melphalan	33-42	RB transcriptional corepressor 1	Homo sapiens	91-93
25220100-5	2014	In 43 patients treated with melphalan and prednisolone, the overall response rate was significantly higher in the high LAT1 expression group (60.0%) than in the low LAT1 expression group (17.6%) (P = 0.03).	Melphalan	28-37	solute carrier family 7 member 5	Homo sapiens	119-123
25220100-5	2014	In 43 patients treated with melphalan and prednisolone, the overall response rate was significantly higher in the high LAT1 expression group (60.0%) than in the low LAT1 expression group (17.6%) (P = 0.03).	Melphalan	28-37	solute carrier family 7 member 5	Homo sapiens	165-169
25046000-4	2014	Seven of them (melphalan, cisplatin, vincristine, etoposide, paclitaxel, methotrexate, and cytarabine) caused the production of IL-1beta in cells pretreated with lipopolysaccharide.	Melphalan	15-24	interleukin 1 beta	Homo sapiens	128-136
25037433-4	2014	It was found that the molecular weight of O,N-carboxymethyl chitosan (O,N-CMCS) and the peptide spacer played a crucial role in controlling the drug content, diameter and drug release properties of O,N-carboxymethyl chitosan-peptide-melphalan conjugates.	Melphalan	233-242	G protein signaling modulator 2	Homo sapiens	74-78
24687382-3	2014	Using immunohistochemical (IHC) staining on paraffin-embedded bone marrow sections, the expression of CRBN protein in myeloma cells (MCs) was assessed in 40 relapsed/refractory MM (RRMM) patients who received lenalidomide/dexamethasone (LD) and 45 and 22 newly diagnosed MM (NDMM) patients who received thalidomide/dexamethasone (TD) and melphalan/bortezomib/prednisolone (MVP), respectively.	Melphalan	338-347	cereblon	Homo sapiens	102-106
25051404-6	2014	Moreover, we found that melphalan-induced apoptosis inversely correlated with the repair efficiency of the TS, with the duration of the inhibition of mRNA synthesis, phosphorylation of p53 at serine 15 and apoptosis rates being higher in responders than in non-responders (all P<0.001).	Melphalan	24-33	tumor protein p53	Homo sapiens	185-188
25007036-8	2014	Median OPN plasma level were associated with number of organs involved, renal function, eligibility for high-dose melphalan chemotherapy and autologous stem cell transplantation, and severity of cardiac amyloidosis.	Melphalan	114-123	secreted phosphoprotein 1	Homo sapiens	7-10
25042558-3	2014	Among them, compounds 8q, 8t, and 8w with excellent Chk1 inhibitory activities (IC50 values of 4.05, 6.23, and 2.33nM, respectively) displayed strong synergistic effects with melphalan, a DNA-damaging agent in the cell-based assay.	Melphalan	175-184	checkpoint kinase 1	Homo sapiens	52-56
24308434-3	2014	Sensitivity of HMCLs to both drugs was correlated to p53: the BDM and melphalan median LD50 values of TP53(wild-type) HMCLs were more than two-fold lower than those of TP53(abnormal) HMCLs (p < 0.001), and p53 silencing in TP53(wt) NCI-H929 cells inhibited BDM- and melphalan-induced cell death.	Melphalan	70-79	tumor protein p53	Homo sapiens	53-56
24308434-3	2014	Sensitivity of HMCLs to both drugs was correlated to p53: the BDM and melphalan median LD50 values of TP53(wild-type) HMCLs were more than two-fold lower than those of TP53(abnormal) HMCLs (p < 0.001), and p53 silencing in TP53(wt) NCI-H929 cells inhibited BDM- and melphalan-induced cell death.	Melphalan	70-79	tumor protein p53	Homo sapiens	102-106
24911220-1	2014	Propylene Glycol-Free melphalan HCL for Injection (PGF-Mel) is a new formulation that incorporates Captisol, a specially modified cyclodextrin, to improve melphalan stability.	Melphalan	22-31	placental growth factor	Homo sapiens	51-54
24704384-0	2014	A single nucleotide polymorphism in SLC7A5 is associated with gastrointestinal toxicity after high-dose melphalan and autologous stem cell transplantation for multiple myeloma.	Melphalan	104-113	solute carrier family 7 member 5	Homo sapiens	36-42
24913980-3	2014	Our findings indicate that sublethal doses of doxorubicin and melphalan initiate a DNA damage response (DDR) controlling ligand upregulation on MM cell lines and patient-derived malignant plasma cells in Chk1/2-dependent and p53-independent manner.	Melphalan	62-71	checkpoint kinase 1	Homo sapiens	204-208
24913980-3	2014	Our findings indicate that sublethal doses of doxorubicin and melphalan initiate a DNA damage response (DDR) controlling ligand upregulation on MM cell lines and patient-derived malignant plasma cells in Chk1/2-dependent and p53-independent manner.	Melphalan	62-71	tumor protein p53	Homo sapiens	225-228
24704384-4	2014	The amino acid transporters LAT1 and LAT2 encoded by the SLC7A5 and SLC7A8 genes, respectively, are the principal mediators of melphalan uptake into cells.	Melphalan	127-136	solute carrier family 7 member 5	Homo sapiens	28-32
24704384-4	2014	The amino acid transporters LAT1 and LAT2 encoded by the SLC7A5 and SLC7A8 genes, respectively, are the principal mediators of melphalan uptake into cells.	Melphalan	127-136	linker for activation of T cells family member 2	Homo sapiens	37-41
24704384-4	2014	The amino acid transporters LAT1 and LAT2 encoded by the SLC7A5 and SLC7A8 genes, respectively, are the principal mediators of melphalan uptake into cells.	Melphalan	127-136	solute carrier family 7 member 5	Homo sapiens	57-63
24704384-4	2014	The amino acid transporters LAT1 and LAT2 encoded by the SLC7A5 and SLC7A8 genes, respectively, are the principal mediators of melphalan uptake into cells.	Melphalan	127-136	solute carrier family 7 member 8	Homo sapiens	68-74
24746827-2	2014	We sought to develop a nonsurgical method of permanent sterilization for male animals by administering the gonadotoxicant melphalan conjugated to peptides derived from the beta-chain of FSHbeta.	Melphalan	122-131	follicle stimulating hormone beta	Mus musculus	186-193
24746827-6	2014	Of the conjugates tested, melphalan conjugated to a 20-amino acid peptide derived from human FSHbeta consisting of amino acids 33 to 53 (FSHbeta (33-53)-melphalan) was very potent, with cell cytotoxicity and lactate dehydrogenase release roughly one-half that of melphalan.	Melphalan	26-35	follicle stimulating hormone subunit beta	Homo sapiens	93-100
24746827-6	2014	Of the conjugates tested, melphalan conjugated to a 20-amino acid peptide derived from human FSHbeta consisting of amino acids 33 to 53 (FSHbeta (33-53)-melphalan) was very potent, with cell cytotoxicity and lactate dehydrogenase release roughly one-half that of melphalan.	Melphalan	26-35	follicle stimulating hormone subunit beta	Homo sapiens	137-144
24746827-6	2014	Of the conjugates tested, melphalan conjugated to a 20-amino acid peptide derived from human FSHbeta consisting of amino acids 33 to 53 (FSHbeta (33-53)-melphalan) was very potent, with cell cytotoxicity and lactate dehydrogenase release roughly one-half that of melphalan.	Melphalan	153-162	follicle stimulating hormone subunit beta	Homo sapiens	93-100
24746827-6	2014	Of the conjugates tested, melphalan conjugated to a 20-amino acid peptide derived from human FSHbeta consisting of amino acids 33 to 53 (FSHbeta (33-53)-melphalan) was very potent, with cell cytotoxicity and lactate dehydrogenase release roughly one-half that of melphalan.	Melphalan	153-162	follicle stimulating hormone subunit beta	Homo sapiens	137-144
24746827-6	2014	Of the conjugates tested, melphalan conjugated to a 20-amino acid peptide derived from human FSHbeta consisting of amino acids 33 to 53 (FSHbeta (33-53)-melphalan) was very potent, with cell cytotoxicity and lactate dehydrogenase release roughly one-half that of melphalan.	Melphalan	153-162	follicle stimulating hormone subunit beta	Homo sapiens	93-100
24746827-6	2014	Of the conjugates tested, melphalan conjugated to a 20-amino acid peptide derived from human FSHbeta consisting of amino acids 33 to 53 (FSHbeta (33-53)-melphalan) was very potent, with cell cytotoxicity and lactate dehydrogenase release roughly one-half that of melphalan.	Melphalan	153-162	follicle stimulating hormone subunit beta	Homo sapiens	137-144
24746827-8	2014	Four weeks after intraperitoneal injection, all mice treated with either FSHbeta (33-53)-melphalan or melphalan had approximately 75% reductions in testicular spermatid counts compared with control animals.	Melphalan	89-98	follicle stimulating hormone beta	Mus musculus	73-80
24706190-3	2014	Melphalan showed the best performance with bortezomib under all culture conditions tested (liquid culture, on fibronectin-coated plates, and co-culture with bone marrow stromal cells), whereas cyclophosphamide was antagonistic with bortezomib especially in the presence of stromal cells.	Melphalan	0-9	fibronectin 1	Homo sapiens	110-121
24706190-6	2014	Consistent with these results, caspase-3 was activated more strongly by melphalan than by other agents in combination with bortezomib.	Melphalan	72-81	caspase 3	Homo sapiens	31-40
24980763-2	2014	The aim of the study was to evaluate the myeloprotective possibilities of carbon enterosorbents in the case of usage of alkilating drug melphalan (L-PAM).	Melphalan	136-145	peptidylglycine alpha-amidating monooxygenase	Rattus norvegicus	149-152
24510345-11	2014	In glioma-derived cell lines, overexpression of PTPN6 caused increase resistance (p < 0.05) to the chemotherapeutic drugs bortezomib, cisplatin, and melphalan.	Melphalan	152-161	protein tyrosine phosphatase non-receptor type 6	Homo sapiens	48-53
24089038-4	2014	Following ex vivo treatment with melphalan, a gradual suppression of the apoptotic pathway occurred in samples collected at different stages of myelomagenesis, with the severity and duration of the inhibition of RNA synthesis, p53 phosphorylation at serine15 and induction of apoptosis being higher in MGUS than SMM and lowest in MM patients (all P<0.0103).	Melphalan	33-42	tumor protein p53	Homo sapiens	227-230
24849305-7	2014	The combination of bortezomib, melphalan and prednisone (VMP) was shown to significantly improve overall survival (OS) compared to melphalan and prednisone (MP, 56.4 vs. 43.1 months, p = < 0.01).	Melphalan	31-40	neurensin 1	Homo sapiens	57-60
24658332-7	2014	Importantly, both CD138++ and CD138low subpopulations have similar sensitivity to bortezomib, melphalan and doxorubicin.	Melphalan	94-103	syndecan 1	Homo sapiens	18-23
24554720-5	2014	Furthermore, we show that disabling CDK12 function in ovarian cancer cells reduces BRCA1 levels, disrupts HR repair, and sensitizes these cells to the cross-linking agents melphalan and cisplatin and to the poly(ADP-ribose) polymerase (PARP) inhibitor veliparib (ABT-888).	Melphalan	172-181	cyclin dependent kinase 12	Homo sapiens	36-41
24210940-0	2014	[Superselective intra-arterial chemotherapy with melphalan for retinoblastoma].	Melphalan	49-58	RB transcriptional corepressor 1	Homo sapiens	63-78
24281418-0	2014	SRC family kinase inhibition as a novel strategy to augment melphalan-based regional chemotherapy of advanced extremity melanoma.	Melphalan	60-69	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	0-3
24281418-3	2014	The goal of this study was to determine if Src kinase inhibition using dasatinib could enhance the efficacy of regionally administered melphalan in advanced extremity melanoma.	Melphalan	135-144	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	43-46
24400589-0	2014	Functional analysis of the involvement of apurinic/apyrimidinic endonuclease 1 in the resistance to melphalan in multiple myeloma.	Melphalan	100-109	apurinic/apyrimidinic endodeoxyribonuclease 1	Homo sapiens	42-78
24465398-7	2014	RESULTS: By univariate analysis, both melphalan and topotecan appear to be associated with changes in ERG amplitude at both 3 and 12 months; but for the most part, these changes are minimal and likely clinically insignificant.	Melphalan	38-47	ETS transcription factor ERG	Homo sapiens	102-105
24465398-8	2014	By multivariate analysis, maximum and cumulative melphalan have a modest, temporary effect on the ERG amplitude change, which is apparent at 3 months but no longer evident at 12 months after completing treatment.	Melphalan	49-58	ETS transcription factor ERG	Homo sapiens	98-101
23933759-0	2014	High-dose melphalan produces favorable response in a patient with multiple myeloma and coexisting essential thrombocythemia with JAK2 mutation.	Melphalan	10-19	Janus kinase 2	Homo sapiens	129-133
22025197-2	2013	Previous findings showed that the anticancer drugs p-N,N-bis(2-chloroethyl) amino-l-phenylalanine (melphalan, MEL) and p-N,N-bis(2-chloroethyl)aminophenylbutyric acid (chlorambucil, CAB) belonging to the nitrogen mustard group, in addition to their clastogenic activity, also exert aneugenic potential, nondisjunction and chromosome delay.	Melphalan	99-108	neural proliferation, differentiation and control 1	Homo sapiens	182-185
23932230-5	2013	Treatment of ARH-77 cells with the NF-kappaB inhibitor dimethyl fumarate or the mTOR inhibitor rapamycin suppressed NF-kappaB p65 nuclear translocation and enhanced the cytotoxic effect of melphalan.	Melphalan	189-198	low density lipoprotein receptor adaptor protein 1	Homo sapiens	13-16
23932230-5	2013	Treatment of ARH-77 cells with the NF-kappaB inhibitor dimethyl fumarate or the mTOR inhibitor rapamycin suppressed NF-kappaB p65 nuclear translocation and enhanced the cytotoxic effect of melphalan.	Melphalan	189-198	nuclear factor kappa B subunit 1	Homo sapiens	35-44
23932230-5	2013	Treatment of ARH-77 cells with the NF-kappaB inhibitor dimethyl fumarate or the mTOR inhibitor rapamycin suppressed NF-kappaB p65 nuclear translocation and enhanced the cytotoxic effect of melphalan.	Melphalan	189-198	mechanistic target of rapamycin kinase	Homo sapiens	80-84
23954667-8	2013	[(3)H]l-Leucine uptake and cellular growth activities in CMeC-1 were inhibited in a dose-dependent manner by selective LAT1 inhibitors (2-amino-2-norbornane-carboxylic acid, BCH and melphalan, LPM).	Melphalan	182-191	solute carrier family 7 member 5	Homo sapiens	119-123
23954667-8	2013	[(3)H]l-Leucine uptake and cellular growth activities in CMeC-1 were inhibited in a dose-dependent manner by selective LAT1 inhibitors (2-amino-2-norbornane-carboxylic acid, BCH and melphalan, LPM).	Melphalan	182-191	NK2 homeobox 1	Homo sapiens	174-177
23942968-9	2013	Although KZ-41 blocked both NF-kappaB- and p38 MAPK-dependent ICAM-1 stimulation; the p38 MAPK/ICAM-1 pathway appears to be the primary pathway involved in melphalan-induced REC apoptosis.	Melphalan	156-165	mitogen-activated protein kinase 14	Homo sapiens	86-89
23942968-9	2013	Although KZ-41 blocked both NF-kappaB- and p38 MAPK-dependent ICAM-1 stimulation; the p38 MAPK/ICAM-1 pathway appears to be the primary pathway involved in melphalan-induced REC apoptosis.	Melphalan	156-165	intercellular adhesion molecule 1	Homo sapiens	95-101
23942968-10	2013	CONCLUSIONS: KZ-41 protects REC against melphalan-induced upregulation of ICAM-1 and apoptosis through p38 MAPK-dependent pathways.	Melphalan	40-49	intercellular adhesion molecule 1	Homo sapiens	74-80
23942968-10	2013	CONCLUSIONS: KZ-41 protects REC against melphalan-induced upregulation of ICAM-1 and apoptosis through p38 MAPK-dependent pathways.	Melphalan	40-49	mitogen-activated protein kinase 14	Homo sapiens	103-106
24156020-1	2013	L19-tumor necrosis factor alpha (L19mTNF-alpha; L), a fusion protein consisting of mouse TNFalpha and the human antibody fragment L19 directed to the extra domain-B (ED-B) of fibronectin, is able to selectively target tumor vasculature and to exert a long-lasting therapeutic activity in combination with melphalan (M) in syngeneic mouse tumor models.	Melphalan	305-314	fibronectin 1	Mus musculus	175-186
23485394-7	2013	In addition, although Bax deficiency rendered cells resistant to PU-H71, combined treatment with the anticancer drugs cisplatin or melphalan greatly sensitized these cells to PU-H71.	Melphalan	131-140	BCL2 associated X, apoptosis regulator	Homo sapiens	22-25
23633493-4	2013	We found that an mTOR-selective kinase inhibitor, AZD8055, significantly enhanced sensitivity of a pediatric rhabdomyosarcoma xenograft to radiotherapy and sensitized rhabdomyosarcoma cells to the DNA interstrand cross-linker (ICL) melphalan.	Melphalan	232-241	mechanistic target of rapamycin kinase	Homo sapiens	17-21
23584492-7	2013	Mechanistic studies show that siRNA knockdown of aminopeptidase N, a key enzyme mediating intracellular conversion of mel-flufen to melphalan, attenuates anti-multiple myeloma activity of mel-flufen.	Melphalan	132-141	alanyl aminopeptidase, membrane	Homo sapiens	49-65
23613505-5	2013	These transfected cells, together with control RPMI-8226 cells, were treated with 20 micromol/l melphalan for 24 h. Knockdown of DEPTOR exacerbated melphalan-induced growth inhibition and apoptosis, increased levels of cleaved caspase-3 and cleaved PARP, and reduced levels of phosphor-AKT.	Melphalan	96-105	DEP domain containing MTOR interacting protein	Homo sapiens	129-135
23613505-5	2013	These transfected cells, together with control RPMI-8226 cells, were treated with 20 micromol/l melphalan for 24 h. Knockdown of DEPTOR exacerbated melphalan-induced growth inhibition and apoptosis, increased levels of cleaved caspase-3 and cleaved PARP, and reduced levels of phosphor-AKT.	Melphalan	148-157	DEP domain containing MTOR interacting protein	Homo sapiens	129-135
23613505-5	2013	These transfected cells, together with control RPMI-8226 cells, were treated with 20 micromol/l melphalan for 24 h. Knockdown of DEPTOR exacerbated melphalan-induced growth inhibition and apoptosis, increased levels of cleaved caspase-3 and cleaved PARP, and reduced levels of phosphor-AKT.	Melphalan	148-157	poly(ADP-ribose) polymerase 1	Homo sapiens	249-253
23613505-5	2013	These transfected cells, together with control RPMI-8226 cells, were treated with 20 micromol/l melphalan for 24 h. Knockdown of DEPTOR exacerbated melphalan-induced growth inhibition and apoptosis, increased levels of cleaved caspase-3 and cleaved PARP, and reduced levels of phosphor-AKT.	Melphalan	148-157	AKT serine/threonine kinase 1	Homo sapiens	286-289
22674435-8	2013	CONCLUSIONS: ILP with L19-TNF had a favorable safety and a promising activity profile at a dose of 650 microg of L19-TNF, supporting the exploration of higher L19-TNF doses and a Phase II trial comparing L19-TNF ILP with standard melphalan-containing ILP.	Melphalan	230-239	immunoglobulin kappa variable 1-12	Homo sapiens	22-29
23481354-7	2013	We determined that antisense downregulation of BRCA2 synergistically potentiated drugs with mechanisms of action related to BRCA2 function (cisplatin, melphalan), a phenomenon we named "complementary lethality."	Melphalan	151-160	BRCA2 DNA repair associated	Homo sapiens	47-52
23481354-7	2013	We determined that antisense downregulation of BRCA2 synergistically potentiated drugs with mechanisms of action related to BRCA2 function (cisplatin, melphalan), a phenomenon we named "complementary lethality."	Melphalan	151-160	BRCA2 DNA repair associated	Homo sapiens	124-129
22674435-8	2013	CONCLUSIONS: ILP with L19-TNF had a favorable safety and a promising activity profile at a dose of 650 microg of L19-TNF, supporting the exploration of higher L19-TNF doses and a Phase II trial comparing L19-TNF ILP with standard melphalan-containing ILP.	Melphalan	230-239	immunoglobulin kappa variable 1-12	Homo sapiens	113-120
22674435-8	2013	CONCLUSIONS: ILP with L19-TNF had a favorable safety and a promising activity profile at a dose of 650 microg of L19-TNF, supporting the exploration of higher L19-TNF doses and a Phase II trial comparing L19-TNF ILP with standard melphalan-containing ILP.	Melphalan	230-239	immunoglobulin kappa variable 1-12	Homo sapiens	22-25
22674435-8	2013	CONCLUSIONS: ILP with L19-TNF had a favorable safety and a promising activity profile at a dose of 650 microg of L19-TNF, supporting the exploration of higher L19-TNF doses and a Phase II trial comparing L19-TNF ILP with standard melphalan-containing ILP.	Melphalan	230-239	immunoglobulin kappa variable 1-12	Homo sapiens	113-116
22674435-8	2013	CONCLUSIONS: ILP with L19-TNF had a favorable safety and a promising activity profile at a dose of 650 microg of L19-TNF, supporting the exploration of higher L19-TNF doses and a Phase II trial comparing L19-TNF ILP with standard melphalan-containing ILP.	Melphalan	230-239	tumor necrosis factor	Homo sapiens	117-120
22453252-0	2012	Melphalan 180 mg/m2 can be safely administered as conditioning regimen before an autologous stem cell transplantation (ASCT) in multiple myeloma patients with creatinine clearance 60 mL/min/1.73 m2 or lower with use of palifermin for cytoprotection: results of a phase I trial.	Melphalan	0-9	CD59 molecule (CD59 blood group)	Homo sapiens	186-191
23689541-0	2013	Waldenstrom"s macroglobulinemia associated with serum amyloid A protein amyloidosis: pitfalls in diagnosis and successful treatment with melphalan-based autologous stem cell transplant.	Melphalan	137-146	serum amyloid A1	Homo sapiens	48-71
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.	Melphalan	156-165	glutathione S-transferase kappa 1	Homo sapiens	10-35
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.	Melphalan	158-167	TNF receptor superfamily member 17	Homo sapiens	82-86
22781767-10	2012	The miRNA-15a/-16 expressions of myeloma cells were up-regulated after the treatment of melphalan and bortezomib (all P < 0.05).	Melphalan	88-97	microRNA 15a	Homo sapiens	4-13
22653969-5	2012	The Chk1/2 inhibitor AZD7762 potentiated the antiproliferative effects of bendamustine, melphalan, and doxorubicin but not bortezomib in multiple myeloma cell lines that were p53-deficient.	Melphalan	88-97	checkpoint kinase 1	Homo sapiens	4-8
22653969-8	2012	In summary, the cytotoxic effects of bendamustine, melphalan and doxorubicin on p53-deficient multiple myeloma cell lines were enhanced by the coadministration of AZD7762.	Melphalan	51-60	tumor protein p53	Homo sapiens	80-83
22474168-4	2012	Unexpectedly, A2A and beta2AR agonists also synergize with melphalan, lenalidomide, bortezomib, and doxorubicin.	Melphalan	59-68	immunoglobulin kappa variable 2D-29	Homo sapiens	14-17
22474168-4	2012	Unexpectedly, A2A and beta2AR agonists also synergize with melphalan, lenalidomide, bortezomib, and doxorubicin.	Melphalan	59-68	adrenoceptor beta 2	Homo sapiens	22-29
22356805-0	2012	Melphalan exposure induces an interleukin-6 deficit in bone marrow stromal cells and osteoblasts.	Melphalan	0-9	interleukin 6	Homo sapiens	30-43
22356805-8	2012	Decreased IL-6 protein is the most pronounced following melphalan exposure compared to several other chemotherapeutic agents tested.	Melphalan	56-65	interleukin 6	Homo sapiens	10-14
22356805-9	2012	We also observed that melphalan decreased IL-6 mRNA in both BMSC and HOB.	Melphalan	22-31	interleukin 6	Homo sapiens	42-46
22356805-10	2012	Finally, using a model of BMSC or HOB co-cultured with myeloma cells exposed to melphalan, we observed that IL-6 protein was also decreased, consistent with treatment of adherent cells alone.	Melphalan	80-89	interleukin 6	Homo sapiens	108-112
22139971-4	2012	In this study, we evaluated the association between genetic variations in the VEGF gene in patients with multiple myeloma and time to treatment failure (TTF) after high-dose melphalan and stem cell support (HDT), overall survival (OS) and efficacy of the anti-angiogenic drug thalidomide.	Melphalan	174-183	vascular endothelial growth factor A	Homo sapiens	78-82
22415970-8	2012	The treatment with RSV or MEL increased the levels of p-Chk2.	Melphalan	26-29	checkpoint kinase 2	Homo sapiens	56-60
22415970-11	2012	While the levels of cyclin dependent kinase 2 (CDK2) remained unchanged by treatments, its active form (Thr(160) -phosphorylated CDK2) was decreased by treatment with RSV and by the combination of RSV with MEL.	Melphalan	206-209	cyclin dependent kinase 2	Homo sapiens	20-45
22415970-11	2012	While the levels of cyclin dependent kinase 2 (CDK2) remained unchanged by treatments, its active form (Thr(160) -phosphorylated CDK2) was decreased by treatment with RSV and by the combination of RSV with MEL.	Melphalan	206-209	cyclin dependent kinase 2	Homo sapiens	129-133
22415970-12	2012	The activity of CDK7, kinase that phosphorylates CDK2 at Thr(160), was inhibited by RSV and by the combination of RSV with MEL.	Melphalan	123-126	cyclin dependent kinase 7	Homo sapiens	16-20
22415970-12	2012	The activity of CDK7, kinase that phosphorylates CDK2 at Thr(160), was inhibited by RSV and by the combination of RSV with MEL.	Melphalan	123-126	cyclin dependent kinase 2	Homo sapiens	49-53
22427570-7	2012	Both melphalan and carboplatin triggered human retinal endothelial cell migration, proliferation, apoptosis, and increased expression of adhesion proteins intracellullar adhesion molecule-1 [ICAM-1] and soluble chemotactic factors (IL-8).	Melphalan	5-14	intercellular adhesion molecule 1	Homo sapiens	191-197
22427570-7	2012	Both melphalan and carboplatin triggered human retinal endothelial cell migration, proliferation, apoptosis, and increased expression of adhesion proteins intracellullar adhesion molecule-1 [ICAM-1] and soluble chemotactic factors (IL-8).	Melphalan	5-14	C-X-C motif chemokine ligand 8	Homo sapiens	232-236
21378390-0	2011	Melphalan as a treatment for BRCA-related ovarian carcinoma: can you teach an old drug new tricks?	Melphalan	0-9	BRCA1 DNA repair associated	Homo sapiens	29-33
22301101-4	2012	In particular, GDF15 conferred resistance to melphalan, bortezomib, and to a lesser extent, lenalidomide in both stroma-dependent and stroma-independent multiple myeloma cells.	Melphalan	45-54	growth differentiation factor 15	Homo sapiens	15-20
21358679-10	2012	Overall, our results suggest that meaningful long-term survival rates and disease control can be achieved with acceptable non-relapse mortality in patients with mature T-cell lymphomas, including CTCL using reduced-intensity conditioning with melphalan and fludarabine.	Melphalan	243-252	TSPY like 2	Homo sapiens	196-200
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.	Melphalan	59-68	interleukin 2 receptor, alpha chain	Mus musculus	188-193
22363485-3	2012	We determined that treatment of human primary osteoblasts (HOB) with melphalan or VP-16 resulted in increased phospho-Smad2, consistent with increased TGF-beta1 activity.	Melphalan	69-78	SMAD family member 2	Homo sapiens	118-123
22363485-3	2012	We determined that treatment of human primary osteoblasts (HOB) with melphalan or VP-16 resulted in increased phospho-Smad2, consistent with increased TGF-beta1 activity.	Melphalan	69-78	transforming growth factor beta 1	Homo sapiens	151-160
21860026-3	2011	CRBN depletion is initially cytotoxic to human myeloma cells, but surviving cells with stable CRBN depletion become highly resistant to both lenalidomide and pomalidomide, but not to the unrelated drugs bortezomib, dexamethasone, and melphalan.	Melphalan	234-243	cereblon	Homo sapiens	0-4
22781604-11	2012	G-CSF alone could obtain satisfactory mobilization results and most of patients well tolerated to the conditioning regimen of melphalan doses from 140 mg/m(2) to 200 mg/m(2).	Melphalan	126-135	colony stimulating factor 3	Homo sapiens	0-5
21863286-2	2011	We present a case of a 3-month-old girl with Munc13-4 mutation (FHL3), who underwent bone marrow transplantation (BMT) from her human leukocyte antigen-haploidentical mother following reduced intensity conditioning (RIC) with fludarabine, melphalan, and busulfan.	Melphalan	239-248	unc-13 homolog D	Homo sapiens	45-53
21599548-0	2011	CD4(+) CD28(+) lymphocytes on day 5 after high-dose melphalan for multiple myeloma predict a low risk of infections during severe neutropenia and are associated with the number of reinfused T lymphocytes of the autologous stem cell graft.	Melphalan	52-61	CD4 molecule	Homo sapiens	0-3
21599548-0	2011	CD4(+) CD28(+) lymphocytes on day 5 after high-dose melphalan for multiple myeloma predict a low risk of infections during severe neutropenia and are associated with the number of reinfused T lymphocytes of the autologous stem cell graft.	Melphalan	52-61	CD28 molecule	Homo sapiens	7-11
21863286-2	2011	We present a case of a 3-month-old girl with Munc13-4 mutation (FHL3), who underwent bone marrow transplantation (BMT) from her human leukocyte antigen-haploidentical mother following reduced intensity conditioning (RIC) with fludarabine, melphalan, and busulfan.	Melphalan	239-248	four and a half LIM domains 3	Homo sapiens	64-68
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.	Melphalan	91-100	CD44 molecule (Indian blood group)	Homo sapiens	150-154
21799030-3	2011	Here we report that chromogranin A (CgA), a protein present in variable amounts in the blood of normal subjects and cancer patients, inhibits the synergism of NGR-TNF with doxorubicin and melphalan in mouse models of lymphoma and melanoma.	Melphalan	188-197	chromogranin A	Homo sapiens	20-34
21799030-3	2011	Here we report that chromogranin A (CgA), a protein present in variable amounts in the blood of normal subjects and cancer patients, inhibits the synergism of NGR-TNF with doxorubicin and melphalan in mouse models of lymphoma and melanoma.	Melphalan	188-197	chromogranin A	Homo sapiens	36-39
21042310-1	2011	We evaluated the efficacy and safety of the conditioning regimen that consisted of TBI and melphalan (L-PAM), followed by hematopoietic SCT (HSCT) in 23 children with advanced hematological malignancies.	Melphalan	91-100	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	104-107
21241278-2	2011	We therefore sought to determine whether the IL-6-neutralizing monoclonal antibody siltuximab, formerly CNTO 328, could enhance the activity of melphalan, and to examine some of the mechanisms underlying this interaction.	Melphalan	144-153	interleukin 6	Homo sapiens	45-49
21288924-5	2011	RESULTS: We showed that DNA-damaging drugs, doxorubicin and melphalan, induce caspase-dependent apoptosis and concurrently trigger Beclin 1-regulated autophagy in human MM cell lines H929 and RPMI 8226.	Melphalan	60-69	beclin 1	Homo sapiens	131-139
21474670-4	2011	Functionally, we have found that shRNA-mediated silencing of ITGB7 reduces MM-cell adhesion to extra-cellular matrix elements (fibronectin, E-cadherin) and reverses cell-adhesion-mediated drug resistance (CAM-DR) sensitizing them to bortezomib and melphalan.	Melphalan	248-257	integrin subunit beta 7	Homo sapiens	61-66
21241278-5	2011	Siltuximab with melphalan enhanced activation of caspase-8, caspase-9, and the downstream effector caspase-3 compared with either of the single agents.	Melphalan	16-25	caspase 8	Homo sapiens	49-58
21241278-5	2011	Siltuximab with melphalan enhanced activation of caspase-8, caspase-9, and the downstream effector caspase-3 compared with either of the single agents.	Melphalan	16-25	caspase 9	Homo sapiens	60-69
21241278-5	2011	Siltuximab with melphalan enhanced activation of caspase-8, caspase-9, and the downstream effector caspase-3 compared with either of the single agents.	Melphalan	16-25	caspase 3	Homo sapiens	99-108
21156464-1	2010	PURPOSE: Aggressive treatment of amyloid light chain (AL) amyloidosis with high-dose intravenous melphalan followed by autologous stem cell transplantation (HDM/SCT) is effective in inducing hematologic remission and clinical improvement.	Melphalan	97-106	secretin	Homo sapiens	161-164
21198861-3	2011	The highest cytotoxic effect was seen when the TKI was followed by MEL; our results indicate that inhibition of BCR/ABL activity by IM increased the cytotoxicity of MEL by favoring the DNA damage induced by this drug and by shortening the time for DNA repair at the G2/M checkpoint.	Melphalan	67-70	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
21198861-5	2011	The drugs association was further tested in a type of BaF3 cells (TonB.210) where the BCR-ABL expression is inducible by doxycycline; in this model it was confirmed that a reduction of BCR/ABL activity resulted in an increased susceptibility to the cytotoxic effect of MEL.	Melphalan	269-272	BCR activator of RhoGEF and GTPase	Homo sapiens	86-89
21198861-5	2011	The drugs association was further tested in a type of BaF3 cells (TonB.210) where the BCR-ABL expression is inducible by doxycycline; in this model it was confirmed that a reduction of BCR/ABL activity resulted in an increased susceptibility to the cytotoxic effect of MEL.	Melphalan	269-272	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-93
21198861-5	2011	The drugs association was further tested in a type of BaF3 cells (TonB.210) where the BCR-ABL expression is inducible by doxycycline; in this model it was confirmed that a reduction of BCR/ABL activity resulted in an increased susceptibility to the cytotoxic effect of MEL.	Melphalan	269-272	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	185-192
21129433-4	2011	Exposure to melphalan induced an early burst of the pro-inflammatory cytokines interleukin (IL)-1beta, IL-6 and IL-23 in airways, followed by extensive infiltration of neutrophils in the lung tissue and airways within 24h.	Melphalan	12-21	interleukin 1 beta	Mus musculus	79-101
