PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
2599104-1	1989	The administration of hydroxyurea (3 x 10(-4) M) and cytosine arabinoside (10(-7) M) greatly induces the expression of the vimentin gene in human promonocytic leukemia U-937 cells.	Cytarabine	53-73	vimentin	Homo sapiens	123-131
2599104-4	1989	Since hydroxyurea and cytosine arabinoside trigger the phenotypic differentiation of U-937 cells, as demonstrated by the induction of the differentiation-specific CD11b and CD11c antigens, it is concluded that vimentin expression might be implicated in the maturation of these cells.	Cytarabine	22-42	integrin subunit alpha M	Homo sapiens	163-168
2599104-4	1989	Since hydroxyurea and cytosine arabinoside trigger the phenotypic differentiation of U-937 cells, as demonstrated by the induction of the differentiation-specific CD11b and CD11c antigens, it is concluded that vimentin expression might be implicated in the maturation of these cells.	Cytarabine	22-42	integrin subunit alpha X	Homo sapiens	173-178
2599104-4	1989	Since hydroxyurea and cytosine arabinoside trigger the phenotypic differentiation of U-937 cells, as demonstrated by the induction of the differentiation-specific CD11b and CD11c antigens, it is concluded that vimentin expression might be implicated in the maturation of these cells.	Cytarabine	22-42	vimentin	Homo sapiens	210-218
2478221-6	1989	These studies strongly suggest that a protocol designed to administer F-ara-A monophosphate prior to ara-C infusion will augment ara-CTP accumulation by leukemia cells.	Cytarabine	101-106	solute carrier family 25 member 1	Homo sapiens	133-136
2539852-13	1989	Our study indicates that deoxycytidine kinase is a dimer with two subunits and has phosphorylating activity for deoxyguanosine, deoxyadenosine, cytidine, and cytosine arabinoside.	Cytarabine	158-178	deoxycytidine kinase	Homo sapiens	25-45
2659542-12	1989	5-Aza-2"-deoxycytidine (Aza-d-Cyd) was very effective on both tumors, etoposide (VP-16) and cytosine arabinoside (Ara-C) had no activity and Adriamycin (ADR) was weakly effective.	Cytarabine	114-119	cytochrome b-245, beta polypeptide	Mus musculus	30-33
2654494-0	1989	Granulocyte-macrophage colony-stimulating factor enhances the cytotoxic effects of cytosine arabinoside in acute myeloblastic leukemia and in the myeloid blast crisis phase of chronic myeloid leukemia.	Cytarabine	83-103	colony stimulating factor 2	Homo sapiens	0-48
2654494-3	1989	In seven patients studied, GM-CSF increased the fraction of myeloid leukemic blasts in S phase as measured by propidium iodide DNA staining, bromodeoxyuridine incorporation, or ARA-C suicide techniques.	Cytarabine	177-182	colony stimulating factor 2	Homo sapiens	27-33
2473850-3	1989	5-Azacytidine (5-Aza-C) and its congeners are potent DNA hypomethylating agents, an action closely associated with the reexpression of certain genes such as that for deoxycytidine kinase (dCk) in ara-C-resistant mouse and human leukemic cells.	Cytarabine	196-201	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	188-191
2558539-0	1989	Reduction of ara-C cytotoxicity in HL 60 cells by addition of deoxycytidine, cytidine or increased level of cytidine deaminase.	Cytarabine	13-18	cytidine deaminase	Homo sapiens	108-126
2502896-1	1989	Amsacrine with high-dose cytarabine is effective therapy for Philadelphia chromosome (Ph1)-negative acute lymphoblastic leukemia (ALL).	Cytarabine	25-35	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	86-89
2473850-4	1989	Reexpression of dCk could increase the cellular ara-CTP concentrations and the sensitivity to ara-C.	Cytarabine	48-53	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	16-19
2473850-3	1989	5-Azacytidine (5-Aza-C) and its congeners are potent DNA hypomethylating agents, an action closely associated with the reexpression of certain genes such as that for deoxycytidine kinase (dCk) in ara-C-resistant mouse and human leukemic cells.	Cytarabine	196-201	deoxycytidine kinase	Mus musculus	166-186
2606728-3	1989	Exposure of KMOE cells to cytosine arabinoside and hemin leads to over 20-fold increases in beta- and gamma-globin mRNA steady-state levels, and an over 60-fold increase in epsilon-globin mRNA level.	Cytarabine	26-46	hemoglobin subunit beta	Homo sapiens	92-114
2676187-0	1989	Flow cytometric correlation of the c-myc oncoprotein and cell cycle kinetics of HL60 leukaemia during induced maturation with cytosine arabinoside and dimethylsulphoxide.	Cytarabine	126-146	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	35-40
2676187-9	1989	ARA-c treatment of HL60 cells leads to a slowing and an accumulation of cells in S phase with a moderate decrease in mean mRNA and only a slight decrease in mean c-myc protein levels.	Cytarabine	0-5	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	162-167
2606728-4	1989	Exposure to cytosine arabinoside alone induced beta- and epsilon-globin but not gamma-globin gene expression.	Cytarabine	12-32	hemoglobin subunit beta	Homo sapiens	47-71
2643680-1	1989	Cytosine arabinoside (ARA C), a competitive inhibitor of the incorporation of 2"-deoxycytidine into DNA in other cell types, caused a concentration-dependent inhibition of KCl- and insulin-stimulated survival of postmitotic ciliary parasympathetic ganglion neurons, and the nerve growth factor (NGF)-stimulated survival of postmitotic dorsal root ganglion (DRG) sensory neurons in vitro.	Cytarabine	0-20	nerve growth factor	Homo sapiens	274-293
2643680-1	1989	Cytosine arabinoside (ARA C), a competitive inhibitor of the incorporation of 2"-deoxycytidine into DNA in other cell types, caused a concentration-dependent inhibition of KCl- and insulin-stimulated survival of postmitotic ciliary parasympathetic ganglion neurons, and the nerve growth factor (NGF)-stimulated survival of postmitotic dorsal root ganglion (DRG) sensory neurons in vitro.	Cytarabine	0-20	nerve growth factor	Homo sapiens	295-298
3264363-7	1988	The differential effect of rGM-CSF on the phosphorylation of Ara-C in normal BMMCs versus leukemic blasts has potential implications for the use of a regimen consisting of rGM-CSF and high dose Ara-C in the treatment of ANLL with chemotherapy or autologous bone marrow transplantation.	Cytarabine	61-66	colony stimulating factor 2	Rattus norvegicus	27-34
2643680-1	1989	Cytosine arabinoside (ARA C), a competitive inhibitor of the incorporation of 2"-deoxycytidine into DNA in other cell types, caused a concentration-dependent inhibition of KCl- and insulin-stimulated survival of postmitotic ciliary parasympathetic ganglion neurons, and the nerve growth factor (NGF)-stimulated survival of postmitotic dorsal root ganglion (DRG) sensory neurons in vitro.	Cytarabine	22-27	nerve growth factor	Homo sapiens	274-293
2643680-1	1989	Cytosine arabinoside (ARA C), a competitive inhibitor of the incorporation of 2"-deoxycytidine into DNA in other cell types, caused a concentration-dependent inhibition of KCl- and insulin-stimulated survival of postmitotic ciliary parasympathetic ganglion neurons, and the nerve growth factor (NGF)-stimulated survival of postmitotic dorsal root ganglion (DRG) sensory neurons in vitro.	Cytarabine	22-27	nerve growth factor	Homo sapiens	295-298
2643680-3	1989	The inhibition of DRG survival by ARA C in the presence of varying concentrations of NGF indicated that ARA C acted as an apparent noncompetitive antagonist of NGF.	Cytarabine	104-109	nerve growth factor	Homo sapiens	160-163
2488733-1	1989	Interaction of the antileukemic drugs, cytosine-arabinoside (Ara-C) and adenosine-arabinoside (Ara-A) and a structural analogue, cytidine, with aromatic dipeptides has been studied by fluorescence and NMR spectroscopy.	Cytarabine	39-59	p21 (RAC1) activated kinase 3	Homo sapiens	61-64
3264363-0	1988	Effect of recombinant GM-CSF on the metabolism of cytosine arabinoside in normal and leukemic human bone marrow cells.	Cytarabine	50-70	colony stimulating factor 2	Homo sapiens	22-28
3264363-2	1988	We determined the effect of rGM-CSF on the metabolism of high dose Ara-C in bone marrow mononuclear cells (BMMCs) from healthy volunteers and patients with ANLL.	Cytarabine	67-72	colony stimulating factor 2	Rattus norvegicus	28-35
3264363-5	1988	Exposure to rGM-CSF in conjunction with Ara-C corrected Ara-C-mediated declines in dCTP levels and decreased cytosine arabinoside triphosphate (Ara-CTP) accumulation in normal BMMCs but not in their leukemic counterparts.	Cytarabine	56-61	colony stimulating factor 2	Rattus norvegicus	12-19
3264363-6	1988	Furthermore, when exposure to Ara-C was preceded by treatment with rGM-CSF for 18 hr, an even greater reduction in the Ara-CTP/dCTP pool ratio was observed in normal versus leukemic elements; however, this did not significantly change Ara-C DNA incorporation in the two cell types.	Cytarabine	30-35	colony stimulating factor 2	Rattus norvegicus	67-74
3264363-6	1988	Furthermore, when exposure to Ara-C was preceded by treatment with rGM-CSF for 18 hr, an even greater reduction in the Ara-CTP/dCTP pool ratio was observed in normal versus leukemic elements; however, this did not significantly change Ara-C DNA incorporation in the two cell types.	Cytarabine	119-124	colony stimulating factor 2	Rattus norvegicus	67-74
3264363-7	1988	The differential effect of rGM-CSF on the phosphorylation of Ara-C in normal BMMCs versus leukemic blasts has potential implications for the use of a regimen consisting of rGM-CSF and high dose Ara-C in the treatment of ANLL with chemotherapy or autologous bone marrow transplantation.	Cytarabine	61-66	colony stimulating factor 2	Rattus norvegicus	172-179
3264363-7	1988	The differential effect of rGM-CSF on the phosphorylation of Ara-C in normal BMMCs versus leukemic blasts has potential implications for the use of a regimen consisting of rGM-CSF and high dose Ara-C in the treatment of ANLL with chemotherapy or autologous bone marrow transplantation.	Cytarabine	194-199	colony stimulating factor 2	Rattus norvegicus	27-34
3201826-3	1988	The synthesis of protein p12 is sensitive to cytosine arabinoside.	Cytarabine	45-65	DNA polymerase epsilon 4, accessory subunit	Homo sapiens	25-28
3191030-3	1988	In any patient, PE2 or clonogenic cells in suspension were more sensitive to Ara-C than PE1.	Cytarabine	77-82	ETS2 repressor factor	Homo sapiens	16-19
3191030-4	1988	The results indicate that Ara-C effectively suppresses not only terminal divisions but also self-renewal of blast progenitors D10 Ara-C value, the dose required to reduce survival to 10% of control, for PE1, PE2 and clonogenic cells in suspension showed marked patient-to-patient variation.	Cytarabine	26-31	ETS variant transcription factor 3	Homo sapiens	203-206
3191030-4	1988	The results indicate that Ara-C effectively suppresses not only terminal divisions but also self-renewal of blast progenitors D10 Ara-C value, the dose required to reduce survival to 10% of control, for PE1, PE2 and clonogenic cells in suspension showed marked patient-to-patient variation.	Cytarabine	26-31	ETS2 repressor factor	Homo sapiens	208-211
3191030-4	1988	The results indicate that Ara-C effectively suppresses not only terminal divisions but also self-renewal of blast progenitors D10 Ara-C value, the dose required to reduce survival to 10% of control, for PE1, PE2 and clonogenic cells in suspension showed marked patient-to-patient variation.	Cytarabine	130-135	ETS variant transcription factor 3	Homo sapiens	203-206
3191030-4	1988	The results indicate that Ara-C effectively suppresses not only terminal divisions but also self-renewal of blast progenitors D10 Ara-C value, the dose required to reduce survival to 10% of control, for PE1, PE2 and clonogenic cells in suspension showed marked patient-to-patient variation.	Cytarabine	130-135	ETS2 repressor factor	Homo sapiens	208-211