21129433-4	2011	Exposure to melphalan induced an early burst of the pro-inflammatory cytokines interleukin (IL)-1beta, IL-6 and IL-23 in airways, followed by extensive infiltration of neutrophils in the lung tissue and airways within 24h.	Melphalan	12-21	interleukin 6	Mus musculus	103-107
21129433-4	2011	Exposure to melphalan induced an early burst of the pro-inflammatory cytokines interleukin (IL)-1beta, IL-6 and IL-23 in airways, followed by extensive infiltration of neutrophils in the lung tissue and airways within 24h.	Melphalan	12-21	interleukin 23, alpha subunit p19	Mus musculus	112-117
20683012-5	2010	RT-qPCR was performed to confirm whether E7 biomarkers would be modulated by melphalan treatment in E7-Tg mice, revealing that up-regulated E7 markers such as cyclin B1, CD166, and actin alpha1 were down-regulated, whereas expression of down-regulated E7 markers such as vimentin was restored by melphalan treatment.	Melphalan	77-86	cyclin B1	Mus musculus	159-168
20429035-9	2010	CONCLUSIONS: In the case of locally advanced disease, the addition of low-dose TNF to melphalan-based isolated limb perfusion appears safe and particularly useful.	Melphalan	86-95	tumor necrosis factor	Homo sapiens	79-82
20447761-7	2010	Furthermore, studies on DNA damage response revealed that phospho-histone H2A.X (gammaH2A.X), a hall marker of DNA double strand break, along with phosphorylated CHK1 (P-CHK1) and CHK2 (P-CHK2) was dramatically induced by SNDX-275 or melphalan.	Melphalan	234-243	checkpoint kinase 1	Homo sapiens	162-166
20683012-5	2010	RT-qPCR was performed to confirm whether E7 biomarkers would be modulated by melphalan treatment in E7-Tg mice, revealing that up-regulated E7 markers such as cyclin B1, CD166, and actin alpha1 were down-regulated, whereas expression of down-regulated E7 markers such as vimentin was restored by melphalan treatment.	Melphalan	77-86	activated leukocyte cell adhesion molecule	Mus musculus	170-175
20067771-0	2010	The alkylating prodrug J1 can be activated by aminopeptidase N, leading to a possible target directed release of melphalan.	Melphalan	113-122	alanyl aminopeptidase, membrane	Homo sapiens	46-62
20221597-6	2010	Furthermore, intraperitoneal (ip) administration of a very small amount of melphalan (L: -phenylalanine mustard; L: -PAM) (0.25 mg/kg) in LPS-stimulated 33D1(+) DC-deleted mice helped to induce H-2K(b)-restricted epitope-specific CD8(+) cytotoxic T lymphocytes (CTLs) among tumor-infiltrating lymphocytes against already established syngeneic E.G7-OVA lymphoma.	Melphalan	75-84	histocompatibility 2, K1, K region	Mus musculus	194-200
20466543-2	2010	Several analogs had K(i) values in the range 2.1-8.5 microM with greater affinities than that of either L-phenylalanine (K(i)=11 microM) or melphalan (K(i)=55 microM), but lower than DL-2-NAM-7 (K(i)=0.08 microM).	Melphalan	140-149	SH3 and cysteine rich domain 3	Homo sapiens	188-191
20514414-9	2010	These results suggest that melphalan inhibits carcinogenesis via modulating K-ras-specific genes and proteins expressed in the lung tissues of K-ras Tg mice.	Melphalan	27-36	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	76-81
20514414-9	2010	These results suggest that melphalan inhibits carcinogenesis via modulating K-ras-specific genes and proteins expressed in the lung tissues of K-ras Tg mice.	Melphalan	27-36	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	143-148
20012043-1	2010	High-dose melphalan chemotherapy and autologous peripheral blood stem cell transplantation (HDM/SCT) has been shown to result in a durable hematologic response and prolonged overall survival in systemic amyloid light-chain (AL) amyloidosis as well as multiple myeloma.	Melphalan	10-19	secretin	Homo sapiens	96-99
20028416-9	2010	These data show impressive synergistic action of the novel HSP90 inhibitor NVP-AUY922 with melphalan, doxorubicin, NVP-LBH589, and SAHA in multiple myeloma and build the frame work for clinical trials.	Melphalan	91-100	heat shock protein 90 alpha family class A member 1	Homo sapiens	59-64
21122307-8	2010	RESULTS: Melphalan treatment induced 45% of CD45(+) and 30% of CD45(-) U266 cells apoptosis.	Melphalan	9-18	protein tyrosine phosphatase receptor type C	Homo sapiens	44-48
21122307-8	2010	RESULTS: Melphalan treatment induced 45% of CD45(+) and 30% of CD45(-) U266 cells apoptosis.	Melphalan	9-18	protein tyrosine phosphatase receptor type C	Homo sapiens	63-67
21122307-12	2010	After melphalan treatment, 60% of the CD45(+) U266 cells lost MMP, while only 30% of CD45(-) U266 cells, and 10% of control cells did so.	Melphalan	6-15	protein tyrosine phosphatase receptor type C	Homo sapiens	38-42
19922338-1	2009	A male patient with primary AL amyloidosis who had been suffering from systemic lymphadenopathy with IgMkappa-type M-proteinemia received two courses of VAD and high-dose melphalan with in vivo elimination of CD20(+) cells using rituximab followed by autologous peripheral blood stem cell transplantation.	Melphalan	171-180	keratin 20	Homo sapiens	209-213
19858394-0	2009	VMP (Bortezomib, Melphalan, and Prednisone) is active and well tolerated in newly diagnosed patients with multiple myeloma with moderately impaired renal function, and results in reversal of renal impairment: cohort analysis of the phase III VISTA study.	Melphalan	17-26	neurensin 1	Homo sapiens	0-3
19934314-5	2009	Specifically, our findings point to constitutive phosphorylation of IkappaB kinase alpha and subsequent alterations in FANCD2 expression and function as underlying events leading to melphalan resistance in repeatedly exposed multiple myeloma cells.	Melphalan	182-191	component of inhibitor of nuclear factor kappa B kinase complex	Homo sapiens	68-88
19934314-5	2009	Specifically, our findings point to constitutive phosphorylation of IkappaB kinase alpha and subsequent alterations in FANCD2 expression and function as underlying events leading to melphalan resistance in repeatedly exposed multiple myeloma cells.	Melphalan	182-191	FA complementation group D2	Homo sapiens	119-125
20149656-4	2010	Methyl N-arylfumaramates showed the highest cytotoxic potencies and, in particular, methyl N-(3,4-dichlorophenyl)fumaramate is six times more potent than melphalan towards L1210 cells and is equipotent with this drug in the Molt 4/C8 assay.	Melphalan	154-163	cell division cycle associated 3	Mus musculus	224-233
20124446-10	2010	Furthermore, V1810 reverses NF-kappaB activation induced by the genotoxic drugs melphalan and doxorubicin.	Melphalan	80-89	nuclear factor kappa B subunit 1	Homo sapiens	28-37
20124446-13	2010	Moreover, V1810 reverses NF-kappaB activation by alkylating drugs and overcomes NF-kappaB-mediated resistance to melphalan.	Melphalan	113-122	nuclear factor kappa B subunit 1	Homo sapiens	80-89
20008842-8	2010	RESULTS: Three alkylators-chlorambucil, melphalan, and nimustine-displayed strong and specific toxicity against BRCA2-deficient cells.	Melphalan	40-49	breast cancer 2, early onset	Mus musculus	112-117
19098271-3	2009	In this study, we show that myeloma cells treated with low doses of therapeutic agents commonly used in the management of patients with MM, such as doxorubicin, melphalan, and bortezomib, up-regulate DNAM-1 and NKG2D ligands.	Melphalan	161-170	CD226 molecule	Homo sapiens	200-206
19447222-11	2009	In conclusion, tumor-specific variations in the expression of the efflux transporter MDR1, but not of the influx transporter LAT1, affect the intracellular accumulation of melphalan and thus determine its cytotoxicity.	Melphalan	172-181	ATP binding cassette subfamily B member 1	Homo sapiens	85-89
19362368-6	2009	Moreover, H3K9 acetylation at c-myc and CCND1 promoters was increased in individual MM patients after melphalan treatment.	Melphalan	102-111	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	30-35
19362368-6	2009	Moreover, H3K9 acetylation at c-myc and CCND1 promoters was increased in individual MM patients after melphalan treatment.	Melphalan	102-111	cyclin D1	Homo sapiens	40-45
19900371-0	2009	[The significance and function of IFN-gamma on the changes of peripheral blood platelet count during tumor-rejection induced by a low dose of melphalan in C57BL/6 mice].	Melphalan	142-151	interferon gamma	Mus musculus	34-43
19900371-1	2009	AIM: To investigate the significance and function of IFN-gamma on the changes of peripheral blood platelet count during tumor-rejection induced by a low dose of melphalan in C57BL/6 mice.	Melphalan	161-170	interferon gamma	Mus musculus	53-62
19900371-11	2009	The number of blood PLT in IFN-gamma(+/-) mice increased to (1935+/-378) x 10(9)/L 6 h after melphalan treatment, significantly higher than before (P<0.01); While in IFN-gamma(-/-) mice it was (1183+/-186) x 10(9)/L 6 h after melphalan treatment, no obvious increase than before.	Melphalan	93-102	interferon gamma	Mus musculus	27-36
19900371-11	2009	The number of blood PLT in IFN-gamma(+/-) mice increased to (1935+/-378) x 10(9)/L 6 h after melphalan treatment, significantly higher than before (P<0.01); While in IFN-gamma(-/-) mice it was (1183+/-186) x 10(9)/L 6 h after melphalan treatment, no obvious increase than before.	Melphalan	229-238	interferon gamma	Mus musculus	27-36
19900371-12	2009	There was significant difference in blood PLT 6 h after melphalan treatment between IFN-gamma(+/-) and IFN-gamma(-/-) mice (P<0.01).	Melphalan	56-65	interferon gamma	Mus musculus	84-93
19900371-16	2009	These data indicated that the increase of blood PLT count was related to the function of IFN-gamma in tumor-bearing mice in vivo during tumor rejection induced by a low dose of melphalan.	Melphalan	177-186	interferon gamma	Mus musculus	89-98
19572781-7	2009	A single intraperitoneal injection of dexamethasone (10 mg/kg body weight) 1 hour after melphalan exposure significantly reduced interleukin (IL)-1 and IL-6 in bronchoalveolar lavage fluid (BALF) and diminished the acute airway inflammation.	Melphalan	88-97	interleukin 1 complex	Mus musculus	129-147
19572781-7	2009	A single intraperitoneal injection of dexamethasone (10 mg/kg body weight) 1 hour after melphalan exposure significantly reduced interleukin (IL)-1 and IL-6 in bronchoalveolar lavage fluid (BALF) and diminished the acute airway inflammation.	Melphalan	88-97	interleukin 6	Mus musculus	152-156
19447222-5	2009	High expression of the efflux transporter MDR1 was associated with low intracellular accumulation and low cytotoxicity of melphalan (r(2)=0.56, P=0.03 and r(2)=0.62, P=0.02, respectively).	Melphalan	122-131	ATP binding cassette subfamily B member 1	Homo sapiens	42-46
19447222-7	2009	In addition, the MDR1 overexpressing HL-60 cell line showed 10-fold higher resistance to melphalan than the non-MDR1 expressing one.	Melphalan	89-98	ATP binding cassette subfamily B member 1	Homo sapiens	17-21
19447222-10	2009	Down-regulation of LAT1 by siRNA reduced the melphalan uptake by 58% and toxicity by 3.5-fold, but natural variation in expression between the tumor cell lines was not associated with accumulation or cytotoxicity of melphalan.	Melphalan	45-54	solute carrier family 7 member 5	Homo sapiens	19-23
19417135-1	2009	The repair of melphalan-induced N-alkylpurine monoadducts and interstrand cross-links was examined in different repair backgrounds, focusing on four genes (beta-actin, p53, N-ras, and delta-globin) with dissimilar transcription activities.	Melphalan	14-23	POTE ankyrin domain family member F	Homo sapiens	156-166
19417135-1	2009	The repair of melphalan-induced N-alkylpurine monoadducts and interstrand cross-links was examined in different repair backgrounds, focusing on four genes (beta-actin, p53, N-ras, and delta-globin) with dissimilar transcription activities.	Melphalan	14-23	tumor protein p53	Homo sapiens	168-171
19417135-1	2009	The repair of melphalan-induced N-alkylpurine monoadducts and interstrand cross-links was examined in different repair backgrounds, focusing on four genes (beta-actin, p53, N-ras, and delta-globin) with dissimilar transcription activities.	Melphalan	14-23	NRAS proto-oncogene, GTPase	Homo sapiens	173-178
19375650-7	2009	RESULTS: Combined treatment of AS101 with melphalan in vitro resulted in a synergistic inhibitory effect on growth, G(2)/M phase growth arrest, reduced IgG(2b) secretion, apoptotic cell death, and reduced fibronectin-mediated adhesion of MM cells.	Melphalan	42-51	immunoglobulin heavy constant gamma 2B	Mus musculus	152-158
19375650-7	2009	RESULTS: Combined treatment of AS101 with melphalan in vitro resulted in a synergistic inhibitory effect on growth, G(2)/M phase growth arrest, reduced IgG(2b) secretion, apoptotic cell death, and reduced fibronectin-mediated adhesion of MM cells.	Melphalan	42-51	fibronectin 1	Mus musculus	205-216
19375650-9	2009	Combined treatment using AS101 and low dose of melphalan in vivo resulted in modest survival improvement of myeloma-bearing mice and in reduced IgG(2b) and VEGF serum levels.	Melphalan	47-56	immunoglobulin heavy constant gamma 2B	Mus musculus	144-150
19375650-9	2009	Combined treatment using AS101 and low dose of melphalan in vivo resulted in modest survival improvement of myeloma-bearing mice and in reduced IgG(2b) and VEGF serum levels.	Melphalan	47-56	vascular endothelial growth factor A	Mus musculus	156-160
19098271-3	2009	In this study, we show that myeloma cells treated with low doses of therapeutic agents commonly used in the management of patients with MM, such as doxorubicin, melphalan, and bortezomib, up-regulate DNAM-1 and NKG2D ligands.	Melphalan	161-170	killer cell lectin like receptor K1	Homo sapiens	211-216
19406725-1	2009	BACKGROUND: Initial analysis of the combination melphalan, prednisone, plus lenalidomide (MPR) showed significant antimyeloma activity in patients with untreated multiple myeloma, with neutropenia and thrombocytopenia as the most frequent side effects.	Melphalan	48-57	progesterone receptor membrane component 1	Homo sapiens	90-93
19590992-1	2009	A male patient with primary AL amyloidosis who had been suffering from systemic lymphadenopathy with IgMkappa-type M-proteinemia received two courses of VAD and high-dose melphalan with in vivo elimination of CD20(+) cells using rituximab followed by autologous peripheral blood stem cell transplantation.	Melphalan	171-180	keratin 20	Homo sapiens	209-213
19190342-6	2009	Uptake of the organic cation [(3)H]MPP (4-methyl-pyridinium iodide) into these cells and also into hOCT3 stably transfected Chinese hamster ovary (CHO) cells was inhibited by irinotecan, vincristine, and melphalan.	Melphalan	204-213	solute carrier family 22 member 3	Homo sapiens	99-104
19190342-10	2009	Melphalan produced 20% to 30% more inhibition in hOCT3-expressing cells compared with nonexpressing control cells.	Melphalan	0-9	solute carrier family 22 member 3	Homo sapiens	49-54
20067882-7	2009	In this study we shown down regulation of Shc and FAK proteins in cells treated with echistatin and melphalan.	Melphalan	100-109	SHC adaptor protein 1	Homo sapiens	42-45
19200007-4	2009	The inhibition of P-gp in MM patients treated with melphalan (PAM) has been associated to increased toxicity, whereas defective apoptosis due to down-modulation of the NF-kB is a feature of MDR+ myeloma cells.	Melphalan	51-60	ATP binding cassette subfamily B member 1	Homo sapiens	18-22
19707399-3	2009	In the near future melphalan-prednisone-lenalidomide (Revlimid((R)), MPR) will also provide a third therapeutic option (MPT, MPV, and MPR), in elderly multiple myeloma, eventually.	Melphalan	19-28	progesterone receptor membrane component 1	Homo sapiens	134-137
20067882-7	2009	In this study we shown down regulation of Shc and FAK proteins in cells treated with echistatin and melphalan.	Melphalan	100-109	protein tyrosine kinase 2	Homo sapiens	50-53
18852129-8	2008	Melphalan, but not camptothecin, caused similar inhibition of GA-induced HSF-1-mediated Hsp70 up-regulation.	Melphalan	0-9	heat shock transcription factor 1	Homo sapiens	73-78
19020753-7	2008	Treatment with anti-myeloma drugs (melphalan, dexamethasone, bortezomib and immunomodulatory compounds) induced apoptosis earlier in D1 transfectants compared with RPMI8226 and mock control via the activation of both caspase-8 and -9.	Melphalan	35-44	caspase 8	Homo sapiens	217-233
18981585-5	2008	LAT1-mediated [3H]L-phenylalanine (Phe) uptake by TR-iBRB2 cells was inhibited in a competitive manner by tyrosine-mustard and phenylglycine-mustard as well as melphalan (phenylalanine-mustard).	Melphalan	160-169	solute carrier family 7 member 5	Rattus norvegicus	0-4
18953432-9	2008	Further, inducible expression of p16(INK4a) sensitized a melanoma cell line to death induced by melphalan or actinomycin-D.	Melphalan	96-105	cyclin dependent kinase inhibitor 2A	Homo sapiens	33-36
18953432-9	2008	Further, inducible expression of p16(INK4a) sensitized a melanoma cell line to death induced by melphalan or actinomycin-D.	Melphalan	96-105	cyclin dependent kinase inhibitor 2A	Homo sapiens	37-42
18656534-3	2008	Only a few drugs (less than 10) are substrates of LAT1 and LAT2, including L-DOPA, alpha-methyldopa, melphalan, and gabapentin.	Melphalan	101-110	solute carrier family 7 member 5	Homo sapiens	50-54
18999930-2	2008	In this paper, we report on the modification of the anticancer drugs, methotrexate (MTX) and melphalan (L-PAM), covalently linked to PEGs for drug delivery.	Melphalan	93-102	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	106-109
18852129-8	2008	Melphalan, but not camptothecin, caused similar inhibition of GA-induced HSF-1-mediated Hsp70 up-regulation.	Melphalan	0-9	heat shock protein family A (Hsp70) member 4	Homo sapiens	88-93
18503584-6	2008	Inhibition of the HSP70 expression decreased 8226 cell adhesion to stroma or FN and induced more apoptosis in FN-adhered 8226 cells than in suspension cultures at 24 h. Further, HSP70 inhibitors enhanced melphalan-induced apoptosis and reversed melphalan-induced cell adhesion-mediated drug resistance (CAM-DR) phenotype.	Melphalan	204-213	heat shock protein family A (Hsp70) member 4	Homo sapiens	18-23
18503584-6	2008	Inhibition of the HSP70 expression decreased 8226 cell adhesion to stroma or FN and induced more apoptosis in FN-adhered 8226 cells than in suspension cultures at 24 h. Further, HSP70 inhibitors enhanced melphalan-induced apoptosis and reversed melphalan-induced cell adhesion-mediated drug resistance (CAM-DR) phenotype.	Melphalan	204-213	heat shock protein family A (Hsp70) member 4	Homo sapiens	178-183
18503584-6	2008	Inhibition of the HSP70 expression decreased 8226 cell adhesion to stroma or FN and induced more apoptosis in FN-adhered 8226 cells than in suspension cultures at 24 h. Further, HSP70 inhibitors enhanced melphalan-induced apoptosis and reversed melphalan-induced cell adhesion-mediated drug resistance (CAM-DR) phenotype.	Melphalan	245-254	heat shock protein family A (Hsp70) member 4	Homo sapiens	18-23
18503584-6	2008	Inhibition of the HSP70 expression decreased 8226 cell adhesion to stroma or FN and induced more apoptosis in FN-adhered 8226 cells than in suspension cultures at 24 h. Further, HSP70 inhibitors enhanced melphalan-induced apoptosis and reversed melphalan-induced cell adhesion-mediated drug resistance (CAM-DR) phenotype.	Melphalan	245-254	heat shock protein family A (Hsp70) member 4	Homo sapiens	178-183
18575761-7	2008	The results also demonstrate that MUC1: i) contributes to KMS28PE cell proliferation, and ii) protects against apoptosis and loss of self-renewal in the response to melphalan and dexamethasone.	Melphalan	165-174	mucin 1, cell surface associated	Homo sapiens	34-38
18483261-3	2008	N-cadherin-expressing human melanoma-derived cell lines were used to generate xenografts in animal models to study isolated limb infusion with melphalan and systemic chemotherapy with temozolomide.	Melphalan	143-152	cadherin 2	Homo sapiens	0-10
18083229-5	2008	Further, we demonstrate that the sole incubation of MM cells with melphalan or doxorubicin leads to a vast activation of NFkappaB activity.	Melphalan	66-75	nuclear factor kappa B subunit 1	Homo sapiens	121-129
18083229-6	2008	Additionally, we show that the co-incubation of bortezomib with melphalan or doxorubicin reduces activation of NFkappaB.	Melphalan	64-73	nuclear factor kappa B subunit 1	Homo sapiens	111-119
18083229-7	2008	These data suggest that the drug-sensitizing effect of bortezomib on MM cells is due to inhibition of melphalan- and doxorubicin-induced activation of NFkappaB activity.	Melphalan	102-111	nuclear factor kappa B subunit 1	Homo sapiens	151-159
17899085-10	2008	Cytotoxicity of cisplatin, chlorambucil, and melphalan was enhanced 1.8-2.7-fold by HEL at 10 muM.	Melphalan	45-54	latexin	Homo sapiens	94-97
17989720-1	2008	We investigated the hypothesis that gemtuzumab ozogamicin (GO), an anti-CD33 immunotoxin would improve the efficacy of fludarabine/melphalan as a preparative regimen for allogeneic hematopoietic stem cell transplantation (HSCT) in a phase I/II trial.	Melphalan	131-140	CD33 molecule	Homo sapiens	72-76
18843977-7	2008	BDNF protected KM3 cells from melphalan and vincristine.	Melphalan	30-39	brain derived neurotrophic factor	Homo sapiens	0-4
18843977-8	2008	The viability of KM3 cells exposed to varying concentrations of melphalan with and without 50 microg/L BDNF showed that BDNF induced almost a 2-fold and a 3-fold increase in melphalan and vincristine toxicity respectively.	Melphalan	64-73	brain derived neurotrophic factor	Homo sapiens	120-124
18843977-8	2008	The viability of KM3 cells exposed to varying concentrations of melphalan with and without 50 microg/L BDNF showed that BDNF induced almost a 2-fold and a 3-fold increase in melphalan and vincristine toxicity respectively.	Melphalan	174-183	brain derived neurotrophic factor	Homo sapiens	120-124
17653083-9	2008	To verify further these findings, we next compared effects triggered by Bortezomib, doxorubicin and melphalan in Mcl-1(wt/wt) and Mcl-1(Delta/null) murine embryonic fibroblasts (MEFs).	Melphalan	100-109	myeloid cell leukemia sequence 1	Mus musculus	113-118
18095870-6	2008	Cells expressing the p53 mutants were either more sensitive to cisplatin and melphalan or more resistant than the untransfected cells, depending on the mutation.	Melphalan	77-86	tumor protein p53	Homo sapiens	21-24
17982021-4	2008	Gene-expression studies and a stringently supervised analysis identified calreticulin as having significantly higher expression in the pretreatment plasma cells of patients with systemic AL-amyloidosis who then had a complete response to high-dose melphalan.	Melphalan	248-257	calreticulin	Homo sapiens	73-85
18028419-10	2008	Finally, western blotting experiments revealed that incubation of myeloma cells with cytotoxic drugs like melphalan or doxorubicin leads to increased phosphorylation and therefore degradation of inhibitor of nuclear factor kappa B (IkappaB) and release of nuclear factor kappa B (NFkappaB).	Melphalan	106-115	nuclear factor kappa B subunit 1	Homo sapiens	208-230
18028419-10	2008	Finally, western blotting experiments revealed that incubation of myeloma cells with cytotoxic drugs like melphalan or doxorubicin leads to increased phosphorylation and therefore degradation of inhibitor of nuclear factor kappa B (IkappaB) and release of nuclear factor kappa B (NFkappaB).	Melphalan	106-115	nuclear factor kappa B subunit 1	Homo sapiens	256-278
18028419-10	2008	Finally, western blotting experiments revealed that incubation of myeloma cells with cytotoxic drugs like melphalan or doxorubicin leads to increased phosphorylation and therefore degradation of inhibitor of nuclear factor kappa B (IkappaB) and release of nuclear factor kappa B (NFkappaB).	Melphalan	106-115	nuclear factor kappa B subunit 1	Homo sapiens	280-288
18066703-3	2007	High response rates and limb salvage rates have been reported in multicenter trials, which combined ILP with TNF-alpha plus melphalan, which resulted in the approval of TNF-alpha for this indication in Europe in 1998.	Melphalan	124-133	tumor necrosis factor	Homo sapiens	169-178
18022863-1	2007	Treatment of tumor-bearing mice with mouse (m)TNF-alpha, targeted to tumor vasculature by the anti-ED-B fibronectin domain antibody L19(scFv) and combined with melphalan, induces a therapeutic immune response.	Melphalan	160-169	tumor necrosis factor	Mus musculus	46-55
17560100-3	2007	Prophalan-L cytotoxicity in B16-F10 cells was lower (GI50=221 microM) than that of melphalan (GI50=173 microM).	Melphalan	83-92	icos ligand	Mus musculus	94-98
18024399-2	2007	DESIGN AND METHODS: Melphalan-induced damage formation and repair of monoadducts and interstrand cross-links in the p53 gene were studied in peripheral blood mononuclear cells obtained from 32 patients prior to therapy.	Melphalan	20-29	tumor protein p53	Homo sapiens	116-119
18024399-9	2007	INTERPRETATION AND CONCLUSIONS: An in vitro assay to quantify melphalan-induced p53-specific damage formation/repair can be used to select those patients with MM who are more likely to benefit from HDM supported by ASCT.	Melphalan	62-71	tumor protein p53	Homo sapiens	80-83
17558306-0	2007	Genetic polymorphisms in the amino acid transporters LAT1 and LAT2 in relation to the pharmacokinetics and side effects of melphalan.	Melphalan	123-132	solute carrier family 7 member 5	Homo sapiens	53-57
17377743-1	2007	PURPOSE: To determine the bioactivation and uptake of prolidase-targeted proline prodrugs of melphalan in six cancer cell lines with variable prolidase expression and to evaluate prolidase-dependence of prodrug cytotoxicity in the cell lines compared to that of the parent drug, melphalan.	Melphalan	93-102	peptidase D	Homo sapiens	54-63
17558306-0	2007	Genetic polymorphisms in the amino acid transporters LAT1 and LAT2 in relation to the pharmacokinetics and side effects of melphalan.	Melphalan	123-132	linker for activation of T cells family member 2	Homo sapiens	62-66
17377743-1	2007	PURPOSE: To determine the bioactivation and uptake of prolidase-targeted proline prodrugs of melphalan in six cancer cell lines with variable prolidase expression and to evaluate prolidase-dependence of prodrug cytotoxicity in the cell lines compared to that of the parent drug, melphalan.	Melphalan	93-102	peptidase D	Homo sapiens	142-151
17377743-1	2007	PURPOSE: To determine the bioactivation and uptake of prolidase-targeted proline prodrugs of melphalan in six cancer cell lines with variable prolidase expression and to evaluate prolidase-dependence of prodrug cytotoxicity in the cell lines compared to that of the parent drug, melphalan.	Melphalan	93-102	peptidase D	Homo sapiens	142-151
17558306-3	2007	As melphalan is a phenylalanine derivative, the pharmacokinetic variability may be determined by genetic polymorphisms in the L-type amino acid transporters LAT1 (SLC7A5) and LAT2 (SLC7A8).	Melphalan	3-12	solute carrier family 7 member 5	Homo sapiens	157-161
17558306-3	2007	As melphalan is a phenylalanine derivative, the pharmacokinetic variability may be determined by genetic polymorphisms in the L-type amino acid transporters LAT1 (SLC7A5) and LAT2 (SLC7A8).	Melphalan	3-12	solute carrier family 7 member 5	Homo sapiens	163-169
17558306-3	2007	As melphalan is a phenylalanine derivative, the pharmacokinetic variability may be determined by genetic polymorphisms in the L-type amino acid transporters LAT1 (SLC7A5) and LAT2 (SLC7A8).	Melphalan	3-12	linker for activation of T cells family member 2	Homo sapiens	175-179
17558306-3	2007	As melphalan is a phenylalanine derivative, the pharmacokinetic variability may be determined by genetic polymorphisms in the L-type amino acid transporters LAT1 (SLC7A5) and LAT2 (SLC7A8).	Melphalan	3-12	solute carrier family 7 member 8	Homo sapiens	181-187
17785116-2	2007	METHODS: Mouse lymphoma cells of the line E14 were cultured and melphalan resistant EL4 cell line (EL4/melphalan) was established by culturing EL4 cells with continuous low-concentration and intermittent gradually-increasing-concentration of melphalan in vitro.	Melphalan	64-73	epilepsy 4	Mus musculus	84-87
17785116-2	2007	METHODS: Mouse lymphoma cells of the line E14 were cultured and melphalan resistant EL4 cell line (EL4/melphalan) was established by culturing EL4 cells with continuous low-concentration and intermittent gradually-increasing-concentration of melphalan in vitro.	Melphalan	64-73	epilepsy 4	Mus musculus	99-102
17785116-2	2007	METHODS: Mouse lymphoma cells of the line E14 were cultured and melphalan resistant EL4 cell line (EL4/melphalan) was established by culturing EL4 cells with continuous low-concentration and intermittent gradually-increasing-concentration of melphalan in vitro.	Melphalan	64-73	epilepsy 4	Mus musculus	99-102
17785116-11	2007	After the treatment of melphalan of the dose 7.5 mg/kg, the tumor sizes of the treatment groups and control groups inoculated with both EL4 cells and the EL4/melphalan cells gradually decreased at the similar speed, and about one week later all tumors disappeared.	Melphalan	23-32	epilepsy 4	Mus musculus	136-139
17785116-11	2007	After the treatment of melphalan of the dose 7.5 mg/kg, the tumor sizes of the treatment groups and control groups inoculated with both EL4 cells and the EL4/melphalan cells gradually decreased at the similar speed, and about one week later all tumors disappeared.	Melphalan	23-32	epilepsy 4	Mus musculus	154-157
17236186-1	2007	A patient with multiple myeloma (MM) was being maintained on human recombinant interferon-alpha (INF-alpha) after VAD and autologous bone marrow transplantation (pretreated with melphalan).	Melphalan	178-187	interferon alpha 17	Homo sapiens	97-106
17330231-1	2007	Tumor necrosis factor (TNF) causes regression of advanced cancers when used in isolation perfusion with melphalan; evidence suggests these effects are mediated via selective yet uncharacterized actions on tumor neovasculature.	Melphalan	104-113	tumor necrosis factor	Mus musculus	23-26
17351391-9	2007	The GI50 values for melphalan and camptothecin correlated positively with the activity of glutathione-S-transferase, whereas GI50 values for methotrexate correlated positively with the cellular activities of both glutathione reductase and thioredoxin reductase.	Melphalan	20-29	glutathione S-transferase kappa 1	Homo sapiens	90-115
17428385-4	2007	Twelve days later, 7.5 mg/kg melphalan was used intraperitoneally to treat the tumor-bearing mice with TNFR1(+/+), TNFR1(+/-) and TNFR1(-/-).	Melphalan	29-38	tumor necrosis factor receptor superfamily, member 1a	Mus musculus	103-108
16896966-2	2007	Likewise, ILP with interleukin-2 (IL-2) resulted in OR of 67%, when combined to melphalan, in the same experimental model.	Melphalan	80-89	interleukin 2	Rattus norvegicus	19-32
16896966-2	2007	Likewise, ILP with interleukin-2 (IL-2) resulted in OR of 67%, when combined to melphalan, in the same experimental model.	Melphalan	80-89	interleukin 2	Rattus norvegicus	34-38
16896966-9	2007	Melphalan accumulation in the tumor when both Hi and IL-2 were added (3.1-fold) was very similar to accumulation with Hi only (2.8-fold), or IL-2 only (3.5-fold) combined to melphalan.	Melphalan	0-9	interleukin 2	Rattus norvegicus	53-57
17428385-4	2007	Twelve days later, 7.5 mg/kg melphalan was used intraperitoneally to treat the tumor-bearing mice with TNFR1(+/+), TNFR1(+/-) and TNFR1(-/-).	Melphalan	29-38	tumor necrosis factor receptor superfamily, member 1a	Mus musculus	115-120
17428385-4	2007	Twelve days later, 7.5 mg/kg melphalan was used intraperitoneally to treat the tumor-bearing mice with TNFR1(+/+), TNFR1(+/-) and TNFR1(-/-).	Melphalan	29-38	tumor necrosis factor receptor superfamily, member 1a	Mus musculus	115-120
17478923-3	2007	Oligonucleotide microarray-based gene expression analysis was applied to CD138-enriched plasma cells from newly diagnosed patients with symptomatic or progressive multiple myeloma treated with melphalan-based high-dose therapy.	Melphalan	193-202	syndecan 1	Homo sapiens	73-78
17109898-0	2007	Effect of p53 haploinsufficiency on melphalan-induced genotoxic effects in mouse bone marrow and peripheral blood.	Melphalan	36-45	transformation related protein 53, pseudogene	Mus musculus	10-13
16920737-6	2007	Here, we show for the first time that MGST1 can protect cells from several cytostatic drugs, chlorambucil, melphalan and cisplatin in an acute toxicity test (MTT assay) as well as a long-term colony forming efficiency cytotoxicity test.	Melphalan	107-116	microsomal glutathione S-transferase 1	Homo sapiens	38-43
17324338-7	2007	It was also confirmed that the amount of APE1 protein in KM3 cells was positively correlated with the dose and action time of melphalan.	Melphalan	126-135	apurinic/apyrimidinic endodeoxyribonuclease 1	Homo sapiens	41-45
17324338-10	2007	A decrease in APE1 levels in siRNA-treated KM3 cells led to enhanced cell sensitization to melphalan.	Melphalan	91-100	apurinic/apyrimidinic endodeoxyribonuclease 1	Homo sapiens	14-18
16953214-0	2006	MBL2 polymorphism and risk of severe infections in multiple myeloma patients receiving high-dose melphalan and autologous stem cell transplantation.	Melphalan	97-106	mannose binding lectin 2	Homo sapiens	0-4