3044574-10	1988	Both Ara-C and hemin-exposed cells showed a decrease in c-myc and c-myb transcripts, suggesting that altered levels of these proto-oncogenes may be associated with erythroid maturation, regardless of the rate of cell division.	Cytarabine	5-10	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	56-61
3044574-10	1988	Both Ara-C and hemin-exposed cells showed a decrease in c-myc and c-myb transcripts, suggesting that altered levels of these proto-oncogenes may be associated with erythroid maturation, regardless of the rate of cell division.	Cytarabine	5-10	MYB proto-oncogene, transcription factor	Homo sapiens	66-71
3263144-0	1988	Interleukin 3 enhances the cytotoxic activity of 1-beta-D-arabinofuranosylcytosine (ara-C) on acute myeloblastic leukaemia (AML) cells.	Cytarabine	49-82	interleukin 3	Homo sapiens	0-13
3263144-0	1988	Interleukin 3 enhances the cytotoxic activity of 1-beta-D-arabinofuranosylcytosine (ara-C) on acute myeloblastic leukaemia (AML) cells.	Cytarabine	84-89	interleukin 3	Homo sapiens	0-13
3263144-3	1988	The results showed that ara-C exposure inhibits the proliferation of a higher proportion of clonogenic cells in cultures pretreated with growth factors than in the controls (mean inhibitory values: in the absence of growth factors = 49.8%; with IL-1 beta = 58.3%; with IL-3 78.9%).	Cytarabine	24-29	interleukin 1 beta	Homo sapiens	245-254
3263144-3	1988	The results showed that ara-C exposure inhibits the proliferation of a higher proportion of clonogenic cells in cultures pretreated with growth factors than in the controls (mean inhibitory values: in the absence of growth factors = 49.8%; with IL-1 beta = 58.3%; with IL-3 78.9%).	Cytarabine	24-29	interleukin 3	Homo sapiens	269-273
3411602-4	1988	These new prodrugs of ara-C include ara-CDP-L-dipalmitin, ara-CDP-D-dipalmitin, and ara-CDP-DL-dipalmitin.	Cytarabine	22-27	cut-like homeobox 1	Mus musculus	40-43
3411602-4	1988	These new prodrugs of ara-C include ara-CDP-L-dipalmitin, ara-CDP-D-dipalmitin, and ara-CDP-DL-dipalmitin.	Cytarabine	22-27	cut-like homeobox 1	Mus musculus	62-65
3411602-4	1988	These new prodrugs of ara-C include ara-CDP-L-dipalmitin, ara-CDP-D-dipalmitin, and ara-CDP-DL-dipalmitin.	Cytarabine	22-27	cut-like homeobox 1	Mus musculus	62-65
2905925-3	1988	A prolonged exposure to normally used concentration of cytosine arabinoside (Ara-C; 10 microM) was toxic to both astroglial and neuronal cells, while a brief treatment (48 h) with a low level (4 microM) of Ara-C failed to eliminate these astrocytes, as judged by glutamine synthetase activity and GFAP-positive cell count.	Cytarabine	55-75	glutamate-ammonia ligase	Rattus norvegicus	263-283
2457505-4	1988	Cytosine arabinoside induces an early DNA hypermethylation, which is however reversible and drops to the original level after 24 h. Hydroxyurea induces DNA hypermethylation after a lag period of more than 48 h and the DNA polymerase alpha inhibitor aphidicolin has no effect on the DNA methylation level.	Cytarabine	0-20	DNA polymerase alpha 1, catalytic subunit	Homo sapiens	218-238
2905925-3	1988	A prolonged exposure to normally used concentration of cytosine arabinoside (Ara-C; 10 microM) was toxic to both astroglial and neuronal cells, while a brief treatment (48 h) with a low level (4 microM) of Ara-C failed to eliminate these astrocytes, as judged by glutamine synthetase activity and GFAP-positive cell count.	Cytarabine	55-75	glial fibrillary acidic protein	Rattus norvegicus	297-301
3071344-0	1988	GM-CSF enhances sensitivity of leukemic clonogenic cells to long-term low dose cytosine arabinoside with sparing of the normal clonogenic cells.	Cytarabine	79-99	colony stimulating factor 2	Homo sapiens	0-6
3071344-5	1988	Interesting was the observation that secondary leukemic colony forming cells were more or at least equally sensitive to Ara-C in the presence of GM-CSF when compared to the primary leukemic clonogenic cells.	Cytarabine	120-125	colony stimulating factor 2	Homo sapiens	145-151
2905925-3	1988	A prolonged exposure to normally used concentration of cytosine arabinoside (Ara-C; 10 microM) was toxic to both astroglial and neuronal cells, while a brief treatment (48 h) with a low level (4 microM) of Ara-C failed to eliminate these astrocytes, as judged by glutamine synthetase activity and GFAP-positive cell count.	Cytarabine	206-211	glutamate-ammonia ligase	Rattus norvegicus	263-283
3071344-7	1988	This indicates that GM-CSF induces leukemic clonogenic cells with selfrenewal capacity into proliferation, and in doing so, it may enhance the cytotoxicity of a cell cycle specific drug like Ara-C with sparing of the normal clonogenic cells.	Cytarabine	191-196	colony stimulating factor 2	Homo sapiens	20-26
2905925-3	1988	A prolonged exposure to normally used concentration of cytosine arabinoside (Ara-C; 10 microM) was toxic to both astroglial and neuronal cells, while a brief treatment (48 h) with a low level (4 microM) of Ara-C failed to eliminate these astrocytes, as judged by glutamine synthetase activity and GFAP-positive cell count.	Cytarabine	206-211	glial fibrillary acidic protein	Rattus norvegicus	297-301
3291772-11	1988	A synergistic increase in the cytotoxic effects of rH-TNF and anti-cancer drugs was demonstrated in vitro The cytotoxicity of rH-TNF against L-M cells in combination with MMC, ADM, Ara-C, ACD, DM, CDDP, VCR and 5-FU was 4 to 347 times as high as that of rH-TNF alone.	Cytarabine	181-186	tumor necrosis factor	Homo sapiens	54-57
3208989-10	1988	Cytosine-arabinoside (ARAc) treatment of the cultures reduced the DNA content per culture dish, corresponding to a fall in the number of GFAp-positive cells (astrocytes) and to a decrease in GS.	Cytarabine	0-20	glutamine fructose-6-phosphate transaminase 1	Rattus norvegicus	137-141
3208989-10	1988	Cytosine-arabinoside (ARAc) treatment of the cultures reduced the DNA content per culture dish, corresponding to a fall in the number of GFAp-positive cells (astrocytes) and to a decrease in GS.	Cytarabine	22-26	glutamine fructose-6-phosphate transaminase 1	Rattus norvegicus	137-141
2896069-7	1988	In contrast, HT1080 DOXR cells display cross-resistance to vincristine, actinomycin D, vinblastine, and etoposide; however, they are not cross-resistant to gramicidin D, and show an increased (approximately 18-fold) cross-resistance to 1-beta-D-arabinofuranosylcytosine.	Cytarabine	236-269	ATP binding cassette subfamily B member 1	Homo sapiens	20-24
3165492-3	1988	While cytosine arabinoside inhibited colony formation and terminal differentiation of the CFU-E cells responding to epo, herbimycin, which is a drug that inhibits src-related phosphorylation, inhibited colony formation only.	Cytarabine	6-26	erythropoietin	Mus musculus	116-119
2900045-4	1988	On the other hand, the exposure of cultures to cytosine arabinoside resulted in a marked increase in choline acetyltransferase enzyme activity.	Cytarabine	47-67	choline O-acetyltransferase	Rattus norvegicus	101-126
3382195-1	1988	A phase II clinical trial on MDS was conducted in a cooperative study with orally administrable ara-C analogue, PLAC, which is resistant to cytidine deaminase and had shown an anti-tumor activity on various experimental tumors by oral route.	Cytarabine	96-101	cytidine deaminase	Homo sapiens	140-158
3291772-11	1988	A synergistic increase in the cytotoxic effects of rH-TNF and anti-cancer drugs was demonstrated in vitro The cytotoxicity of rH-TNF against L-M cells in combination with MMC, ADM, Ara-C, ACD, DM, CDDP, VCR and 5-FU was 4 to 347 times as high as that of rH-TNF alone.	Cytarabine	181-186	tumor necrosis factor	Homo sapiens	129-132
3291772-11	1988	A synergistic increase in the cytotoxic effects of rH-TNF and anti-cancer drugs was demonstrated in vitro The cytotoxicity of rH-TNF against L-M cells in combination with MMC, ADM, Ara-C, ACD, DM, CDDP, VCR and 5-FU was 4 to 347 times as high as that of rH-TNF alone.	Cytarabine	181-186	tumor necrosis factor	Homo sapiens	129-132
3137398-0	1988	Differentiation of human leukaemic cell lines and fresh leukaemia cells by low dose Ara-C: monitoring by expression of c-myc and c-fos oncogenes.	Cytarabine	84-89	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	119-124
3350002-12	1988	The results of the subcellular distribution of this mRNA in proliferating myoblasts following inhibition of DNA synthesis by cytosine arabinoside have shown that translation of P-40 mRNA continued in absence of DNA synthesis.	Cytarabine	125-145	LanC like 1	Rattus norvegicus	177-181
3288838-2	1988	The ara-C-resistant subclones, 707DKE and 707DK48, had respective deoxycytidine kinase activities of 6.7 and 5.4% the values found in wild-type cells.	Cytarabine	4-9	deoxycytidine kinase	Mus musculus	66-86
3335008-1	1988	Previous studies have indicated that deoxycytidine kinase (dCK) is requisite and rate limiting in the phosphorylation of 1-beta-D-arabinofuranosylcytosine (ara-C) and 9-beta-D-arabinofuranosyl-2-fluoroadenine (F-ara-A) on the pathway to their respective cytotoxic 5"-triphosphates.	Cytarabine	121-154	deoxycytidine kinase	Homo sapiens	37-57
3335008-1	1988	Previous studies have indicated that deoxycytidine kinase (dCK) is requisite and rate limiting in the phosphorylation of 1-beta-D-arabinofuranosylcytosine (ara-C) and 9-beta-D-arabinofuranosyl-2-fluoroadenine (F-ara-A) on the pathway to their respective cytotoxic 5"-triphosphates.	Cytarabine	121-154	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	59-62
3335008-1	1988	Previous studies have indicated that deoxycytidine kinase (dCK) is requisite and rate limiting in the phosphorylation of 1-beta-D-arabinofuranosylcytosine (ara-C) and 9-beta-D-arabinofuranosyl-2-fluoroadenine (F-ara-A) on the pathway to their respective cytotoxic 5"-triphosphates.	Cytarabine	156-161	deoxycytidine kinase	Homo sapiens	37-57
3335008-1	1988	Previous studies have indicated that deoxycytidine kinase (dCK) is requisite and rate limiting in the phosphorylation of 1-beta-D-arabinofuranosylcytosine (ara-C) and 9-beta-D-arabinofuranosyl-2-fluoroadenine (F-ara-A) on the pathway to their respective cytotoxic 5"-triphosphates.	Cytarabine	156-161	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	59-62
27519637-7	1987	In these experiments, ARA-CDP-D,L-PTBA, ARA-CDP-D,L-PBA, ARA-CDP-L-dipalmitin and ARA-CDP-D,L-PCA were more active than either the parent compounds ARA-C and ET-18-OCH3 alone or their equimolar mixtures.	Cytarabine	22-27	cut-like homeobox 1	Mus musculus	44-47
27519637-7	1987	In these experiments, ARA-CDP-D,L-PTBA, ARA-CDP-D,L-PBA, ARA-CDP-L-dipalmitin and ARA-CDP-D,L-PCA were more active than either the parent compounds ARA-C and ET-18-OCH3 alone or their equimolar mixtures.	Cytarabine	22-27	cut-like homeobox 1	Mus musculus	44-47
27519637-7	1987	In these experiments, ARA-CDP-D,L-PTBA, ARA-CDP-D,L-PBA, ARA-CDP-L-dipalmitin and ARA-CDP-D,L-PCA were more active than either the parent compounds ARA-C and ET-18-OCH3 alone or their equimolar mixtures.	Cytarabine	22-27	cut-like homeobox 1	Mus musculus	44-47
3444389-6	1987	In these experiments, ARA-CDP-D,L-PTBA, ARA-CDP-D,L-PBA, ARA-CDP-L-dipalmitin and ARA-CDP-D,L-PCA were more active than either the parent compounds ARA-C and ET-18-OCH3 alone or their equimolar mixtures.	Cytarabine	22-27	cut-like homeobox 1	Mus musculus	44-47
3444389-6	1987	In these experiments, ARA-CDP-D,L-PTBA, ARA-CDP-D,L-PBA, ARA-CDP-L-dipalmitin and ARA-CDP-D,L-PCA were more active than either the parent compounds ARA-C and ET-18-OCH3 alone or their equimolar mixtures.	Cytarabine	22-27	cut-like homeobox 1	Mus musculus	44-47
3444389-6	1987	In these experiments, ARA-CDP-D,L-PTBA, ARA-CDP-D,L-PBA, ARA-CDP-L-dipalmitin and ARA-CDP-D,L-PCA were more active than either the parent compounds ARA-C and ET-18-OCH3 alone or their equimolar mixtures.	Cytarabine	22-27	cut-like homeobox 1	Mus musculus	44-47
3681903-4	1987	Our results suggest that the inhibition of DNA repair, including the inhibition in G2 phase, plays an important role in the expression of FRA3B, supporting other authors" data on the effect of other DNA repair inhibitors, such as aphidicolin, caffeine, 1-beta-D-arabinofuranosylcytosine, and 5-fluorodeoxyuridine, on the expression of FRA3B.	Cytarabine	253-286	fragile histidine triad diadenosine triphosphatase	Homo sapiens	138-143
3137398-0	1988	Differentiation of human leukaemic cell lines and fresh leukaemia cells by low dose Ara-C: monitoring by expression of c-myc and c-fos oncogenes.	Cytarabine	84-89	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	129-134
3475975-3	1987	Employing an enzyme-linked immunosorbent assay with cytarabine coated onto the wells in bovine serum albumin, specific IgE antibodies to this drug could be demonstrated.	Cytarabine	52-62	albumin	Homo sapiens	95-108
3115933-4	1987	The sensitivity of the leukemic cell lines to ara-C, which was measured in terms of decrease of clonogenic survival, correlated with the amount of ara-CTP formed.	Cytarabine	46-51	solute carrier family 25 member 1	Homo sapiens	151-154
2444837-2	1987	KMOE cells exposed to cytosine arabinofuranoside (Ara-C) synthesized beta-globin gene transcripts, however, in the presence of hemin gamma-globin gene transcripts.	Cytarabine	22-48	hemoglobin subunit beta	Homo sapiens	69-80
2444837-2	1987	KMOE cells exposed to cytosine arabinofuranoside (Ara-C) synthesized beta-globin gene transcripts, however, in the presence of hemin gamma-globin gene transcripts.	Cytarabine	22-48	hemoglobin subunit gamma 1	Homo sapiens	133-145
2444837-2	1987	KMOE cells exposed to cytosine arabinofuranoside (Ara-C) synthesized beta-globin gene transcripts, however, in the presence of hemin gamma-globin gene transcripts.	Cytarabine	50-55	hemoglobin subunit beta	Homo sapiens	69-80
2444837-3	1987	An increase in alpha-globin gene transcripts was also detectable in KMOE cells treated with both Ara-C and hemin.	Cytarabine	97-102	hemoglobin subunit alpha 2	Homo sapiens	15-27
2444837-4	1987	Upon exposure to hemin after exposure to Ara-C, or exposure to Ara-C after hemin, there was a 5-10-fold increase in gamma-globin gene transcripts compared to that of cells induced by hemin alone.	Cytarabine	41-46	hemoglobin subunit gamma 1	Homo sapiens	116-128
2444837-4	1987	Upon exposure to hemin after exposure to Ara-C, or exposure to Ara-C after hemin, there was a 5-10-fold increase in gamma-globin gene transcripts compared to that of cells induced by hemin alone.	Cytarabine	63-68	hemoglobin subunit gamma 1	Homo sapiens	116-128
2439659-7	1987	The effectiveness of VP-16/5-Az combination therapy in patients refractory to anthracyclines and cytarabine indicates a potential role for these compounds in first-line treatment of patients with ANLL.	Cytarabine	97-107	host cell factor C1	Homo sapiens	21-26
3669771-1	1987	The cytotoxic effect of cytosine arabinoside (ara-C) is presumably mediated by cytosine arabinoside 5"-triphosphate (ara-CTP).	Cytarabine	24-44	solute carrier family 25 member 1	Homo sapiens	121-124
3669771-1	1987	The cytotoxic effect of cytosine arabinoside (ara-C) is presumably mediated by cytosine arabinoside 5"-triphosphate (ara-CTP).	Cytarabine	46-51	solute carrier family 25 member 1	Homo sapiens	121-124
3107809-6	1987	These findings contrast with those obtained with CDDP and aphidicolin (the latter agent resembles ara-C in competing with dCTP for binding to DNA polymerase alpha but, unlike ara-C, is not incorporated into DNA).	Cytarabine	98-103	DNA polymerase alpha 1, catalytic subunit	Homo sapiens	142-162
3607288-1	1987	We examined the ability of high concentrations of the naturally occurring nucleoside deoxycytidine (dCyd) to reverse the cytotoxicity of high (eg, greater than or equal to 10(-5) mol/L) concentrations of 1-B-D arabinofuranosylcytosine (Ara-C) toward normal (CFU-GM) and leukemic myeloid progenitor cells (L-CFU).	Cytarabine	236-241	Cyd	Drosophila melanogaster	100-104
3607288-5	1987	When higher concentrations of Ara-C (eg, 5 X 10(-5) mol/L) were administered, dCyd-mediated protection toward CFU-GM decreased, but remained significantly greater than that observed for L-CFU.	Cytarabine	30-35	Cyd	Drosophila melanogaster	78-82
3607288-6	1987	Incubation with 10(-3) mol/L of dCyd reduced the 4-hour intracellular accumulation of the triphosphate derivative of Ara-C (Ara-CTP) in both normal and leukemic cells by greater than 98%; under identical conditions, a significant expansion of the intracellular of the triphosphate derivative of dCyd (dCTP) pools was observed in normal bone marrow mononuclear cells but not in leukemic blasts.	Cytarabine	117-122	Cyd	Drosophila melanogaster	32-36
3607288-8	1987	These in vitro studies suggest that dCyd may preferentially protect normal v leukemic myeloid progenitor cells from the lethal actions of high-dose Ara-C.	Cytarabine	148-153	Cyd	Drosophila melanogaster	36-40
3472650-0	1987	The effect of cytosine-arabinoside treatment on the overexpression of c-myc protooncogene in a case of prolymphocytic leukemia.	Cytarabine	14-34	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	70-75
3472650-3	1987	Treatment with cytosine-arabinoside at high doses abolished this altered expression of c-myc and resulted in a twofold increase in the expression of a gene sequence encoding the invariant gamma-chain of class II histocompatibility antigens, preferentially expressed in resting B lymphocytes.	Cytarabine	15-35	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	87-92
3473677-3	1987	Preliminary data indicate that the development of ara-C resistance is related with decreased intracellular levels of deoxycytidine kinase.	Cytarabine	50-55	deoxycytidine kinase	Homo sapiens	117-137
3037013-5	1987	The p68 was synthesized shortly after infection and in the presence of cytosine arabinoside, an inhibitor of viral DNA replication.	Cytarabine	71-91	KH RNA binding domain containing, signal transduction associated 1	Homo sapiens	4-7
3585446-1	1987	In order to test the toxicity and efficacy of intensive postremission therapy with high-dose cytosine arabinoside with L-asparaginase and amsacrine with etoposide in adults with acute nonlymphocytic leukemia (ANL), 100 adults (ages 19 to 75) with previously untreated ANL were entered into a study using six sequential cycles of chemotherapy.	Cytarabine	93-113	asparaginase and isoaspartyl peptidase 1	Homo sapiens	119-133
2967076-0	1987	Inhibition of thymidylate synthase in intact L1210 cells by ara-C, daunomycin, hydroxyurea and 3,4-dihydroxybenzylamine.	Cytarabine	60-65	thymidylate synthase	Mus musculus	14-34
2967076-1	1987	The use of an in situ assay for thymidylate synthase has shown that a variety of clinically important drugs, including arabinofuranosylcytosine, hydroxyurea, and daunomycin, inhibit thymidylate synthase in intact cells.	Cytarabine	119-143	thymidylate synthase	Mus musculus	32-52
2967076-1	1987	The use of an in situ assay for thymidylate synthase has shown that a variety of clinically important drugs, including arabinofuranosylcytosine, hydroxyurea, and daunomycin, inhibit thymidylate synthase in intact cells.	Cytarabine	119-143	thymidylate synthase	Mus musculus	182-202
2461052-0	1987	Differential expression of c-myc and c-fos oncogenes during the differentiation of human leukemic cells by Ara-C.	Cytarabine	107-112	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	27-32
3298663-5	1987	It was shown that neuronal densities similar to those with uninhibited media may be retained in the presence of cytosine arabinoside if fibronectin-coated substrata are prepared.	Cytarabine	112-132	fibronectin 1	Mus musculus	136-147
2461052-0	1987	Differential expression of c-myc and c-fos oncogenes during the differentiation of human leukemic cells by Ara-C.	Cytarabine	107-112	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	37-42
2461052-5	1987	On the other hand, in the bipotential promyelocytic HL-60 cells, Ara-C induces only 40% monocytic differentiation after 7 days; this is associated to a weaker decrement of c-myc expression; c-fos is however greatly induced 3 log after 2 days treatment, but before monocytic phenotype is observed.	Cytarabine	65-70	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	172-177
2461052-5	1987	On the other hand, in the bipotential promyelocytic HL-60 cells, Ara-C induces only 40% monocytic differentiation after 7 days; this is associated to a weaker decrement of c-myc expression; c-fos is however greatly induced 3 log after 2 days treatment, but before monocytic phenotype is observed.	Cytarabine	65-70	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	190-195
2461052-7	1987	The rapid inducement of c-fos expression may allow to foresee a rapid prescreening of Ara-C sensitive-blasts.	Cytarabine	86-91	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	24-29
3467840-1	1987	The treatment of K562 human myeloblastic leukemia cells and YAC-1 murine lymphoma cells with cadeguomycin at concentrations over 0.6 microM significantly enhanced the cytotoxicity of 1-beta-D-arabinofuranosylcytosine (ara-C).	Cytarabine	183-216	ADP-ribosyltransferase 1	Mus musculus	60-65
3664332-1	1987	Deamination of cytosine arabinoside (ara-C) by cytidine deaminase (Cyt DA) is the main mode of the inactivation of this drug in vivo.	Cytarabine	15-35	cytidine deaminase	Mus musculus	47-65
3664332-1	1987	Deamination of cytosine arabinoside (ara-C) by cytidine deaminase (Cyt DA) is the main mode of the inactivation of this drug in vivo.	Cytarabine	15-35	cytidine deaminase	Mus musculus	67-73
3664332-1	1987	Deamination of cytosine arabinoside (ara-C) by cytidine deaminase (Cyt DA) is the main mode of the inactivation of this drug in vivo.	Cytarabine	37-42	cytidine deaminase	Mus musculus	47-65
3664332-1	1987	Deamination of cytosine arabinoside (ara-C) by cytidine deaminase (Cyt DA) is the main mode of the inactivation of this drug in vivo.	Cytarabine	37-42	cytidine deaminase	Mus musculus	67-73
3664332-5	1987	The control peak plasma levels of ara-C and ara-U were 3.3 and 0.78 mM and they were eliminated with a half life (t 1/2) of 1.26 and 1.43 hours, respectively.	Cytarabine	34-39	brachyury, T-box transcription factor T	Mus musculus	114-134
3023059-9	1986	Myeloid leukemic cells induced to differentiate by normal myeloid cell differentiation factor MGI-2 (= DF), or by low doses of actinomycin D or cytosine arabinoside, showed an up-regulation of the number of MGI-1GM and IL-3 receptors.	Cytarabine	144-164	interleukin 3	Homo sapiens	219-223
3470578-1	1987	The cytotoxic effect of cytosine arabinoside (ara-C) depends on the capacity of cells to form and retain intracellularly the phosphorylated metabolite cytosine arabinoside triphosphate (ara-CTP).	Cytarabine	24-44	solute carrier family 25 member 1	Homo sapiens	190-193
3470578-1	1987	The cytotoxic effect of cytosine arabinoside (ara-C) depends on the capacity of cells to form and retain intracellularly the phosphorylated metabolite cytosine arabinoside triphosphate (ara-CTP).	Cytarabine	46-51	solute carrier family 25 member 1	Homo sapiens	190-193
3470578-4	1987	Phosphorylation of ara-C to ara-CTP appeared to be a saturable process.	Cytarabine	19-24	solute carrier family 25 member 1	Homo sapiens	32-35
3536078-0	1986	Terminal erythroid differentiation in the K-562 cell line by 1-beta-D-arabinofuranosylcytosine: accompaniment by c-myc messenger RNA decrease.	Cytarabine	61-94	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	113-118