17143522-2	2007	Present studies in K562 human myelogenous leukemia show that RALBP1 overexpression confers broad resistance to multiple chemotherapy drugs including cisplatin, melphalan, doxorubicin, daunorubicin, vincristine, vinblastine, vinorelbine, and mitomycin-C.	Melphalan	160-169	ralA binding protein 1	Homo sapiens	61-67
17176891-0	2006	[Cryotherapy is useful and safe in the prevention of oral mucositis after high-dose melphalan (L-PAM)].	Melphalan	84-93	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	97-100
16740717-4	2006	In addition, LBH589 potentiated the action of drugs, such as bortezomib, dexamethasone, or melphalan.	Melphalan	91-100	LBH regulator of WNT signaling pathway	Homo sapiens	13-16
16948903-4	2006	Twelve days later, 7.5 mg/kg melphalan was used intraperitoneally to treat all these IFN-gamma(+/+), IFN-gamma(+/-) and IFN-gamma(-/-) tumor-bearing mice.	Melphalan	29-38	interferon gamma	Mus musculus	85-94
16948903-4	2006	Twelve days later, 7.5 mg/kg melphalan was used intraperitoneally to treat all these IFN-gamma(+/+), IFN-gamma(+/-) and IFN-gamma(-/-) tumor-bearing mice.	Melphalan	29-38	interferon gamma	Mus musculus	101-110
16948903-4	2006	Twelve days later, 7.5 mg/kg melphalan was used intraperitoneally to treat all these IFN-gamma(+/+), IFN-gamma(+/-) and IFN-gamma(-/-) tumor-bearing mice.	Melphalan	29-38	interferon gamma	Mus musculus	101-110
16948903-6	2006	RESULTS: After melphalan (7.5 mg/kg) treatment, tumor size decreased at a similar rate in IFN-gamma(-/-), IFN-gamma(+/-) and IFN-gamma(+/+) mice within the first 3 d. Tumors shrank further or completely disappeared in most of IFN-gamma(+/-) and IFN-gamma(+/+) mice, whereas tumors grew gradually in all IFN-gamma(-/-) mice.	Melphalan	15-24	interferon gamma	Mus musculus	90-99
16948903-6	2006	RESULTS: After melphalan (7.5 mg/kg) treatment, tumor size decreased at a similar rate in IFN-gamma(-/-), IFN-gamma(+/-) and IFN-gamma(+/+) mice within the first 3 d. Tumors shrank further or completely disappeared in most of IFN-gamma(+/-) and IFN-gamma(+/+) mice, whereas tumors grew gradually in all IFN-gamma(-/-) mice.	Melphalan	15-24	interferon gamma	Mus musculus	106-115
16948903-6	2006	RESULTS: After melphalan (7.5 mg/kg) treatment, tumor size decreased at a similar rate in IFN-gamma(-/-), IFN-gamma(+/-) and IFN-gamma(+/+) mice within the first 3 d. Tumors shrank further or completely disappeared in most of IFN-gamma(+/-) and IFN-gamma(+/+) mice, whereas tumors grew gradually in all IFN-gamma(-/-) mice.	Melphalan	15-24	interferon gamma	Mus musculus	106-115
16948903-6	2006	RESULTS: After melphalan (7.5 mg/kg) treatment, tumor size decreased at a similar rate in IFN-gamma(-/-), IFN-gamma(+/-) and IFN-gamma(+/+) mice within the first 3 d. Tumors shrank further or completely disappeared in most of IFN-gamma(+/-) and IFN-gamma(+/+) mice, whereas tumors grew gradually in all IFN-gamma(-/-) mice.	Melphalan	15-24	interferon gamma	Mus musculus	106-115
16948903-6	2006	RESULTS: After melphalan (7.5 mg/kg) treatment, tumor size decreased at a similar rate in IFN-gamma(-/-), IFN-gamma(+/-) and IFN-gamma(+/+) mice within the first 3 d. Tumors shrank further or completely disappeared in most of IFN-gamma(+/-) and IFN-gamma(+/+) mice, whereas tumors grew gradually in all IFN-gamma(-/-) mice.	Melphalan	15-24	interferon gamma	Mus musculus	106-115
16948903-6	2006	RESULTS: After melphalan (7.5 mg/kg) treatment, tumor size decreased at a similar rate in IFN-gamma(-/-), IFN-gamma(+/-) and IFN-gamma(+/+) mice within the first 3 d. Tumors shrank further or completely disappeared in most of IFN-gamma(+/-) and IFN-gamma(+/+) mice, whereas tumors grew gradually in all IFN-gamma(-/-) mice.	Melphalan	15-24	interferon gamma	Mus musculus	106-115
16827882-9	2006	Serial evaluation of CD33 expression showed that the amount of CD33 significantly increased after a variety of treatment including melphalan and steroid in individual patients.	Melphalan	131-140	CD33 molecule	Homo sapiens	21-25
16827882-9	2006	Serial evaluation of CD33 expression showed that the amount of CD33 significantly increased after a variety of treatment including melphalan and steroid in individual patients.	Melphalan	131-140	CD33 molecule	Homo sapiens	63-67
16737912-5	2006	Among five patients receiving more than 2 g of melphalan, three developed MDS, and two of them showed der(1;7)(q10;p10) before or at the time of MDS diagnosis.	Melphalan	47-56	S100 calcium binding protein A10	Homo sapiens	115-118
16940805-5	2006	Co-administration of tumor necrosis factor-alpha in the isolated limb perfusion with melphalan induced a six-fold enhanced drug accumulation of melphalan in the tumor compared with isolated limb perfusion with melphalan alone.	Melphalan	85-94	tumor necrosis factor	Rattus norvegicus	21-48
16940805-5	2006	Co-administration of tumor necrosis factor-alpha in the isolated limb perfusion with melphalan induced a six-fold enhanced drug accumulation of melphalan in the tumor compared with isolated limb perfusion with melphalan alone.	Melphalan	144-153	tumor necrosis factor	Rattus norvegicus	21-48
16940805-5	2006	Co-administration of tumor necrosis factor-alpha in the isolated limb perfusion with melphalan induced a six-fold enhanced drug accumulation of melphalan in the tumor compared with isolated limb perfusion with melphalan alone.	Melphalan	144-153	tumor necrosis factor	Rattus norvegicus	21-48
16730667-7	2006	The expression of beta(1)-integrin receptor, as well as Sos-1 and phosphorylated MAPK, ERK(1) and ERK(2) but not FAK, Shc, and Grb-2 was significantly decreased in cells incubated for 24h with 20 microM AB4 compared to the control, not treated cells, whereas in the same conditions melphalan did not evoke any changes in expression of all these signaling proteins, as shown by Western immunoblot analysis.	Melphalan	282-291	integrin subunit beta 1	Homo sapiens	18-34
16730667-7	2006	The expression of beta(1)-integrin receptor, as well as Sos-1 and phosphorylated MAPK, ERK(1) and ERK(2) but not FAK, Shc, and Grb-2 was significantly decreased in cells incubated for 24h with 20 microM AB4 compared to the control, not treated cells, whereas in the same conditions melphalan did not evoke any changes in expression of all these signaling proteins, as shown by Western immunoblot analysis.	Melphalan	282-291	mitogen-activated protein kinase 3	Homo sapiens	87-93
16507262-8	2006	RESULTS: A single dose of melphalan (7.5 mg/kg) could cure EL4 tumor-bearing wild type C57BL/6 mice, but could not induce tumor regression in EL4 tumor-bearing nude C57BL/6 mice.	Melphalan	26-35	epilepsy 4	Mus musculus	59-62
16507262-9	2006	CONCLUSION: A single dose of melphalan has obvious anti-tumor effect on mouse lymphoma EL4 tumor-bearing wild type C57BL/6mice, which requires the involvement of T lymphocytes in the host probably related to their killing functions.	Melphalan	29-38	epilepsy 4	Mus musculus	87-90
16462850-4	2006	High response rates and limb-salvage rates have been reported in multicenter trials that combined ILP with TNF-alpha plus melphalan; these trials resulted in the approval of TNF-alpha for bulky melanoma metastases and soft tissue sarcomas in Europe in 1998.	Melphalan	122-131	tumor necrosis factor	Homo sapiens	174-183
16475717-0	2006	TRAIL-induced cytotoxicity in a melphalan-resistant rhabdomyosarcoma cell line via activation of caspase-2.	Melphalan	32-41	TNF superfamily member 10	Homo sapiens	0-5
16475717-0	2006	TRAIL-induced cytotoxicity in a melphalan-resistant rhabdomyosarcoma cell line via activation of caspase-2.	Melphalan	32-41	caspase 2	Homo sapiens	97-106
16569345-0	2006	c-MYC deregulation is involved in melphalan resistance of multiple myeloma: role of PDGF-BB.	Melphalan	34-43	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	0-5
16314190-0	2006	Thyroid hormone and insulin-like growth factor-I in patients with multiple myeloma treated with melphalan and prednisone.	Melphalan	96-105	insulin like growth factor 1	Homo sapiens	20-48
16314190-11	2006	CONCLUSIONS: Euthyroid sick syndrome can exist in MM patients, and the therapy with melphalan plus prednisone is accompanied by slightly expressed serum changes of thyroid hormone concentrations and IGF-I levels.	Melphalan	84-93	insulin like growth factor 1	Homo sapiens	199-204
16397040-1	2006	PURPOSE: Subnanogram doses of NGR-tumor necrosis factor (TNF), a TNF-alpha derivative able to target tumor neovessels, can enhance the antitumor activity of doxorubicin and melphalan in murine models.	Melphalan	173-182	tumor necrosis factor	Mus musculus	30-55
16397040-1	2006	PURPOSE: Subnanogram doses of NGR-tumor necrosis factor (TNF), a TNF-alpha derivative able to target tumor neovessels, can enhance the antitumor activity of doxorubicin and melphalan in murine models.	Melphalan	173-182	tumor necrosis factor	Mus musculus	57-60
16397040-1	2006	PURPOSE: Subnanogram doses of NGR-tumor necrosis factor (TNF), a TNF-alpha derivative able to target tumor neovessels, can enhance the antitumor activity of doxorubicin and melphalan in murine models.	Melphalan	173-182	tumor necrosis factor	Mus musculus	65-74
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.	Melphalan	124-133	fms related receptor tyrosine kinase 1	Homo sapiens	31-35
16148157-4	2005	Neutralization of TNF prevented melphalan-induced apoptosis and liver cells derived from mice genetically deficient in either TNFR 1 or 2, but not from lpr mice lacking a functional CD95 receptor, were completely resistant.	Melphalan	32-41	tumor necrosis factor	Mus musculus	18-21
16148157-6	2005	Melphalan increased membrane-bound but not secreted TNF in Kupffer cells and inhibited recombinant TNF-alpha converting enzyme in vitro.	Melphalan	0-9	tumor necrosis factor	Mus musculus	52-55
16148157-6	2005	Melphalan increased membrane-bound but not secreted TNF in Kupffer cells and inhibited recombinant TNF-alpha converting enzyme in vitro.	Melphalan	0-9	tumor necrosis factor	Mus musculus	99-102
16148157-8	2005	In conclusion, this study shows that melphalan elicits membrane TNF on Kupffer cells due to inhibition of TNF processing and thereby initiates apoptosis of hepatocytes via obligatory activation of both TNFRs.	Melphalan	37-46	tumor necrosis factor	Mus musculus	64-67
16148157-8	2005	In conclusion, this study shows that melphalan elicits membrane TNF on Kupffer cells due to inhibition of TNF processing and thereby initiates apoptosis of hepatocytes via obligatory activation of both TNFRs.	Melphalan	37-46	tumor necrosis factor	Mus musculus	106-109
16085187-7	2005	We next found, however, that nitrogen mustards (chlorambucil and melphalan) and alkyl sulfonates (busulfan) efficiently inhibited TrxR while these compounds, surprisingly, did not inhibit GR.	Melphalan	65-74	peroxiredoxin 5	Homo sapiens	130-134
16091744-0	2005	Melphalan-induced apoptosis in multiple myeloma cells is associated with a cleavage of Mcl-1 and Bim and a decrease in the Mcl-1/Bim complex.	Melphalan	0-9	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	87-92
16091744-0	2005	Melphalan-induced apoptosis in multiple myeloma cells is associated with a cleavage of Mcl-1 and Bim and a decrease in the Mcl-1/Bim complex.	Melphalan	0-9	BCL2 like 11	Homo sapiens	97-100
16091744-0	2005	Melphalan-induced apoptosis in multiple myeloma cells is associated with a cleavage of Mcl-1 and Bim and a decrease in the Mcl-1/Bim complex.	Melphalan	0-9	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	123-128
16091744-0	2005	Melphalan-induced apoptosis in multiple myeloma cells is associated with a cleavage of Mcl-1 and Bim and a decrease in the Mcl-1/Bim complex.	Melphalan	0-9	BCL2 like 11	Homo sapiens	129-132
16091744-3	2005	In the current study, we demonstrate that melphalan induces a drastic downregulation of Mcl-1L, Bcl-x(L) and BimEL in human melphalan-sensitive myeloma cells while the most potent proapoptotic isoforms, BimL and S, are affected to a lesser extent.	Melphalan	42-51	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	88-94
16091744-3	2005	In the current study, we demonstrate that melphalan induces a drastic downregulation of Mcl-1L, Bcl-x(L) and BimEL in human melphalan-sensitive myeloma cells while the most potent proapoptotic isoforms, BimL and S, are affected to a lesser extent.	Melphalan	42-51	BCL2 like 1	Homo sapiens	96-104
16091744-6	2005	In this study, we demonstrate that melphalan disrupts the Mcl-1/Bim complex whereas the Bcl-2/Bim complex is not modified.	Melphalan	35-44	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	58-63
16091744-6	2005	In this study, we demonstrate that melphalan disrupts the Mcl-1/Bim complex whereas the Bcl-2/Bim complex is not modified.	Melphalan	35-44	BCL2 like 11	Homo sapiens	64-67
16091744-8	2005	Thus, we can hypothesize that the cleaved 26 kDa proapoptotic Mcl-1 and the 19 and 12 kDa of Bim, generated during melphalan treatment could contribute to the amplification loop of apoptosis.	Melphalan	115-124	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	62-67
16091744-8	2005	Thus, we can hypothesize that the cleaved 26 kDa proapoptotic Mcl-1 and the 19 and 12 kDa of Bim, generated during melphalan treatment could contribute to the amplification loop of apoptosis.	Melphalan	115-124	BCL2 like 11	Homo sapiens	93-96
16178815-3	2005	An elegant approach to circumvent these problems consists in the local application of TNF in an isolated limb or organ setting, preferentially in the presence of cytostatic and alkylating agents, such as melphalan.	Melphalan	204-213	tumor necrosis factor	Homo sapiens	86-89
15726362-3	2005	Using multivariate Cox regression analysis BEAM conditioning (carmustine, cytarabine, etoposide and melphalan) was predictive for favourable outcome, better disease-/progression-free survival and a significantly lower risk for relapse.	Melphalan	100-109	cytochrome c oxidase subunit 8A	Homo sapiens	19-22
15843498-3	2005	The Rad51-guided homologous recombination repair system plays an important role in the recognition and repair of DNA interstrand crosslinks (ICLs), and cells deficient in this repair pathway become hypersensitive to ICL-inducing agents such as cisplatin and melphalan.	Melphalan	258-267	RAD51 recombinase	Homo sapiens	4-9
15843498-5	2005	Xrcc3 overexpression in MCF-7 cells resulted in 1) a 2- to 6-fold resistance to cisplatin/melphalan, 2) a 2-fold increase in drug-induced Rad51 foci, 3) an increased cisplatin-induced S-phase arrest, 4) decreased cisplatin-induced apoptosis, and 5) increased cisplatin-induced DNA synthesis arrest.	Melphalan	90-99	X-ray repair cross complementing 3	Homo sapiens	0-5
15883412-0	2005	Extent of damage and repair in the p53 tumor-suppressor gene after treatment of myeloma patients with high-dose melphalan and autologous blood stem-cell transplantation is individualized and may predict clinical outcome.	Melphalan	112-121	tumor protein p53	Homo sapiens	35-38
16025434-4	2005	However, exposure to melphalan also induces activation of intracellular signal transduction pathways, as indicated by phosphorylation of extracellular signal-regulated kinase (ERK1/2) and p38 (proteins belonging to the family of stress-induced mitogen-activated phosphorylated kinases, MAPK) within 5 min, as well as translocation of the transcription factor nuclear factor (NF)-kappaB to the nucleus within 45 min.	Melphalan	21-30	mitogen-activated protein kinase 3	Homo sapiens	176-182
16025434-4	2005	However, exposure to melphalan also induces activation of intracellular signal transduction pathways, as indicated by phosphorylation of extracellular signal-regulated kinase (ERK1/2) and p38 (proteins belonging to the family of stress-induced mitogen-activated phosphorylated kinases, MAPK) within 5 min, as well as translocation of the transcription factor nuclear factor (NF)-kappaB to the nucleus within 45 min.	Melphalan	21-30	mitogen-activated protein kinase 1	Homo sapiens	188-191
16025434-4	2005	However, exposure to melphalan also induces activation of intracellular signal transduction pathways, as indicated by phosphorylation of extracellular signal-regulated kinase (ERK1/2) and p38 (proteins belonging to the family of stress-induced mitogen-activated phosphorylated kinases, MAPK) within 5 min, as well as translocation of the transcription factor nuclear factor (NF)-kappaB to the nucleus within 45 min.	Melphalan	21-30	mitogen-activated protein kinase 3	Homo sapiens	286-290
16025434-4	2005	However, exposure to melphalan also induces activation of intracellular signal transduction pathways, as indicated by phosphorylation of extracellular signal-regulated kinase (ERK1/2) and p38 (proteins belonging to the family of stress-induced mitogen-activated phosphorylated kinases, MAPK) within 5 min, as well as translocation of the transcription factor nuclear factor (NF)-kappaB to the nucleus within 45 min.	Melphalan	21-30	nuclear factor kappa B subunit 1	Homo sapiens	359-385
16025434-5	2005	This early activation was followed by elevated levels of tumor necrosis factor (TNF)-alpha mRNA within 2 h. We also observed increased expression of intercellular adhesion molecule-1 (ICAM-1) on the surface of both cell lines 18 h after exposure to 25 microM melphalan and an increased adhesion of monocytes to the epithelial cells in vitro.In conclusion, we have demonstrated that alkylating compounds not only cause cell death of lung epithelial cells but also activate stress-associated MAPK signal transduction pathways and induce expression of mediators known to participate in the recruitment of inflammatory cells.	Melphalan	259-268	tumor necrosis factor	Homo sapiens	57-90
16025434-5	2005	This early activation was followed by elevated levels of tumor necrosis factor (TNF)-alpha mRNA within 2 h. We also observed increased expression of intercellular adhesion molecule-1 (ICAM-1) on the surface of both cell lines 18 h after exposure to 25 microM melphalan and an increased adhesion of monocytes to the epithelial cells in vitro.In conclusion, we have demonstrated that alkylating compounds not only cause cell death of lung epithelial cells but also activate stress-associated MAPK signal transduction pathways and induce expression of mediators known to participate in the recruitment of inflammatory cells.	Melphalan	259-268	intercellular adhesion molecule 1	Homo sapiens	149-182
16025434-5	2005	This early activation was followed by elevated levels of tumor necrosis factor (TNF)-alpha mRNA within 2 h. We also observed increased expression of intercellular adhesion molecule-1 (ICAM-1) on the surface of both cell lines 18 h after exposure to 25 microM melphalan and an increased adhesion of monocytes to the epithelial cells in vitro.In conclusion, we have demonstrated that alkylating compounds not only cause cell death of lung epithelial cells but also activate stress-associated MAPK signal transduction pathways and induce expression of mediators known to participate in the recruitment of inflammatory cells.	Melphalan	259-268	intercellular adhesion molecule 1	Homo sapiens	184-190
15883412-2	2005	PATIENTS AND METHODS: The formation and subsequent repair of DNA damage (monoadducts and interstrand cross-links) in the p53 tumor-suppressor gene, the proto-oncogene N-ras, and the housekeeping gene beta-actin during the first 24 hours after treatment with high-dose melphalan (HDM; 200 mg/m2) supported by autologous blood stem-cell transplantation (ABSCT) was measured in blood leukocytes of 26 patients with MM.	Melphalan	268-277	tumor protein p53	Homo sapiens	121-124
15883412-2	2005	PATIENTS AND METHODS: The formation and subsequent repair of DNA damage (monoadducts and interstrand cross-links) in the p53 tumor-suppressor gene, the proto-oncogene N-ras, and the housekeeping gene beta-actin during the first 24 hours after treatment with high-dose melphalan (HDM; 200 mg/m2) supported by autologous blood stem-cell transplantation (ABSCT) was measured in blood leukocytes of 26 patients with MM.	Melphalan	268-277	POTE ankyrin domain family member F	Homo sapiens	200-210
15899822-8	2005	Additionally, increased levels of TNF mRNA were found in tumors treated with IL-2 and IL-2 plus melphalan.	Melphalan	96-105	tumor necrosis factor	Rattus norvegicus	34-37
15735676-2	2005	We have previously shown that lysophosphatidic acid acyltransferase (LPAAT)-beta inhibitor CT-32615 triggers caspase-dependent apoptosis, and can overcome resistance to conventional therapeutics (i.e., dexamethasone, doxorubicin, melphalan) in MM cells.	Melphalan	230-239	1-acylglycerol-3-phosphate O-acyltransferase 2	Homo sapiens	30-80
15308759-7	2004	Levels of p53 were quantified by sensitive fluorogenic enzyme-linked immunosorbent assay at intervals up to 24 h after exposure of cells to various concentrations of melphalan and monohydroxymelphalan.	Melphalan	166-175	tumor protein p53	Homo sapiens	10-13
15779864-8	2005	In an acute (24-hour) melphalan exposure assay, MGSTII conferred about a twofold selective advantage.	Melphalan	22-31	microsomal glutathione S-transferase 2	Homo sapiens	48-54
15843040-4	2005	While ERK1/2 activation was a general phenomenon, irrespective of the used cell type or antitumour drug, the MEK/ERK inhibitors only reduced cisplatin toxicity in human myeloid cells (THP-1, HL-60 and NB-4), but not in RAW 264.7 mouse macrophages and NRK-52E rat renal tubular cells; and failed to reduce the toxicity etoposide, camptothecin, melphalan and arsenic trioxide, in U-937 cells.	Melphalan	343-352	mitogen-activated protein kinase kinase 7	Homo sapiens	109-112
15840383-0	2005	Metabolism of melphalan by rat liver microsomal glutathione S-transferase.	Melphalan	14-23	hematopoietic prostaglandin D synthase	Rattus norvegicus	48-73
15840383-6	2005	We demonstrated that rat liver microsomal GST presented a strong catalytic effect on the reaction as determined by the increase of monoglutathionyl and diglutathionyl melphalan derivatives and the decrease of melphalan.	Melphalan	167-176	hematopoietic prostaglandin D synthase	Rattus norvegicus	42-45
15840383-7	2005	We showed that microsomal GST was activated by melphalan in a concentration- and time-dependent manner.	Melphalan	47-56	hematopoietic prostaglandin D synthase	Rattus norvegicus	26-29
15840383-8	2005	Microsomal GST which was stimulated approximately 1.5-fold with melphalan had a stronger catalytic effect.	Melphalan	64-73	hematopoietic prostaglandin D synthase	Rattus norvegicus	11-14
15840383-9	2005	Thus microsomal GST may play a potential role in the metabolism of melphalan in biological membranes, and in the development of ADR.	Melphalan	67-76	hematopoietic prostaglandin D synthase	Rattus norvegicus	16-19
15779864-0	2005	Overexpression of glutathione-S-transferase, MGSTII, confers resistance to busulfan and melphalan.	Melphalan	88-97	microsomal glutathione S-transferase 2	Homo sapiens	45-51
15308759-8	2004	The level of initially formed DNA adducts needed to cause elevation of p53 from a baseline level of 0.5 ng/mg total protein to 2 ng/mg was 5- to 8-fold higher for monohydroxymelphalan than melphalan.	Melphalan	174-183	tumor protein p53	Homo sapiens	71-74
15256247-1	2004	BACKGROUND: Addition of tumour necrosis factor-alpha (TNF) to hypoxic abdominal perfusion (HAP) and hypoxic pelvic perfusion (HPP) with chemotherapeutic agents for treatment of un-resectable malignancies may lead to similar enhanced anti-tumour effects as are observed when TNF is added to isolated limb perfusions (ILP) with Melphalan.	Melphalan	326-335	tumor necrosis factor	Sus scrofa	54-57
15138161-7	2004	However, therapeutic administration of the antibody combined with melphalan significantly suppressed serum IgG2b levels and tumor burden in bone.	Melphalan	66-75	immunoglobulin heavy constant gamma 2B	Mus musculus	107-112
15325612-9	2004	A strong correlation was seen between in vitro melphalan dose and resultant GSH level and GST activity.	Melphalan	47-56	glutathione S-transferase kappa 1	Homo sapiens	90-93
15144226-7	2004	A relatively minor phospholipid species, phosphatidylserine (PS), was markedly oxidized 3 h after Mel treatment in HL-60 cells (but not in HP100 cells) where it was significantly inhibited by exogenously added CAT.	Melphalan	98-101	catalase	Homo sapiens	210-213
15215163-6	2004	Furthermore, down-regulation of PDZK1 with an anti-sense oligonucleotide sensitized a cell line KMS-11 to melphalan, cis-platin, and vincristin.	Melphalan	106-115	PDZ domain containing 1	Homo sapiens	32-37
15135647-5	2004	In this work, the standard comet assay and an assay modified by prolonging the electrophoresis time have been applied to evaluate DNA lesions induced by single, 4 or 26 weekly oral administrations of melphalan to p53(+/-) knockout and to isotype parental mice.	Melphalan	200-209	transformation related protein 53, pseudogene	Mus musculus	213-216
15147213-8	2004	The melphalan prodrug was essentially nontoxic to CHO, F9 teratocarcinoma, MCF7 breast adenocarcinoma, and p3U1 mouse myeloma cells up to millimolar concentrations, while prodrug incubation with the engineered prolyl endopeptidase mutant led to a cell killing profile superimposable to the one of melphalan.	Melphalan	4-13	prolyl endopeptidase	Homo sapiens	210-230
15005346-1	2004	To investigate whether combination chemotherapy with vincristine, cyclophosphamide, prednisolone, and melphalan (COP/ MP) with the addition of ranimustine (MCNU) (MCNU-COP/MP) is superior to the slightly modified COP/MP (mCOP/MP) regimen in multiple myeloma (MM), a multicenter randomized study was performed.	Melphalan	102-111	caspase recruitment domain family member 16	Homo sapiens	113-116
15053862-5	2004	The combination of pNGR-TNF or pRGD-TNF with doxorubicin or melphalan induced stronger effects than single agents.	Melphalan	60-69	tumor necrosis factor	Homo sapiens	36-39
15153331-2	2004	By using three M14-derived c-Myc low-expressing clones, we demonstrate that alkylating agents, cisplatin and melphalan, trigger apoptosis in the c-Myc antisense transfectants, but not in the parental line.	Melphalan	109-118	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	27-32
15153331-2	2004	By using three M14-derived c-Myc low-expressing clones, we demonstrate that alkylating agents, cisplatin and melphalan, trigger apoptosis in the c-Myc antisense transfectants, but not in the parental line.	Melphalan	109-118	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	145-150
15153331-8	2004	Indeed, GSH ethyl ester-mediated increase of GSH abrogated apoptosis induced by cisplatin and melphalan by inhibition of Bax/cytochrome c redistribution.	Melphalan	94-103	BCL2 associated X, apoptosis regulator	Homo sapiens	121-124
15153331-8	2004	Indeed, GSH ethyl ester-mediated increase of GSH abrogated apoptosis induced by cisplatin and melphalan by inhibition of Bax/cytochrome c redistribution.	Melphalan	94-103	cytochrome c, somatic	Homo sapiens	125-137
15152941-4	2004	Other changes in glucose metabolism that may affect 2-DG as an antimetabolite were observed, including increases in glucose-6-phosphate dehydrogenase of 10-fold and 100-fold for taxol- and melphalan-resistant variants, respectively, suggesting higher pentose phosphate activity; increased glutamine utilisation and greater sensitivity to iodoacetic acid-induced depletion of ATP levels in the parent relative to the resistant variants.	Melphalan	189-198	glucose-6-phosphate dehydrogenase	Homo sapiens	116-149
14761920-1	2004	BACKGROUND: Melphalan (L-PAM) hyperthermic isolated limb perfusion (HILP) is currently considered the standard treatment for patients with in-transit metastases from cutaneous melanoma.	Melphalan	12-21	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	25-28
12941846-4	2003	Here we report that coculture of immature DCs with tumor cells treated with the alkylating agents melphalan and chlorambucil leads to enhanced autologous and allogeneic T-cell activation, up-regulation of surface expression of MHC and costimulatory molecules, and increased interleukin (IL)-12 secretion.	Melphalan	98-107	major histocompatibility complex, class I, C	Homo sapiens	227-230
16767914-3	2003	Recently, Tumor Necrosis Factor (TNFalpha) has been employed at high dosages (3-4 mg) in association to Melphalan and hyperthermia.	Melphalan	104-113	tumor necrosis factor	Homo sapiens	10-31
16767914-3	2003	Recently, Tumor Necrosis Factor (TNFalpha) has been employed at high dosages (3-4 mg) in association to Melphalan and hyperthermia.	Melphalan	104-113	tumor necrosis factor	Homo sapiens	33-41
16767914-5	2003	A phase I - II study was undertaken in order to assess the MTD of TNFalpha in association to true hyperthermia (41.5 degrees C) and Melphalan.	Melphalan	132-141	tumor necrosis factor	Homo sapiens	66-74
14633719-5	2003	In contrast, cells adhered to fibronectin accumulate similar amounts of DNA damage compared with drug-sensitive cells but are protected from melphalan-induced mitochondrial perturbations and caspase activation.	Melphalan	141-150	fibronectin 1	Homo sapiens	30-41
14555520-4	2003	RESULTS: When lymphocytes were treated in vitro with biologically relevant doses of melphalan, monoadducts accumulated rapidly in both p53 and N-ras genes, reaching maximal levels within 2 h, whereas the highest interstrand cross-link levels were found within 8 h. Thereafter, the adducts were repaired with half-lives of 14.5 +/- 0.3 h (p53) or 18.8 +/- 1.5 h (N-ras) for monoadducts and 12.4 +/- 0.8 h (p53) or 14.1 +/- 2.2 h (N-ras) for interstrand cross-links.	Melphalan	84-93	tumor protein p53	Homo sapiens	135-138
14555520-4	2003	RESULTS: When lymphocytes were treated in vitro with biologically relevant doses of melphalan, monoadducts accumulated rapidly in both p53 and N-ras genes, reaching maximal levels within 2 h, whereas the highest interstrand cross-link levels were found within 8 h. Thereafter, the adducts were repaired with half-lives of 14.5 +/- 0.3 h (p53) or 18.8 +/- 1.5 h (N-ras) for monoadducts and 12.4 +/- 0.8 h (p53) or 14.1 +/- 2.2 h (N-ras) for interstrand cross-links.	Melphalan	84-93	NRAS proto-oncogene, GTPase	Homo sapiens	143-148
14555520-4	2003	RESULTS: When lymphocytes were treated in vitro with biologically relevant doses of melphalan, monoadducts accumulated rapidly in both p53 and N-ras genes, reaching maximal levels within 2 h, whereas the highest interstrand cross-link levels were found within 8 h. Thereafter, the adducts were repaired with half-lives of 14.5 +/- 0.3 h (p53) or 18.8 +/- 1.5 h (N-ras) for monoadducts and 12.4 +/- 0.8 h (p53) or 14.1 +/- 2.2 h (N-ras) for interstrand cross-links.	Melphalan	84-93	tumor protein p53	Homo sapiens	338-341
14555520-4	2003	RESULTS: When lymphocytes were treated in vitro with biologically relevant doses of melphalan, monoadducts accumulated rapidly in both p53 and N-ras genes, reaching maximal levels within 2 h, whereas the highest interstrand cross-link levels were found within 8 h. Thereafter, the adducts were repaired with half-lives of 14.5 +/- 0.3 h (p53) or 18.8 +/- 1.5 h (N-ras) for monoadducts and 12.4 +/- 0.8 h (p53) or 14.1 +/- 2.2 h (N-ras) for interstrand cross-links.	Melphalan	84-93	NRAS proto-oncogene, GTPase	Homo sapiens	362-367
14555520-4	2003	RESULTS: When lymphocytes were treated in vitro with biologically relevant doses of melphalan, monoadducts accumulated rapidly in both p53 and N-ras genes, reaching maximal levels within 2 h, whereas the highest interstrand cross-link levels were found within 8 h. Thereafter, the adducts were repaired with half-lives of 14.5 +/- 0.3 h (p53) or 18.8 +/- 1.5 h (N-ras) for monoadducts and 12.4 +/- 0.8 h (p53) or 14.1 +/- 2.2 h (N-ras) for interstrand cross-links.	Melphalan	84-93	tumor protein p53	Homo sapiens	338-341
14555520-4	2003	RESULTS: When lymphocytes were treated in vitro with biologically relevant doses of melphalan, monoadducts accumulated rapidly in both p53 and N-ras genes, reaching maximal levels within 2 h, whereas the highest interstrand cross-link levels were found within 8 h. Thereafter, the adducts were repaired with half-lives of 14.5 +/- 0.3 h (p53) or 18.8 +/- 1.5 h (N-ras) for monoadducts and 12.4 +/- 0.8 h (p53) or 14.1 +/- 2.2 h (N-ras) for interstrand cross-links.	Melphalan	84-93	NRAS proto-oncogene, GTPase	Homo sapiens	362-367
12805482-4	2003	Transfection of the GSTP1-1 antisense expression vector into a human cholangiocarcinoma cell line (HuCCT1) apparently decreased its intracellular GSTP1-1 concentration, and the sensitivity of transfectants to adriamycin (ADR), cisplatin, and alkylating agents such as melphalan and 4-hydroxyperoxycyclophosphamide (4-HC) was increased significantly, compared with that of mock transfectants.	Melphalan	268-277	glutathione S-transferase pi 1	Homo sapiens	20-27
14734721-1	2004	In this study, we show that engagement of CTLA-4 on tumor-infiltrating lymphocytes from low-dose melphalan (L-phenylalanine mustard (L-PAM))-treated MOPC-315 tumor bearers led to IL-10 secretion.	Melphalan	97-106	cytotoxic T-lymphocyte-associated protein 4	Mus musculus	42-48
14734721-1	2004	In this study, we show that engagement of CTLA-4 on tumor-infiltrating lymphocytes from low-dose melphalan (L-phenylalanine mustard (L-PAM))-treated MOPC-315 tumor bearers led to IL-10 secretion.	Melphalan	97-106	interleukin 10	Mus musculus	179-184
14734721-1	2004	In this study, we show that engagement of CTLA-4 on tumor-infiltrating lymphocytes from low-dose melphalan (L-phenylalanine mustard (L-PAM))-treated MOPC-315 tumor bearers led to IL-10 secretion.	Melphalan	133-138	cytotoxic T-lymphocyte-associated protein 4	Mus musculus	42-48
14734721-1	2004	In this study, we show that engagement of CTLA-4 on tumor-infiltrating lymphocytes from low-dose melphalan (L-phenylalanine mustard (L-PAM))-treated MOPC-315 tumor bearers led to IL-10 secretion.	Melphalan	133-138	interleukin 10	Mus musculus	179-184
14734721-4	2004	The percentage of MOPC-315 tumor-bearing mice cured following administration of neutralizing anti-IL-10 mAb to low-dose L-PAM-treated MOPC-315 tumor bearers was comparable to that observed following administration of blocking anti-CTLA-4 mAb.	Melphalan	120-125	interleukin 10	Mus musculus	98-103
14734721-6	2004	Taken together, these results indicate that CTLA-4 blockade improves the therapeutic outcome of low-dose L-PAM for MOPC-315 tumor bearers by inhibiting IL-10 secretion as a consequence of blocking CTLA-4 ligation.	Melphalan	105-110	cytotoxic T-lymphocyte-associated protein 4	Mus musculus	44-50
14734721-6	2004	Taken together, these results indicate that CTLA-4 blockade improves the therapeutic outcome of low-dose L-PAM for MOPC-315 tumor bearers by inhibiting IL-10 secretion as a consequence of blocking CTLA-4 ligation.	Melphalan	105-110	interleukin 10	Mus musculus	152-157
14734721-6	2004	Taken together, these results indicate that CTLA-4 blockade improves the therapeutic outcome of low-dose L-PAM for MOPC-315 tumor bearers by inhibiting IL-10 secretion as a consequence of blocking CTLA-4 ligation.	Melphalan	105-110	cytotoxic T-lymphocyte-associated protein 4	Mus musculus	197-203
15068672-5	2004	Two esophageal adenocarcinoma and one esophageal squamous cell line, expressing LAT-1 on Western blot analysis, were sensitive to therapeutic doses of melphalan (P <.001).	Melphalan	151-160	solute carrier family 7 (cationic amino acid transporter, y+ system), member 5	Mus musculus	80-85
15068672-6	2004	Simultaneous treatment with the competitive inhibitor, BCH [2-aminobicyclo-(2,1,1)-heptane-2-carboxylic acid], decreased sensitivity to melphalan (P <.05).	Melphalan	136-145	chimerin 2	Mus musculus	55-58
15068672-9	2004	These results demonstrate that LAT-1 is highly expressed in a subset of esophageal adenocarcinomas and that Barrett"s adenocarcinoma cell lines expressing LAT-1 are sensitive to melphalan.	Melphalan	178-187	solute carrier family 7 (cationic amino acid transporter, y+ system), member 5	Mus musculus	155-160
15068672-10	2004	LAT-1 expression is also retained in cell lines grown in nude mice providing a model to evaluate melphalan as a chemotherapeutic agent against esophageal adenocarcinomas expressing LAT-1.	Melphalan	97-106	solute carrier family 7 (cationic amino acid transporter, y+ system), member 5	Mus musculus	0-5
15068672-10	2004	LAT-1 expression is also retained in cell lines grown in nude mice providing a model to evaluate melphalan as a chemotherapeutic agent against esophageal adenocarcinomas expressing LAT-1.	Melphalan	97-106	solute carrier family 7 (cationic amino acid transporter, y+ system), member 5	Mus musculus	181-186
14572862-0	2003	Proline analogue of melphalan as a prodrug susceptible to the action of prolidase in breast cancer MDA-MB 231 cells.	Melphalan	20-29	peptidase D	Homo sapiens	72-81
14572862-1	2003	Proline analogue of melphalan (Mel-pro) was synthesized as a prodrug susceptible to the action of ubiquitously distributed, cytosolic imidodipeptidase-prolidase [E.C.3.4.13.9].	Melphalan	20-29	peptidase D	Homo sapiens	151-160
14572862-2	2003	Conjugation of melphalan (Mel) with proline (Pro) through imido-bond resulted in formation of a good substrate for prolidase.	Melphalan	15-24	peptidase D	Homo sapiens	115-124
12846887-6	2003	Importantly, N-BP-resistant myeloma cells also remained sensitive to conventional myeloma chemotherapeutics (melphalan, doxorubicin and vincristine).	Melphalan	109-118	Coenzyme A synthase	Homo sapiens	13-17
12862438-1	2003	To gain insight into the strategy to target PBR ligand-drug conjugates to brain tumors, novel N-imidazopyridinacetyl-melphalan conjugates and the corresponding ethyl esters have been prepared and evaluated for their cytotoxicity in melphalan-sensitive human (SF126, SF188) and rat (RG-2) glioma cell lines.	Melphalan	117-126	translocator protein	Homo sapiens	44-47
12393461-9	2003	Curcumin-induced down-regulation of NF-kappaB, a factor that has been implicated in chemoresistance, also induced chemosensitivity to vincristine and melphalan.	Melphalan	150-159	nuclear factor kappa B subunit 1	Homo sapiens	36-45
12962637-3	2003	Melphalan-resistant L1210/L-PAM1, adriamycin-resistant P388/ADR, and adriamycin-resistant HL-60/ADR leukemia cells were markedly less sensitive to CV-PDT than their wild-type counterparts, whereas cisplatin-resistant H69/CDDP cells were more sensitive than wild-type H69 cells.	Melphalan	0-9	F11 receptor	Homo sapiens	28-32
12850194-6	2003	They have identified TNFalpha-mediated vasculotoxic effects on the tumour vasculature and have shown that addition of TNFalpha to the perfusate results in an increase of three to six times in uptake of melphalan or doxorubicin by tumours.	Melphalan	202-211	tumor necrosis factor	Homo sapiens	21-29
12850194-6	2003	They have identified TNFalpha-mediated vasculotoxic effects on the tumour vasculature and have shown that addition of TNFalpha to the perfusate results in an increase of three to six times in uptake of melphalan or doxorubicin by tumours.	Melphalan	202-211	tumor necrosis factor	Homo sapiens	118-126
12649745-0	2003	Melphalan-induced up-regulation of B7-1 surface expression on normal splenic B cells.	Melphalan	0-9	CD80 antigen	Mus musculus	35-39
12388254-1	2003	High-dose TNF with melphalan has significant antitumor activity in regional perfusion of the limbs and liver in human malignancies.	Melphalan	19-28	tumor necrosis factor	Homo sapiens	10-13
12872149-12	2003	CIB was relatively well tolerated although febrile neutropenia or septicaemia occurred in 5% of the cycles and a dose-reduction of cyclophosphamide due to grade IV neutropenia was performed in 11% of the patients.CIB seems to be an effective regimen for remission induction in MM patients aged up to 75 years as an alternative to VAD (vincristine, doxorubicin, dexamethasone) if a regimen with intensity higher than that of oral melphalan/prednisone is warranted.	Melphalan	429-438	calcium and integrin binding 1	Homo sapiens	0-3
12094545-3	2002	Here, we determined the cytotoxic effect of TNF-alpha on several tumor cell lines in vitro in combination with doxorubicin (cell-cycle dependent) or melphalan (cell-cycle independent), and its effect on cell-cycle progression.	Melphalan	149-158	tumor necrosis factor	Rattus norvegicus	44-53
12036601-6	2002	In the present study, we tested the effect of PRL on a U266 human myeloma cell line and demonstrated constitutive and melphalan-stimulated intracytoplasmic PRL in U266 cells.	Melphalan	118-127	prolactin	Homo sapiens	46-49
12036601-6	2002	In the present study, we tested the effect of PRL on a U266 human myeloma cell line and demonstrated constitutive and melphalan-stimulated intracytoplasmic PRL in U266 cells.	Melphalan	118-127	prolactin	Homo sapiens	156-159
11901210-5	2002	Although most of the compounds that inhibited LAT1-mediated uptake were able to induce the efflux of [(14)C]phenylalanine preloaded to the oocytes expressing LAT1 through the obligatory exchange mechanism, melphalan, triiodothyronine, and thyroxine did not induce the significant efflux.	Melphalan	206-215	solute carrier family 7 member 5 L homeolog	Xenopus laevis	46-50
11901210-5	2002	Although most of the compounds that inhibited LAT1-mediated uptake were able to induce the efflux of [(14)C]phenylalanine preloaded to the oocytes expressing LAT1 through the obligatory exchange mechanism, melphalan, triiodothyronine, and thyroxine did not induce the significant efflux.	Melphalan	206-215	solute carrier family 7 member 5 L homeolog	Xenopus laevis	158-162
12017294-0	2002	Interleukin-6 affects melphalan-induced DNA damage and repair in human multiple myeloma cells.	Melphalan	22-31	interleukin 6	Homo sapiens	0-13
12130494-5	2002	Similarly, reduced SSB repair activity in CD34(+) cells was detected following melphalan or cisplatin application.	Melphalan	79-88	small RNA binding exonuclease protection factor La	Homo sapiens	19-22
12130494-5	2002	Similarly, reduced SSB repair activity in CD34(+) cells was detected following melphalan or cisplatin application.	Melphalan	79-88	CD34 molecule	Homo sapiens	42-46
12130494-9	2002	Because CD34(+) cells also displayed higher frequencies of apoptosis in response to melphalan or cisplatin, these findings may help to explain the myelosuppression after exposure to alkylating agents.	Melphalan	84-93	CD34 molecule	Homo sapiens	8-12
12189530-0	2002	Synergistic cytotoxicity of buthionine sulfoximine (BSO) and intensive melphalan (L-PAM) for neuroblastoma cell lines established at relapse after myeloablative therapy.	Melphalan	71-80	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	84-87
11986187-13	2002	CONCLUSIONS: A good correlation between RISA leakage measurement and TNF alpha exposure during and after hyperthermic isolated limb perfusion with TNF alpha and melphalan was demonstrated.	Melphalan	161-170	tumor necrosis factor	Homo sapiens	69-78
12040471-6	2002	Starting G-CSF on day +1 does not result in faster neutrophil engraftment but in later onset and consequently, slightly shorter duration of neutropenia in patients who receive melphalan 200 mg/m(2) and CD34(+) cell doses >3.0 x 10(6)/kg.	Melphalan	176-185	colony stimulating factor 3	Homo sapiens	9-14
11901210-3	2002	LAT1-mediated [(14)C]phenylalanine uptake was strongly inhibited in a competitive manner by aromatic-amino acid derivatives including L-dopa, alpha-methyldopa, melphalan, triiodothyronine, and thyroxine, whereas phenylalanine methyl ester, N-methyl phenylalanine, dopamine, tyramine, carbidopa, and droxidopa did not inhibit [(14)C]phenylalanine uptake.	Melphalan	160-169	solute carrier family 7 member 5 L homeolog	Xenopus laevis	0-4
11788894-1	2002	We studied the consequences of interfering with DNA topoisomerase IIalpha (topo IIalpha) activity on melphalan-induced cytotoxicity.	Melphalan	101-110	DNA topoisomerase 2-alpha	Cricetulus griseus	48-73
11878777-2	2001	Buthionine sulfoximine (BSO) can deplete glutathione and synergistically enhance in vitro sensitivity to the alkylating agent melphalan (L-PAM) for many neuroblastoma cell lines, but optimal use of this combination needs to be defined because clinical responses have been less frequent and not durable.	Melphalan	126-135	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	139-142
11673494-0	2001	Melphalan-induced expression of IFN-beta in MOPC-315 tumor-bearing mice and its importance for the up-regulation of TNF-alpha expression.	Melphalan	0-9	interferon beta 1, fibroblast	Mus musculus	32-40
11673494-0	2001	Melphalan-induced expression of IFN-beta in MOPC-315 tumor-bearing mice and its importance for the up-regulation of TNF-alpha expression.	Melphalan	0-9	tumor necrosis factor	Mus musculus	116-125
11673494-1	2001	We have previously shown that administration of a low-dose of melphalan (L-phenylalanine mustard; L-PAM) to mice bearing a large s.c. MOPC-315 tumor leads to up-regulation of TNF-alpha expression, which is first evident at the mRNA level at 24 h after the chemotherapy.	Melphalan	62-71	peptidylglycine alpha-amidating monooxygenase	Mus musculus	100-103
11673494-1	2001	We have previously shown that administration of a low-dose of melphalan (L-phenylalanine mustard; L-PAM) to mice bearing a large s.c. MOPC-315 tumor leads to up-regulation of TNF-alpha expression, which is first evident at the mRNA level at 24 h after the chemotherapy.	Melphalan	62-71	tumor necrosis factor	Mus musculus	175-184
11584063-6	2001	Homologous recombinational repair involving Rad51-related proteins was investigated by determining the levels of Rad51, Rad52, and Xrcc3 proteins and the density of nuclear melphalan-induced Rad51 foci, which represent sites of homologous recombinational repair.	Melphalan	173-182	RAD51 recombinase	Homo sapiens	44-49
11584063-10	2001	RESULTS: Melphalan resistance was correlated with Xrcc3 levels (r =.587; P =.027) and the density of melphalan-induced Rad51 foci (r =.848; P =.008).	Melphalan	9-18	X-ray repair cross complementing 3	Homo sapiens	50-55
11507071-3	2001	We determined p53 function by measuring induction of p21 and/or MDM2 proteins in response to melphalan (L-PAM) in seven L-PAM-sensitive and 11 L-PAM-resistant neuroblastoma cell lines.	Melphalan	104-109	MDM2 proto-oncogene	Homo sapiens	64-68
11584063-10	2001	RESULTS: Melphalan resistance was correlated with Xrcc3 levels (r =.587; P =.027) and the density of melphalan-induced Rad51 foci (r =.848; P =.008).	Melphalan	101-110	RAD51 recombinase	Homo sapiens	119-124
11680815-1	2001	Proline analogue of melphalan (MEL-PRO) was synthesised as a prodrug susceptible to the action of ubiquitously distributed, cytosolic imidodipeptidase--prolidase [E.C.3.4.13.9].	Melphalan	20-29	peptidase D	Homo sapiens	152-161
11680815-2	2001	Conjugation of melphalan (MEL) with proline (PRO) through an imido-bond resulted in formation of a good substrate for prolidase.	Melphalan	15-24	peptidase D	Homo sapiens	118-127
11507071-3	2001	We determined p53 function by measuring induction of p21 and/or MDM2 proteins in response to melphalan (L-PAM) in seven L-PAM-sensitive and 11 L-PAM-resistant neuroblastoma cell lines.	Melphalan	93-102	tumor protein p53	Homo sapiens	14-17
11507071-3	2001	We determined p53 function by measuring induction of p21 and/or MDM2 proteins in response to melphalan (L-PAM) in seven L-PAM-sensitive and 11 L-PAM-resistant neuroblastoma cell lines.	Melphalan	120-125	tumor protein p53	Homo sapiens	14-17
11507071-3	2001	We determined p53 function by measuring induction of p21 and/or MDM2 proteins in response to melphalan (L-PAM) in seven L-PAM-sensitive and 11 L-PAM-resistant neuroblastoma cell lines.	Melphalan	93-102	H3 histone pseudogene 16	Homo sapiens	53-56
11507071-3	2001	We determined p53 function by measuring induction of p21 and/or MDM2 proteins in response to melphalan (L-PAM) in seven L-PAM-sensitive and 11 L-PAM-resistant neuroblastoma cell lines.	Melphalan	93-102	MDM2 proto-oncogene	Homo sapiens	64-68
11507071-3	2001	We determined p53 function by measuring induction of p21 and/or MDM2 proteins in response to melphalan (L-PAM) in seven L-PAM-sensitive and 11 L-PAM-resistant neuroblastoma cell lines.	Melphalan	120-125	tumor protein p53	Homo sapiens	14-17
11507071-3	2001	We determined p53 function by measuring induction of p21 and/or MDM2 proteins in response to melphalan (L-PAM) in seven L-PAM-sensitive and 11 L-PAM-resistant neuroblastoma cell lines.	Melphalan	104-109	tumor protein p53	Homo sapiens	14-17
11507071-3	2001	We determined p53 function by measuring induction of p21 and/or MDM2 proteins in response to melphalan (L-PAM) in seven L-PAM-sensitive and 11 L-PAM-resistant neuroblastoma cell lines.	Melphalan	104-109	H3 histone pseudogene 16	Homo sapiens	53-56
11507071-9	2001	Loss of p53 function was selectively achieved by transduction of human papillomavirus 16 E6 (which degrades p53) into two drug-sensitive neuroblastoma cell lines with intact p53, causing high-level drug resistance to L-PAM, carboplatin, and etoposide.	Melphalan	217-222	tumor protein p53	Homo sapiens	8-11
11389822-6	2001	High-dose TNF destructs tumor vasculature, and, most importantly, it enhances tumor-selective drug uptake (ie, melphalan and doxorubicin) by threefold to sixfold.	Melphalan	111-120	tumor necrosis factor	Homo sapiens	10-13
11468181-3	2001	TRAIL/Apo2L potently induced apoptosis of MM cells from patients and the majority of MM cell lines, including cells sensitive or resistant to dexamethasone (Dex), doxorubicin (Dox), melphalan, and mitoxantrone.	Melphalan	182-191	TNF superfamily member 10	Homo sapiens	0-5
11468181-3	2001	TRAIL/Apo2L potently induced apoptosis of MM cells from patients and the majority of MM cell lines, including cells sensitive or resistant to dexamethasone (Dex), doxorubicin (Dox), melphalan, and mitoxantrone.	Melphalan	182-191	TNF superfamily member 10	Homo sapiens	6-11
11509930-14	2001	This study showed that in pediatric patients with AML consolidation of CR1 with high-dose melphalan allows survival and EFS to be obtained comparable to other auto-HSCT or chemotherapy published series with a potential sparing effect both on duration of treatment (with respect to chemotherapy) and on long-term side-effects (with respect to auto-HSCT with TBI or busulfan containing regimens).	Melphalan	90-99	complement C3b/C4b receptor 1 (Knops blood group)	Homo sapiens	71-74
11359799-1	2001	We have previously shown that exposure of P815 tumor cells to melphalan (L-phenylalanine mustard; L-PAM) leads to up-regulation of B7-1 surface expression, and this L-PAM-induced up-regulation requires de novo RNA synthesis and is associated with accumulation of B7-1 mRNA.	Melphalan	98-103	CD80 antigen	Mus musculus	131-135
11497396-1	2001	The object of this study was to determine the efficacy and safety of glycosylated recombinant human granulocyte colony-stimulating factor (rHuG-CSF; lenograstim) after combination chemotherapy consisting of ranimustine, vindesine, melphalan and prednisolone (MCNU-VMP).	Melphalan	231-240	colony stimulating factor 3	Homo sapiens	100-137
11417986-13	2001	This may be caused by increased thermal enhancement of melphalan due to the higher tissue temperatures (39--40 degrees C) at which the melphalan in the TNF alpha-ILPs was administered or by an interaction between high-dose TNF alpha and melphalan.	Melphalan	55-64	tumor necrosis factor	Homo sapiens	152-161
11417986-13	2001	This may be caused by increased thermal enhancement of melphalan due to the higher tissue temperatures (39--40 degrees C) at which the melphalan in the TNF alpha-ILPs was administered or by an interaction between high-dose TNF alpha and melphalan.	Melphalan	55-64	tumor necrosis factor	Homo sapiens	223-232
11438975-8	2001	Combined ifosfamide/epirubicin and standard G-CSF is able to mobilize sufficient PBPC without serious side-effects for patients with MM and for purging procedures resulting in a high proportion of complete remissions after tandem high-dose melphalan chemotherapy.	Melphalan	240-249	colony stimulating factor 3	Homo sapiens	44-49
11359799-1	2001	We have previously shown that exposure of P815 tumor cells to melphalan (L-phenylalanine mustard; L-PAM) leads to up-regulation of B7-1 surface expression, and this L-PAM-induced up-regulation requires de novo RNA synthesis and is associated with accumulation of B7-1 mRNA.	Melphalan	98-103	CD80 antigen	Mus musculus	263-267
11359799-2	2001	Here we show that the effect of L-PAM on B7-1 surface expression can be mimicked by exposing P815 tumor cells to oxidative stress but not to heat shock.	Melphalan	32-37	CD80 antigen	Mus musculus	41-45
11359799-3	2001	Moreover, the antioxidant N-acetyl-L-cysteine prevented the L-PAM-induced accumulation of B7-1 mRNA in P815 tumor cells, suggesting that reactive oxygen species are involved in the transcriptional regulation of L-PAM-induced B7-1 gene expression.	Melphalan	60-65	CD80 antigen	Mus musculus	90-94
11359799-3	2001	Moreover, the antioxidant N-acetyl-L-cysteine prevented the L-PAM-induced accumulation of B7-1 mRNA in P815 tumor cells, suggesting that reactive oxygen species are involved in the transcriptional regulation of L-PAM-induced B7-1 gene expression.	Melphalan	60-65	CD80 antigen	Mus musculus	225-229
11359799-3	2001	Moreover, the antioxidant N-acetyl-L-cysteine prevented the L-PAM-induced accumulation of B7-1 mRNA in P815 tumor cells, suggesting that reactive oxygen species are involved in the transcriptional regulation of L-PAM-induced B7-1 gene expression.	Melphalan	211-216	CD80 antigen	Mus musculus	90-94
11359799-3	2001	Moreover, the antioxidant N-acetyl-L-cysteine prevented the L-PAM-induced accumulation of B7-1 mRNA in P815 tumor cells, suggesting that reactive oxygen species are involved in the transcriptional regulation of L-PAM-induced B7-1 gene expression.	Melphalan	211-216	CD80 antigen	Mus musculus	225-229
11359799-4	2001	Although AP-1 and NF-kappaB are regarded as redox-sensitive transcription factors and the promoter/enhancer region of the B7-1 gene contains an AP-1 and an NF-kappaB binding site, exposure of P815 tumor cells to L-PAM led to rapid and transient activation only of NF-kappaB, but not AP-1, that bound specifically to a probe containing the respective binding site in the murine or human B7-1 gene.	Melphalan	212-217	CD80 antigen	Mus musculus	122-126
11359799-5	2001	Moreover, exposure of P815 tumor cells to a cell-permeable peptide that selectively inhibits NF-kappaB activation by blocking the activation of the IkappaB-kinase complex was found to inhibit the L-PAM-induced B7-1 mRNA accumulation, indicating that NF-kappaB activation is essential for the L-PAM-induced B7-1 gene expression.	Melphalan	196-201	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	93-102
11359799-5	2001	Moreover, exposure of P815 tumor cells to a cell-permeable peptide that selectively inhibits NF-kappaB activation by blocking the activation of the IkappaB-kinase complex was found to inhibit the L-PAM-induced B7-1 mRNA accumulation, indicating that NF-kappaB activation is essential for the L-PAM-induced B7-1 gene expression.	Melphalan	196-201	CD80 antigen	Mus musculus	210-214
11359799-5	2001	Moreover, exposure of P815 tumor cells to a cell-permeable peptide that selectively inhibits NF-kappaB activation by blocking the activation of the IkappaB-kinase complex was found to inhibit the L-PAM-induced B7-1 mRNA accumulation, indicating that NF-kappaB activation is essential for the L-PAM-induced B7-1 gene expression.	Melphalan	196-201	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	250-259
11359799-5	2001	Moreover, exposure of P815 tumor cells to a cell-permeable peptide that selectively inhibits NF-kappaB activation by blocking the activation of the IkappaB-kinase complex was found to inhibit the L-PAM-induced B7-1 mRNA accumulation, indicating that NF-kappaB activation is essential for the L-PAM-induced B7-1 gene expression.	Melphalan	196-201	CD80 antigen	Mus musculus	306-310
11359799-5	2001	Moreover, exposure of P815 tumor cells to a cell-permeable peptide that selectively inhibits NF-kappaB activation by blocking the activation of the IkappaB-kinase complex was found to inhibit the L-PAM-induced B7-1 mRNA accumulation, indicating that NF-kappaB activation is essential for the L-PAM-induced B7-1 gene expression.	Melphalan	292-297	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	93-102
11359799-5	2001	Moreover, exposure of P815 tumor cells to a cell-permeable peptide that selectively inhibits NF-kappaB activation by blocking the activation of the IkappaB-kinase complex was found to inhibit the L-PAM-induced B7-1 mRNA accumulation, indicating that NF-kappaB activation is essential for the L-PAM-induced B7-1 gene expression.	Melphalan	292-297	CD80 antigen	Mus musculus	210-214
11359799-6	2001	Taken together, these results indicate that L-PAM leads to activation of B7-1 gene expression by activating NF-kappaB via a pathway that involves reactive oxygen species.	Melphalan	44-49	CD80 antigen	Mus musculus	73-77
11359799-6	2001	Taken together, these results indicate that L-PAM leads to activation of B7-1 gene expression by activating NF-kappaB via a pathway that involves reactive oxygen species.	Melphalan	44-49	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	108-117
11313680-2	2001	The aim of this study was to evaluate the tolerance, pharmacokinetics (PK) and pharmacodynamics (PD) of HD single-agent melphalan administered over two consecutive courses (C1 and C2) in children.	Melphalan	120-129	heterogeneous nuclear ribonucleoprotein C	Homo sapiens	173-182
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.	Melphalan	10-19	colony stimulating factor 3	Homo sapiens	25-30
11422413-7	2001	Cost per QALY gained by the treatment with high-dose melphalan and autologous blood stem cell support was estimated at NOK 249,000 (USD 27,000).	Melphalan	53-62	serine/threonine/tyrosine kinase 1	Homo sapiens	119-122
11309322-2	2001	However, the contribution of TNF to the efficacy of isolation perfusion with melphalan has not been demonstrated conclusively in random assignment trials.	Melphalan	77-86	tumor necrosis factor	Homo sapiens	29-32
11309322-13	2001	CONCLUSIONS: Addition of TNF to melphalan during IHP results in significant differences in post-IHP production of IL-6 and IL-8 with associated changes in mean arterial blood pressure and greater regional toxicity, as reflected in higher levels of serum bilirubin.	Melphalan	32-41	interleukin 6	Homo sapiens	114-118
11309322-13	2001	CONCLUSIONS: Addition of TNF to melphalan during IHP results in significant differences in post-IHP production of IL-6 and IL-8 with associated changes in mean arterial blood pressure and greater regional toxicity, as reflected in higher levels of serum bilirubin.	Melphalan	32-41	C-X-C motif chemokine ligand 8	Homo sapiens	123-127
11481854-11	2001	After treatment with melphalan-prednisolone therapy, the neurological symptoms improved along with decrease of serum VEGF levels as well as the size of pulmonary plasmacytoma.	Melphalan	21-30	vascular endothelial growth factor A	Homo sapiens	117-121
11236942-8	2001	Doxorubicin and melphalan were able to suppress bcl-XL expression only in the presence of IL-6.	Melphalan	16-25	BCL2 like 1	Homo sapiens	48-54
11236942-8	2001	Doxorubicin and melphalan were able to suppress bcl-XL expression only in the presence of IL-6.	Melphalan	16-25	interleukin 6	Homo sapiens	90-94
11236942-5	2001	An interleukin-6-dependent myeloma cell line ANBL6 was used and treated with dexamethasone, doxorubicin, and melphalan in the presence of bone marrow stromal cells.	Melphalan	109-118	interleukin 6	Homo sapiens	3-16
11820612-0	2001	Proline analogue of melphalan as a prolidase-convertible pro-drug in breast cancer MCF-7 cells.	Melphalan	20-29	peptidase D	Homo sapiens	35-44
11050000-5	2000	Expression of wt p53 also leads to cell cycle arrest and protection from doxorubicin (Dox)- and melphalan (Mel)-induced apoptosis.	Melphalan	96-105	tumor protein p53	Homo sapiens	17-20
11096420-0	2000	Abrogation of G(2)/M-phase block enhances the cytotoxicity of daunorubicin, melphalan and cisplatin in TP53 mutant human tumor cells.	Melphalan	76-85	tumor protein p53	Homo sapiens	103-107
11096420-3	2000	In the TP53-mutated cell lines MeWo and 4451, the survival ratio at 7 Gy measured by colony formation was 2.3-2.8, 8.6-85 and 52-74 for daunorubicin, melphalan and cisplatin, respectively.	Melphalan	150-159	tumor protein p53	Homo sapiens	7-11
11107118-4	2000	RESULTS: Loss of p53 function (p53-LOF), defined as a failure to induce p21 and/or MDM2 in response to melphalan, was seen in 1/8 drug-sensitive and 6/10 drug-resistant cell lines.	Melphalan	103-112	tumor protein p53	Homo sapiens	17-20
11107118-4	2000	RESULTS: Loss of p53 function (p53-LOF), defined as a failure to induce p21 and/or MDM2 in response to melphalan, was seen in 1/8 drug-sensitive and 6/10 drug-resistant cell lines.	Melphalan	103-112	tumor protein p53	Homo sapiens	31-34
11050000-5	2000	Expression of wt p53 also leads to cell cycle arrest and protection from doxorubicin (Dox)- and melphalan (Mel)-induced apoptosis.	Melphalan	107-110	tumor protein p53	Homo sapiens	17-20
11079271-1	2000	The use of high-dose melphalan (L-phenyalalanine mustard or L-PAM) has been shown to be associated with both hematological and non-hematological toxicity.	Melphalan	21-30	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	62-65
10860939-4	2000	Cross-resistance to melphalan occurred, but not to doxorubicin (Adriamycin), taxol, and gamma-glutamyl-S-(benzyl)cysteinyl-R(-)-phenyl glycine diethyl ester, a GSTP1-1 inhibitor.	Melphalan	20-29	glutathione S-transferase pi 1	Homo sapiens	160-167
10956394-1	2000	It has previously been demonstrated in the setting of an isolated limb perfusion that application of high-dose TNF-alpha in combination with chemotherapy (melphalan, doxorubicin) results in strong synergistic antitumor effects in both the clinical and preclinical settings.	Melphalan	155-164	tumor necrosis factor	Rattus norvegicus	111-120
10953327-6	2000	Melphalan transport was inhibited by 2-amino-bicyclo[2,2,1] heptane-2-carboxylic acid(BCH) in both cell lines, indicating that the amino acid transport (System L, which is sodium independent and inhibited by BCH) is functional in these two cell lines.	Melphalan	0-9	NK2 homeobox 1	Homo sapiens	86-89
10953327-6	2000	Melphalan transport was inhibited by 2-amino-bicyclo[2,2,1] heptane-2-carboxylic acid(BCH) in both cell lines, indicating that the amino acid transport (System L, which is sodium independent and inhibited by BCH) is functional in these two cell lines.	Melphalan	0-9	NK2 homeobox 1	Homo sapiens	208-211
10953327-7	2000	Only a minor degree of inhibition of melphalan transport was noted after sodium depletion (System ASC, which is sodium dependent and unaffected by BCH).	Melphalan	37-46	PYD and CARD domain containing	Homo sapiens	98-101
10907648-4	2000	Engraftment data in the melphalan + TBI cohorts confirmed that HSC doses above the threshold dose of 0.8 x 10(6) CD34+Thy1+ HSCs/ kg provided prompt engraftment (absolute neutrophil count >0.5 x 10(9)/L day 10; platelet count >50 x 10(9)/L day 13).	Melphalan	24-33	fucosyltransferase 1 (H blood group)	Homo sapiens	63-66
10916754-9	2000	When TNF was added to melphalan, a dramatic anti-tumor effect was observed.	Melphalan	22-31	tumor necrosis factor	Rattus norvegicus	5-8
10828874-3	2000	Melphalan therapy followed by reinfusion of haemopoietic blood stem cells collected from the patient led to the improvement of the clinical status, although mixed chimerism and an elevated serum IgA persisted.	Melphalan	0-9	CD79a molecule	Homo sapiens	195-198
10789721-1	2000	A phase I dose-escalation study was performed to determine whether isolated hepatic perfusion (IHP) with melphalan (L-PAM) allows exposure of the liver to much higher drug concentrations than clinically achievable after systemic administration and leads to higher tumour concentrations of L-PAM.	Melphalan	105-114	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	118-121
10843675-1	2000	In this study, we show that administration of low-dose melphalan (l -PAM, l -phenylalanine mustard) to mice bearing a large MOPC-315 plasmacytoma led to a rapid up-regulation of B7-1 (CD80), but not B7-2 (CD86), expression on the surface of MOPC-315 tumor cells.	Melphalan	55-64	CD80 antigen	Mus musculus	178-182
10843675-1	2000	In this study, we show that administration of low-dose melphalan (l -PAM, l -phenylalanine mustard) to mice bearing a large MOPC-315 plasmacytoma led to a rapid up-regulation of B7-1 (CD80), but not B7-2 (CD86), expression on the surface of MOPC-315 tumor cells.	Melphalan	55-64	CD80 antigen	Mus musculus	184-188
10843675-1	2000	In this study, we show that administration of low-dose melphalan (l -PAM, l -phenylalanine mustard) to mice bearing a large MOPC-315 plasmacytoma led to a rapid up-regulation of B7-1 (CD80), but not B7-2 (CD86), expression on the surface of MOPC-315 tumor cells.	Melphalan	55-64	CD86 antigen	Mus musculus	199-203
10843675-1	2000	In this study, we show that administration of low-dose melphalan (l -PAM, l -phenylalanine mustard) to mice bearing a large MOPC-315 plasmacytoma led to a rapid up-regulation of B7-1 (CD80), but not B7-2 (CD86), expression on the surface of MOPC-315 tumor cells.	Melphalan	55-64	CD86 antigen	Mus musculus	205-209
10843675-1	2000	In this study, we show that administration of low-dose melphalan (l -PAM, l -phenylalanine mustard) to mice bearing a large MOPC-315 plasmacytoma led to a rapid up-regulation of B7-1 (CD80), but not B7-2 (CD86), expression on the surface of MOPC-315 tumor cells.	Melphalan	66-72	CD80 antigen	Mus musculus	178-182
10843675-1	2000	In this study, we show that administration of low-dose melphalan (l -PAM, l -phenylalanine mustard) to mice bearing a large MOPC-315 plasmacytoma led to a rapid up-regulation of B7-1 (CD80), but not B7-2 (CD86), expression on the surface of MOPC-315 tumor cells.	Melphalan	66-72	CD80 antigen	Mus musculus	184-188
10843675-1	2000	In this study, we show that administration of low-dose melphalan (l -PAM, l -phenylalanine mustard) to mice bearing a large MOPC-315 plasmacytoma led to a rapid up-regulation of B7-1 (CD80), but not B7-2 (CD86), expression on the surface of MOPC-315 tumor cells.	Melphalan	66-72	CD86 antigen	Mus musculus	199-203