3536078-6	1986	In contrast to what is seen for other inducers (sodium butyrate and hemin), one of the early effects of ara-C treatment is the marked decrease of c-myc mRNA expression after the first 4 hours of induction, whereas N-ras and histone 4 expression remain constant during the first 48 h. Our results suggest that ara-C treatment can irreversibly activate the erythroid differentiative program of K-562 cells.	Cytarabine	104-109	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	146-151
3793108-0	1986	The effect of 1-beta-D-arabinofuranosyl-cytosine on the expression of the common fragile site at 3p14.	Cytarabine	14-48	ribonuclease P/MRP subunit p14	Homo sapiens	98-101
3793108-1	1986	The effect of the G2-treatment of 1-beta-D-arabino-furanosyl-cytosine (araC) on the expression of the common fragile site at 3p14 (FRA3B) was studied.	Cytarabine	34-69	ribonuclease P/MRP subunit p14	Homo sapiens	126-129
3793108-1	1986	The effect of the G2-treatment of 1-beta-D-arabino-furanosyl-cytosine (araC) on the expression of the common fragile site at 3p14 (FRA3B) was studied.	Cytarabine	34-69	fragile histidine triad diadenosine triphosphatase	Homo sapiens	131-136
3793108-1	1986	The effect of the G2-treatment of 1-beta-D-arabino-furanosyl-cytosine (araC) on the expression of the common fragile site at 3p14 (FRA3B) was studied.	Cytarabine	71-75	ribonuclease P/MRP subunit p14	Homo sapiens	126-129
3793108-1	1986	The effect of the G2-treatment of 1-beta-D-arabino-furanosyl-cytosine (araC) on the expression of the common fragile site at 3p14 (FRA3B) was studied.	Cytarabine	71-75	fragile histidine triad diadenosine triphosphatase	Homo sapiens	131-136
3531806-3	1986	The results demonstrate that ara-C inhibits both U-937 proliferation and c-myc expression in a concentration- and time-dependent manner.	Cytarabine	29-34	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	73-78
3531806-4	1986	At non-toxic concentrations of ara-C, these decreases in c-myc RNA occur in the absence of changes in the level of actin transcripts.	Cytarabine	31-36	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	57-62
3531806-5	1986	The results also demonstrate that ara-C increases c-fos but not c-fms expression.	Cytarabine	34-39	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	50-55
3798365-0	1986	Prevention of polydactyly manifestation in Polydactyly Nagoya (Pdn) mice by administration of cytosine arabinoside during pregnancy.	Cytarabine	94-114	GLI-Kruppel family member GLI3	Mus musculus	43-61
3798365-0	1986	Prevention of polydactyly manifestation in Polydactyly Nagoya (Pdn) mice by administration of cytosine arabinoside during pregnancy.	Cytarabine	94-114	GLI-Kruppel family member GLI3	Mus musculus	63-66
3798365-9	1986	In the vitally stained specimens at 6 and 24 hours after injection of Ara-C, preaxial marginal necrotic zones (fMI) were observed in almost all of the treated embryos from +/+ x Pdn/+ matings.	Cytarabine	70-75	GLI-Kruppel family member GLI3	Mus musculus	178-181
3798365-12	1986	These findings indicated that a subteratogenic dose of Ara-C prevented the genetic expression of polydactyly in almost all Pdn/+ and some cases of Pdn/Pdn mice.	Cytarabine	55-60	GLI-Kruppel family member GLI3	Mus musculus	123-126
3798365-12	1986	These findings indicated that a subteratogenic dose of Ara-C prevented the genetic expression of polydactyly in almost all Pdn/+ and some cases of Pdn/Pdn mice.	Cytarabine	55-60	GLI-Kruppel family member GLI3	Mus musculus	147-150
3798365-12	1986	These findings indicated that a subteratogenic dose of Ara-C prevented the genetic expression of polydactyly in almost all Pdn/+ and some cases of Pdn/Pdn mice.	Cytarabine	55-60	GLI-Kruppel family member GLI3	Mus musculus	147-150
3461882-4	1986	CSF ara-c concentrations ranged from 1.2 microM at 4 g to 4.1 microM at 18 g; the ratio of CSF to plasma ara-c decreased progressively from 0.33 at 4 g to 0.18 at 18 g. The toxic effects were significant and included myelosuppression, nausea, and vomiting in all patients.	Cytarabine	4-9	colony stimulating factor 2	Homo sapiens	0-3
3017738-4	1986	This processing of vimentin occurred mainly in dense cell cultures and it could not be induced in sparse cell cultures by inhibiting DNA synthesis with ara C, or by arresting cell growth in medium containing 0.1% serum.	Cytarabine	152-157	vimentin	Homo sapiens	19-27
3718702-2	1986	Following inhibition of DNA synthesis in L6 myoblasts with cytosine arabinoside, a coordinate and exaggerated rate of degradation of histone mRNAs occurs while other mRNAs, encoding ribosomal protein L32 and actin, are unaffected.	Cytarabine	59-79	ribosomal protein L32	Homo sapiens	182-203
3087388-5	1986	Cytosine arabinoside and dideoxythymidine also stimulated the increase of NAT activity and advanced the time of peak activity with glands cultured in the dark from midphotoperiod.	Cytarabine	0-20	arylamine N-acetyltransferase, liver isozyme	Gallus gallus	74-77
3457603-0	1986	Treatment of TdT+ myeloid blast crisis of chronic granulocytic leukemia with low dose cytosine arabinoside.	Cytarabine	86-106	DNA nucleotidylexotransferase	Homo sapiens	13-16
2874992-9	1986	Proliferating cells arrested at the G1-S boundary by exposure to cytosine arabinoside showed an increased PCNA immunofluorescence as compared to unstimulated cells.	Cytarabine	65-85	proliferating cell nuclear antigen	Homo sapiens	106-110
3456425-8	1986	The one-hour AMSA/continuous VP-16 combination is effective for patients with relapsing AML and shows no cross-resistance in a proportion of patients refractory to the standard anthracycline-cytarabine combination.	Cytarabine	191-201	host cell factor C1	Homo sapiens	29-34
2932216-4	1985	This suggests an approach to the treatment of human tumors possessing elevated levels of cytidine deaminase such as certain leukemias, bronchogenic carcinoma of the lung, adenocarcinomas of the colon and rectum, astrocytomas, and certain tumors which are refractory to chemotherapy with 1-beta-D-arabinofuranosylcytosine.	Cytarabine	287-320	cytidine deaminase	Homo sapiens	89-107
3090830-0	1986	Antithrombin III during high-dose cytosine arabinoside therapy with or without asparaginase.	Cytarabine	34-54	serpin family C member 1	Homo sapiens	0-16
2429121-3	1986	HL-60/Ara-C were also highly cross-resistant to both DAZ and AAC.	Cytarabine	6-11	deleted in azoospermia 1	Homo sapiens	53-56
2992752-5	1985	The results of the use of this assay report for SCCL spheroid responses to various concentrations of doxorubicin hydrochloride, cytosine arabinoside, mechlorethamine hydrochloride, cisplatin, or etoposide.	Cytarabine	128-148	SCLC1	Homo sapiens	48-52
2992834-9	1985	Furthermore, the suppression of induced strand break accumulation is partly due to a suppression by novobiocin of the uptake and phosphorylation of cytosine arabinoside; breaks accumulated in u.v.-irradiated cells in the presence of aphidicolin, an inhibitor of DNA polymerase alpha that does not require phosphorylation, are less novobiocin-sensitive.	Cytarabine	148-168	DNA polymerase alpha 1, catalytic subunit	Homo sapiens	262-282
3856968-3	1985	A high response rate to low-dose cytosine-arabinoside (LD-CAR) was observed in myeloblastic and promyelocytic leukaemias, but the complete remission rate was low.	Cytarabine	33-53	CXADR pseudogene 1	Homo sapiens	58-61
3862119-6	1985	When cells were serum-stimulated in the presence of an inhibitor of DNA synthesis, 1-beta-D-arabinofuranosylcytosine (araC), the levels of hsp70 mRNA were induced to only 20% of the maximal level detected in the absence of the inhibitor.	Cytarabine	83-116	heat shock protein family A (Hsp70) member 4	Homo sapiens	139-144
3862119-6	1985	When cells were serum-stimulated in the presence of an inhibitor of DNA synthesis, 1-beta-D-arabinofuranosylcytosine (araC), the levels of hsp70 mRNA were induced to only 20% of the maximal level detected in the absence of the inhibitor.	Cytarabine	118-122	heat shock protein family A (Hsp70) member 4	Homo sapiens	139-144
2990754-3	1985	The ADPRT activities of the various marrow cell preparations correlated to the morphological diagnoses, in vitro growth patterns, in vitro drug sensitivities to cytosine arabinoside, and to the prognoses of the AML patients.	Cytarabine	161-181	poly(ADP-ribose) polymerase 1	Homo sapiens	4-9
2413049-6	1985	It was subsequently found that inhibition of the M2 subunit of ribonucleotide reductase in CCRF-CEM cells with 5 X 10(-5) M hydroxyurea, which is not an iron chelator, also enhanced TfR expression, as did thymidine and cytosine arabinoside, which have different enzyme targets.	Cytarabine	219-239	transferrin receptor	Homo sapiens	182-185
3858662-2	1985	The present study extends these findings by demonstrating that ara-C treatment of K562 cells results in both increased heme synthesis and accumulation of alpha-, gamma-, epsilon-, and zeta-globin RNA.	Cytarabine	63-68	hemoglobin subunit alpha 2	Homo sapiens	154-195
3858662-4	1985	Furthermore, we demonstrate that phorbol ester (12-O-tetradecanoylphorbol-13-acetate; TPA) inhibits the effects of ara-C on heme production, accumulation of globin RNA, and glycophorin expression.	Cytarabine	115-120	plasminogen activator, tissue type	Homo sapiens	86-89
3858662-5	1985	The inhibitory effect occurs maximally when K562 cells are treated with TPA before undergoing ara-C-induced commitment to erythroid differentiation.	Cytarabine	94-99	plasminogen activator, tissue type	Homo sapiens	72-75
3930450-4	1985	Therefore, the synergistic cell kill of HU and ara-C may be the consequence of greater inhibition of DNA polymerase by the increased level of ara-CTP in the presence of the decreased concentration of the natural substrate of this enzyme, dCTP.	Cytarabine	47-52	cut up	Drosophila melanogaster	146-149
4012338-3	1985	We therefore, attempted to improve the complete remission rate in patients with low ara-CTP levels by decreasing the intermittent ara-C dosing interval, thereby raising the minimum ara-CTP level in leukemic cells between doses.	Cytarabine	84-89	solute carrier family 25 member 1	Homo sapiens	185-188
3019066-8	1985	An apparent Km of 13 microM for deoxycytidine and Ki of 55 microM for arabinosyl-cytosine were found for the tonsillar deoxycytidine kinase.	Cytarabine	70-89	deoxycytidine kinase	Homo sapiens	119-139
3980658-1	1985	Currently available high-performance liquid chromatographic assays for cytosine arabinoside (ara-C) and its metabolites suffer from two major shortcomings: inability to resolve both ara-C and its nucleotides in a single chromatographic step and/or inadequate sensitivity to allow quantitation of intracellular cytosine arabinofuranoside-5"-triphosphate (ara-CTP) without the use of radiolabelled drug.	Cytarabine	93-98	solute carrier family 25 member 1	Homo sapiens	358-361
2986054-4	1985	), a synthetic derivative of thyrotropin-releasing hormone (TRH), significantly increased [3H]GABA binding in the cerebellum of cytosine arabinoside-induced ataxic rats.	Cytarabine	128-148	thyrotropin releasing hormone	Rattus norvegicus	29-58
2986054-4	1985	), a synthetic derivative of thyrotropin-releasing hormone (TRH), significantly increased [3H]GABA binding in the cerebellum of cytosine arabinoside-induced ataxic rats.	Cytarabine	128-148	thyrotropin releasing hormone	Rattus norvegicus	60-63
3980658-2	1985	In this paper, we describe a new ion-pairing high-performance liquid chromatographic assay for ara-C in biological samples that can separate ara-C from its nucleotides, metabolites, and naturally occurring ribonucleotides in a single chromatographic step with a lower limit of quantitation of 5 pmol for ara-C and 10 pmol for ara-CTP.	Cytarabine	95-100	solute carrier family 25 member 1	Homo sapiens	330-333
3013572-5	1985	Nonproliferating astrocytes in cultures treated with 0.4 microM 1-beta-D-arabinofuranosyl-cytosine were refractory to EGF treatment, indicating that their responsiveness to EGF is cell cycle-dependent.	Cytarabine	64-98	epidermal growth factor like 1	Rattus norvegicus	173-176