10843675-1	2000	In this study, we show that administration of low-dose melphalan (l -PAM, l -phenylalanine mustard) to mice bearing a large MOPC-315 plasmacytoma led to a rapid up-regulation of B7-1 (CD80), but not B7-2 (CD86), expression on the surface of MOPC-315 tumor cells.	Melphalan	66-72	CD86 antigen	Mus musculus	205-209
10843675-2	2000	This l -PAM-induced preferential up-regulation of B7-1 surface expression was due, at least in part, to a direct effect of l -PAM on the tumor cells, as in vitro exposure of MOPC-315 tumor cells to l -PAM led to the preferential up-regulation of B7-1 surface expression.	Melphalan	5-11	CD80 antigen	Mus musculus	50-54
10843675-2	2000	This l -PAM-induced preferential up-regulation of B7-1 surface expression was due, at least in part, to a direct effect of l -PAM on the tumor cells, as in vitro exposure of MOPC-315 tumor cells to l -PAM led to the preferential up-regulation of B7-1 surface expression.	Melphalan	5-11	CD80 antigen	Mus musculus	246-250
10843675-2	2000	This l -PAM-induced preferential up-regulation of B7-1 surface expression was due, at least in part, to a direct effect of l -PAM on the tumor cells, as in vitro exposure of MOPC-315 tumor cells to l -PAM led to the preferential up-regulation of B7-1 surface expression.	Melphalan	123-129	CD80 antigen	Mus musculus	50-54
10843675-2	2000	This l -PAM-induced preferential up-regulation of B7-1 surface expression was due, at least in part, to a direct effect of l -PAM on the tumor cells, as in vitro exposure of MOPC-315 tumor cells to l -PAM led to the preferential up-regulation of B7-1 surface expression.	Melphalan	123-129	CD80 antigen	Mus musculus	246-250
10843675-2	2000	This l -PAM-induced preferential up-regulation of B7-1 surface expression was due, at least in part, to a direct effect of l -PAM on the tumor cells, as in vitro exposure of MOPC-315 tumor cells to l -PAM led to the preferential up-regulation of B7-1 surface expression.	Melphalan	123-129	CD80 antigen	Mus musculus	50-54
10843675-2	2000	This l -PAM-induced preferential up-regulation of B7-1 surface expression was due, at least in part, to a direct effect of l -PAM on the tumor cells, as in vitro exposure of MOPC-315 tumor cells to l -PAM led to the preferential up-regulation of B7-1 surface expression.	Melphalan	123-129	CD80 antigen	Mus musculus	246-250
10843675-5	2000	The up-regulation of B7-1 surface expression following in vitro exposure of tumor cells to l -PAM, gamma-irradiation, or mitomycin C required de novo protein and RNA synthesis, and was associated with the accumulation of mRNA for B7-1 within 4-8 h, indicating that the regulation of B7-1 expression is at the RNA transcriptional level.	Melphalan	91-97	CD80 antigen	Mus musculus	21-25
10843675-5	2000	The up-regulation of B7-1 surface expression following in vitro exposure of tumor cells to l -PAM, gamma-irradiation, or mitomycin C required de novo protein and RNA synthesis, and was associated with the accumulation of mRNA for B7-1 within 4-8 h, indicating that the regulation of B7-1 expression is at the RNA transcriptional level.	Melphalan	91-97	CD80 antigen	Mus musculus	230-234
10843675-5	2000	The up-regulation of B7-1 surface expression following in vitro exposure of tumor cells to l -PAM, gamma-irradiation, or mitomycin C required de novo protein and RNA synthesis, and was associated with the accumulation of mRNA for B7-1 within 4-8 h, indicating that the regulation of B7-1 expression is at the RNA transcriptional level.	Melphalan	91-97	CD80 antigen	Mus musculus	230-234
10848839-10	2000	Tandem transplants or the use of multiple agents (busulphan and melphalan) in the preparative regimen resulted in a higher CR1 level; none of the biological factors explored influenced the possibility of achieving CR1.	Melphalan	64-73	complement C3b/C4b receptor 1 (Knops blood group)	Homo sapiens	123-126
10789721-1	2000	A phase I dose-escalation study was performed to determine whether isolated hepatic perfusion (IHP) with melphalan (L-PAM) allows exposure of the liver to much higher drug concentrations than clinically achievable after systemic administration and leads to higher tumour concentrations of L-PAM.	Melphalan	105-114	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	291-294
10800168-17	2000	Repeated melphalan infusion hampered subsequent CD34(+) harvests.	Melphalan	9-18	CD34 molecule	Homo sapiens	48-52
10940652-8	2000	Expression of CD98, which was recently cloned as an L-phenylalanine transporter, was 6-fold decreased in KHM-11(EMS), suggesting that CD98 may be correlated with the incorporation of melphalan.	Melphalan	183-192	solute carrier family 3 member 2	Homo sapiens	14-18
10782862-0	2000	B7-2 expression on tumor cells is important for the acquisition of cytotoxic T lymphocyte activity by spleen cells from low-dose-melphalan-treated MOPC-315 tumor bearers via a mechanism that requires either B7-1 or B7-2 expression on host antigen-presenting cells.	Melphalan	129-138	CD86 antigen	Mus musculus	0-4
10782862-0	2000	B7-2 expression on tumor cells is important for the acquisition of cytotoxic T lymphocyte activity by spleen cells from low-dose-melphalan-treated MOPC-315 tumor bearers via a mechanism that requires either B7-1 or B7-2 expression on host antigen-presenting cells.	Melphalan	129-138	CD80 antigen	Mus musculus	207-219
10782862-1	2000	We have previously shown that B7-2 (CD86) and, to a lesser extent, B7-1 (CD80) contribute to the curative effectiveness of low-dose melphalan (L-phenylalanine mustard) for mice bearing a large MOPC-315 tumor under conditions that lead to the acquisition of potent cytotoxic T lymphocyte (CTL) activity at the tumor site.	Melphalan	132-141	CD86 antigen	Mus musculus	30-34
10782862-1	2000	We have previously shown that B7-2 (CD86) and, to a lesser extent, B7-1 (CD80) contribute to the curative effectiveness of low-dose melphalan (L-phenylalanine mustard) for mice bearing a large MOPC-315 tumor under conditions that lead to the acquisition of potent cytotoxic T lymphocyte (CTL) activity at the tumor site.	Melphalan	132-141	CD86 antigen	Mus musculus	36-40
10782862-1	2000	We have previously shown that B7-2 (CD86) and, to a lesser extent, B7-1 (CD80) contribute to the curative effectiveness of low-dose melphalan (L-phenylalanine mustard) for mice bearing a large MOPC-315 tumor under conditions that lead to the acquisition of potent cytotoxic T lymphocyte (CTL) activity at the tumor site.	Melphalan	132-141	CD80 antigen	Mus musculus	67-71
10782862-1	2000	We have previously shown that B7-2 (CD86) and, to a lesser extent, B7-1 (CD80) contribute to the curative effectiveness of low-dose melphalan (L-phenylalanine mustard) for mice bearing a large MOPC-315 tumor under conditions that lead to the acquisition of potent cytotoxic T lymphocyte (CTL) activity at the tumor site.	Melphalan	132-141	CD80 antigen	Mus musculus	73-77
10782862-6	2000	Thus, it is likely that B7-2, which is expressed at high levels on MOPC-315 tumor cells, promotes the rapid lysis of MOPC-315 stimulator tumor cells, thereby making tumor-associated antigens more readily available for efficient presentation by B7-expressing host APC which, in turn, stimulate the acquisition of CTL activity by spleen cells from low-dose-melphalan-treated MOPC-315 tumor bearers.	Melphalan	355-364	CD86 antigen	Mus musculus	24-28
10683851-3	2000	The cellular A beta 42 increase was caused by 3-day treatments with H2O2, etoposide or melphalan, all of which induce genotoxic apoptosis, but not by treatment with sodium azide, which causes necrosis.	Melphalan	87-96	amyloid beta precursor protein	Homo sapiens	13-19
10737727-2	2000	Chang liver cells with highest GSH content and highest activities of GST, GSH-RD, GSHpx and GS-X pump were found to be most resistant to melphalan.	Melphalan	137-146	ATP binding cassette subfamily C member 1	Homo sapiens	92-96
10940652-8	2000	Expression of CD98, which was recently cloned as an L-phenylalanine transporter, was 6-fold decreased in KHM-11(EMS), suggesting that CD98 may be correlated with the incorporation of melphalan.	Melphalan	183-192	solute carrier family 3 member 2	Homo sapiens	134-138
10658480-1	1999	We encountered a 65-year-old woman with diffuse large B-cell lymphoma showing t(8;14)(q24;q32) and c-myc gene rearrangement that developed following 12 years of melphalan-based chemotherapy for multiple myeloma.	Melphalan	161-170	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	99-104
10643540-5	1999	ASCT1 was conditioned with CBV + mitoxantrone (30 mg/m2) and ASCT2 (cytarabine 6 g/m2 melphalan 140 mg/m2 and total body irradiation at 12 Gy or busulfan 16 (n = 4) than 12 mg/kg).	Melphalan	86-95	solute carrier family 1 member 4	Homo sapiens	0-5
10717383-3	2000	We show here that three different strains deficient in either the Ku80 (xrs-6) or DNA-PKcs (V-3, scid) component of DNA-PK are markedly sensitive (3.5- to 5-fold) to a group of DNA cross-linking agents, the nitrogen mustards (NMs) (melphalan and mechlorethamine) as compared to their parental cell line.	Melphalan	232-241	X-ray repair cross complementing 5	Homo sapiens	66-70
10717383-3	2000	We show here that three different strains deficient in either the Ku80 (xrs-6) or DNA-PKcs (V-3, scid) component of DNA-PK are markedly sensitive (3.5- to 5-fold) to a group of DNA cross-linking agents, the nitrogen mustards (NMs) (melphalan and mechlorethamine) as compared to their parental cell line.	Melphalan	232-241	protein kinase, DNA-activated, catalytic subunit	Homo sapiens	82-90
10717383-3	2000	We show here that three different strains deficient in either the Ku80 (xrs-6) or DNA-PKcs (V-3, scid) component of DNA-PK are markedly sensitive (3.5- to 5-fold) to a group of DNA cross-linking agents, the nitrogen mustards (NMs) (melphalan and mechlorethamine) as compared to their parental cell line.	Melphalan	232-241	protein kinase, DNA-activated, catalytic subunit	Homo sapiens	82-88
10590370-1	1999	BACKGROUND: The primary purpose of this study was to establish the maximum tolerated dose (MTD) of intravenous melphalan in combination with paclitaxel and cisplatin plus granulocyte-colony stimulating factor (G-CSF) in patients with suboptimal advanced epithelial ovarian carcinoma or primary peritoneal carcinoma.	Melphalan	111-120	colony stimulating factor 3	Homo sapiens	210-215
10499614-1	1999	Expression of the lung resistance protein (LRP) is associated with resistance to various anticancer drugs including melphalan and, therefore, may affect the clinical outcome in multiple myeloma (MM).	Melphalan	116-125	major vault protein	Homo sapiens	43-46
10583236-14	1999	12 patients received a median of 3.9 x 106 CD34+ B-lin- cells/kg after conditioning with high-dose melphalan and showed a rapid reconstitution of haemopoiesis.	Melphalan	99-108	CD34 molecule	Homo sapiens	43-47
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.	Melphalan	113-122	CD34 molecule	Homo sapiens	0-4
10452985-3	1999	Here, we show that NE inhibits the production of TNF-alpha protein and mRNA by l -PAM TuB spleen cells stimulated in vitro with mitomycin C-treated tumor cells.	Melphalan	79-85	tumor necrosis factor	Mus musculus	49-58
10413303-7	1999	A combination of annexin V labeling and propidium iodide staining revealed that even the higher concentration of L-PAM (420 microM) did not induce apoptosis until 48 hr after treatment, but that induction of cell death was markedly accelerated as a result of GSH depletion: 48 hours after L-PAM (420 microM) treatment, GSH-depleted cells showed a 4-fold increase in DNA fragmentation and a 7-fold increase in the fraction of apoptotic (annexin V-positive) cells as compared to cells with normal GSH levels.	Melphalan	113-118	annexin A5	Homo sapiens	17-26
10413303-7	1999	A combination of annexin V labeling and propidium iodide staining revealed that even the higher concentration of L-PAM (420 microM) did not induce apoptosis until 48 hr after treatment, but that induction of cell death was markedly accelerated as a result of GSH depletion: 48 hours after L-PAM (420 microM) treatment, GSH-depleted cells showed a 4-fold increase in DNA fragmentation and a 7-fold increase in the fraction of apoptotic (annexin V-positive) cells as compared to cells with normal GSH levels.	Melphalan	113-118	annexin A5	Homo sapiens	436-445
10389992-7	1999	Synergy between TNF and melphalan was lost at a dose of TNF below 10 microg in 5 ml perfusate.	Melphalan	24-33	tumor necrosis factor	Rattus norvegicus	56-59
10198218-3	1999	In contrast, over-expression of GRP78 under the conditions outlined above is found to be associated with hypersensitivity to several clinically-relevant DNA cross-linking agents, namely, 1,3-bis (2-chloroethyl)-1-nitrosourea (BCNU), cisplatin, and melphalan.	Melphalan	248-257	heat shock protein family A (Hsp70) member 5	Homo sapiens	32-37
9973225-11	1999	In contrast, melphalan and paclitaxel augmented TRAIL-induced apoptosis in few cell lines, and methotrexate did not augment it in any cell line.	Melphalan	13-22	TNF superfamily member 10	Homo sapiens	48-53
10412944-3	1999	We studied the effect of BSO in rats bearing intrahepatically implanted tumors of the CC531 colorectal cancer cell line on the antitumor activity of melphalan (L-PAM).	Melphalan	149-158	peptidylglycine alpha-amidating monooxygenase	Rattus norvegicus	162-165
10037044-4	1999	Lower CD34 values (P = 0.002) were seen in patients treated with potent stem cell toxins (BCNU, melphalan, CCNU and mustine), designated toxicity factor 4 agents (TF4).	Melphalan	96-105	CD34 molecule	Homo sapiens	6-10
10100597-5	1999	TNF was delivered as a 24-h intravenous infusion, 48 h prior to the combination of L-PAM and WBH; L-PAM was given over 10 min at target temperature at a dose of 17.5 mg/ m2 based on a previous phase I WBH/L-PAM trial.	Melphalan	83-88	tumor necrosis factor	Homo sapiens	0-3
9923544-4	1999	RESULTS: D-283 Med (4-HCR) was cross-resistant to melphalan and 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), with O6-alkylguanine-DNA alkyltransferase (AGT) levels of 466+/-164 fmol/mg protein; AGT levels in the parental line, D-283 Med, were 76+/-96 fmol/mg.	Melphalan	50-59	coiled-coil alpha-helical rod protein 1	Homo sapiens	22-25
9850053-5	1998	In addition, we show here that anti-CTLA-4 monoclonal antibody enhanced antitumor cytotoxicity when the anti-CTLA-4 monoclonal antibody was added to stimulation cultures of spleen cells from low-dose melphalan-treated MOPC-315 tumor-bearing mice but not from untreated tumor-bearing mice.	Melphalan	200-209	cytotoxic T-lymphocyte-associated protein 4	Mus musculus	36-42
9892492-1	1998	Exposure of A2780 human ovarian tumor cells to a low concentration of melphalan in vitro for 7 d results in the development of melphalan resistance, which is dependent on elevated cellular levels of glutathione and glutathione S-transferase.	Melphalan	70-79	glutathione S-transferase kappa 1	Homo sapiens	215-240
9892492-1	1998	Exposure of A2780 human ovarian tumor cells to a low concentration of melphalan in vitro for 7 d results in the development of melphalan resistance, which is dependent on elevated cellular levels of glutathione and glutathione S-transferase.	Melphalan	127-136	glutathione S-transferase kappa 1	Homo sapiens	215-240
9892492-4	1998	It also prevented the increase in the expression of the glutathione S-transferase gene, suggesting that this may be the mechanism by which it prevents the development of melphalan resistance.	Melphalan	170-179	glutathione S-transferase kappa 1	Homo sapiens	56-81
9850053-5	1998	In addition, we show here that anti-CTLA-4 monoclonal antibody enhanced antitumor cytotoxicity when the anti-CTLA-4 monoclonal antibody was added to stimulation cultures of spleen cells from low-dose melphalan-treated MOPC-315 tumor-bearing mice but not from untreated tumor-bearing mice.	Melphalan	200-209	cytotoxic T-lymphocyte-associated protein 4	Mus musculus	109-115
9850053-6	1998	These results suggest that the therapeutic benefits of CTLA-4 blockade depend on the ability of drugs such as melphalan to promote an immunogenic environment by altering the cytokine profile of tumor-specific T cells.	Melphalan	110-119	cytotoxic T-lymphocyte-associated protein 4	Mus musculus	55-61
9840918-7	1998	Cisplatin and melphalan, the UV-mimetic agents known to elicit UV-type DNA damage, also induced apoptosis but differed from UV in that both of the former agents engaged the caspase cascade at a level distal to FADD.	Melphalan	14-23	Fas associated via death domain	Homo sapiens	210-214
9951688-1	1998	Resistance of myeloma cells to melphalan (L-PAM) is a serious problem.	Melphalan	31-40	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	44-47
9751079-2	1998	Previous studies showed that L-2-oxothiazolidine-4-carboxylate (OTZ), a 5-oxo-L-proline analog that is metabolized by 5-OPase, can preferentially decrease the cellular GSH levels in vivo in rat mammary tumors and sensitizes the tumors to the alkylating agent melphalan.	Melphalan	259-268	5-oxoprolinase (ATP-hydrolysing)	Rattus norvegicus	118-125
9809994-15	1998	The scattered tumor cell necrosis in the latter type may be explained by a TNF-alpha-induced increase in permeability of the tumor vascular bed, which results in higher intratumoral concentrations of melphalan or in a prolongation of its effect.	Melphalan	200-209	tumor necrosis factor	Homo sapiens	75-84
9827813-6	1998	Previous treatment with melphalan or carmustine was associated with a significantly lower yield of CD34-positive cells (P= 0.0001).	Melphalan	24-33	CD34 molecule	Homo sapiens	99-103
9751079-7	1998	We also observed that the expression of 5-OPase in the stably transfected MCF7 cells decreased the cellular GSH contents, sensitized the cells to melphalan toxicity, and diminished the sensitizing effect of OTZ.	Melphalan	146-155	5-oxoprolinase, ATP-hydrolysing	Homo sapiens	40-47
9751079-5	1998	When the cells were treated with OTZ plus melphalan, the cytotoxicity of melphalan was increased as compared with that of melphalan alone, and this effect could be reversed by the addition of glutamate, which is the product of 5-OPase reaction and a critical substrate in GSH synthesis.	Melphalan	42-51	5-oxoprolinase, ATP-hydrolysing	Homo sapiens	227-234
9751079-5	1998	When the cells were treated with OTZ plus melphalan, the cytotoxicity of melphalan was increased as compared with that of melphalan alone, and this effect could be reversed by the addition of glutamate, which is the product of 5-OPase reaction and a critical substrate in GSH synthesis.	Melphalan	73-82	5-oxoprolinase, ATP-hydrolysing	Homo sapiens	227-234
9751079-5	1998	When the cells were treated with OTZ plus melphalan, the cytotoxicity of melphalan was increased as compared with that of melphalan alone, and this effect could be reversed by the addition of glutamate, which is the product of 5-OPase reaction and a critical substrate in GSH synthesis.	Melphalan	73-82	5-oxoprolinase, ATP-hydrolysing	Homo sapiens	227-234
9704736-1	1998	PURPOSE: In a randomized trial conducted by the National Cancer Institute of Canada Clinical Trials Group (NCIC CTG), interferon alpha-2b (IFN) maintenance therapy (2 mU/m2 subcutaneously three times per week) after successful induction with melphalan and prednisone was found to prolong time to progression in patients with multiple myeloma.	Melphalan	242-251	interferon alpha 2	Homo sapiens	118-137
9692813-10	1998	Pretreatment with six or more cycles of melphalan yielded a smaller number of CD34+ cells than pretreatment with fewer than six cycles (2.5 vs 5.3 x 10(6)/kg; p = 0.001).	Melphalan	40-49	CD34 molecule	Homo sapiens	78-82
9733636-12	1998	CONCLUSION: TBI and the associated reduction in WBC count decreased the tumor response by TNFalpha and melphalan significantly and abrogated the immediate response of skin necrosis at the tumor site, as found in rats treated with TNFalpha and melphalan without TBI.	Melphalan	103-112	tumor necrosis factor	Rattus norvegicus	230-238
9679558-4	1998	Phase I clinical trials of BSO + melphalan (L-PAM)have been carried out and observed little toxicity with BSO alone and increased myelosuppression with BSO + L-PAM.	Melphalan	33-42	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	46-49
9679558-4	1998	Phase I clinical trials of BSO + melphalan (L-PAM)have been carried out and observed little toxicity with BSO alone and increased myelosuppression with BSO + L-PAM.	Melphalan	33-42	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	160-163
9602861-7	1998	In line with a genotoxic mechanism and absence of additional cytotoxic effects, the DNA fragments generated by gamma-irradiation as well as by etoposide and melphalan displayed a distribution between 1 and 4 Mbp with a peak around 2 Mbp.	Melphalan	157-166	myelin basic protein	Homo sapiens	208-211
18020561-5	1998	Our results, using the combination of high dose rTNFalpha, interferon-gamma and melphalan (TIM), produced an overall objective response rate of 100% in 2 successive studies on melanoma, with 90% and 78% complete response, respectively.	Melphalan	80-89	Rho guanine nucleotide exchange factor 5	Homo sapiens	91-94
9621525-2	1998	Several studies have shown that when TNF is used with melphalan in closed circuit perfusion treatment for multiple melanoma metastases confined to a limb, a response rate of 80% can be achieved compared to a best response rate of 40% with melphalan alone.	Melphalan	54-63	tumor necrosis factor	Homo sapiens	37-40
9621525-2	1998	Several studies have shown that when TNF is used with melphalan in closed circuit perfusion treatment for multiple melanoma metastases confined to a limb, a response rate of 80% can be achieved compared to a best response rate of 40% with melphalan alone.	Melphalan	239-248	tumor necrosis factor	Homo sapiens	37-40
9548610-6	1998	Because alkylating agents generally have steep dose-response curves, mitomycin C (MMC) and melphalan (L-PAM) entered phase I/II studies on IHP.	Melphalan	91-100	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	104-107
9602861-7	1998	In line with a genotoxic mechanism and absence of additional cytotoxic effects, the DNA fragments generated by gamma-irradiation as well as by etoposide and melphalan displayed a distribution between 1 and 4 Mbp with a peak around 2 Mbp.	Melphalan	157-166	myelin basic protein	Homo sapiens	233-236
9443402-6	1998	BCL-X expression in malignant plasma cells strongly correlated with decreased response rates in patient groups treated with either melphalan and prednisone or vincristine, Adriamycin, and dexamethasone.	Melphalan	131-140	BCL2 like 1	Homo sapiens	0-5
9446640-9	1998	Measurement of HGF may identify a group of patients with poor response to melphalan-prednisone treatment and short survival.	Melphalan	74-83	hepatocyte growth factor	Homo sapiens	15-18
9469448-0	1998	Importance of the B7-2 molecule for low dose melphalan-induced acquisition of tumor-eradicating immunity by mice bearing a large MOPC-315 tumor.	Melphalan	45-54	CD86 antigen	Mus musculus	18-22
9469448-1	1998	We have previously shown that low dose melphalan (L-phenylalanine mustard; L-PAM) therapy of hitherto immunosuppressed mice bearing a large (20-mm) s.c. MOPC-315 tumor leads to the acquisition of potent CD8+ T cell-mediated antitumor immunity which in turn eradicates the large tumor burden not eradicated by the direct antitumor effects of the drug.	Melphalan	39-48	peptidylglycine alpha-amidating monooxygenase	Mus musculus	77-80
9344321-6	1997	In 55 patients treated with the combination of high-dose rTNF alpha + interferon-gamma + melphalan an overall objective response rate of 87% with 36% complete responses was observed; it was 81% and 28%, respectively, in a group treated with TNF alpha and melphalan (n = 85).	Melphalan	255-264	interferon gamma	Homo sapiens	70-86
9460989-2	1998	The present study details for the first time MRP1-mediated ATP-dependent transport of various glutathione S-conjugates of the bifunctional alkylating agents chlorambucil and melphalan.	Melphalan	174-183	ATP binding cassette subfamily C member 1	Homo sapiens	45-49
9488598-5	1998	RESULTS: The present investigations provide data indicating that Pro-Gln-Gly-Ile-Mel-Gly (melphalan hexapeptide, MHP) is a substrate for both bacterial and 72-kDa type IV collagenases and that in this way it can generate Ile-Mel-Gly (melphalan tripeptide, MTP) of higher cytotoxic potency.	Melphalan	90-99	metallothionein 1B	Homo sapiens	256-259
9488598-7	1998	In a comparison of equimolar concentrations of melphalan and its two peptide derivatives (MHP and MTP), superior antiproliferative action of MTP was seen in HT-29, HT-1080, and HT-168 tumor cell cultures.	Melphalan	47-56	metallothionein 1B	Homo sapiens	98-101
9488598-7	1998	In a comparison of equimolar concentrations of melphalan and its two peptide derivatives (MHP and MTP), superior antiproliferative action of MTP was seen in HT-29, HT-1080, and HT-168 tumor cell cultures.	Melphalan	47-56	metallothionein 1B	Homo sapiens	141-144
9384474-2	1997	The efficacy of an intensified regimen, TAM (TBI, high-dose cytosine arabinoside and melphalan), is evaluated by analyzing long-term follow-up of a homogenous group of 42 high-risk ALL patients allografted in first CR.	Melphalan	85-94	Myeloproliferative syndrome, transient (transient abnormal myelopoiesis)	Homo sapiens	40-43
9670271-2	1998	In this overview we present our experimental and clinical results with mitomycin C (MMC) and melphalan (L-Pam).	Melphalan	93-102	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	106-109
9371511-5	1997	Subsequently, these GRP78-overexpressing cells were trypsinized, plated in regular medium without GRP78-inducing agents, and allowed a 5-h attachment time before being treated with melphalan, BCNU, or cisplatin for 1 h to determine clonogenic survivals.	Melphalan	181-190	endoplasmic reticulum chaperone BiP	Cricetulus griseus	20-25
9516845-0	1997	Buthionine sulphoximine alone and in combination with melphalan (L-PAM) is highly cytotoxic for human neuroblastoma cell lines.	Melphalan	54-63	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	67-70
9516845-1	1997	Buthionine sulphoximine (BSO) selectively inhibits glutathione (GSH) synthesis and may enhance the antineuroblastoma activity of melphalan (L-PAM).	Melphalan	129-138	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	142-145
9313875-11	1997	The 112 patients receiving the melphalan autografts fared significantly better than the rest of the patients with OS and PFS (from high-dose treatment) of 6.6 years and 27 months, respectively (P < 0.005), and the 57 patients also receiving IFN have a OS yet to reach a median at 8 years and a PFS of 44 months, significantly better than non IFN high-dose patients (P < 0.0036).	Melphalan	31-40	interferon alpha 1	Homo sapiens	244-247
9313875-11	1997	The 112 patients receiving the melphalan autografts fared significantly better than the rest of the patients with OS and PFS (from high-dose treatment) of 6.6 years and 27 months, respectively (P < 0.005), and the 57 patients also receiving IFN have a OS yet to reach a median at 8 years and a PFS of 44 months, significantly better than non IFN high-dose patients (P < 0.0036).	Melphalan	31-40	interferon alpha 1	Homo sapiens	345-348
9266941-4	1997	IL4 sensitized alkylator-resistant B-CLL cells to the cytotoxic effects of melphalan (L-phenylalanine mustard) but had no influence on melphalan-induced cytotoxicity against normal B lymphocytes.	Melphalan	75-84	interleukin 4	Homo sapiens	0-3
9339752-7	1997	Multivariate analysis revealed that cyclophosphamide and G-CSF priming before collection of hematopoietic precursors (P < 0.001) was a positive predictor of rapid engraftment and prior exposure to melphalan given orally (P = 0.02) was a negative predictor of subsequent platelet engraftment.	Melphalan	200-209	colony stimulating factor 3	Homo sapiens	57-62
9329556-1	1997	Dramatic clinical results have been obtained in malignant melanoma and sarcoma using hyperthermic limb perfusion in combination with tumor necrosis factor (TNF) and melphalan (L-PAM).	Melphalan	165-174	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	178-181
21528210-5	1997	Lisofylline alone or along with G-CSF was effective in protecting animals from the weight loss caused by high dose melphalan but not from weight loss caused by other cytotoxic therapies.	Melphalan	115-124	peripheral blood stem cell response to granulocyte colony stimulating factor 1	Mus musculus	32-37
9225006-5	1997	Finally, TNF and GM-CSF may cooperate in enhancing the in vivo generation of CTL activity in MOPC-315 tumor bearers because low-dose melphalan (L-phenylalanine mustard) therapy, which was previously shown to lead to the rapid up-regulation of TNF production at the tumor site and the subsequent TNF-dependent in vivo acquisition of potent CTL activity, is shown here to lead to the rapid up-regulation of GM-CSF production at the tumor site.	Melphalan	133-142	tumor necrosis factor	Mus musculus	9-12
9225006-5	1997	Finally, TNF and GM-CSF may cooperate in enhancing the in vivo generation of CTL activity in MOPC-315 tumor bearers because low-dose melphalan (L-phenylalanine mustard) therapy, which was previously shown to lead to the rapid up-regulation of TNF production at the tumor site and the subsequent TNF-dependent in vivo acquisition of potent CTL activity, is shown here to lead to the rapid up-regulation of GM-CSF production at the tumor site.	Melphalan	133-142	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	17-23
9074631-3	1997	Preincubation of HL-60 cells with the hydrogen peroxide-scavenging enzyme catalase (500 U/ml) inhibited apoptosis due to UV irradiation or low concentrations of camptothecin, etoposide or melphalan, but did not protect against higher concentrations.	Melphalan	188-197	catalase	Homo sapiens	74-82
9092631-1	1997	Previous work showed that melphalan-induced mutations in the aprt gene of CHO cells are primarily transversions and occur preferentially at G-G-C sequences, which are potential sites for various bifunctional alkylations involving guanine N-7.	Melphalan	26-35	adenine phosphoribosyltransferase	Cricetulus griseus	61-65
9092631-2	1997	To identify the DNA lesion(s) which may be responsible for these mutations, an end-labeled DNA duplex containing a frequent site of melphalan-induced mutation in the aprt gene was treated with melphalan, mechlorethamine or phosphoramide mustard.	Melphalan	132-141	adenine phosphoribosyltransferase	Cricetulus griseus	166-170
9092631-2	1997	To identify the DNA lesion(s) which may be responsible for these mutations, an end-labeled DNA duplex containing a frequent site of melphalan-induced mutation in the aprt gene was treated with melphalan, mechlorethamine or phosphoramide mustard.	Melphalan	193-202	adenine phosphoribosyltransferase	Cricetulus griseus	166-170
9171882-3	1997	A PBR ligand-melphalan conjugate (PBR-MEL) was synthesized and evaluated for cytotoxicity and affinity for PBRs.	Melphalan	13-22	translocator protein	Rattus norvegicus	2-5
9171882-3	1997	A PBR ligand-melphalan conjugate (PBR-MEL) was synthesized and evaluated for cytotoxicity and affinity for PBRs.	Melphalan	13-22	translocator protein	Rattus norvegicus	34-37
9135501-3	1997	The present study investigated the in vivo antitumour activity of a combination of tallimustine and melphalan (L-PAM).	Melphalan	100-109	peptidylglycine alpha-amidating monooxygenase	Mus musculus	113-116
9053491-0	1997	Prospective randomized placebo-controlled study of granulocyte-macrophage colony-stimulating factor without stem-cell transplantation after high-dose melphalan in patients with multiple myeloma.	Melphalan	150-159	colony stimulating factor 2	Homo sapiens	51-99
9778589-15	1997	This fact makes melphalan an adequate choice for TNF perfusion in advanced limb malignancies.	Melphalan	16-25	tumor necrosis factor-like	Rattus norvegicus	49-52
9166943-0	1997	Liver and tumour tissue concentrations of TNF-alpha in cancer patients treated with TNF-alpha and melphalan by isolated liver perfusion.	Melphalan	98-107	tumor necrosis factor	Homo sapiens	42-51
9166943-1	1997	In this study we determined the level of tumour necrosis factor alpha (TNF-alpha) in liver and tumour tissue samples obtained from patients with colorectal metastases confined to the liver, who were treated with isolated liver perfusion with TNF-alpha and melphalan.	Melphalan	256-265	tumor necrosis factor	Homo sapiens	71-80
8996517-5	1997	This antiserum was used in vivo to inactivate LOX after it had depleted the large neutral amino acids, thereby preventing LOX-mediated catabolism of melphalan.	Melphalan	149-158	interleukin 4 induced 1B	Mus musculus	46-49
8996517-5	1997	This antiserum was used in vivo to inactivate LOX after it had depleted the large neutral amino acids, thereby preventing LOX-mediated catabolism of melphalan.	Melphalan	149-158	interleukin 4 induced 1B	Mus musculus	122-125