3980658-2	1985	In this paper, we describe a new ion-pairing high-performance liquid chromatographic assay for ara-C in biological samples that can separate ara-C from its nucleotides, metabolites, and naturally occurring ribonucleotides in a single chromatographic step with a lower limit of quantitation of 5 pmol for ara-C and 10 pmol for ara-CTP.	Cytarabine	141-146	solute carrier family 25 member 1	Homo sapiens	330-333
3980658-2	1985	In this paper, we describe a new ion-pairing high-performance liquid chromatographic assay for ara-C in biological samples that can separate ara-C from its nucleotides, metabolites, and naturally occurring ribonucleotides in a single chromatographic step with a lower limit of quantitation of 5 pmol for ara-C and 10 pmol for ara-CTP.	Cytarabine	141-146	solute carrier family 25 member 1	Homo sapiens	330-333
3871104-7	1985	Furthermore, highly purified IL 2 can restore cytolytic activity, even when cytosine arabinoside is present to inhibit clonal expansion.	Cytarabine	76-96	interleukin 2	Mus musculus	29-33
3896977-3	1985	In the second study the addition of the epipodophyllotoxin VP16-213 to conventional doses of doxorubicin and cytosine arabinoside improved complete remission rate and median duration of survival.	Cytarabine	109-129	host cell factor C1	Homo sapiens	59-63
6487363-0	1984	Involvement of tryptophan residues of lysozyme in its binding with cytosine arabinoside.	Cytarabine	67-87	lysozyme	Homo sapiens	38-46
4068748-4	1985	When MTX at the dose of 12 mg/kg was preceded 6 h and 3 h to ara-C at the dose of 25 mg/kg, the intracellular levels of ara-CTP were found to be significantly higher as compared with those of ara-C alone as control group.	Cytarabine	61-66	metaxin 1	Mus musculus	5-8
4068748-4	1985	When MTX at the dose of 12 mg/kg was preceded 6 h and 3 h to ara-C at the dose of 25 mg/kg, the intracellular levels of ara-CTP were found to be significantly higher as compared with those of ara-C alone as control group.	Cytarabine	120-125	metaxin 1	Mus musculus	5-8
4068748-5	1985	At 1 h after ara-C, ara-CTP was measured about 165 and 130% of the control levels, respectively, and at 12 h, ara-CTP was over 4 times higher of control level with group of mice to which MTX was preceded 6 h prior to MTX.	Cytarabine	13-18	metaxin 1	Mus musculus	187-190
4068748-2	1985	The mechanism of this combination effect not well elucidated but the intracellular uptake of ara-C was higher when cells were pre-exposed to MTX.	Cytarabine	93-98	metaxin 1	Mus musculus	141-144
6397235-4	1984	GalC-positive oligodendrocytes rarely incorporate [3H]thymidine so that the use of a mitotic inhibitor (5 X 10(-6)M AraC) reduced the number of non-oligodendrocytes so as to maintain the purity of oligodendrocytes at more than 75% for 14 days in culture.	Cytarabine	116-120	galactosylceramidase	Mus musculus	0-4
6487363-8	1984	Ara-C inhibited lysozyme activity noncompetitively.	Cytarabine	0-5	lysozyme	Homo sapiens	16-24
6308437-1	1983	Chinese hamster ovary cell strains deficient in deoxycytidine kinase activity were selected by isolating mutants resistant to high concentrations of the analogue arabinosyl cytosine.	Cytarabine	162-181	deoxycytidine kinase	Cricetulus griseus	48-68
6094841-8	1984	The neonatal administration of ara-C caused an elevation of CNPase activity and myelin protein content in the cerebellum, suggesting a relative increase in myelin concentration as a result of hypoplasia of granule cells.	Cytarabine	31-36	2',3'-cyclic nucleotide 3' phosphodiesterase	Rattus norvegicus	60-66
6727776-0	1984	Anaphylactic reaction to cytarabine: in vitro evidence that the response is immunoglobulin E mediated.	Cytarabine	25-35	immunoglobulin heavy constant epsilon	Homo sapiens	76-92
6727776-2	1984	In this report we present the first in vitro evidence that such a reaction to cytarabine can be associated with the release of histamine and therefore might be immunoglobulin E (IgE) mediated.	Cytarabine	78-88	immunoglobulin heavy constant epsilon	Homo sapiens	160-176
6727776-2	1984	In this report we present the first in vitro evidence that such a reaction to cytarabine can be associated with the release of histamine and therefore might be immunoglobulin E (IgE) mediated.	Cytarabine	78-88	immunoglobulin heavy constant epsilon	Homo sapiens	178-181
6230394-6	1984	In the presence of cytosine arabinoside, which effectively inhibited proliferation, IL 2 was capable of reactivating memory CTL as efficiently as antigen, thus implying a differentiative role for IL 2 in secondary CTL activation.	Cytarabine	19-39	interleukin 2	Mus musculus	196-200
6423305-2	1984	damage in human fibroblasts is more sensitive to inhibitors of DNA polymerase alpha (cytosine arabinoside, aphidicolin) than to an inhibitor of polymerase beta (dideoxythymidine), which indicates a greater role in repair for polymerase alpha than for polymerase beta.	Cytarabine	85-105	DNA polymerase alpha 1, catalytic subunit	Homo sapiens	63-83
6629738-7	1983	Measurement of deoxycytidine kinase activity in cell-free extracts of cell cultures stimulated by antibody, however, did not reveal enhanced enzymatic activity due to stimulated enzyme synthesis, but, rather indicated that antibody and complement altered the intracellular concentrations of nucleotides which affected the interaction of cytosine arabinoside with deoxycytidine kinase in intact cells.	Cytarabine	337-357	deoxycytidine kinase	Homo sapiens	15-35
6656988-5	1983	The neonatal administration of ara-C caused an elevation of 2",3"-cyclic nucleotide 3"-phosphodiesterase (CNPase) (EC 3.1.4.37) activity and myelin protein content in the cerebellum, suggesting a relative increase in myelin concentration as a result of hypoplasia of granule cells.	Cytarabine	31-36	2',3'-cyclic nucleotide 3' phosphodiesterase	Rattus norvegicus	60-104
6656988-5	1983	The neonatal administration of ara-C caused an elevation of 2",3"-cyclic nucleotide 3"-phosphodiesterase (CNPase) (EC 3.1.4.37) activity and myelin protein content in the cerebellum, suggesting a relative increase in myelin concentration as a result of hypoplasia of granule cells.	Cytarabine	31-36	2',3'-cyclic nucleotide 3' phosphodiesterase	Rattus norvegicus	106-112
6224699-13	1983	HK II disappears after induction with ARA-C and mitomycin-C but not with hemin.	Cytarabine	38-43	hexokinase 2	Homo sapiens	0-5
6576907-4	1983	We consider that ara-C sensitivity could be predicted by measuring the plateau ara-CTP level before commencement of chemotherapy.	Cytarabine	17-22	solute carrier family 25 member 1	Homo sapiens	83-86
6189497-0	1983	Kinetics of deamination of 5-aza-2"-deoxycytidine and cytosine arabinoside by human liver cytidine deaminase and its inhibition by 3-deazauridine, thymidine or uracil arabinoside.	Cytarabine	54-74	cytidine deaminase	Homo sapiens	90-108
6403037-1	1983	Excision repair of ultraviolet damage in human fibroblasts was partially inhibited by drugs that block DNA polymerases alpha or beta (cytosine arabinoside, aphidicolin and dideoxythymidine) causing a reduction in unscheduled synthesis and an accumulation of single-strand breaks.	Cytarabine	134-154	DNA polymerase alpha 1, catalytic subunit	Homo sapiens	103-124
6762195-3	1982	CROP (cytosine arabinoside, daunorubicin, vincristine, prednisolone) produced CR in 41% of patients, 7 and 3 (cytosine arabinoside, daunorubicin) in 42% and 7 and 3 plus hydroxyurea in 52%.	Cytarabine	6-26	LUC7 like 3 pre-mRNA splicing factor	Homo sapiens	0-4
6306422-0	1983	Role of deoxycytidine kinase in the inhibitory activity of 5-substituted 2"-deoxycytidines and cytosine arabinosides on tumor cell growth.	Cytarabine	95-116	deoxycytidine kinase	Mus musculus	8-28
7161328-2	1982	One of the proposed mechanisms for the effectiveness of this drug in treating leukemias suggests that a metabolite of ara-C, i.e., 2"-deoxycytidine 5"-triphosphate (araCTP), competes with cytosine arabinoside 5"-triphosphate (dCTP) for binding to DNA polymerase.	Cytarabine	118-123	cut up	Drosophila melanogaster	226-230
7161328-3	1982	The ratio of the drug metabolite to the endogenous nucleotide (araCTP/dCTP) may, therefore, be important in determining the effectiveness of ara-C therapy.	Cytarabine	141-146	cut up	Drosophila melanogaster	70-74
6958361-0	1982	Kinetics of appearance of differentiation-associated characteristics in ML-1, a line of human myeloblastic leukemia cells, after treatment with 12-O-tetradecanoylphorbol-13-acetate, dimethyl sulfoxide or 1-beta-D-arabinofuranosylcytosine.	Cytarabine	204-237	interleukin 17F	Homo sapiens	72-76
6762195-3	1982	CROP (cytosine arabinoside, daunorubicin, vincristine, prednisolone) produced CR in 41% of patients, 7 and 3 (cytosine arabinoside, daunorubicin) in 42% and 7 and 3 plus hydroxyurea in 52%.	Cytarabine	110-130	LUC7 like 3 pre-mRNA splicing factor	Homo sapiens	0-4
7152024-0	1982	An NMR study of the interaction of cytosine arabinoside and lysozyme.	Cytarabine	35-55	lysozyme	Homo sapiens	60-68
6753603-3	1982	Under conditions in which at least 95% of [3H]thymidine incorporation was blocked by cytosine arabinoside, there was a 5- to 10-fold increase in the extent of differentiation (determined as fusion or creatine kinase elevation) on addition of insulin or multiplication-stimulating activity.	Cytarabine	85-105	insulin	Coturnix japonica	242-249
7162528-4	1982	The single exception was a pair of CS strains from sibling donors in which the rate of uncoupled incision due to the presence of either araC or the specific inhibitor of DNA polymerase alpha, aphidicolin, was slightly faster than in other cells studied.	Cytarabine	136-140	citrate synthase	Homo sapiens	35-37
7184462-3	1982	The ara-CTP level was certified to be determined by the capacity for not only ara-C phosphorylation but also the ara-CTP degradation in the B-cell lines, and, in addition, by the ara-C deamination in the T-cell lines.	Cytarabine	4-9	solute carrier family 25 member 1	Homo sapiens	117-120
7184462-3	1982	The ara-CTP level was certified to be determined by the capacity for not only ara-C phosphorylation but also the ara-CTP degradation in the B-cell lines, and, in addition, by the ara-C deamination in the T-cell lines.	Cytarabine	78-83	solute carrier family 25 member 1	Homo sapiens	8-11
6191711-1	1982	Ara-C should be converted to ara-CTP to inhibit DNA polymerase in the malignant cells but is rapidly inactivated to uracil arabinoside (ara-U) by cytidine deaminase in human tissue.	Cytarabine	0-5	cytidine deaminase	Homo sapiens	146-164
7152202-4	1982	In combinations of Hu IFN-alpha with anticancer agents such as bleomycin, mitomycin C, and cytosine arabinoside in certain concentration ranges, antagonism was noticed when Hu IFN-alpha and anticancer agents were added simultaneously to the cell culture.	Cytarabine	91-111	interferon alpha 1	Homo sapiens	22-31
7152202-4	1982	In combinations of Hu IFN-alpha with anticancer agents such as bleomycin, mitomycin C, and cytosine arabinoside in certain concentration ranges, antagonism was noticed when Hu IFN-alpha and anticancer agents were added simultaneously to the cell culture.	Cytarabine	91-111	interferon alpha 1	Homo sapiens	176-185
7102674-2	1982	Inhibition of polymerization and/or ligation of repaired regions with inhibitors of DNA polymerase alpha (cytosine arabinoside and aphidicolin) resulted in the accumulation of single-strand breaks, delayed reconstruction of DNA supercoiling, and maintenance of the staphylococcal nuclease digestibility.	Cytarabine	106-126	DNA polymerase alpha 1, catalytic subunit	Homo sapiens	84-104
7083175-9	1982	This conclusion was supported by the fact that, in Raji and Daudi cells exposed to 0.1 microM ara-C in the presence of 1 mM hydroxyurea, the plateau levels of ara-CTP increased 3-fold through inhibition of the nucleotide degradation.	Cytarabine	94-99	solute carrier family 25 member 1	Homo sapiens	163-166