8996517-7	1997	In three separate studies using groups of eight to ten mice bearing intracranial human glioma xenografts, pretreatment with LOX followed by anti-LOX serum increased the antitumor activity of melphalan as compared with treatments with melphalan plus LOX, melphalan plus anti-LOX serum, or melphalan alone.	Melphalan	191-200	lysyl oxidase	Homo sapiens	124-127
8996517-7	1997	In three separate studies using groups of eight to ten mice bearing intracranial human glioma xenografts, pretreatment with LOX followed by anti-LOX serum increased the antitumor activity of melphalan as compared with treatments with melphalan plus LOX, melphalan plus anti-LOX serum, or melphalan alone.	Melphalan	191-200	lysyl oxidase	Homo sapiens	145-148
8996517-7	1997	In three separate studies using groups of eight to ten mice bearing intracranial human glioma xenografts, pretreatment with LOX followed by anti-LOX serum increased the antitumor activity of melphalan as compared with treatments with melphalan plus LOX, melphalan plus anti-LOX serum, or melphalan alone.	Melphalan	191-200	lysyl oxidase	Homo sapiens	145-148
8996517-7	1997	In three separate studies using groups of eight to ten mice bearing intracranial human glioma xenografts, pretreatment with LOX followed by anti-LOX serum increased the antitumor activity of melphalan as compared with treatments with melphalan plus LOX, melphalan plus anti-LOX serum, or melphalan alone.	Melphalan	191-200	lysyl oxidase	Homo sapiens	145-148
8980389-15	1996	In conclusion, our findings suggest that the enhanced anti-tumour effect after the combination of TNF-alpha with melphalan results from potentiation of the TNF-alpha-induced vascular changes accompanied by increased vascular permeability and platelet aggregation.	Melphalan	113-122	tumor necrosis factor	Rattus norvegicus	156-165
8980391-0	1996	Effect of melphalan and hyperthermia on p34cdc2 kinase activity in human melanoma cells.	Melphalan	10-19	cyclin dependent kinase 1	Homo sapiens	40-47
8980391-4	1996	At a concentration of 8.5 micrograms ml-1, which reduced cell growth by 50% at 37 degrees C, melphalan inhibited p34cdc2 kinase activity as a consequence of an increased tyrosine phosphorylation of the protein.	Melphalan	93-102	cyclin dependent kinase 1	Homo sapiens	113-120
8980391-5	1996	A similar inhibitory effect on p34cdc2 kinase was obtained when the lowest melphalan concentration (2.5 micrograms ml-1) was used under hyperthermic conditions.	Melphalan	75-84	cyclin dependent kinase 1	Homo sapiens	31-38
8706243-3	1996	Sublines that were resistant to melphalan, pyrazafurin, mitoxantrone, etoposide and PALA all retained expression of wild-type p53.	Melphalan	32-41	tumor protein p53	Homo sapiens	126-129
8932839-0	1996	Role of CD34+ cells in engraftment after high-dose melphalan in multiple myeloma patients given peripheral blood stem cell rescue.	Melphalan	51-60	CD34 molecule	Homo sapiens	8-12
9014745-0	1996	High-dose melphalan with re-infusion of unprocessed, G-CSF-primed whole blood is effective and non-toxic therapy in multiple myeloma.	Melphalan	10-19	colony stimulating factor 3	Homo sapiens	53-58
8779461-9	1996	All 3 had been treated with melphalan.	Melphalan	28-37	paired box 5	Homo sapiens	0-5
8739794-3	1996	The serum IgA concentration fell from 3.42 g/dl to 1.24 g/dl following chemotherapy with melphalan and prednisolone, and a concomitant decrease in both the serum cholesterol and triglyceride levels was observed.	Melphalan	89-98	CD79a molecule	Homo sapiens	10-13
8647649-3	1996	We confirmed that ERCC1 and ERCC4 play a role in the repair of cis-diamminedichloroplatinum (DDP)- and Melphalan (L-PAM)-induced DNA damage, while a marginal role of ERCC2 and ERCC3 in the cellular response to DDP and L-PAM treatment has been observed.	Melphalan	103-112	DNA excision repair protein ERCC-1	Cricetulus griseus	18-23
8647649-3	1996	We confirmed that ERCC1 and ERCC4 play a role in the repair of cis-diamminedichloroplatinum (DDP)- and Melphalan (L-PAM)-induced DNA damage, while a marginal role of ERCC2 and ERCC3 in the cellular response to DDP and L-PAM treatment has been observed.	Melphalan	103-112	DNA repair endonuclease XPF	Cricetulus griseus	28-33
8647649-3	1996	We confirmed that ERCC1 and ERCC4 play a role in the repair of cis-diamminedichloroplatinum (DDP)- and Melphalan (L-PAM)-induced DNA damage, while a marginal role of ERCC2 and ERCC3 in the cellular response to DDP and L-PAM treatment has been observed.	Melphalan	114-119	DNA excision repair protein ERCC-1	Cricetulus griseus	18-23
8647649-3	1996	We confirmed that ERCC1 and ERCC4 play a role in the repair of cis-diamminedichloroplatinum (DDP)- and Melphalan (L-PAM)-induced DNA damage, while a marginal role of ERCC2 and ERCC3 in the cellular response to DDP and L-PAM treatment has been observed.	Melphalan	114-119	DNA repair endonuclease XPF	Cricetulus griseus	28-33
8647649-3	1996	We confirmed that ERCC1 and ERCC4 play a role in the repair of cis-diamminedichloroplatinum (DDP)- and Melphalan (L-PAM)-induced DNA damage, while a marginal role of ERCC2 and ERCC3 in the cellular response to DDP and L-PAM treatment has been observed.	Melphalan	218-223	DNA excision repair protein ERCC-1	Cricetulus griseus	18-23
8647649-3	1996	We confirmed that ERCC1 and ERCC4 play a role in the repair of cis-diamminedichloroplatinum (DDP)- and Melphalan (L-PAM)-induced DNA damage, while a marginal role of ERCC2 and ERCC3 in the cellular response to DDP and L-PAM treatment has been observed.	Melphalan	218-223	DNA repair endonuclease XPF	Cricetulus griseus	28-33
8612685-5	1996	Concentrations and durations of exposure to phorbol esters that downregulated PKC activity correlated with inhibition of VP-16 or melphalan-induced morphological apoptosis and generation of the 30-to-50-kbp DNA fragments.	Melphalan	130-139	protein kinase C alpha	Homo sapiens	78-81
7882302-5	1995	Non-cytotoxic doses of TNF had a super-additive interaction with L-PAM/heat.	Melphalan	65-70	tumor necrosis factor	Mus musculus	23-26
8568824-2	1996	DNA cross-linking was detected in the reaction of linearized pBR322 DNA with 1,12-diaziridinyl-4,9-diazadodecane at concentrations comparable with that required for cross-linking by two nitrogen mustard drugs, mechlorethamine and melphalan.	Melphalan	230-239	resistance to Paracoccidioides brasiliensis	Mus musculus	61-64
8548883-8	1996	TER 117 DEE enhanced melphalan effects on xenografts of HT4-1 in mice to a similar extent as that achieved with the previously described nonspecific GST inhibitor, ethacrynic acid.	Melphalan	21-30	oxidative stress induced growth inhibitor family member 2	Homo sapiens	56-61
7585502-5	1995	A direct correlation (P < 0.01) between intracellular GSH levels and the LD99 dose of melphalan was observed, signifying that elevation of the thiol secondary to GCS expression is sufficient to confer the resistance phenotype.	Melphalan	89-98	glutamate-cysteine ligase catalytic subunit	Homo sapiens	165-168
21597830-2	1995	Incubation with 100 ng/ml human recombinant IL-1 beta for 20 hours prior to a one hour exposure to L-phenylalanine mustard (L-PAM) provided significant protection of bone marrow colony forming cells when compared to bone marrow cells not exposed to IL-1.	Melphalan	99-122	interleukin 1 beta	Homo sapiens	44-53
21597830-2	1995	Incubation with 100 ng/ml human recombinant IL-1 beta for 20 hours prior to a one hour exposure to L-phenylalanine mustard (L-PAM) provided significant protection of bone marrow colony forming cells when compared to bone marrow cells not exposed to IL-1.	Melphalan	99-122	interleukin 1 alpha	Homo sapiens	44-48
21597830-2	1995	Incubation with 100 ng/ml human recombinant IL-1 beta for 20 hours prior to a one hour exposure to L-phenylalanine mustard (L-PAM) provided significant protection of bone marrow colony forming cells when compared to bone marrow cells not exposed to IL-1.	Melphalan	124-129	interleukin 1 beta	Homo sapiens	44-53
21597830-2	1995	Incubation with 100 ng/ml human recombinant IL-1 beta for 20 hours prior to a one hour exposure to L-phenylalanine mustard (L-PAM) provided significant protection of bone marrow colony forming cells when compared to bone marrow cells not exposed to IL-1.	Melphalan	124-129	interleukin 1 alpha	Homo sapiens	44-48
21597830-4	1995	Similar results demonstrating greater protection with IL-1 incubation from L-PAM were seen when murine bone marrow cells were assayed for long-term culture-initiating cells.	Melphalan	75-80	interleukin 1 complex	Mus musculus	54-58
21597830-5	1995	Furthermore, IL-1 protects long-term repopulating hematopoietic stem cells from L-PAM when studied using an in vivo irradiated mouse assay.	Melphalan	80-85	interleukin 1 complex	Mus musculus	13-17
21597830-8	1995	This result indicates that IL-1 may increase the amount of glutathione in hematopoietic cells and be responsible for the observed protection from L-PAM.	Melphalan	146-151	interleukin 1 alpha	Homo sapiens	27-31
7651367-2	1995	Using a mouse mast cell line (IC.DP), we previously showed that v-Abl PTK induced resistance to the anti-cancer drugs melphalan and hydroxyurea by the suppression of apoptosis.	Melphalan	118-127	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	66-69
7706732-0	1995	Importance of TNF production for the curative effectiveness of low dose melphalan therapy for mice bearing a large MOPC-315 tumor.	Melphalan	72-81	tumor necrosis factor	Mus musculus	14-17
7706732-1	1995	We have previously shown the importance of the acquisition of CD8+ T cell-dependent tumor-eradicating immunity for the curative effectiveness of low dose melphalan (L-PAM, L-phenylalanine mustard) for mice bearing a large MOPC-315 tumor.	Melphalan	154-163	peptidylglycine alpha-amidating monooxygenase	Mus musculus	167-170
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.	Melphalan	111-120	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	70-73
8636747-13	1996	CONCLUSION: CTX, at a maximum total dose of 6,000 mg/m2, administered sequentially with melphalan and followed by ABMR was tolerable in children with recurrent brain tumors who had not been heavily pretreated.	Melphalan	88-97	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	12-15
8635194-0	1995	Low-dose-melphalan-induced up-regulation of type-1 cytokine expression in the s.c. tumor nodule of MOPC-315 tumor bearers and the role of interferon gamma in the therapeutic outcome.	Melphalan	9-18	interferon gamma	Mus musculus	138-154
8635194-1	1995	We have previously shown the importance of endogenous tumor necrosis factor (TNF) production for the curative effectiveness of low-dose melphalan (L-phenylalanine mustard) for mice bearing a large MOPC-315 tumor.	Melphalan	136-145	tumor necrosis factor	Mus musculus	54-75
8635194-1	1995	We have previously shown the importance of endogenous tumor necrosis factor (TNF) production for the curative effectiveness of low-dose melphalan (L-phenylalanine mustard) for mice bearing a large MOPC-315 tumor.	Melphalan	136-145	tumor necrosis factor	Mus musculus	77-80
8635194-2	1995	In the current study we demonstrate that low-dose melphalan is actually associated with enhanced expression of mRNA for TNF alpha in the s.c. tumor nodule.	Melphalan	50-59	tumor necrosis factor	Mus musculus	120-129
8635194-5	1995	Moreover, neutralizing anti-IFN gamma mAb, like neutralizing anti-TNF mAb but not neutralizing anti-IL-12 mAb, reduced the curative effectiveness of low-dose melphalan for MOPC-315 tumor bearers.	Melphalan	158-167	interferon gamma	Mus musculus	28-37
8635194-5	1995	Moreover, neutralizing anti-IFN gamma mAb, like neutralizing anti-TNF mAb but not neutralizing anti-IL-12 mAb, reduced the curative effectiveness of low-dose melphalan for MOPC-315 tumor bearers.	Melphalan	158-167	tumor necrosis factor	Mus musculus	66-69
8635194-6	1995	Studies into the mechanism through which IFN gamma mediates its antitumor effect in low-dose-melphalan-treated MOPC-315 tumor-bearing mice revealed that MOPC-315 tumor cells, which are not sensitive to the direct antitumor effects of TNF, display some sensitivity to the antiproliferative activity of high concentrations of IFN gamma.	Melphalan	93-102	interferon gamma	Mus musculus	41-50
8635194-8	1995	Taken together, our studies illustrate that low-dose melphalan therapy of MOPC-315 tumor bearers is associated with the rapid elevation in the expression of mRNA for IFN gamma and TNF, two cytokines which are important for the curative effectiveness of low-dose melphalan, and which mediate their antitumor effect, in part, through distinct mechanisms.	Melphalan	53-62	interferon gamma	Mus musculus	166-175
8635194-8	1995	Taken together, our studies illustrate that low-dose melphalan therapy of MOPC-315 tumor bearers is associated with the rapid elevation in the expression of mRNA for IFN gamma and TNF, two cytokines which are important for the curative effectiveness of low-dose melphalan, and which mediate their antitumor effect, in part, through distinct mechanisms.	Melphalan	53-62	tumor necrosis factor	Mus musculus	180-183
8635194-8	1995	Taken together, our studies illustrate that low-dose melphalan therapy of MOPC-315 tumor bearers is associated with the rapid elevation in the expression of mRNA for IFN gamma and TNF, two cytokines which are important for the curative effectiveness of low-dose melphalan, and which mediate their antitumor effect, in part, through distinct mechanisms.	Melphalan	262-271	interferon gamma	Mus musculus	166-175
7591283-7	1995	ILP with TNF, IFN gamma and melphalan induced a rapid increase in plasma TN-C levels, peaking in most patients between 24 or 48 hr after ILP.	Melphalan	28-37	tenascin C	Homo sapiens	73-77
7622292-2	1995	The cell-cycle phase perturbations induced by the drug were investigated and compared with those caused by melphalan (L-PAM) in SW626 human ovarian-cancer cells.	Melphalan	107-116	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	120-123
7534716-0	1995	G-CSF is a major component of colony-stimulating activity (CSA) in the plasma of patients with multiple myeloma after treatment with high-dose melphalan (HDM).	Melphalan	143-152	colony stimulating factor 3	Homo sapiens	0-5
7880833-1	1995	Rabbit liver metallothionein-2 is shown to form covalent bonds with the anticancer agent melphalan, in support of the hypothesis that covalent sequestration by metallothionein constitutes one mechanism for the cross-resistance acquired by cancer patients to therapeutic alkylating agents.	Melphalan	89-98	metallothionein 2A	Homo sapiens	13-30
7882302-6	1995	Conversely, non-cytotoxic doses of L-PAM had super-additive interactions with TNF followed by hyperthermia.	Melphalan	35-40	tumor necrosis factor	Mus musculus	78-81
7634379-5	1995	Conditions were found under which LOX-mediated degradation of melphalan was minimized and LNAA depletion was maximized, resulting in a potentiation of the antitumor effect of melphalan on human glioma xenografts in nude mice.	Melphalan	62-71	lysyl oxidase	Homo sapiens	34-37
7530507-4	1995	We have analyzed the prognostic significance of serum immunoreactive IL-6, as measured by a sensitive immunosorbent assay, in 210 patients with newly diagnosed MM subsequently treated with intermittent melphalan and prednisone.	Melphalan	202-211	interleukin 6	Homo sapiens	69-73
7634379-5	1995	Conditions were found under which LOX-mediated degradation of melphalan was minimized and LNAA depletion was maximized, resulting in a potentiation of the antitumor effect of melphalan on human glioma xenografts in nude mice.	Melphalan	175-184	lysyl oxidase	Homo sapiens	34-37
8089490-1	1994	We have previously shown that depletion of TCR-V beta 8+ T cells by treatment with mAb reduces the curative effectiveness of low dose melphalan (L-phenylalanine mustard; L-PAM) for mice bearing a large MOPC-315 tumor and extensive metastases.	Melphalan	134-143	peptidylglycine alpha-amidating monooxygenase	Mus musculus	172-175
7954458-7	1994	These TGF-beta-resistant cells also exhibited progressively increasing levels of expression of the c-fos and and myc mRNA, and increased resistance to the cytotoxicity of Adriamycin and melphalan.	Melphalan	186-195	transforming growth factor, beta 1	Rattus norvegicus	6-14
7923130-1	1994	Cells with a temperature-sensitive mutant of the v-abl oncoprotein (IC.DP) were treated with the anticancer drugs melphalan or hydroxyurea.	Melphalan	114-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-54
7812943-6	1994	When MCF-7 cells or human SW2 small cell lung cancer cells were exposed to a concentration of melphalan or cis-diamminedichloroplatinum(II) that killed 1-2 logs of cells followed by exposure to a concentration range of the same drug for 24 h or 7 days later resistance to the second drug exposure was evident in both cell lines.	Melphalan	94-103	WD repeat domain 82 pseudogene 1	Homo sapiens	26-29
7969079-3	1994	Using melphalan-resistant DU 145/M4.5 human prostate carcinoma cells, which express elevated GSH levels, GCS enzyme activity, and GCS mRNA levels, we sought to determine the mechanism(s) responsible for the increased GCS mRNA expression.	Melphalan	6-15	glutamate-cysteine ligase catalytic subunit	Homo sapiens	105-108
7969079-3	1994	Using melphalan-resistant DU 145/M4.5 human prostate carcinoma cells, which express elevated GSH levels, GCS enzyme activity, and GCS mRNA levels, we sought to determine the mechanism(s) responsible for the increased GCS mRNA expression.	Melphalan	6-15	glutamate-cysteine ligase catalytic subunit	Homo sapiens	130-133
7969079-3	1994	Using melphalan-resistant DU 145/M4.5 human prostate carcinoma cells, which express elevated GSH levels, GCS enzyme activity, and GCS mRNA levels, we sought to determine the mechanism(s) responsible for the increased GCS mRNA expression.	Melphalan	6-15	glutamate-cysteine ligase catalytic subunit	Homo sapiens	130-133
8044831-5	1994	In addition, by day 2 after low-dose L-PAM therapy a drastic decrease in the amount of IL-10 secreted by the s.c. tumor nodules was noted, which preceded the accumulation of tumor-infiltrating lymphocytes capable of secreting IFN gamma.	Melphalan	37-42	interleukin 10	Mus musculus	87-92
8044831-0	1994	Low-dose melphalan-induced shift in the production of a Th2-type cytokine to a Th1-type cytokine in mice bearing a large MOPC-315 tumor.	Melphalan	9-18	heart and neural crest derivatives expressed 2	Mus musculus	56-59
8083225-6	1994	The resistance conferred by ALDH to mafosfamide is OAP-specific since the 3A1-31A line is also resistant to 4-hydroperoxycyclophosphamide (2.9-fold) and 4-hydroperoxyifosfamide (3.2-fold) but not to the non-oxazaphosphorine drugs phosphoramide mustard and melphalan, which cannot be detoxified by aldehyde dehydrogenase enzymes.	Melphalan	256-265	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	28-32
8044831-5	1994	In addition, by day 2 after low-dose L-PAM therapy a drastic decrease in the amount of IL-10 secreted by the s.c. tumor nodules was noted, which preceded the accumulation of tumor-infiltrating lymphocytes capable of secreting IFN gamma.	Melphalan	37-42	interferon gamma	Mus musculus	226-235
8044831-0	1994	Low-dose melphalan-induced shift in the production of a Th2-type cytokine to a Th1-type cytokine in mice bearing a large MOPC-315 tumor.	Melphalan	9-18	negative elongation factor complex member C/D, Th1l	Mus musculus	79-82
8044831-6	1994	Thus, low-dose L-PAM therapy of mice bearing a large MOPC-315 tumor leads to a shift in cytokine production from a Th2-type cytokine to a Th1-type cytokine, and it is conceivable that this shift in cytokine production plays an important role in the low-dose L-PAM-induced acquisition of antitumor immunity by hitherto immunosuppressed mice bearing a large MOPC-315 tumor.	Melphalan	15-20	heart and neural crest derivatives expressed 2	Mus musculus	115-118
8044831-3	1994	In contrast, addition of monoclonal anti-IL-10 antibody to the in vitro stimulation cultures of splenic cells from mice that are in the final stages of immune-mediated tumor eradication as a consequence of low-dose melphalan (L-phenylalanine mustard; L-PAM) therapy (and whose spleens no longer contain metastatic tumor cells) did not lead to enhancement in the in vitro generation of antitumor cytotoxicity.	Melphalan	215-224	interleukin 10	Mus musculus	41-46
8044831-4	1994	The cessation of IL-10 secretion as a consequence of low-dose L-PAM therapy of MOPC-315 tumor bearers was found to be accompanied by the acquisition of the ability to secrete interferon gamma (IFN gamma) by the splenic cells.	Melphalan	62-67	interleukin 10	Mus musculus	17-22
8044831-6	1994	Thus, low-dose L-PAM therapy of mice bearing a large MOPC-315 tumor leads to a shift in cytokine production from a Th2-type cytokine to a Th1-type cytokine, and it is conceivable that this shift in cytokine production plays an important role in the low-dose L-PAM-induced acquisition of antitumor immunity by hitherto immunosuppressed mice bearing a large MOPC-315 tumor.	Melphalan	15-20	negative elongation factor complex member C/D, Th1l	Mus musculus	138-141
8044831-4	1994	The cessation of IL-10 secretion as a consequence of low-dose L-PAM therapy of MOPC-315 tumor bearers was found to be accompanied by the acquisition of the ability to secrete interferon gamma (IFN gamma) by the splenic cells.	Melphalan	62-67	interferon gamma	Mus musculus	193-202
8144932-1	1994	We have recently demonstrated the importance of V beta 8+/CD8+ cells for the curative effectiveness of a suboptimal low dose (0.75 mg/kg) of melphalan (L-phenylalanine mustard; L-PAM) for mice bearing a large s.c. MOPC-315 tumor and extensive metastases.	Melphalan	141-150	peptidylglycine alpha-amidating monooxygenase	Mus musculus	179-182
8168116-4	1994	Moreover, even spleen cells from MOPC-315 tumor-bearing mice, which had received L-PAM therapy 7 days earlier and had acquired CTL activity in vivo, were sensitive to the inhibitory activity of TGF-beta upon culture for as little as 1 day, with or without stimulator tumor cells.	Melphalan	81-86	transforming growth factor, beta 1	Mus musculus	194-202
8168116-6	1994	Thus, the curative effectiveness of low-dose L-PAM therapy for MOPC-315 tumor-bearing mice may be due, at least in part, to a reduction in TGF-beta production that enables the development of tumor-eradicating immunity.	Melphalan	45-50	transforming growth factor, beta 1	Mus musculus	139-147
7910660-12	1994	LYC5 cells were slightly more sensitive to Melphalan and doxorubicin (2.8- and 2.3-fold, respectively) but not to cisplatin or dideazatetrahydrofolic acid.	Melphalan	43-52	sperm acrosome associated 5	Homo sapiens	0-4
8004757-4	1994	The addition of each of the modulator combinations for 1 h or 24 h to treatment with melphalan (L-PAM) or carmustine (BCNU) resulted in greater-than-additive cytotoxicity with each of four regimens.	Melphalan	85-94	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	98-101
8011697-7	1994	Renewed interest has developed in hyperthermic limb perfusion for the treatment of transit and locally advanced recurrent disease because of the availability of melphalan and the recent reports of higher response rates with the addition of tumor necrosis factor and interferon gamma to melphalan.	Melphalan	286-295	interferon gamma	Homo sapiens	266-282
8038591-11	1994	We conclude that high-dose rTNF-alpha associated with melphalan in isolation perfusion is the therapy of choice for in-transit melanoma metastases.	Melphalan	54-63	tumor necrosis factor	Rattus norvegicus	27-37
7513621-1	1994	Levels of intracellular glutathione (GSH) and the GSH-related enzymes gamma-glutamylcysteine synthetase (gamma-GCS) and gamma-glutamyltranspeptidase (gamma-GT) were measured in the melphalan-resistant human multiple myeloma cell line 8226/LR-5 and were compared to those measured in the drug-sensitive 8226/S and doxorubicin-resistant 8226/Dox40 cell lines.	Melphalan	181-190	glutamate-cysteine ligase catalytic subunit	Homo sapiens	70-103
8262669-0	1994	Receptor-mediated cytotoxicity of alpha-MSH fragments containing melphalan in a human melanoma cell line.	Melphalan	65-74	proopiomelanocortin	Homo sapiens	34-43
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.	Melphalan	195-204	protein disulfide isomerase associated 4	Mus musculus	18-21
8422666-0	1993	Characterization of the exogenous interleukin-2 requirements for the generation of enhanced antitumor cytotoxicity by thymocytes from low-dose melphalan-treated MOPC-315 tumor bearers.	Melphalan	143-152	interleukin 2	Mus musculus	34-47
8298434-8	1993	After melphalan treatment down regulation of c-myc and of the H2A histone was seen at high doses, while no significant alteration of their expression was seen with the other drugs.	Melphalan	6-15	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	45-50
8409442-1	1993	We have previously shown that the curative efficacy of low dose melphalan (L-phenylalanine mustard; L-PAM) for mice bearing a large s.c. MOPC-315 tumor requires the participation of CD8+ (but not CD4+) T cell-dependent antitumor immunity.	Melphalan	64-73	peptidylglycine alpha-amidating monooxygenase	Mus musculus	102-105
8402679-7	1993	The clones expressing recombinant GST Yc were more resistant to melphalan (6- to 12-fold), mechlorethamine (10- to 16-fold), and chlorambucil (7- to 30-fold).	Melphalan	64-73	hematopoietic prostaglandin D synthase	Rattus norvegicus	34-37
8324733-1	1993	Previous studies of ERCC-1 gene expression levels in chronic lymphocytic leukemia and ovarian carcinoma tumor specimens indicated that increased gene expression may correlate with a lack of response to the alkylating agents, melphalan, and cis-diamminedichloroplatinum (II).	Melphalan	225-234	DNA excision repair protein ERCC-1	Cricetulus griseus	20-26
7513621-2	1994	Both GSH and gamma-GCS activity, the rate-limiting step in the de novo synthesis of GSH, were elevated by a factor of approximately 2 in the melphalan-resistant 8226/LR-5 cells relative to the other two lines.	Melphalan	141-150	glutamate-cysteine ligase catalytic subunit	Homo sapiens	13-22
7517149-0	1994	The costs of peripheral blood progenitor cell reinfusion mobilised by granulocyte colony-stimulating factor following high dose melphalan as compared with conventional therapy in multiple myeloma.	Melphalan	128-137	colony stimulating factor 3	Homo sapiens	70-107
8019062-1	1994	Two different chlorinated drugs, chlorambucil and melphalan, have been linked to the carrier alpha-melanocyte-stimulating hormone at the end of the solid-phase peptide synthesis of the hormone.	Melphalan	50-59	proopiomelanocortin	Homo sapiens	93-129
8492420-12	1993	Treatment with prednisolone and melphalan resulted in improvement of clinical findings such as anemia, lymph node swelling and hypergammaglobulinemia in concurrence with decrease in serum levels of IL-6.	Melphalan	32-41	interleukin 6	Homo sapiens	198-202
8462127-0	1993	Glutathione depletion increases the cytotoxicity of melphalan to PC-3, an androgen-insensitive prostate cancer cell line.	Melphalan	52-61	chromobox 8	Homo sapiens	65-69
8422666-2	1993	Here we characterize the rIL-2 requirements for the generation of enhanced antitumor cytotoxicity by L-PAM TuB thymocytes relative to normal thymocytes upon in vitro stimulation with MOPC-315 tumor cells.	Melphalan	101-106	interleukin 2	Rattus norvegicus	25-30
8422666-2	1993	Here we characterize the rIL-2 requirements for the generation of enhanced antitumor cytotoxicity by L-PAM TuB thymocytes relative to normal thymocytes upon in vitro stimulation with MOPC-315 tumor cells.	Melphalan	101-106	tubby bipartite transcription factor	Mus musculus	107-110
8422666-4	1993	However, even when rIL-2 was added on day 2 after culture initiation, thymocytes from L-PAM TuB mice generated a more potent antitumor cytotoxicity than did thymocytes from normal mice.	Melphalan	86-91	interleukin 2	Rattus norvegicus	19-24
8422666-4	1993	However, even when rIL-2 was added on day 2 after culture initiation, thymocytes from L-PAM TuB mice generated a more potent antitumor cytotoxicity than did thymocytes from normal mice.	Melphalan	86-91	tubby bipartite transcription factor	Mus musculus	92-95
8422666-5	1993	In addition, when rIL-2 was added at the time of culture initiation, replacement of the conditioned medium with fresh medium lacking rIL-2 on day 3 of the 5-day in vitro stimulation culture period eliminated the ability of normal thymocytes, and reduced (but did not eliminate) the ability of L-PAM TuB thymocytes, to generate a significant level of antitumor cytotoxicity.	Melphalan	293-298	interleukin 2	Rattus norvegicus	18-23
8422666-6	1993	A low concentration of fresh rIL-2 was sufficient to restore completely the generation of antitumor cytotoxicity by normal or L-PAM TuB thymocytes when added to the stimulation cultures immediately after the removal of the rIL-2-containing conditioned medium.	Melphalan	126-131	interleukin 2	Rattus norvegicus	29-34
8422666-7	1993	The same low concentration of rIL-2 was also sufficient for restoring the generation of antitumor cytotoxicity by cultures of L-PAM TuB thymocytes, but not normal thymocytes, from which the rIL-2-containing medium was removed 1 day earlier.	Melphalan	126-131	interleukin 2	Rattus norvegicus	30-35
8422666-7	1993	The same low concentration of rIL-2 was also sufficient for restoring the generation of antitumor cytotoxicity by cultures of L-PAM TuB thymocytes, but not normal thymocytes, from which the rIL-2-containing medium was removed 1 day earlier.	Melphalan	126-131	tubby bipartite transcription factor	Mus musculus	132-135
8422666-8	1993	At the same time, conditioned medium from stimulation cultures of L-PAM TuB thymocytes was not superior to conditioned medium from stimulation cultures of normal thymocytes in supporting the generation of antitumor cytotoxicity by either normal or L-PAM TuB thymocytes.	Melphalan	66-71	tubby bipartite transcription factor	Mus musculus	72-75
1372807-1	1992	The alkylating agent melphalan is actively transported in mammalian cells by two amino acid transport carriers: the sodium-dependent carrier with substrate preference for alanine-serine-cysteine (system ASC), and a sodium-independent carrier with preference for leucine (system L).	Melphalan	21-30	PYD and CARD domain containing	Homo sapiens	203-206
1733553-10	1992	The most marked reduction in [3H]-thymidine incorporation into SCC-25 cells occurred following treatment with the combination of beta-carotene and melphalan.	Melphalan	147-156	serpin family B member 3	Homo sapiens	63-66
1545395-6	1992	We conclude that although liver cytosol contains enzymes that significantly enhance the rate of glutathione conjugation with melphalan, in the case of the tumor cells studied, cellular glutathione S-transferase-catalyzed activity appears to be, at best, a very minor determinant of the overall rate of melphalan-glutathione conjugate formation.	Melphalan	302-311	glutathione S-transferase kappa 1	Homo sapiens	185-210
1561804-6	1992	rIFN-gamma was given subcutaneously on days -2 and -1 and in the perfusate, with rTNF alpha, at the dose of 0.2 mg. Melphalan was administered in the perfusate at dose giving a concentration of 40 micrograms/ml.	Melphalan	116-125	interferon gamma	Rattus norvegicus	0-10
1564957-5	1992	Moreover, melphalan was equally effective in inhibiting CFU-L growth in both PE1 and PE2 assays, with D10 values of 1.53 +/- 0.17 micrograms/ml and 1.59 +/- 0.21 micrograms/ml for PE1 and PE2, respectively (p = 0.48).	Melphalan	10-19	ETS variant transcription factor 3	Homo sapiens	77-80
1564957-5	1992	Moreover, melphalan was equally effective in inhibiting CFU-L growth in both PE1 and PE2 assays, with D10 values of 1.53 +/- 0.17 micrograms/ml and 1.59 +/- 0.21 micrograms/ml for PE1 and PE2, respectively (p = 0.48).	Melphalan	10-19	ETS2 repressor factor	Homo sapiens	85-88
1764367-3	1991	The compound maintains activity on melphalan (L-PAM)-resistant cells, whereas cross-resistance is observed on doxorubicin-(DX)-resistant cells.	Melphalan	35-44	peptidylglycine alpha-amidating monooxygenase	Mus musculus	48-51
1730428-3	1992	Therefore, a phase I study of intravenous melphalan utilizing GM-CSF (recombinant granulocyte-macrophage colony-stimulating factor) support was initiated.	Melphalan	42-51	colony stimulating factor 2	Homo sapiens	82-130
1730428-8	1992	Utilizing 20 micrograms/kg/day GM-CSF, the maximum tolerated dose (MTD) of melphalan is 30 mg/m2 and, with 10 mg/kg/day GM-CSF, the maximum tolerated melphalan dose is only 20 mg/m2.	Melphalan	75-84	colony stimulating factor 2	Homo sapiens	31-37
1730428-2	1992	It was postulated that GM-CSF would permit the use of higher dose melphalan with only moderate myelosuppression easily manageable in an outpatient setting.	Melphalan	66-75	colony stimulating factor 2	Homo sapiens	23-29
1730428-3	1992	Therefore, a phase I study of intravenous melphalan utilizing GM-CSF (recombinant granulocyte-macrophage colony-stimulating factor) support was initiated.	Melphalan	42-51	colony stimulating factor 2	Homo sapiens	62-68
1681052-2	1991	The cytotoxic drug combination of methotrexate and melphalan, or nifedipine alone (0.2-25 micrograms mL-1), caused a concentration-related reduction of NC cell growth in culture.	Melphalan	51-60	L1 cell adhesion molecule	Mus musculus	101-105