7083175-10	1982	Thus, not only ara-C phosphorylation but also subsequent ara-CTP dephosphorylation was important in the accumulation and maintenance of ara-CTP and in the sensitivity to ara-C.	Cytarabine	15-20	solute carrier family 25 member 1	Homo sapiens	140-143
7083175-10	1982	Thus, not only ara-C phosphorylation but also subsequent ara-CTP dephosphorylation was important in the accumulation and maintenance of ara-CTP and in the sensitivity to ara-C.	Cytarabine	57-62	solute carrier family 25 member 1	Homo sapiens	140-143
7049670-1	1982	The effect of cytotoxic therapy (including cytosine-arabinoside and thioguanine) on the adrenal response to insulin-induced hypoglycemia has been investigated in 15 newly diagnosed patients with an acute form of leukemia.	Cytarabine	43-63	insulin	Homo sapiens	108-115
6949626-3	1982	A literature review provided two more cases of pancreatitis associated with Ara-c therapy in patients previously treated with L-asparaginase.	Cytarabine	76-81	asparaginase and isoaspartyl peptidase 1	Homo sapiens	126-140
6949626-4	1982	In view of th extreme rarity of pancreatitis in patients receiving Ara-c, the possibility arises that prior treatment with L-asparaginase may predispose the pancreas to this complication.	Cytarabine	67-72	asparaginase and isoaspartyl peptidase 1	Homo sapiens	123-137
7067928-2	1982	Extensive inhibition of DNA synthesis (61-78%) with hydroxyurea or cytosine arabinoside resulted in only 28-33% decrease in estrogen-induced prolactin synthesis.	Cytarabine	67-87	prolactin	Homo sapiens	141-150
6761307-5	1982	Three immunosuppressive drugs, HCA, cyclophosphamide, and Ara-C, depleted the thymus of cells expressing a large quantity of Thy-1.	Cytarabine	58-63	thymus cell antigen 1, theta	Mus musculus	125-130
6281786-3	1982	The presence of histone encoding regions in the lambda HHG clones was demonstrated by several independent criteria including hybridization with specific DNA probes, hybrid selection/in vitro translation, and hybridization of lambda HHG DNAs to reserve Southern blots containing cytoplasmic RNAs from G1-, S-, and arabinofuranosylcytosine (cytosine arabinoside)-treated S-phase cells.	Cytarabine	313-337	luteinizing hormone/choriogonadotropin receptor	Homo sapiens	55-58
6281786-3	1982	The presence of histone encoding regions in the lambda HHG clones was demonstrated by several independent criteria including hybridization with specific DNA probes, hybrid selection/in vitro translation, and hybridization of lambda HHG DNAs to reserve Southern blots containing cytoplasmic RNAs from G1-, S-, and arabinofuranosylcytosine (cytosine arabinoside)-treated S-phase cells.	Cytarabine	339-359	luteinizing hormone/choriogonadotropin receptor	Homo sapiens	55-58
6761307-10	1982	Treatment with Ara-C or 15(S)-methyl PGE1 produced a very modest evaluation in Lyt-1+2- cells.	Cytarabine	15-20	CD5 antigen	Mus musculus	79-84
6948608-7	1982	The sensitivity of DNA polymerase alpha of blast cells to 1-beta-D-arabinofuranosylcytosine 5"-triphosphate may be one of the determinants of the clinical response to 1-beta-D-arabinofuranosylcytosine treatment.	Cytarabine	58-91	DNA polymerase alpha 1, catalytic subunit	Homo sapiens	19-39
6806308-3	1982	Addition of cytosine-beta-D-arabinofuranoside to the explant cultures suppresses both hormonally induced DNA synthesis and enhanced production of milk protein.	Cytarabine	12-45	casein alpha s2-like A	Mus musculus	146-158
6958391-9	1982	Even in patients with low phosphorylation increasing Ara-C concentration increased Ara-CTP levels proportionally, but up to 10 times conventional doses may be necessary to exceed endogenous dCTP levels.	Cytarabine	53-58	cut up	Drosophila melanogaster	87-90
7062908-7	1982	Ara-C (10(-6) M) abolished also the PHA induced elevation of DNA polymerase alpha and thymidine kinase activities without influencing protein synthesis of the cell.	Cytarabine	0-5	DNA polymerase alpha 1, catalytic subunit	Homo sapiens	61-81
6272978-2	1981	One mutant that lacked deoxycytidine kinase activity, designated CEM/ara-C, retained about 10% of wild-type deoxyadenosine kinase and deoxyguanosine kinase activity each but maintained normal adenosine kinase or thymidine kinase activity.	Cytarabine	69-74	deoxycytidine kinase	Homo sapiens	23-43
6272978-2	1981	One mutant that lacked deoxycytidine kinase activity, designated CEM/ara-C, retained about 10% of wild-type deoxyadenosine kinase and deoxyguanosine kinase activity each but maintained normal adenosine kinase or thymidine kinase activity.	Cytarabine	69-74	adenosine kinase	Homo sapiens	113-129
6976970-2	1981	It was found that the induction process by TPA, which included increase in cells with receptors to sheep red blood cells (E--rosette positive--E+) and decrease in the levels of the marker enzyme terminal deoxynucleotidyl transferase (TdT) was not affected by the presence of DNA synthesis inhibitor arabinofuranosylcytosine (Ara-C).	Cytarabine	299-323	DNA nucleotidylexotransferase	Homo sapiens	234-237
6976970-2	1981	It was found that the induction process by TPA, which included increase in cells with receptors to sheep red blood cells (E--rosette positive--E+) and decrease in the levels of the marker enzyme terminal deoxynucleotidyl transferase (TdT) was not affected by the presence of DNA synthesis inhibitor arabinofuranosylcytosine (Ara-C).	Cytarabine	325-330	DNA nucleotidylexotransferase	Homo sapiens	234-237
7459369-10	1980	Against a P388 ara-C-resistant cell line (P/Ara-C, kinase deficient) in mice, ara-CDPdiacylglycerol prolonged survival times by 34% at a dose of 50 mg/kg per day times 4 and by 55% at 75 mg/kg per day times 4; the drug was not active against two other ara-C-resistant murine leukemia mutants (CA 55, CA5b).	Cytarabine	78-83	carbonic anhydrase 5b, mitochondrial	Mus musculus	300-304
7448798-9	1981	We suggest that MTX, by attenuating the ara-C-induced increase in dCTP, caused a change in the allosteric regulation of either deoxycytidine kinase or deoxycytidylate deaminase (or both), thereby potentiating the activity of ara-C.	Cytarabine	40-45	deoxycytidine kinase	Mus musculus	127-147
7448798-9	1981	We suggest that MTX, by attenuating the ara-C-induced increase in dCTP, caused a change in the allosteric regulation of either deoxycytidine kinase or deoxycytidylate deaminase (or both), thereby potentiating the activity of ara-C.	Cytarabine	40-45	dCMP deaminase	Mus musculus	151-176
7448798-9	1981	We suggest that MTX, by attenuating the ara-C-induced increase in dCTP, caused a change in the allosteric regulation of either deoxycytidine kinase or deoxycytidylate deaminase (or both), thereby potentiating the activity of ara-C.	Cytarabine	225-230	deoxycytidine kinase	Mus musculus	127-147
7448798-9	1981	We suggest that MTX, by attenuating the ara-C-induced increase in dCTP, caused a change in the allosteric regulation of either deoxycytidine kinase or deoxycytidylate deaminase (or both), thereby potentiating the activity of ara-C.	Cytarabine	225-230	dCMP deaminase	Mus musculus	151-176
7266020-0	1981	Thymidine enhancement of 1-beta-d-arabinofuranosylcytosine activity for mouse EL4 tumors.	Cytarabine	25-58	epilepsy 4	Mus musculus	78-81
6786736-0	1981	Diamine oxidase as a plasma marker of rat intestinal mucosal injury and regeneration after administration of 1-beta-D-arabinofuranosylcytosine.	Cytarabine	109-142	amine oxidase, copper containing 1	Rattus norvegicus	0-15
6786736-2	1981	The present study was designed to investigate whether plasma and mucosal DAO could be used to monitor the timing and severity of injury and recovery of the intestinal mucosa after administration of the chemotherapeutic agent 1-beta-D-arabinofuranosylcytosine (ara-C).	Cytarabine	225-258	amine oxidase, copper containing 1	Rattus norvegicus	73-76
6786736-2	1981	The present study was designed to investigate whether plasma and mucosal DAO could be used to monitor the timing and severity of injury and recovery of the intestinal mucosa after administration of the chemotherapeutic agent 1-beta-D-arabinofuranosylcytosine (ara-C).	Cytarabine	260-265	amine oxidase, copper containing 1	Rattus norvegicus	73-76
6786736-7	1981	With increasing dosage and/or increasing duration of ara-C treatment, mucosal injury was progressive, with increasing loss of both plasma and mucosal DAO levels as compared to controls (N = 38, p less than 0.005).	Cytarabine	53-58	amine oxidase, copper containing 1	Rattus norvegicus	150-153
6786736-8	1981	Plasma DAO levels in three patients with leukemia following ara-C chemotherapy decreased markedly to less than 30% of basal pretreatment levels (p less than 0.05) by Days 9 to 12, with a time course that was compatible with clinical intestinal mucosal injury.	Cytarabine	60-65	D-amino acid oxidase	Homo sapiens	7-10
6786736-9	1981	Our data document that plasma DAO levels reflect the mucosal injury and subsequent recovery after ara-C treatment in the rat and humans.	Cytarabine	98-103	amine oxidase, copper containing 1	Rattus norvegicus	30-33
6937239-3	1980	During separate courses of continuous infusion of different therapeutic doses of ara-C, ara-CTP accumulated in the leukemic bone marrow cells of a patient with acute myelogenous leukemia in proportion to the dose of ara-C.	Cytarabine	81-86	solute carrier family 25 member 1	Homo sapiens	92-95
20227960-1	1980	Cytidine deaminase, an enzyme found in the supernatant fluid of hepatocytes, granulocytes and tumor cells, and in plasma, degrades the antitumor agents cytosine arabinoside and 5-azacytidine.	Cytarabine	152-172	cytidine deaminase	Homo sapiens	0-18
6937239-5	1980	A priming dose of ara-C(125 to 250 mg/sq m) followed by a 1-hr infusion of an equal dose of ara-C to patients with acute myelogenous leukemia facilitated the determination of ara-CTP retention in bone marrow and peripheral blood leukemic cells in vivo.	Cytarabine	18-23	solute carrier family 25 member 1	Homo sapiens	179-182
6821557-2	1980	In additional studies, the cytostatic effects of activated macrophages markedly reduced the cytotoxic effects of the chemotherapeutic agent cytosine arabinoside on EMT-6 target cells.	Cytarabine	140-160	IL2 inducible T cell kinase	Mus musculus	164-167
118258-4	1979	They were demonstrated to be enzymatically hydrolyzed to the corresponding steroid and ara-CMP and the latter was further shown to be hydrolyzed to ara-C by phosphodiesterase I, snake venom, 5"-nucleotidase, and acid phosphatase.	Cytarabine	87-92	5'-nucleotidase, cytosolic IB	Mus musculus	191-206
7355245-2	1980	Behenoyl ara-C was resistant to deamination by cytidine deaminase, which was supposed to be liable for inactivating ara-C in vivo.	Cytarabine	9-14	cytidine deaminase	Mus musculus	47-65
510847-5	1979	Some regimens which did not include adriamycin, such as MFC (mitomycin-C, 5-fluorouracil, and cytosine arabinoside) had a good effect on the ER-positive cases, whereas the response to regimens including adriamycin was not influenced by the ER positiveness of the tumors.	Cytarabine	94-114	estrogen receptor 1	Homo sapiens	141-143
36105-2	1979	Equilibrium dialysis measurements were carried out to study the binding of 1-beta-D-arabinofuranosyl cytosine (ara-C) to human and bovine serum albumin (HSA, BSA) and to chemically modified albumin.	Cytarabine	75-109	albumin	Homo sapiens	138-151
427759-6	1979	Phosphorylation and incorporation of psi l Cyd into nucleic acids of P815 cells and of a P815 subline resistant to 1-beta-D-arabinofuranosylcytosine are about 2- to 20-fold higher than in P815 sublines resistant to psi l Cyd or to both 5-azacytidine and 1-beta-D-arabinofuranosylcytosine.	Cytarabine	115-148	cytochrome b-245, beta polypeptide	Mus musculus	43-46