2015603-2	1991	We have isolated and purified GST isozymes from mouse liver (M. Warholm et al., Biochemistry, 25: 4119-4125, 1986) and analyzed the metabolic products of the reaction of L-phenylalanine mustard (L-PAM) with glutathione in the presence of GST isozymes, using reverse phase high performance liquid chromatography.	Melphalan	195-200	hematopoietic prostaglandin D synthase	Mus musculus	30-33
1668532-0	1991	Human melanoma targeting with alpha-MSH-melphalan conjugate.	Melphalan	40-49	proopiomelanocortin	Homo sapiens	30-39
1668532-6	1991	alpha-MSH receptor recognition properties also remained unchanged with a better apparent affinity of the conjugate probably due to the alkylating activity of melphalan itself.	Melphalan	158-167	proopiomelanocortin	Homo sapiens	0-9
1668532-7	1991	Using human melanoma dendritic cells expressing more than 10,000 alpha-MSH binding sites per cell as an in vitro model, we were able to demonstrate higher cytotoxicities as compared to melphalan-treated cells.	Melphalan	185-194	proopiomelanocortin	Homo sapiens	65-74
2015603-5	1991	Only isozymes of the alpha GST class catalyze the conjugation of L-PAM with glutathione.	Melphalan	65-70	hematopoietic prostaglandin D synthase	Mus musculus	27-30
1901031-7	1991	The apparent specificity of the lytic activity exerted by the PMA-stimulated L-PAM TuB spleen cells was illustrated not only by the inability of the spleen cells to lyse an allogeneic, antigenically unrelated thymoma (EL4), but also by their relatively weak lytic activity for two antigenically related syngeneic plasmacytomas.	Melphalan	77-82	epilepsy 4	Mus musculus	218-221
1760820-3	1991	In addition, the ability of melphalan TuB thymocytes to generate an enhanced level of anti-MOPC-315 cytotoxicity correlated with their ability to proliferate more readily than thymocytes from untreated tumor-bearing mice and thymocytes from untreated or melphalan-treated normal mice in response to stimulation with MOPC-315 tumor cells plus a low concentration of rIL-2.	Melphalan	28-37	tubby bipartite transcription factor	Mus musculus	38-41
1760820-3	1991	In addition, the ability of melphalan TuB thymocytes to generate an enhanced level of anti-MOPC-315 cytotoxicity correlated with their ability to proliferate more readily than thymocytes from untreated tumor-bearing mice and thymocytes from untreated or melphalan-treated normal mice in response to stimulation with MOPC-315 tumor cells plus a low concentration of rIL-2.	Melphalan	28-37	interleukin 2	Rattus norvegicus	365-370
1901031-8	1991	In addition, when EL4 target cells were admixed with MOPC-315 tumor cells, the lytic activity triggered in the L-PAM TuB spleen cells by the MOPC-315 tumor cells plus PMA was not effective in lysing the antigenically unrelated target cells.	Melphalan	111-116	epilepsy 4	Mus musculus	18-21
2123740-4	1990	Treatment of MOPC-315 tumor bearers with low-dose L-PAM in conjunction with monoclonal anti-Thy-1.2 or anti-Lyt-2.2 antibody, in contrast to treatment with monoclonal anti-L3T4 antibody, prevented the appearance of the massive CD8+ T-cell infiltrate in the s.c. tumor nodules.	Melphalan	50-55	thymus cell antigen 1, theta	Mus musculus	92-99
27463358-3	1991	Six years later, an increased serum M-protein became evident (IgG$LD, 3 gr/dl) associated with 35% plasma cells in the bone marrow, which necessitated melphalan/prednisone therapy.	Melphalan	151-160	myomesin 2	Homo sapiens	36-45
2260990-0	1990	Enhancement of melphalan (L-PAM) toxicity by reductive metabolites of 1-methyl-2-nitroimidazole, a model nitroimidazole chemosensitizing agent.	Melphalan	15-24	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	28-31
1977668-3	1990	Five patients resistant to protocols including vincristine, melphalan and doxorubicin were found to express P-glycoprotein.	Melphalan	60-69	ATP binding cassette subfamily B member 1	Homo sapiens	108-122
2208589-1	1990	Previous studies have demonstrated that three cancer chemotherapeutic compounds of the nitrogen mustard class, melphalan (L-PAM), nitrogen mustard (HN2) and chlorambucil (CBC), each generated DNA lesions that prematurely terminate in vitro transcription.	Melphalan	111-120	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	124-127
2200536-2	1990	In an attempt to stimulate earlier granulocyte recovery, recombinant human granulocyte-macrophage colony-stimulating factor (GM-CSF) was administered subcutaneously to 23 patients with refractory myeloma who had been treated with melphalan at a high dose of 100 mg/m2.	Melphalan	230-239	colony stimulating factor 2	Homo sapiens	75-123
2200536-8	1990	These results support the usefulness of low-dose GM-CSF (0.25 mg/m2) in stimulating marrow recovery in selected patients with adequate marrow reserve treated with high-dose melphalan for refractory multiple myeloma.	Melphalan	173-182	colony stimulating factor 2	Homo sapiens	49-55
2201402-0	1990	Colony stimulating activity in the serum of patients with multiple myeloma is enhanced by interleukin 3: a possible role for interleukin 3 after high dose melphalan and autologous bone marrow transplantation for multiple myeloma.	Melphalan	155-164	interleukin 3	Homo sapiens	125-138
1703510-0	1990	CAV chemotherapy (CCNU, melphalan, etoposide) as salvage treatment for relapsing or resistant Hodgkin"s disease.	Melphalan	24-33	caveolin 2	Homo sapiens	0-3
1692472-0	1990	Granulocyte-macrophage colony stimulating factor (GM-CSF) after high-dose melphalan in patients with advanced colon cancer.	Melphalan	74-83	colony stimulating factor 2	Homo sapiens	0-48
1692472-0	1990	Granulocyte-macrophage colony stimulating factor (GM-CSF) after high-dose melphalan in patients with advanced colon cancer.	Melphalan	74-83	colony stimulating factor 2	Homo sapiens	50-56
2171755-1	1990	alpha-MSH fragments containing melphalan were tested in vivo on L1210 leukemia and on human amelanotic melanoma xenograft in mice and in vitro on human amelanotic melanoma cell lines.	Melphalan	31-40	proopiomelanocortin	Homo sapiens	0-9
2177734-1	1990	For chemical affinity labeling of the melanotropin receptor several alpha-MSH fragments containing phenylalanine mustard were synthesized in solution.	Melphalan	99-120	melanocortin 1 receptor	Homo sapiens	38-59
2177734-1	1990	For chemical affinity labeling of the melanotropin receptor several alpha-MSH fragments containing phenylalanine mustard were synthesized in solution.	Melphalan	99-120	proopiomelanocortin	Homo sapiens	68-77
2116401-2	1990	PC-9/CDDP demonstrated 28-fold resistance to cisplatin, with cross resistance to other chemotherapeutic drugs including chlorambucil (X 6.3), melphalan (X 3.7) and 3-[(4-amino-2-methyl-5-pyrimidinyl)]methyl-1-(2-chloroethyl)-1-nitros our ea (ACNU) (x 3.9).	Melphalan	142-151	proprotein convertase subtilisin/kexin type 9	Homo sapiens	0-4
2381059-8	1990	Plasma exchange was done four times and melphalan was given orally for two weeks, but the level of serum IgA increased further.	Melphalan	40-49	CD79a molecule	Homo sapiens	105-108
2337902-0	1990	Eradication of a large MOPC-315 tumor in athymic nude mice by chemoimmunotherapy with Lyt2+ splenic T cells from melphalan-treated BALB/c mice bearing a large MOPC-315 tumor.	Melphalan	113-122	CD8 antigen, alpha chain	Mus musculus	86-90
2289208-1	1990	We have previously shown that, as a consequence of low-dose melphalan (L-phenylalanine mustard) treatment, thymocytes from mice bearing a large, day-10 MOPC-315 tumor, but not thymocytes from normal mice, acquire the ability to generate an enhanced level of antitumor cytotoxicity upon in vitro stimulation with MOPC-315 tumor cells plus low concentrations (9.0-90 IU/ml) of exogenous interleukin-2 (IL-2).	Melphalan	60-69	interleukin 2	Mus musculus	385-398
2289208-1	1990	We have previously shown that, as a consequence of low-dose melphalan (L-phenylalanine mustard) treatment, thymocytes from mice bearing a large, day-10 MOPC-315 tumor, but not thymocytes from normal mice, acquire the ability to generate an enhanced level of antitumor cytotoxicity upon in vitro stimulation with MOPC-315 tumor cells plus low concentrations (9.0-90 IU/ml) of exogenous interleukin-2 (IL-2).	Melphalan	60-69	interleukin 2	Mus musculus	400-404
33972235-1	2022	BACKGROUND: Current melphalan-based intravitreal regimens for retinoblastoma (RB) vitreous seeds cause retinal toxicity.	Melphalan	20-29	RB transcriptional corepressor 1	Homo sapiens	62-76
2289208-8	1990	Thus, the enhanced level of antitumor cytotoxicity generated by thymocytes from mice that are treated with low-dose melphalan when they have a large, late-stage MOPC-315 tumor is due, at least in part, to the presence of an enlarged pool of CTLp specific for MOPC-315-associated antigens, which mature into CD8+/CD4- effector cells upon stimulation with MOPC-315 tumor cells plus low concentrations of rIL-2.	Melphalan	116-125	interleukin 2	Rattus norvegicus	402-407
34676048-0	2021	TAK1-inhibitors are cytotoxic for multiple myeloma cells alone and in combination with melphalan.	Melphalan	87-96	mitogen-activated protein kinase kinase kinase 7	Homo sapiens	0-4
33771821-9	2021	In addition, blockade of CD304 reversed suppression of the in vitro cytotoxic effect of melphalan by pre-ASCT M-MDSCs.	Melphalan	88-97	neuropilin 1	Homo sapiens	25-30
34832966-10	2021	Treatment with cisplatin, melphalan, or 9-cis RA decreased p53 expression levels in SK-N-FI cells but not in SK-N-Be (2).	Melphalan	26-35	tumor protein p53	Homo sapiens	59-62
34504546-9	2021	Furthermore, DHMEQ enhanced cytotoxicity of the anticancer agent melphalan in SP2/0 cells.	Melphalan	65-74	Sp2 transcription factor	Mus musculus	78-83
34641586-5	2021	Melphalan flufenamide (melflufen) is a highly lipophilic PDC that takes a novel approach by utilizing increased aminopeptidase activity to selectively increase the release and concentration of cytotoxic alkylating agents inside tumor cells.	Melphalan	0-9	carboxypeptidase Q	Homo sapiens	112-126
35190641-7	2022	The Chk1 inhibitor (AZD7762) tested showed good synergism with standard-of-care myeloma drugs, velcade and melphalan, thus further reinforcing the translational potential of this therapeutic approach.	Melphalan	107-116	checkpoint kinase 1	Homo sapiens	4-8
34367999-14	2021	Here, we report a considerable clinical activity of melphalan chemotherapy, more evident in a subset of BRCA1/2 mutated patients.	Melphalan	52-61	BRCA1 DNA repair associated	Homo sapiens	104-111
34262262-8	2021	The aminopeptidase-driven accumulation results in a 50-fold increase in L-PAM cell enrichment as compared with free alkylator.	Melphalan	72-77	carboxypeptidase Q	Homo sapiens	4-18
35546555-3	2022	Here, we show that mucosal barrier injury induced by the mucotoxic chemotherapeutic agent, high-dose melphalan (HDM), is characterized by hyper-active IL-1b/CXCL1/neutrophil signaling.	Melphalan	101-110	interleukin 1 beta	Rattus norvegicus	151-156
35546555-3	2022	Here, we show that mucosal barrier injury induced by the mucotoxic chemotherapeutic agent, high-dose melphalan (HDM), is characterized by hyper-active IL-1b/CXCL1/neutrophil signaling.	Melphalan	101-110	C-X-C motif chemokine ligand 1	Rattus norvegicus	157-162
35427190-1	2022	PURPOSE: Ewing 2008R3 was conducted in 12 countries and evaluated the effect of treosulfan and melphalan high-dose chemotherapy (TreoMel-HDT) followed by reinfusion of autologous hematopoietic stem cells on event-free survival (EFS) and overall survival in high-risk Ewing sarcoma (EWS).	Melphalan	95-104	EWS RNA binding protein 1	Homo sapiens	282-285
34530900-10	2021	Finally, we showed that SETD8 inhibition is strongly synergistic with melphalan and may overcome resistance to this alkylating agent widely used in MM treatment.	Melphalan	70-79	lysine methyltransferase 5A	Homo sapiens	24-29
34530900-12	2021	Moreover, we provide evidences that myeloma cells are dependent on SETD8 activity and its pharmacological inhibition synergizes with melphalan, which could be beneficial to improve MM treatment in high-risk patients whatever their status for p53.	Melphalan	133-142	lysine methyltransferase 5A	Homo sapiens	67-72
34530900-12	2021	Moreover, we provide evidences that myeloma cells are dependent on SETD8 activity and its pharmacological inhibition synergizes with melphalan, which could be beneficial to improve MM treatment in high-risk patients whatever their status for p53.	Melphalan	133-142	tumor protein p53	Homo sapiens	242-245
34136753-7	2021	We hypothesized that increased aminopeptidase B expression in aggressive myeloma clones may be used therapeutically toward elimination of the cells via the use of a novel peptide-drug conjugate, melphalan flufenamide (melflufen).	Melphalan	195-204	arginyl aminopeptidase	Homo sapiens	31-47
35464103-9	2022	In the analysis using a mouse model of DRONJ-like lesion, it was revealed that anti-mouse RANKL monoclonal antibody and melphalan suppress autoimmune regulator (AIRE) expression in the thymus and imbalanced T cell populations.	Melphalan	120-129	autoimmune regulator (autoimmune polyendocrinopathy candidiasis ectodermal dystrophy)	Mus musculus	139-159
35094950-13	2022	In our retrospective analysis of 36 patients we showed that single agent high-dose melphalan can achieve high response rates (ORR 66.7%) even in uncontrolled disease enabling consolidation therapy e.g. with allogeneic stem cell transplantation or CAR T-cell therapy.	Melphalan	83-92	CXADR pseudogene 1	Homo sapiens	247-250
35163680-6	2022	Melphalan derivatives were evaluated for cytotoxicity (resazurin viability assay), genotoxicity (alkaline comet assay), and their ability to induce apoptosis (Hoechst33342/propidium iodide double staining method; phosphatidylserine translocation; and caspase 3/7, 8, and 9 activity measurements).	Melphalan	0-9	caspase 3	Homo sapiens	251-262
34969749-0	2022	A Single Nucleotide Polymorphism (SNP) in the SLC22A3 Transporter Gene Is Associated With the Severity of Oral Mucositis in Multiple Myeloma Patients Receiving Autologous Stem Cell Transplant Followed by Melphalan Therapy.	Melphalan	204-213	solute carrier family 22 member 3	Homo sapiens	46-53
34969749-2	2022	Herein we investigated the association of select single nucleotide polymorphisms in SLC22A3 (gene encoding OCT3) with clinical outcomes in multiple myeloma (MM) patients with hematopoietic autologous stem cell transplants followed by high-dose melphalan therapy.	Melphalan	244-253	solute carrier family 22 member 3	Homo sapiens	84-91
34969749-6	2022	CONCLUSION: OCT3 might be involved in melphalan transport in MM patients.	Melphalan	38-47	solute carrier family 22 member 3	Homo sapiens	12-16
35435039-11	2022	We conclude that curcumin mitigates toxicities of high-dose melphalan, possibly through IL-8 modulation.	Melphalan	60-69	C-X-C motif chemokine ligand 8	Homo sapiens	88-92
2788494-7	1989	The magnitude of lysis of EL4 and WEHI 22.1 tumor cells by MOPC-315 in vitro-immunized (IVI) spleen cells from L-PAM-cured MOPC-315 tumor bearers can be substantially enhanced upon reexposure of the spleen cells to MOPC-315-associated antigens during the 12-h 51Cr release assay.	Melphalan	111-116	epilepsy 4	Mus musculus	26-29
2479474-2	1989	C/CDP-2 was cross-resistant to carboplatin, L-phenylalanine mustard (melphalan), and CdSO4, but not to other anticancer agents.	Melphalan	69-78	cut like homeobox 2	Homo sapiens	2-7
2789274-1	1989	In patients who have not received extensive prior chemotherapy or radiotherapy, it has been previously demonstrated that granulocyte colony-stimulating factor (G-CSF) abrogated the leukopenia following administration of melphalan (25 mg/m2).	Melphalan	220-229	colony stimulating factor 3	Homo sapiens	121-158
2789274-1	1989	In patients who have not received extensive prior chemotherapy or radiotherapy, it has been previously demonstrated that granulocyte colony-stimulating factor (G-CSF) abrogated the leukopenia following administration of melphalan (25 mg/m2).	Melphalan	220-229	colony stimulating factor 3	Homo sapiens	160-165
2789274-6	1989	G-CSF produced a rapid and sustained elevation in neutrophil levels within 24 hours even when started 8 days after melphalan.	Melphalan	115-124	colony stimulating factor 3	Homo sapiens	0-5
2789274-12	1989	We conclude that after melphalan chemotherapy, G-CSF may need to be given for only a short period to prevent chemotherapy-induced neutropenia, and that G-CSF induces a rapid rise in neutrophil levels even when started 8 days after melphalan administration.	Melphalan	231-240	colony stimulating factor 3	Homo sapiens	152-157
2788494-11	1989	Thus, Lyt 2+ T-cells independent of effector macrophages are responsible for lysis of innocent bystander tumor cells by MOPC-315-IVI spleen cells from L-PAM-cured MOPC-315 tumor bearers.	Melphalan	151-156	CD8 antigen, alpha chain	Mus musculus	6-11
2548207-1	1989	The nitrogen mustard derivatives of 4-phenylbutyric acid and L-phenylalanine, called chlorambucil (Chl) and melphalan (Mel), respectively, have been incorporated into several peptide hormones, including luteinizing hormone-releasing hormone (LH-RH).	Melphalan	108-117	gonadotropin releasing hormone 1	Homo sapiens	203-240
2475185-4	1989	When a continuous infusion of G-CSF was administered after melphalan, serum G-CSF levels remained constant for a longer period of time but did decrease during the second phase of a biphasic neutrophil response.	Melphalan	59-68	colony stimulating factor 3	Homo sapiens	30-35
2475185-4	1989	When a continuous infusion of G-CSF was administered after melphalan, serum G-CSF levels remained constant for a longer period of time but did decrease during the second phase of a biphasic neutrophil response.	Melphalan	59-68	colony stimulating factor 3	Homo sapiens	76-81
2568172-2	1989	The MX2 cells are cross-resistant to etoposide, teniposide, bisantrene, dactinomycin, 4"-(9-acridinylamino)methanesulfon-m-anisidide, and the anthracyclines daunorubicin and doxorubicin but retain sensitivity to the Vinca alkaloids melphalan and mitomycin C.	Melphalan	232-241	MX dynamin like GTPase 2	Homo sapiens	4-7
2568174-0	1989	Importance of Lyt 2+ T-cells in the curative effectiveness of a low dose of melphalan for mice bearing a large MOPC-315 tumor.	Melphalan	76-85	CD8 antigen, alpha chain	Mus musculus	14-19
2568174-1	1989	We have previously demonstrated that the curative effectiveness of a low dose (2.5 mg/kg) of melphalan (L-phenylalanine mustard; L-PAM) for mice bearing a large s.c. (approximately 20 mm in diameter) MOPC-315 tumor and extensive metastases requires the participation of T-cell-dependent antitumor immunity in tumor eradication (S. Ben-Efraim et al., Cancer Immunol.	Melphalan	93-102	peptidylglycine alpha-amidating monooxygenase	Mus musculus	131-134
2680579-0	1989	Effect in vivo of recombinant GM-CSF on neutropenia and survival in mice treated by high-dose melphalan.	Melphalan	94-103	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	30-36
2680579-3	1989	However, GM-CSF accelerated the neutrophil recovery and reduced the mortality rate during the neutropenic period compared to melphalan-only treated mice.	Melphalan	125-134	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	9-15
2680579-5	1989	In comparison, GM-CSF further reduced the total CFU-GM population in melphalan-treated mice including the levels in the bone marrow and in the spleen.	Melphalan	69-78	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	15-21
2680579-8	1989	The results suggest that GM-CSF could be used to shorten the neutropenic period and reduce mortality caused by a high dose of melphalan.	Melphalan	126-135	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	25-31
2548207-1	1989	The nitrogen mustard derivatives of 4-phenylbutyric acid and L-phenylalanine, called chlorambucil (Chl) and melphalan (Mel), respectively, have been incorporated into several peptide hormones, including luteinizing hormone-releasing hormone (LH-RH).	Melphalan	108-117	gonadotropin releasing hormone 1	Homo sapiens	242-247
2715802-3	1989	Clinically relevant concentrations of tamoxifen and melphalan reduced colony survival of estrogen receptor (ER)-positive breast cancer cells when used alone in a colony-forming assay.	Melphalan	52-61	estrogen receptor 1	Homo sapiens	89-106
2567207-0	1989	Enhancement of the effectiveness of Lyt-2+ T-cells for adoptive chemoimmunotherapy by short-term exposure of tumor-bearer spleen cells to polyethylene glycol and/or melphalan.	Melphalan	165-174	CD8 antigen, alpha chain	Mus musculus	36-41
2715802-3	1989	Clinically relevant concentrations of tamoxifen and melphalan reduced colony survival of estrogen receptor (ER)-positive breast cancer cells when used alone in a colony-forming assay.	Melphalan	52-61	estrogen receptor 1	Homo sapiens	108-110
2715802-7	1989	Tamoxifen even antagonized melphalan cytotoxicity in ER-negative breast cancer cells and in cultured liver cells.	Melphalan	27-36	estrogen receptor 1	Homo sapiens	53-55
2748937-3	1989	Our results show that the cell killing produced in whole spheroids following a 1-h exposure to melphalan (L-PAM) was enhanced by a 3-h pre-exposure to 5 mM misonidazole (MISO), an enhancement ratio of 1.3-1.7 being obtained.	Melphalan	95-104	peptidylglycine alpha-amidating monooxygenase	Mus musculus	108-111
2715059-2	1989	Treatment of mice with hydralazine (5 mg/kg) 15 mins after melphalan increases by a factor of approximately 2.5 melphalan-induced delay in growth of either the RIF-1 or KHT tumors.	Melphalan	112-121	replication timing regulatory factor 1	Mus musculus	160-165
2783475-1	1989	In vivo mutations at the locus for hypoxanthine phosphoribosyl transferase (hprt) were studied in 6-thioguanine (TG)-resistant T-lymphocyte clones from healthy male and female subjects and ovarian carcinoma patients treated with melphalan.	Melphalan	229-238	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	76-80
2721813-1	1989	K18 is an anticancer drug for oral administration comprising about five molecules of melphalan, an alkylating drug, covalently bonded to human immunoglobulin G. This study measured the in vitro antitumour activity of K18, melphalan and immunoglobulin G on human myeloma cells (RPMI-8226) and the in vivo antitumour effects of K18 and melphalan in BALB/c nude mice bearing human lung cancer cells (LC-10).	Melphalan	85-94	keratin 18	Homo sapiens	0-3
2721813-1	1989	K18 is an anticancer drug for oral administration comprising about five molecules of melphalan, an alkylating drug, covalently bonded to human immunoglobulin G. This study measured the in vitro antitumour activity of K18, melphalan and immunoglobulin G on human myeloma cells (RPMI-8226) and the in vivo antitumour effects of K18 and melphalan in BALB/c nude mice bearing human lung cancer cells (LC-10).	Melphalan	85-94	keratin 18	Homo sapiens	217-220
2721813-1	1989	K18 is an anticancer drug for oral administration comprising about five molecules of melphalan, an alkylating drug, covalently bonded to human immunoglobulin G. This study measured the in vitro antitumour activity of K18, melphalan and immunoglobulin G on human myeloma cells (RPMI-8226) and the in vivo antitumour effects of K18 and melphalan in BALB/c nude mice bearing human lung cancer cells (LC-10).	Melphalan	85-94	keratin 18	Homo sapiens	217-220
2721813-3	1989	This activity of K18 was about half the theoretical value indicating that melphalan molecules are not released easily from the conjugate.	Melphalan	74-83	keratin 18	Homo sapiens	17-20
2783475-1	1989	In vivo mutations at the locus for hypoxanthine phosphoribosyl transferase (hprt) were studied in 6-thioguanine (TG)-resistant T-lymphocyte clones from healthy male and female subjects and ovarian carcinoma patients treated with melphalan.	Melphalan	229-238	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	35-74
2471275-2	1989	Our studies suggest that 10 micrograms/kg/day of G-CSF administered as a continuous subcutaneous infusion abrogates the neutropenia associated with a standard dose of melphalan.	Melphalan	167-176	colony stimulating factor 3	Homo sapiens	49-54
2562921-1	1989	Eight patients with stage III aggressive multiple myeloma, refractory to current chemotherapy in six cases, were treated by high-dose chemotherapy (nitrosourea, etoposide, and melphalan) (HDC) and total body irradiation (TBI), followed by autografting with blood stem cells.	Melphalan	176-185	histidine decarboxylase	Homo sapiens	188-191
2468306-1	1989	The binding and internalization of melphalan-conjugated human immunoglobulin G (K18) to human tumor cell lines were studied using 14C-K18 (IgG conjugated with 14C-melphalan) and were compared with those of 14C-melphalan.	Melphalan	35-44	keratin 18	Homo sapiens	80-83
2468306-1	1989	The binding and internalization of melphalan-conjugated human immunoglobulin G (K18) to human tumor cell lines were studied using 14C-K18 (IgG conjugated with 14C-melphalan) and were compared with those of 14C-melphalan.	Melphalan	35-44	keratin 18	Homo sapiens	134-137
2485138-1	1988	K18 is a newly synthesized antitumor agent which is the conjugate form of human immunoglobulin with p-di (2-chloroethyl)-amino-L-phenylalamine (melphalan).	Melphalan	144-153	keratin 18	Homo sapiens	0-3
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.	Melphalan	119-128	beta-2-microglobulin	Homo sapiens	298-318
3264199-6	1988	In patients nine days after treatment with melphalan and then rG-CSF, progenitor cell levels were very low with doses of rG-CSF at or below 10 micrograms/kg/d, but equaled or exceeded pretreatment values when 30 or 60 micrograms/kg/d of rG-CSF was given.	Melphalan	43-52	colony stimulating factor 3	Rattus norvegicus	121-127
3264199-6	1988	In patients nine days after treatment with melphalan and then rG-CSF, progenitor cell levels were very low with doses of rG-CSF at or below 10 micrograms/kg/d, but equaled or exceeded pretreatment values when 30 or 60 micrograms/kg/d of rG-CSF was given.	Melphalan	43-52	colony stimulating factor 3	Rattus norvegicus	121-127
3416297-10	1988	These studies demonstrate transport parameters confirming facilitated transport of melphalan in human medulloblastoma, a mean murine plasma melphalan concentration (following treatment with melphalan) above the in vitro drug dose at which there is a 90% reduction in the number of colonies in comparison to controls for TE-671 and Daoy for 2 h, and glutathione and glutathione-S-transferase levels in the same range previously reported in other melphalan-sensitive and melphalan-resistant human tumors.	Melphalan	83-92	hematopoietic prostaglandin D synthase	Mus musculus	365-390
3223339-0	1988	M-protein kinetics in multiple myeloma treated with melphalan, ifosfamide, prednisolone, nitrosourea and vincristine in combination.	Melphalan	52-61	myomesin 2	Homo sapiens	0-9
3177368-2	1988	The M-protein and bone pain disappeared within 6 weeks after therapy with melphalan and prednisone was started.	Melphalan	74-83	myomesin 2	Homo sapiens	4-13
3182309-3	1988	Patients with previously untreated myeloma received 12 weeks of melphalan (L-PAM) and prednisone (pred) therapy.	Melphalan	64-73	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	77-80
3178239-3	1988	The KFr cell line proved to be 3.1-fold resistant to L-phenylalanine mustard (L-PAM).	Melphalan	53-76	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	80-83
3261626-1	1988	We have previously shown that mice bearing a large MOPC-315 tumor can be cured by a low dose of melphalan (L-phenylalanine mustard; L-PAM) if T-cell-dependent antitumor immunity also aids in tumor eradication (S. Ben-Efraim et al., Cancer Immunol.	Melphalan	96-105	peptidylglycine alpha-amidating monooxygenase	Mus musculus	134-137
2467651-4	1988	G-CSF was also administered to patients following melphalan and this resulted in a reduction in the duration of the neutropenia that invariably follows melphalan.	Melphalan	50-59	colony stimulating factor 3	Homo sapiens	0-5
2467651-4	1988	G-CSF was also administered to patients following melphalan and this resulted in a reduction in the duration of the neutropenia that invariably follows melphalan.	Melphalan	152-161	colony stimulating factor 3	Homo sapiens	0-5
3367382-1	1988	The average relative dose intensity (DI) of conventional oral melphalan and prednisone therapy received by 93 newly diagnosed multiple myeloma patients was correlated with survival and with percent reduction in M-protein.	Melphalan	62-71	myomesin 2	Homo sapiens	211-220
2453234-2	1988	Melphalan was included in a polychemotherapy treatment with eight 1-h infusions of 230 mg of etoposide (VP 16), then one 5-min infusion of 370 mg of melphalan (200 mg/m2) followed by autologous bone marrow grafting (ABMG).	Melphalan	0-9	host cell factor C1	Homo sapiens	104-109
2895212-6	1988	G-CSF administration following melphalan reduced the period of neutropenia caused by melphalan.	Melphalan	31-40	colony stimulating factor 3	Homo sapiens	0-5
2485136-2	1988	After oral administration of 14C-melphalan and 14C-K-18 to ICR mice with subcutaneously transplanted Ehrlich carcinoma, K-18 was detected at the tumor site by autoradiogram after 48 hrs, but melphalan was not.	Melphalan	33-42	keratin 18	Mus musculus	120-124
3260089-1	1988	Clinical effects of a low dose of behenoyl ara-C (LD-BHAC) and K-18, an IgG-melphalan conjugate, were studied in hypoplastic leukemia (HL).	Melphalan	76-85	keratin 18	Homo sapiens	63-67
3497748-1	1987	In vitro treatment with melphalan (L-PAM, L-phenylalanine mustard), 2 micrograms/2 X 10(6) cells, significantly decreased the total number of E-rosette-positive (E+) T lymphocytes from peripheral blood (PBL) of healthy human donors as well as those of the OKT4 (precursor suppressor/helper/inducer T cells) and OKT17 populations (suppressor cells within the OKT4 subset).	Melphalan	24-33	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	37-40
3396150-3	1988	When L-PAM was given 24 h before DDP, the elimination half-life (t 1/2 beta), plasma clearance (Clp), and volume of distribution (Vd beta) of L-PAM were, respectively: 46.4 +/- 6.7 min, 20.5 +/- 3.7 l/m2, and 306.8 +/- 34.4 ml/min per square meter.	Melphalan	5-10	interleukin 1 receptor like 1	Homo sapiens	65-75
3396150-3	1988	When L-PAM was given 24 h before DDP, the elimination half-life (t 1/2 beta), plasma clearance (Clp), and volume of distribution (Vd beta) of L-PAM were, respectively: 46.4 +/- 6.7 min, 20.5 +/- 3.7 l/m2, and 306.8 +/- 34.4 ml/min per square meter.	Melphalan	5-10	calmodulin like 3	Homo sapiens	96-99
3396150-4	1988	When L-PAM was inoculated 24 h after DDP, t 1/2 beta, Clp, and Vd beta were 47.5 +/- 6.3 min, 20.4 +/- 2.8 l/m2, and 322.0 +/- 54.1 ml/min per square meter.	Melphalan	5-10	interleukin 1 receptor like 1	Homo sapiens	42-52
3396150-4	1988	When L-PAM was inoculated 24 h after DDP, t 1/2 beta, Clp, and Vd beta were 47.5 +/- 6.3 min, 20.4 +/- 2.8 l/m2, and 322.0 +/- 54.1 ml/min per square meter.	Melphalan	5-10	calmodulin like 3	Homo sapiens	54-57
3349564-1	1988	A sensitive high-performance liquid chromatographic assay has been developed for the measurement of the alkylating cytostatic drug melphalan (4-[bis(2-chloroethyl)amino]-L-phenyl-alanine, or L-phenylalanine-mustard, L-PAM) and its two hydrolysis products, monohydroxy melphalan (MOH) and dihydroxy melphalan (DOH).	Melphalan	131-140	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	218-221
2447835-1	1988	Five cases of hypoplastic acute myelocytic leukemia were treated with an IgG-melphalan conjugate, K-18.	Melphalan	77-86	keratin 18	Homo sapiens	98-102
3006735-1	1986	The effect of inhibitors of nuclear ADP-ribosyl transferase (ADPRT) on the cytotoxicity of melphalan (L-PAM) in the RIF-1 tumour in vivo was investigated.	Melphalan	91-100	ADP-ribosyltransferase 1	Mus musculus	36-59
3677124-8	1987	The ability of the L-PAM-cured MOPC-315-tumor bearers to reject the MOPC-315 cells present in the challenge mixture was reduced when the mice were treated with anti-Thy 1.2 antibody but not with carrageenan, indicating that T-cells independent from carrageenan-sensitive effector cells are required for the rejection of the MOPC-315 tumor cells.	Melphalan	19-24	thymus cell antigen 1, theta	Mus musculus	165-172
2944475-1	1986	Both melphalan (L-PAM: L phenylalanine mustard) and 5-fluorouracil (5-FU) expressed a cytotoxic effect in vitro on MOPC-315 plasmacytoma tumour cells.	Melphalan	5-14	peptidylglycine alpha-amidating monooxygenase	Mus musculus	18-21
3486861-1	1986	The effect of several purine nucleoside analogs on the cytotoxicity of melphalan (L-PAM) in the RIF-1 tumor in vivo was investigated.	Melphalan	71-80	replication timing regulatory factor 1	Mus musculus	96-101
3486861-1	1986	The effect of several purine nucleoside analogs on the cytotoxicity of melphalan (L-PAM) in the RIF-1 tumor in vivo was investigated.	Melphalan	82-87	replication timing regulatory factor 1	Mus musculus	96-101
3567896-7	1987	The rate of removal of HN2-induced DNA cross-links was, however, 1.5-2.4 times more rapid than that of melphalan-induced cross-links.	Melphalan	103-112	MT-RNR2 like 2 (pseudogene)	Homo sapiens	23-26