427759-6	1979	Phosphorylation and incorporation of psi l Cyd into nucleic acids of P815 cells and of a P815 subline resistant to 1-beta-D-arabinofuranosylcytosine are about 2- to 20-fold higher than in P815 sublines resistant to psi l Cyd or to both 5-azacytidine and 1-beta-D-arabinofuranosylcytosine.	Cytarabine	254-287	cytochrome b-245, beta polypeptide	Mus musculus	43-46
36105-2	1979	Equilibrium dialysis measurements were carried out to study the binding of 1-beta-D-arabinofuranosyl cytosine (ara-C) to human and bovine serum albumin (HSA, BSA) and to chemically modified albumin.	Cytarabine	111-116	albumin	Homo sapiens	138-151
6236-9	1976	The activities of deoxycytidine kinase, but not of deoxycytidine deaminase, in host tissues of mice inoculated with L1210 leukemic cells sensitive to ara-C were greater than in those of normal mice.	Cytarabine	150-155	deoxycytidine kinase	Mus musculus	18-38
282937-1	1979	Paraplegia following prophylactic intrathecal cytosine arabinoside (Ara-C) is described in a patient with acute myelogenous leukemia in remission who received doses of 100 mg/m2/d for 5 consecutive days.	Cytarabine	46-66	ATP binding cassette subfamily C member 6	Homo sapiens	68-71
287856-0	1979	L-asparaginase used with cytosine arabinoside in treatment of childhood acute lymphocytic leukemia refractory to vincristine and prednisone.	Cytarabine	25-45	asparaginase and isoaspartyl peptidase 1	Homo sapiens	0-14
87370-0	1978	Differential inhibition of mammalian DNA polymerases alpha, beta and gamma and herpes simplex virus-induced DNA polymerase by the 5"-triphosphates of arabinosyladenine and arabinosylcytosine.	Cytarabine	172-190	DNA polymerase alpha 1, catalytic subunit	Homo sapiens	37-58
991148-1	1976	Cytosine arabinoside (CA) was utilized in efforts to synchronize leukemic cells in DNA synthesis for treatment with vincristine, prednisone, and L-asparaginase in children with acute leukemia in relapse.	Cytarabine	0-20	asparaginase and isoaspartyl peptidase 1	Homo sapiens	145-159
328050-1	1977	1-beta-D-Arabinofuranosylcytosine 5"-triphosphate (araCTP), an active form of a inhibitor of DNA replication, 1-beta-D-arabinofuranosylcytosine (araC) was tested for its inhibitory action on the DNA polymerase-alpha and -beta (EC 2.7.7.7) purified from calf thymus.	Cytarabine	51-55	DNA polymerase beta	Bos taurus	195-225
17616-3	1977	Cytosine arabinoside (Ara-C) elicits a significant increase in the level of the enzyme glutamine synthetase (GS) while it markedly reduces overall RNA and protein synthesis in cultures of embryonic chick neural retina.	Cytarabine	0-20	glutamate-ammonia ligase	Gallus gallus	87-107
17616-3	1977	Cytosine arabinoside (Ara-C) elicits a significant increase in the level of the enzyme glutamine synthetase (GS) while it markedly reduces overall RNA and protein synthesis in cultures of embryonic chick neural retina.	Cytarabine	22-27	glutamate-ammonia ligase	Gallus gallus	87-107
191910-1	1977	We have synthesized an analog (ara-CDP-DL-dipalmitin) of cytidine diphosphate diglyceride (CDP-diglyceride) in which the antitumor drug, cytosine arabinoside, is substituted for the cytidine moiety.	Cytarabine	137-157	cut like homeobox 1	Homo sapiens	35-38
191910-1	1977	We have synthesized an analog (ara-CDP-DL-dipalmitin) of cytidine diphosphate diglyceride (CDP-diglyceride) in which the antitumor drug, cytosine arabinoside, is substituted for the cytidine moiety.	Cytarabine	137-157	cut like homeobox 1	Homo sapiens	91-94
1277182-4	1976	They were superior to the parent compound, 1-beta-D-arabinofuranosylcytosine, in that smaller dosages exhibited strong activities regardless of the treatment schedule, and they were also resistant to cytidine deaminase.	Cytarabine	43-76	cytidine deaminase	Mus musculus	200-218
51655-1	1975	Deoxycytidine kinase, which phosphorylates deoxycytidine (CdR) and its analog, cytosine arabinoside (ara-C), has been purified 71-fold from human leukemic cells.	Cytarabine	79-99	deoxycytidine kinase	Homo sapiens	0-20
178873-3	1976	It has now been shown that the 2,2"-anhydro linkage in 1 and 3 can be selectively and efficiently cleaved by treatment with a mixture of pyridine and methanol giving the corresponding 3"-O-acyl derivatives of 1-beta-D-arabinofuranosylcytosine (2,4).	Cytarabine	209-242	inversion, Chr 17	Mus musculus	52-62
51655-1	1975	Deoxycytidine kinase, which phosphorylates deoxycytidine (CdR) and its analog, cytosine arabinoside (ara-C), has been purified 71-fold from human leukemic cells.	Cytarabine	101-106	deoxycytidine kinase	Homo sapiens	0-20
51655-2	1975	Biochemical properties of the partially purified enzyme included a molecular weight of 68,000, Kms of 7.8 muM for CdR and 25.6 muM for ara-C, and optimal activity with ATP and GTP as phosphate donors.	Cytarabine	135-140	latexin	Homo sapiens	127-130
51655-3	1975	Ara-C phosphorylation was strongly inhibited by CdR (Ki = 0.17 muM) and dCTP (Ki = 7.3 muM) and was weakly inhibited by ara-CTP (Ki = 0.13 mM).	Cytarabine	0-5	latexin	Homo sapiens	63-66
51655-3	1975	Ara-C phosphorylation was strongly inhibited by CdR (Ki = 0.17 muM) and dCTP (Ki = 7.3 muM) and was weakly inhibited by ara-CTP (Ki = 0.13 mM).	Cytarabine	0-5	latexin	Homo sapiens	87-90
51655-4	1975	Purification by calcium phosphate gel elution and DEAE chromatography effectively separated this enzyme from cytidine deaminase, which deaminates both CdR and ara-C, and from uridine-cytidine kinase, the enzyme which phosphorylates 5-azacytidine.	Cytarabine	159-164	cytidine deaminase	Homo sapiens	109-127
1109791-9	1975	ara-C was the predominant nucleoside present in hydrolysates of ara-CTP fractions.	Cytarabine	0-5	solute carrier family 25 (mitochondrial carrier, citrate transporter), member 1	Mus musculus	68-71
168963-4	1975	Treatment of MTV-positive and -negative animals with a regimen of cytosine arabinoside designed to inhibit only humoral immunity and leave CMI intact, corrected the deficit in methylated bovine serum albumin reactivity in MTV-positive mice.	Cytarabine	66-86	albumin	Mus musculus	194-207
809135-2	1975	The average inhibition of deaminase activity was 78% for tetrahydrouridine lot AJ39 (1.0 muM) when the concentration of cytosine arabinoside ranged from 44.2 to 170.7 muM; under the same conditions tetrahydrouridine lot AJ22 inhibited deamination by an average of 68%.	Cytarabine	120-140	latexin	Homo sapiens	89-92
809135-2	1975	The average inhibition of deaminase activity was 78% for tetrahydrouridine lot AJ39 (1.0 muM) when the concentration of cytosine arabinoside ranged from 44.2 to 170.7 muM; under the same conditions tetrahydrouridine lot AJ22 inhibited deamination by an average of 68%.	Cytarabine	120-140	latexin	Homo sapiens	167-170
1058044-1	1975	Short courses of cytosine arabinoside (Ara-C), cyclophosphamide, and L-asparaginase were given to seven children with newly diagnosed acute lymphocytic leukemia, who had failed to remit on standard remission induction therapy.	Cytarabine	17-37	ATP binding cassette subfamily C member 6	Homo sapiens	39-42
1174598-1	1975	Suckling mice were injectd with 30 or 50 mg cytosine arabinoside/kg body weight 2, 3 and 4 days after birth.	Cytarabine	44-64	weight 2	Mus musculus	73-81
4151790-2	1974	The analogue of cytidine, cytosine arabinoside (Ara-C), elicited a significant increase in the level of glutamine synthetase (GS) in embryonic chick neural retina in the absence of the steroid inducer of the enzyme.	Cytarabine	26-46	glutamate-ammonia ligase	Gallus gallus	104-124
4474681-0	1974	Comparative reactivity of cytidine and arabinosylcytosine to their 6-methyl derivatives in the presence of cytidine deaminase.	Cytarabine	39-57	cytidine deaminase	Homo sapiens	107-125
4151790-2	1974	The analogue of cytidine, cytosine arabinoside (Ara-C), elicited a significant increase in the level of glutamine synthetase (GS) in embryonic chick neural retina in the absence of the steroid inducer of the enzyme.	Cytarabine	48-53	glutamate-ammonia ligase	Gallus gallus	104-124
33655416-0	2021	Autologous hematopoietic cell transplantation following high-dose cytarabine consolidation for core-binding factor-acute myeloid leukemia in first complete remission: a phase 2 prospective trial.	Cytarabine	66-76	CCAAT enhancer binding protein zeta	Homo sapiens	95-114
4521417-1	1974	Cytidine deaminase, an enzyme that catalyses the deamination of both cytidine and its nucleoside analogues including the antineoplastic agents cytosine arabinoside (ara-C) and 5-azacytidine (5-azaC), has been partially purified from normal and leukemic human granulocytes.	Cytarabine	143-163	cytidine deaminase	Homo sapiens	0-18
4521417-1	1974	Cytidine deaminase, an enzyme that catalyses the deamination of both cytidine and its nucleoside analogues including the antineoplastic agents cytosine arabinoside (ara-C) and 5-azacytidine (5-azaC), has been partially purified from normal and leukemic human granulocytes.	Cytarabine	165-170	cytidine deaminase	Homo sapiens	0-18
4521417-5	1974	Cytidine deaminase from normal human granulocytes has a greater affinity for its physiologic substrate cytidine (K(m) = 1.1 x 10(-5) M) than for ara-C (8.8 x 10(-5) M) or 5-azaC (4.3 x 10(-4) M).	Cytarabine	145-150	cytidine deaminase	Homo sapiens	0-18
33919958-4	2021	The Bcl-2 inhibitor venetoclax, in combination with hypomethylating agents or low dose cytarabine, has produced impressive results for newly diagnosed AML, while its role in R/R disease is not well defined yet.	Cytarabine	87-97	BCL2 apoptosis regulator	Homo sapiens	4-9
33786613-6	2021	Cytarabine decreased cell viability, as determined by MTT assay, and induced cell death and cell cycle arrest in the parental HL-60 cell line, as revealed by Annexin V/propidium iodide (PI) staining and PI DNA incorporation, respectively, whereas no change was observed in the HL-60R cell line.	Cytarabine	0-10	annexin A5	Homo sapiens	158-167
33786613-10	2021	Furthermore, the antitumor effect of LQB-118 pterocarpanquinone was investigated; this compound induced apoptosis, a reduction in cell viability and a decrease in XIAP expression in cytarabine-resistant cells.	Cytarabine	182-192	X-linked inhibitor of apoptosis	Homo sapiens	163-167
33976256-0	2021	IDH2 mutations in patients with normal karyotype AML predict favorable responses to daunorubicin, cytarabine and cladribine regimen.	Cytarabine	98-108	isocitrate dehydrogenase (NADP(+)) 2	Homo sapiens	0-4
34059487-1	2021	INTRODUCTION: Venetoclax is a selective B-cell lymphoma 2 (BCL2) inhibitor, which is approved to treat elderly patients with newly diagnosed acute myeloid leukemia (AML) and high-risk myelodysplastic syndrome (MDS) in combination with either low-dose cytarabine (ARA-C) or hypomethylating agents.	Cytarabine	251-261	BCL2 apoptosis regulator	Homo sapiens	59-63
34059487-1	2021	INTRODUCTION: Venetoclax is a selective B-cell lymphoma 2 (BCL2) inhibitor, which is approved to treat elderly patients with newly diagnosed acute myeloid leukemia (AML) and high-risk myelodysplastic syndrome (MDS) in combination with either low-dose cytarabine (ARA-C) or hypomethylating agents.	Cytarabine	263-268	BCL2 apoptosis regulator	Homo sapiens	59-63
33853292-2	2021	We hypothesized that quizartinib, a selective and potent FLT3 inhibitor, with azacitidine (AZA) or low-dose cytarabine (LDAC) might improve the outcomes in patients with FLT3-ITD-mutated AML.	Cytarabine	108-118	fms related receptor tyrosine kinase 3	Homo sapiens	170-174
33787864-2	2021	We recently reported the results of treating children with AML with a combination of low-dose cytarabine and mitoxantrone or omacetaxine mepesuccinate with concurrent granulocyte colony-stimulating factor (G-CSF) (low-dose chemotherapy [LDC]) for remission induction followed by standard postremission strategies.	Cytarabine	94-104	colony stimulating factor 3	Homo sapiens	206-211