3579919-1	1987	Endogenous thiols such as glutathione (GSH) are known to mediate the activity of bifunctional alkylating agents such as melphalan (L-PAM).	Melphalan	120-129	peptidylglycine alpha-amidating monooxygenase	Mus musculus	133-136
2891627-0	1987	Melphalan-induced appearance of potent antitumor immune reactivity in tumor bearer lymphocytes co-expressing the Lyt 2 and the L3T4 antigens.	Melphalan	0-9	CD8 antigen, alpha chain	Mus musculus	113-118
2891627-0	1987	Melphalan-induced appearance of potent antitumor immune reactivity in tumor bearer lymphocytes co-expressing the Lyt 2 and the L3T4 antigens.	Melphalan	0-9	CD4 antigen	Mus musculus	127-131
2891627-3	1987	This immunopotentiating activity of the Sephadex G-10-adherent spleen cells from L-PAM treated MOPC-315 tumor bearers was attributed to T-cells which co-express the Lyt 2 and the L3T4 antigens based on results of experiments employing negative selection.	Melphalan	81-86	CD8 antigen, alpha chain	Mus musculus	165-170
2891627-3	1987	This immunopotentiating activity of the Sephadex G-10-adherent spleen cells from L-PAM treated MOPC-315 tumor bearers was attributed to T-cells which co-express the Lyt 2 and the L3T4 antigens based on results of experiments employing negative selection.	Melphalan	81-86	CD4 antigen	Mus musculus	179-183
2891627-4	1987	Specifically, depletion of Lyt 2+ cells or of L3T4+ cells abolished the ability of the Sephadex G-10-adherent splenic cell population from L-PAM treated MOPC-315 tumor bearers to bring about the generation of enhanced antitumor cytotoxicity when added to the immunization culture of normal spleen cells.	Melphalan	139-144	CD8 antigen, alpha chain	Mus musculus	27-32
2891627-4	1987	Specifically, depletion of Lyt 2+ cells or of L3T4+ cells abolished the ability of the Sephadex G-10-adherent splenic cell population from L-PAM treated MOPC-315 tumor bearers to bring about the generation of enhanced antitumor cytotoxicity when added to the immunization culture of normal spleen cells.	Melphalan	139-144	CD4 antigen	Mus musculus	46-50
2891627-6	1987	In light of the unusual phenotype of the immunopotentiating cells in the spleens of L-PAM treated MOPC-315 tumor bearing mice (i.e. Lyt 2+ L3T4+), and since the vast majority of thymocytes in normal adult BALB/c mice co-express the Lyt 2 and the L3T4 antigens, we evaluated the effect of low dose L-PAM therapy on the antitumor immune reactivity of thymocytes from MOPC-315 tumor bearing mice.	Melphalan	84-89	CD8 antigen, alpha chain	Mus musculus	132-137
2891627-6	1987	In light of the unusual phenotype of the immunopotentiating cells in the spleens of L-PAM treated MOPC-315 tumor bearing mice (i.e. Lyt 2+ L3T4+), and since the vast majority of thymocytes in normal adult BALB/c mice co-express the Lyt 2 and the L3T4 antigens, we evaluated the effect of low dose L-PAM therapy on the antitumor immune reactivity of thymocytes from MOPC-315 tumor bearing mice.	Melphalan	84-89	CD4 antigen	Mus musculus	139-143
2891627-6	1987	In light of the unusual phenotype of the immunopotentiating cells in the spleens of L-PAM treated MOPC-315 tumor bearing mice (i.e. Lyt 2+ L3T4+), and since the vast majority of thymocytes in normal adult BALB/c mice co-express the Lyt 2 and the L3T4 antigens, we evaluated the effect of low dose L-PAM therapy on the antitumor immune reactivity of thymocytes from MOPC-315 tumor bearing mice.	Melphalan	84-89	CD8 antigen, alpha chain	Mus musculus	232-237
2891627-6	1987	In light of the unusual phenotype of the immunopotentiating cells in the spleens of L-PAM treated MOPC-315 tumor bearing mice (i.e. Lyt 2+ L3T4+), and since the vast majority of thymocytes in normal adult BALB/c mice co-express the Lyt 2 and the L3T4 antigens, we evaluated the effect of low dose L-PAM therapy on the antitumor immune reactivity of thymocytes from MOPC-315 tumor bearing mice.	Melphalan	84-89	CD4 antigen	Mus musculus	246-250
2891627-9	1987	The possibility that the Lyt 2+ L3T4+ immunopotentiating cells in the spleens of L-PAM treated MOPC-315 tumor bearers represent immature cells that have been induced by the chemotherapy to migrate from the thymus into the spleen is discussed.	Melphalan	81-86	CD8 antigen, alpha chain	Mus musculus	25-30
2891627-9	1987	The possibility that the Lyt 2+ L3T4+ immunopotentiating cells in the spleens of L-PAM treated MOPC-315 tumor bearers represent immature cells that have been induced by the chemotherapy to migrate from the thymus into the spleen is discussed.	Melphalan	81-86	CD4 antigen	Mus musculus	32-36
3785141-3	1986	Glutathione had no effect on the rate of hydrolysis of LPAM, consistent with the SN1-like reaction mechanism of LPAM.	Melphalan	112-116	solute carrier family 38, member 3	Mus musculus	81-84
2938728-9	1986	An LD10 of 6-bis-(2-chloroethyl) amino-6-deoxy-D-glucose (C-6) or TGM produced significantly less depression of WBC counts than did an equitoxic dose of the C-1 isomers, HN2, or p-di(2-chloroethyl)amino-L-phenylalanine.	Melphalan	178-218	oogenesin 1	Mus musculus	157-160
3006735-1	1986	The effect of inhibitors of nuclear ADP-ribosyl transferase (ADPRT) on the cytotoxicity of melphalan (L-PAM) in the RIF-1 tumour in vivo was investigated.	Melphalan	91-100	ADP-ribosyltransferase 1	Mus musculus	61-66
3006735-1	1986	The effect of inhibitors of nuclear ADP-ribosyl transferase (ADPRT) on the cytotoxicity of melphalan (L-PAM) in the RIF-1 tumour in vivo was investigated.	Melphalan	91-100	replication timing regulatory factor 1	Mus musculus	116-121
3006735-1	1986	The effect of inhibitors of nuclear ADP-ribosyl transferase (ADPRT) on the cytotoxicity of melphalan (L-PAM) in the RIF-1 tumour in vivo was investigated.	Melphalan	102-107	ADP-ribosyltransferase 1	Mus musculus	36-59
3006735-1	1986	The effect of inhibitors of nuclear ADP-ribosyl transferase (ADPRT) on the cytotoxicity of melphalan (L-PAM) in the RIF-1 tumour in vivo was investigated.	Melphalan	102-107	ADP-ribosyltransferase 1	Mus musculus	61-66
3006735-1	1986	The effect of inhibitors of nuclear ADP-ribosyl transferase (ADPRT) on the cytotoxicity of melphalan (L-PAM) in the RIF-1 tumour in vivo was investigated.	Melphalan	102-107	replication timing regulatory factor 1	Mus musculus	116-121
4017161-6	1985	In tumor cells from patients A, B, D, and F, 2 mM BCH had no significant effect on melphalan uptake at 3 min; it slightly decreased uptake in tumor cells from patient C. At 35 min, 2 mM BCH significantly reduced melphalan transport in tumor cells from patients C and F only.	Melphalan	212-221	NK2 homeobox 1	Homo sapiens	186-189
3840666-0	1985	Human meningeal sarcoma heterotransplants in Nu/Nu mice treated with L-phenylalanine mustard (L-PAM) and dianhydrogalactitol (DAG).	Melphalan	69-92	peptidylglycine alpha-amidating monooxygenase	Mus musculus	96-99
2409315-2	1985	The antitumor effect of a subeffective dose of K-18 or an equivalent dose of melphalan alone was enhanced by local hyperthermia.	Melphalan	77-86	keratin 18	Mus musculus	47-51
2409315-4	1985	Local hyperthermia plus K-18 reduced the dose of melphalan required for tumor growth inhibition by melphalan alone.	Melphalan	49-58	keratin 18	Mus musculus	24-28
2409315-4	1985	Local hyperthermia plus K-18 reduced the dose of melphalan required for tumor growth inhibition by melphalan alone.	Melphalan	99-108	keratin 18	Mus musculus	24-28
3933817-1	1985	Exposure of MOPC-315 cells from the primary tumor nodule to a low concentration (0.5 nmol/ml) of melphalan (L-phenylalanine mustard; L-PAM) rendered the tumor cells capable of bringing about the generation of a potent primary antitumor cytotoxic response.	Melphalan	97-106	peptidylglycine alpha-amidating monooxygenase	Mus musculus	135-138
3971199-1	1985	A patient with IgG3 lambda plasma cell myeloma characterized by anemia, hypercalcemia, hypoalbuminemia, renal insufficiency, osteolytic bone lesions, and serum and urinary light chains inadvertently received a dose of intravenous melphalan considerably greater than standard.	Melphalan	230-239	immunoglobulin heavy constant gamma 3 (G3m marker)	Homo sapiens	15-19
3490305-5	1986	L-PAM-cured MOPC-315 tumor bearers exhibited in vivo immunity against SIg- MOPC-315 tumor cells, which was sufficiently triggered by the SIg- cells to bring about the rejection of a challenge of at least 100-fold the minimal lethal tumor dose of the SIg- MOPC-315 cells.	Melphalan	0-5	sightless	Mus musculus	70-73
3490305-5	1986	L-PAM-cured MOPC-315 tumor bearers exhibited in vivo immunity against SIg- MOPC-315 tumor cells, which was sufficiently triggered by the SIg- cells to bring about the rejection of a challenge of at least 100-fold the minimal lethal tumor dose of the SIg- MOPC-315 cells.	Melphalan	0-5	sightless	Mus musculus	137-140
3490305-5	1986	L-PAM-cured MOPC-315 tumor bearers exhibited in vivo immunity against SIg- MOPC-315 tumor cells, which was sufficiently triggered by the SIg- cells to bring about the rejection of a challenge of at least 100-fold the minimal lethal tumor dose of the SIg- MOPC-315 cells.	Melphalan	0-5	sightless	Mus musculus	137-140
3490305-6	1986	Thus, SIg- MOPC-315 tumor cells present among SIg+ tumor cells in the parental MOPC-315 tumor inoculum can be eradicated in the L-PAM-treated MOPC-315 tumor bearers by the immune response to SIg+ tumor cells as well as by the immune response to SIg- tumor cells themselves.	Melphalan	128-133	sightless	Mus musculus	6-19
3490305-6	1986	Thus, SIg- MOPC-315 tumor cells present among SIg+ tumor cells in the parental MOPC-315 tumor inoculum can be eradicated in the L-PAM-treated MOPC-315 tumor bearers by the immune response to SIg+ tumor cells as well as by the immune response to SIg- tumor cells themselves.	Melphalan	128-133	sightless	Mus musculus	6-9
3490305-6	1986	Thus, SIg- MOPC-315 tumor cells present among SIg+ tumor cells in the parental MOPC-315 tumor inoculum can be eradicated in the L-PAM-treated MOPC-315 tumor bearers by the immune response to SIg+ tumor cells as well as by the immune response to SIg- tumor cells themselves.	Melphalan	128-133	sightless	Mus musculus	46-49
3967079-0	1985	[Induction of drug resistance to sarcolysine in plasmacytoma line MORC/406].	Melphalan	33-44	microrchidia 1	Mus musculus	66-70
6466544-1	1984	In the present studies we have used the RIF-1 tumour in C3H mice to try to identify the mechanism(s) responsible for the enhancement of melphalan (L-PAM) induced tumour cell killing by the 2-nitroimidazole misonidazole (MISO).	Melphalan	136-145	replication timing regulatory factor 1	Mus musculus	40-45
2981183-0	1985	Melphalan potently substitutes the N-terminal Tyr of D-Ala2-Leu5-enkephalin methyl ester.	Melphalan	0-9	tripartite motif containing 13	Homo sapiens	60-64
3918212-2	1985	For the determination of whether chronic alkylating agent treatment of hematopoietic stem cells in vitro was detectably leukemogenic, murine long-term bone marrow cultures (LTBMC) and clonal interleukin 3 (IL-3)-dependent multipotential hematopoietic progenitor cell lines [B6SUtA clone (cl) 27 and Ro cl 3-1] derived from LTBMC were chronically pulse treated in vitro with the alkylating agent melphalan [L-phenylalanine mustard (L-PAM)].	Melphalan	431-436	interleukin 3	Mus musculus	191-210
3918212-4	1985	Weekly, twice weekly, or daily (3 X 10(-6)M) L-PAM treatment of IL-3-dependent cell lines induced gradual L-PAM adaptation in the absence of a detectable change in the maximum binding capacity of 125I-labeled IL-3.	Melphalan	45-50	interleukin 3	Mus musculus	64-68
3918212-4	1985	Weekly, twice weekly, or daily (3 X 10(-6)M) L-PAM treatment of IL-3-dependent cell lines induced gradual L-PAM adaptation in the absence of a detectable change in the maximum binding capacity of 125I-labeled IL-3.	Melphalan	45-50	interleukin 3	Mus musculus	209-213
3918212-4	1985	Weekly, twice weekly, or daily (3 X 10(-6)M) L-PAM treatment of IL-3-dependent cell lines induced gradual L-PAM adaptation in the absence of a detectable change in the maximum binding capacity of 125I-labeled IL-3.	Melphalan	106-111	interleukin 3	Mus musculus	64-68
3918212-7	1985	Thus IL-3-dependent hematopoietic progenitor cells slowly adapt to L-PAM when in suspension culture in vitro.	Melphalan	67-72	interleukin 3	Mus musculus	5-9
3155814-1	1985	The relationship between thiol depletion and its enhancement of melphalan (L-PAM) cytotoxicity was studied with the use of V-79-379A Chinese hamster cells in vitro.	Melphalan	64-73	peptidyl-glycine alpha-amidating monooxygenase	Cricetulus griseus	77-80
6466544-1	1984	In the present studies we have used the RIF-1 tumour in C3H mice to try to identify the mechanism(s) responsible for the enhancement of melphalan (L-PAM) induced tumour cell killing by the 2-nitroimidazole misonidazole (MISO).	Melphalan	136-145	peptidylglycine alpha-amidating monooxygenase	Mus musculus	149-152
6434498-1	1984	CB 1954 potentiates the cytotoxic action of the bifunctional alkylating agent melphalan (L-PAM).	Melphalan	78-87	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	91-94
6090366-0	1984	Enhancement of melphalan cytotoxicity in vivo and in vitro by inhibitors of poly (ADP-ribose) polymerase.	Melphalan	15-24	poly(ADP-ribose) polymerase 1	Homo sapiens	76-104
6090366-1	1984	In these preliminary experiments, we have found enhanced cell killing by the bifunctional alkylating agent L-phenylalanine mustard (L-PAM) in the presence of inhibitors of poly (ADP-ribose) polymerase (ADPRP) in vitro.	Melphalan	132-137	poly(ADP-ribose) polymerase 1	Homo sapiens	172-200
6882665-1	1983	Misonidazole (MISO) given as a large single dose enhanced the action of cyclophosphamide (Cy) and melphalan (L-PAM) in two mouse tumours.	Melphalan	98-107	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	111-114
6466534-1	1984	The response of clonal subpopulations isolated from the RIF-1 mouse sarcoma to melphalan treatment is independent of cell ploidy, whereas a clear relationship exists between ploidy and cell sensitivity to CCNU treatment.	Melphalan	79-88	replication timing regulatory factor 1	Mus musculus	56-61
6541216-2	1984	A single dose of cisplatin (1 mg/kg) enhanced the in vivo tumor killing by melphalan (L-PAM; 8 mg/kg).	Melphalan	75-84	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	88-91
6733699-1	1984	In regional hyperthermic perfusion with melphalan for patients with malignant melanoma of the leg, plasma leakage between the perfusion circuit and the systemic circulation was 4-7 ml X min-1.	Melphalan	40-49	CD59 molecule (CD59 blood group)	Homo sapiens	186-191
6546359-1	1984	Melphalan (L-PAM) was compared to (C) cyclophosphamide, (M) methotrexate, and (F) 5-fluorouracil (CMF) in 413 patients with advanced ovarian carcinoma.	Melphalan	0-9	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	13-16
6712172-6	1984	The MT2 and TEC tumors responded only slightly to melphalan treatment alone.	Melphalan	50-59	metallothionein 2	Mus musculus	4-7
6553510-1	1983	Following inoculation with 1 X 10(6) MOPC-315 tumor cells, a single injection of a very low dose of melphalan (L-PAM, L-phenylalanine mustard), 0.75 mg/kg, cured most of the mice bearing a day 11 large primary tumor (20 mm) and metastases, but failed to cure mice bearing a day 4 nonpalpable tumor.	Melphalan	100-109	peptidylglycine alpha-amidating monooxygenase	Mus musculus	113-116
6897078-0	1982	Effect of melphalan on delta-aminolevulinic acid synthetase in the spleen, bone marrow and liver of rats.	Melphalan	10-19	5'-aminolevulinate synthase 1	Rattus norvegicus	23-59
7139616-4	1982	Compared to estrogen receptor-positive cells, estrogen receptor-negative cells were 2-fold more sensitive to melphalan but were conversely 1.9-fold more resistant to Adriamycin; these differences were statistically significant (p less than 0.001).	Melphalan	109-118	estrogen receptor 1	Homo sapiens	46-63
6897078-1	1982	The effect of melphalan, an antineoplastic alkylating agent, on the activity of delta-aminolevulinic acid synthetase (ALA-S) was studied.	Melphalan	14-23	5'-aminolevulinate synthase 1	Rattus norvegicus	80-116
6897078-1	1982	The effect of melphalan, an antineoplastic alkylating agent, on the activity of delta-aminolevulinic acid synthetase (ALA-S) was studied.	Melphalan	14-23	5'-aminolevulinate synthase 1	Rattus norvegicus	118-123
7073938-0	1982	Effect of misonidazole or metronidazole pretreatment on the response of the RIF-1 mouse sarcoma to melphalan, cyclophosphamide, chlorambucil and CCNU.	Melphalan	99-108	replication timing regulatory factor 1	Mus musculus	76-81
7092953-1	1982	The pharmacokinetics and macromolecular interactions of [14C-ring]melphalan (L-PAM) in blood were studied in rats following a single oral dose (20 mg/kg, 0.1 mCi/kg).	Melphalan	66-75	peptidylglycine alpha-amidating monooxygenase	Rattus norvegicus	79-82
7000345-0	1980	L-phenylalanine mustard (L-PAM): the first 25 years.	Melphalan	0-23	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	27-30
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.	Melphalan	15-24	immunoglobulin heavy constant epsilon	Homo sapiens	81-84
101843-1	1978	A prospective clinical trial of melphalan (L-PAM) versus combination chemotherapy.	Melphalan	32-41	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	45-48
536450-1	1979	A procedure for the separation and quantitation of melphalan (L-PAM) and its hydrolysis products by high-performance liquid chromatography is described.	Melphalan	51-60	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	64-67
762115-0	1979	Active carrier-mediated transport of melphalan by two separate amino acid transport systems in LPC-1 plasmacytoma cells in vitro.	Melphalan	37-46	annexin A1	Homo sapiens	95-100
623430-5	1978	Against MX-1 tumor, both cyclophosphamide and melphalan induced tumor regressions with no recurrence.	Melphalan	46-55	MX dynamin-like GTPase 1	Mus musculus	8-12
565677-5	1978	In contrast, following a 30-min exposure to melphalan, cross-link formation increased for 12 hr and removal was much slower than it was for HN2.	Melphalan	44-53	MT-RNR2 like 2 (pseudogene)	Homo sapiens	140-143
415659-5	1978	Decreased lysozyme activity was determined in the spleen, kidneys and lungs by the 5th day and in the kidneys by the 10th day in the mice treated with sarcolysine in combination with Tio-Tel and in the spleen and lungs by the 5th and 10th days in the animals treated with neocid in combination with sarcolysine or Tio-Tef as compared to the animals treated with sarcolysine.	Melphalan	151-162	thyrotroph embryonic factor	Mus musculus	318-321
415659-6	1978	The lysozyme activity in the kidneys under the effect of sarcolysine combination with Tio-Tef was lower by the 5th days and higher by the 10th day as compared to that under the effect of Tio-Tef.	Melphalan	57-68	thyrotroph embryonic factor	Mus musculus	191-194
576517-10	1977	From coagulation tests studied, only thrombin time and reptilase time was found to be moderately prolonged in the presence of melphalan.	Melphalan	126-135	coagulation factor II, thrombin	Homo sapiens	37-45
597816-1	1977	[14C]melphalan ([14C]L-PAM) was rapidly absorbed from the gut of dogs after oral dosing and reached a maximum concentration in the serum by 30 minutes.	Melphalan	5-14	peptidylglycine alpha-amidating monooxygenase	Canis lupus familiaris	23-26
588739-0	1977	[Effect of sarcolysine on glutathione peroxidase and glutathione reductase activity in sarcoma C-45].	Melphalan	11-22	glutathione-disulfide reductase	Homo sapiens	53-74
588739-2	1977	Repeated sarcolysine injections (1.2 mg/kg, intraperitoneally) caused a sharp fall in the activity of both enzymes with a simultaneous reduction of the ratio of glutathione reductase and glutathione peroxidase activities.	Melphalan	9-20	glutathione-disulfide reductase	Homo sapiens	161-182
14260722-0	1964	[SARCOLYSINE IN A SEMINOMA].	Melphalan	1-12	internexin neuronal intermediate filament protein alpha	Homo sapiens	13-17
1016968-4	1976	Melphalan (L-PAM) inhibits nucleic-acid synthesis but not protein synthesis in L1210/0 and L1210/CPA.	Melphalan	0-9	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	13-16
1016968-4	1976	Melphalan (L-PAM) inhibits nucleic-acid synthesis but not protein synthesis in L1210/0 and L1210/CPA.	Melphalan	0-9	carboxypeptidase A1	Homo sapiens	91-100
1232529-3	1975	The group of patients receiving melphalan and prednisone 0.6 mg/kg had significantly improved responses in hemoglobin, lowering of the M-protein concentration, and reduction of azotemia.	Melphalan	32-41	myomesin 2	Homo sapiens	135-144
33980416-0	2021	Anti-PD-1 checkpoint blockade improves the efficacy of a melphalan-based therapy in experimental melanoma.	Melphalan	57-66	programmed cell death 1	Homo sapiens	5-9
33980416-7	2021	RESULTS: Treatment with melphalan-based therapy significantly induced the expression of PD-1 on CD8+ tumour-infiltrating lymphocytes.	Melphalan	24-33	programmed cell death 1	Mus musculus	88-92
33980416-9	2021	CONCLUSIONS: This study thus suggests that the addition of PD-1 blockade to melphalan-based therapies, such as ILP, may be therapeutically beneficial.	Melphalan	76-85	programmed cell death 1	Mus musculus	59-63
33363008-11	2020	In initial analyses of CD107a degranulation impaired T-cell cytotoxicity was detected in one patient following melphalan and autoSCT.	Melphalan	111-120	lysosomal associated membrane protein 1	Homo sapiens	23-29
33933805-3	2021	The recognition and binding processes of LAT1-ligands, such as amino acids and clinically used small molecules, including l-dopa, gabapentin, and melphalan, are today well-known.	Melphalan	146-155	solute carrier family 7 member 5	Homo sapiens	41-45
33323683-4	2021	O-methylguanine-DNA methyltransferase (MGMT) mRNA was upregulated in cell lines with greater melphalan and temozolomide (TMZ) resistance.	Melphalan	93-102	O-6-methylguanine-DNA methyltransferase	Homo sapiens	0-37
33323683-4	2021	O-methylguanine-DNA methyltransferase (MGMT) mRNA was upregulated in cell lines with greater melphalan and temozolomide (TMZ) resistance.	Melphalan	93-102	O-6-methylguanine-DNA methyltransferase	Homo sapiens	39-43
33000368-2	2021	We report the case of a 12-year-old female patient with C1q deficiency presenting with intractable SLE who successfully underwent bone marrow transplantation from a human leukocyte antigen (HLA)-mismatched unrelated donor with an immunosuppressive conditioning regimen based on fludarabine, melphalan, and anti-thymocyte globulin.	Melphalan	291-300	complement C1q A chain	Homo sapiens	56-59
32512672-19	2020	CONCLUSION: The increased amount of CD34+ autologous hematopoietic stem cell dose after high dose melphalan chemotherapy in MM patients shortens platelet and neutrophil engraftment time and increases overall survival.	Melphalan	98-107	CD34 molecule	Homo sapiens	36-40
33363008-13	2020	Our results point to a preferred interval of more than 3 months until patients should undergo cell separation for CAR-T therapy in the specific situation post-HD melphalan/autoSCT.	Melphalan	162-171	CXADR pseudogene 1	Homo sapiens	114-117
33116152-8	2020	Our finding that HUWE1 might thus be involved in endogenous DNA repair is further supported by strongly enhanced apoptotic effects of the DNA-damaging agent melphalan in HUWE1 depleted cells in vitro and in vivo.	Melphalan	157-166	HECT, UBA and WWE domain containing 1	Mus musculus	17-22
33023948-8	2020	In addition, repair of melphalan-induced DNA damage was inhibited by selinexor, which decreased melphalan-induced monoubiquitination of FANCD2 in MM cells.	Melphalan	23-32	FA complementation group D2	Homo sapiens	136-142
33023948-8	2020	In addition, repair of melphalan-induced DNA damage was inhibited by selinexor, which decreased melphalan-induced monoubiquitination of FANCD2 in MM cells.	Melphalan	96-105	FA complementation group D2	Homo sapiens	136-142
33023948-9	2020	Knockdown of FANCD2 was found to replicate the effect of selinexor when used with melphalan, increasing DNA damage (gammaH2AX) by inhibiting DNA repair.	Melphalan	82-91	FA complementation group D2	Homo sapiens	13-19
32861768-0	2020	Survivin silencing improved the cytotoxicity of carboplatin and melphalan in Y79 and primary retinoblastoma cells.	Melphalan	64-73	RB transcriptional corepressor 1	Homo sapiens	93-107
33153480-9	2020	In addition, several other signaling pathways including the p53 and transforming growth factor-beta signaling pathways were also implicated in melphalan-induced cardiotoxicity according to the proteomic and transcriptomic analyses.	Melphalan	143-152	tumor protein p53	Homo sapiens	60-63
33116152-8	2020	Our finding that HUWE1 might thus be involved in endogenous DNA repair is further supported by strongly enhanced apoptotic effects of the DNA-damaging agent melphalan in HUWE1 depleted cells in vitro and in vivo.	Melphalan	157-166	HECT, UBA and WWE domain containing 1	Mus musculus	170-175
32774473-2	2020	This study aims to investigate the role of aminopeptidase N (ANPEP) in HGOS progression and its targeting with a novel lipophilic peptidase-enhanced cytotoxic compound melphalan flufenamide (melflufen) in HGOS.	Melphalan	168-177	alanyl aminopeptidase, membrane	Homo sapiens	61-66
33054085-6	2020	We found that ATR inhibition is strongly synergistic with melphalan, even in resistant cells.	Melphalan	58-67	ATR serine/threonine kinase	Homo sapiens	14-17
32194286-0	2020	PARP inhibition synergizes with melphalan but does not reverse resistance completely.	Melphalan	32-41	poly(ADP-ribose) polymerase 1	Homo sapiens	0-4
32161295-2	2020	Thus, the object of this study was to generate melphalan derivatives with improved cytotoxic activity in human cancer cells (RPMI8226, HL60 and THP1).	Melphalan	47-56	GLI family zinc finger 2	Homo sapiens	144-148
32377929-6	2020	Thus, the anti-parkinsonian drug, L-Dopa, the anti-cancer drug, melphalan and the anti-epileptic drug gabapentin, all used in clinical practice, utilize LAT1 to reach their target site.	Melphalan	64-73	solute carrier family 7 member 5	Homo sapiens	153-157
31942432-0	2019	Histopathologic findings after selective ophthalmic arterial injection of melphalan for retinoblastoma.	Melphalan	74-83	RB transcriptional corepressor 1	Homo sapiens	88-102
31650359-0	2020	Inhibition of HSP90 overcomes melphalan resistance through downregulation of Src in multiple myeloma cells.	Melphalan	30-39	heat shock protein 90 alpha family class A member 1	Homo sapiens	14-19
31650359-0	2020	Inhibition of HSP90 overcomes melphalan resistance through downregulation of Src in multiple myeloma cells.	Melphalan	30-39	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	77-80
31650359-7	2020	In this study, we assessed the role of HSP90 in MDR using established melphalan-resistant MM cells.	Melphalan	70-79	heat shock protein 90 alpha family class A member 1	Homo sapiens	39-44
31650359-8	2020	We found that expression of HSP90 was higher in melphalan-resistant MM cells than in parent cells and that HSP90 inhibitors KW-2478 and NUV-AUY922 restored drug sensitivity to the level observed in parent cells.	Melphalan	48-57	heat shock protein 90 alpha family class A member 1	Homo sapiens	28-33
31427718-7	2020	The translational significance of NEAT1 targeting is further underlined by its synergistic effects with the most common drugs administered for MM treatment, including bortezomib, carfilzomib, and melphalan.	Melphalan	196-205	nuclear paraspeckle assembly transcript 1 (non-protein coding)	Mus musculus	34-39
31768675-3	2020	Thirty-six patients of median age 74 years old with NDMM initially received 35-day cycles of VMP: oral melphalan (6 mg/m2) and prednisolone (60 mg/m2) on days 1 to 4 and bortezomib (1.3 mg/m2) on days 1, 8, 15, and 22.	Melphalan	103-112	neurensin 1	Homo sapiens	93-96
31942432-1	2019	PURPOSE: The aim is to describe histopathologic observations in eyes enucleated after selective ophthalmic arterial injection (SOAI) of melphalan for retinoblastoma (RB).	Melphalan	136-145	RB transcriptional corepressor 1	Homo sapiens	150-164
31544312-4	2019	In the current study, we investigated the roles of XRCC1, a protein involved in base excision repair and single-strand break repair, in melphalan response in MM cells.	Melphalan	136-145	X-ray repair cross complementing 1	Homo sapiens	51-56
31544312-5	2019	Small interfering RNA knockdown of XRCC1 significantly increased the accumulation of melphalan-induced DNA damage in MM cells and sensitized them to melphalan treatment, indicating that genetic variation in XRCC1 may impact response to melphalan treatment.	Melphalan	85-94	X-ray repair cross complementing 1	Homo sapiens	35-40
31544312-5	2019	Small interfering RNA knockdown of XRCC1 significantly increased the accumulation of melphalan-induced DNA damage in MM cells and sensitized them to melphalan treatment, indicating that genetic variation in XRCC1 may impact response to melphalan treatment.	Melphalan	85-94	X-ray repair cross complementing 1	Homo sapiens	207-212
31544312-5	2019	Small interfering RNA knockdown of XRCC1 significantly increased the accumulation of melphalan-induced DNA damage in MM cells and sensitized them to melphalan treatment, indicating that genetic variation in XRCC1 may impact response to melphalan treatment.	Melphalan	149-158	X-ray repair cross complementing 1	Homo sapiens	35-40
31544312-5	2019	Small interfering RNA knockdown of XRCC1 significantly increased the accumulation of melphalan-induced DNA damage in MM cells and sensitized them to melphalan treatment, indicating that genetic variation in XRCC1 may impact response to melphalan treatment.	Melphalan	149-158	X-ray repair cross complementing 1	Homo sapiens	35-40
31544312-9	2019	Taken together, these results indicate that XRCC1 is involved in the repair of melphalan-induced DNA damage and XRCC1 rs25487 variant with impaired DNA repair function influences the clinical responses of HDM in MM patients.	Melphalan	79-88	X-ray repair cross complementing 1	Homo sapiens	44-49
31703617-4	2019	Melphalan conditioning reduced the levels of total CD14+ as well as classical and non-classical monocytes, whereas intermediate monocytes were not affected.	Melphalan	0-9	CD14 molecule	Homo sapiens	51-55
31756922-7	2019	Furthermore, we observed an increase in ASM expression in MM cell lines treated with melphalan or bortezomib, as well as in their exosomes.	Melphalan	85-94	sphingomyelin phosphodiesterase 1	Homo sapiens	40-43
32002296-7	2020	Peripheral blood mononuclear cells (PBMCs) secreted high levels of CXCL10, CCL2 and IFN-gamma in response to co-culture with melphalan-exposed melanoma cells in vitro.	Melphalan	125-134	C-X-C motif chemokine ligand 10	Homo sapiens	67-73
32002296-7	2020	Peripheral blood mononuclear cells (PBMCs) secreted high levels of CXCL10, CCL2 and IFN-gamma in response to co-culture with melphalan-exposed melanoma cells in vitro.	Melphalan	125-134	C-C motif chemokine ligand 2	Homo sapiens	75-79
32002296-7	2020	Peripheral blood mononuclear cells (PBMCs) secreted high levels of CXCL10, CCL2 and IFN-gamma in response to co-culture with melphalan-exposed melanoma cells in vitro.	Melphalan	125-134	interferon gamma	Homo sapiens	84-93
32002296-9	2020	Furthermore, melphalan-exposed melanoma cells triggered upregulation of CXCR3, CCR4, CCR5 and PD-1 on co-cultured T cells and/or NK cells.	Melphalan	13-22	C-X-C motif chemokine receptor 3	Sus scrofa	72-77
32002296-9	2020	Furthermore, melphalan-exposed melanoma cells triggered upregulation of CXCR3, CCR4, CCR5 and PD-1 on co-cultured T cells and/or NK cells.	Melphalan	13-22	C-C motif chemokine receptor 4	Sus scrofa	79-83
32002296-9	2020	Furthermore, melphalan-exposed melanoma cells triggered upregulation of CXCR3, CCR4, CCR5 and PD-1 on co-cultured T cells and/or NK cells.	Melphalan	13-22	C-C motif chemokine receptor 5	Sus scrofa	85-89
32002296-9	2020	Furthermore, melphalan-exposed melanoma cells triggered upregulation of CXCR3, CCR4, CCR5 and PD-1 on co-cultured T cells and/or NK cells.	Melphalan	13-22	MHC class I antigen 1	Sus scrofa	94-98
31480729-7	2019	Results: AC2 administration promoted significant myeloprotective effect: 1.5-fold increase in leukocytes, 2-fold in neutrophils, 1.5-fold in lymphocytes, and 1.23-fold in platelet count compared to the experimental Melphalan Group.	Melphalan	215-224	adenylate cyclase 2	Rattus norvegicus	9-12
31632904-2	2019	In this study, we show that CASIN, a selective inhibitor of cell division cycle 42 (Cdc42) GTPase, inhibited proliferation and survival of melphalan/bortezomib-resistant MM cells more profoundly than that of the sensitive cells.	Melphalan	139-148	cell division cycle 42	Homo sapiens	84-89
31632904-5	2019	Mechanistically, Cdc42 activity was higher in melphalan/bortezomib-resistant cells than that in the sensitive cells.	Melphalan	46-55	cell division cycle 42	Homo sapiens	17-22
31632904-6	2019	CASIN inhibited mono-ubiquitination of Fanconi anemia (FA) complementation group D2 (FANCD2) of the FA DNA damage repair pathway in melphalan-resistant but not melphalan-sensitive cells, thereby sensitizing melphalan-resistant cells to DNA damage.	Melphalan	132-141	FA complementation group D2	Homo sapiens	85-91