33601148-6	2021	Here, we confirmed that HMGCS1 inhibitor Hymeglusin enhanced cytarabine/Adriamycin (Ara-c/ADR) chemo-sensitivity in AML cells lines.	Cytarabine	61-71	3-hydroxy-3-methylglutaryl-CoA synthase 1	Homo sapiens	24-30
33601148-7	2021	Moreover, Ara-c-resistant HL-60 cells (HL-60/Ara-c) and ADR-resistant HL-60 cells (HL-60/ADR) were more sensitive to HMGCS1 inhibition than HL-60 cells.	Cytarabine	10-15	3-hydroxy-3-methylglutaryl-CoA synthase 1	Homo sapiens	117-123
33601148-7	2021	Moreover, Ara-c-resistant HL-60 cells (HL-60/Ara-c) and ADR-resistant HL-60 cells (HL-60/ADR) were more sensitive to HMGCS1 inhibition than HL-60 cells.	Cytarabine	45-50	3-hydroxy-3-methylglutaryl-CoA synthase 1	Homo sapiens	117-123
33476656-11	2021	On the contrary, knockdown of TBC1D16 resulted in decreased sensitivity to cytarabine in U937 cells.	Cytarabine	75-85	TBC1 domain family member 16	Homo sapiens	30-37
33832283-0	2021	Decitabine combined with medium-dose cytarabine in the treatment of DEK/CAN-positive acute myeloid leukemia: a case report.	Cytarabine	37-47	DEK proto-oncogene	Homo sapiens	68-71
33832283-6	2021	Herein, we reported the first case with DEK/CAN-positive AML who achieved complete remission of molecular biology via decitabine combined with a medium-dose cytarabine regimen.	Cytarabine	157-167	DEK proto-oncogene	Homo sapiens	40-43
33832283-8	2021	We hypothesized that the combination of decitabine and medium-dose cytarabine play an important role in targeting DEK/CAN and it should be verified by the accumulation of clinical cases and basic experiments in the future.	Cytarabine	67-77	DEK proto-oncogene	Homo sapiens	114-117
32554563-0	2021	Targeting GLUT1 in acute myeloid leukemia to overcome cytarabine resistance.	Cytarabine	54-64	solute carrier family 2 member 1	Homo sapiens	10-15
33782537-6	2021	MTSS1 expression was regulated by promoter methylation, and reduced by cytosine arabinoside and the anthracycline daunorubicin.	Cytarabine	71-91	MTSS I-BAR domain containing 1	Homo sapiens	0-5
33837299-5	2021	It induced apoptosis in leukaemia cells by increasing reactive oxygen species (ROS) and potentiated the activity of the chemotherapeutic cytarabine against highly aggressive models of infant MLL-rearranged ALL by enhancing DNA damage accumulation.	Cytarabine	137-147	lysine methyltransferase 2A	Homo sapiens	191-194
33638615-0	2021	Long noncoding RNA DANCR confers cytarabine resistance in acute myeloid leukemia by activating autophagy via the miR-874-3P/ATG16L1 axis.	Cytarabine	33-43	differentiation antagonizing non-protein coding RNA	Homo sapiens	19-24
33638615-0	2021	Long noncoding RNA DANCR confers cytarabine resistance in acute myeloid leukemia by activating autophagy via the miR-874-3P/ATG16L1 axis.	Cytarabine	33-43	microRNA 874	Homo sapiens	113-120
33638615-0	2021	Long noncoding RNA DANCR confers cytarabine resistance in acute myeloid leukemia by activating autophagy via the miR-874-3P/ATG16L1 axis.	Cytarabine	33-43	autophagy related 16 like 1	Homo sapiens	124-131
33638615-3	2021	We report here that cytarabine (Ara-C) treatment elevates DANCR expression in human AML cells.	Cytarabine	20-30	differentiation antagonizing non-protein coding RNA	Homo sapiens	58-63
33638615-3	2021	We report here that cytarabine (Ara-C) treatment elevates DANCR expression in human AML cells.	Cytarabine	32-37	differentiation antagonizing non-protein coding RNA	Homo sapiens	58-63
33638615-4	2021	In addition, DANCR overexpression confers and its knockdown diminishes Ara-C resistance in human AML cells, suggesting that DANCR positively regulates AML chemoresistance to Ara-C.	Cytarabine	71-76	differentiation antagonizing non-protein coding RNA	Homo sapiens	13-18
33638615-4	2021	In addition, DANCR overexpression confers and its knockdown diminishes Ara-C resistance in human AML cells, suggesting that DANCR positively regulates AML chemoresistance to Ara-C.	Cytarabine	71-76	differentiation antagonizing non-protein coding RNA	Homo sapiens	124-129
33638615-4	2021	In addition, DANCR overexpression confers and its knockdown diminishes Ara-C resistance in human AML cells, suggesting that DANCR positively regulates AML chemoresistance to Ara-C.	Cytarabine	174-179	differentiation antagonizing non-protein coding RNA	Homo sapiens	13-18
33638615-4	2021	In addition, DANCR overexpression confers and its knockdown diminishes Ara-C resistance in human AML cells, suggesting that DANCR positively regulates AML chemoresistance to Ara-C.	Cytarabine	174-179	differentiation antagonizing non-protein coding RNA	Homo sapiens	124-129
33638615-5	2021	Moreover, DANCR promotes autophagy in Ara-C-treated human AML cells and acts as a sponge to decrease miR-20a-5p expression, thereby upregulating the expression of ATG16L1, a critical component of the autophagy machinery.	Cytarabine	38-43	differentiation antagonizing non-protein coding RNA	Homo sapiens	10-15
33638615-6	2021	Importantly, ATG16L1 silencing abrogates DANCR-promoted autophagy and markedly restores DANCR-conferred Ara-C resistance, suggesting that DANCR promotes MIR-874-3P/ATG16L1 axis-regulated autophagy to confer Ara-C resistance in human AML cells.	Cytarabine	104-109	autophagy related 16 like 1	Homo sapiens	13-20
33638615-6	2021	Importantly, ATG16L1 silencing abrogates DANCR-promoted autophagy and markedly restores DANCR-conferred Ara-C resistance, suggesting that DANCR promotes MIR-874-3P/ATG16L1 axis-regulated autophagy to confer Ara-C resistance in human AML cells.	Cytarabine	104-109	differentiation antagonizing non-protein coding RNA	Homo sapiens	88-93
33638615-6	2021	Importantly, ATG16L1 silencing abrogates DANCR-promoted autophagy and markedly restores DANCR-conferred Ara-C resistance, suggesting that DANCR promotes MIR-874-3P/ATG16L1 axis-regulated autophagy to confer Ara-C resistance in human AML cells.	Cytarabine	104-109	differentiation antagonizing non-protein coding RNA	Homo sapiens	88-93
33638615-6	2021	Importantly, ATG16L1 silencing abrogates DANCR-promoted autophagy and markedly restores DANCR-conferred Ara-C resistance, suggesting that DANCR promotes MIR-874-3P/ATG16L1 axis-regulated autophagy to confer Ara-C resistance in human AML cells.	Cytarabine	104-109	microRNA 874	Homo sapiens	153-160
33638615-6	2021	Importantly, ATG16L1 silencing abrogates DANCR-promoted autophagy and markedly restores DANCR-conferred Ara-C resistance, suggesting that DANCR promotes MIR-874-3P/ATG16L1 axis-regulated autophagy to confer Ara-C resistance in human AML cells.	Cytarabine	207-212	autophagy related 16 like 1	Homo sapiens	13-20
33638615-6	2021	Importantly, ATG16L1 silencing abrogates DANCR-promoted autophagy and markedly restores DANCR-conferred Ara-C resistance, suggesting that DANCR promotes MIR-874-3P/ATG16L1 axis-regulated autophagy to confer Ara-C resistance in human AML cells.	Cytarabine	207-212	differentiation antagonizing non-protein coding RNA	Homo sapiens	41-46
33638615-6	2021	Importantly, ATG16L1 silencing abrogates DANCR-promoted autophagy and markedly restores DANCR-conferred Ara-C resistance, suggesting that DANCR promotes MIR-874-3P/ATG16L1 axis-regulated autophagy to confer Ara-C resistance in human AML cells.	Cytarabine	207-212	differentiation antagonizing non-protein coding RNA	Homo sapiens	88-93
33638615-6	2021	Importantly, ATG16L1 silencing abrogates DANCR-promoted autophagy and markedly restores DANCR-conferred Ara-C resistance, suggesting that DANCR promotes MIR-874-3P/ATG16L1 axis-regulated autophagy to confer Ara-C resistance in human AML cells.	Cytarabine	207-212	differentiation antagonizing non-protein coding RNA	Homo sapiens	88-93
33638615-6	2021	Importantly, ATG16L1 silencing abrogates DANCR-promoted autophagy and markedly restores DANCR-conferred Ara-C resistance, suggesting that DANCR promotes MIR-874-3P/ATG16L1 axis-regulated autophagy to confer Ara-C resistance in human AML cells.	Cytarabine	207-212	microRNA 874	Homo sapiens	153-160
33638615-6	2021	Importantly, ATG16L1 silencing abrogates DANCR-promoted autophagy and markedly restores DANCR-conferred Ara-C resistance, suggesting that DANCR promotes MIR-874-3P/ATG16L1 axis-regulated autophagy to confer Ara-C resistance in human AML cells.	Cytarabine	207-212	autophagy related 16 like 1	Homo sapiens	164-171
33638615-7	2021	Together, this study identifies DANCR as a positive regulator of Ara-C resistance in human AML cells, suggesting this lncRNA as a potential target for overcoming Ara-C resistance in AML chemotherapy.	Cytarabine	65-70	differentiation antagonizing non-protein coding RNA	Homo sapiens	32-37
33638615-7	2021	Together, this study identifies DANCR as a positive regulator of Ara-C resistance in human AML cells, suggesting this lncRNA as a potential target for overcoming Ara-C resistance in AML chemotherapy.	Cytarabine	162-167	differentiation antagonizing non-protein coding RNA	Homo sapiens	32-37
33709099-0	2021	AHR signaling pathway reshapes the metabolism of AML/MDS cells and potentially leads to cytarabine resistance.	Cytarabine	88-98	aryl hydrocarbon receptor	Homo sapiens	0-3
33709099-8	2021	Activating AHR in MDS/AML cells enhanced the resistance to cytarabine.	Cytarabine	59-69	aryl hydrocarbon receptor	Homo sapiens	11-14
33709099-9	2021	These findings indicated that activating the AHR signaling pathway reshaped the metabolism in MDS/AML cells, thus contributing to the resistance to cytarabine.	Cytarabine	148-158	aryl hydrocarbon receptor	Homo sapiens	45-48
33393145-0	2021	BACH2-mediated FOS confers cytarabine resistance via stromal microenvironment alterations in pediatric ALL.	Cytarabine	27-37	BTB domain and CNC homolog 2	Homo sapiens	0-5
33836581-4	2021	Here we present data demonstrating that AML cell lines deficient in OGG1 have enhanced sensitivity to cytarabine (cytosine arabinoside [Ara-C]) relative to OGG1-proficient cells.	Cytarabine	102-112	8-oxoguanine DNA glycosylase	Homo sapiens	68-72
33836581-4	2021	Here we present data demonstrating that AML cell lines deficient in OGG1 have enhanced sensitivity to cytarabine (cytosine arabinoside [Ara-C]) relative to OGG1-proficient cells.	Cytarabine	114-134	8-oxoguanine DNA glycosylase	Homo sapiens	68-72
33712646-3	2021	Here we report that loss-of-function mutations (LOF) in the histone methyltransferase EZH2 have the potential to confer resistance against the chemotherapeutic agent cytarabine.	Cytarabine	166-176	PR/SET domain 9	Homo sapiens	60-85
33712646-3	2021	Here we report that loss-of-function mutations (LOF) in the histone methyltransferase EZH2 have the potential to confer resistance against the chemotherapeutic agent cytarabine.	Cytarabine	166-176	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	86-90
33712646-6	2021	We confirm that loss of EZH2 induces resistance against cytarabine in the cell lines HEK293T and K562 as well as in a patient-derived xenograft model.	Cytarabine	56-66	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	24-28
33836581-4	2021	Here we present data demonstrating that AML cell lines deficient in OGG1 have enhanced sensitivity to cytarabine (cytosine arabinoside [Ara-C]) relative to OGG1-proficient cells.	Cytarabine	136-141	8-oxoguanine DNA glycosylase	Homo sapiens	68-72
33836581-6	2021	This lethality was highly specific for Ara-C treatment of AML cells deficient in OGG1, with no other replication stress-inducing agents showing a correlation between cell killing and low OGG1 levels.	Cytarabine	39-44	8-oxoguanine DNA glycosylase	Homo sapiens	81-85
33836581-6	2021	This lethality was highly specific for Ara-C treatment of AML cells deficient in OGG1, with no other replication stress-inducing agents showing a correlation between cell killing and low OGG1 levels.	Cytarabine	39-44	8-oxoguanine DNA glycosylase	Homo sapiens	187-191
33836581-7	2021	The mechanism for this preferential toxicity was addressed using in vitro replication assays in which DNA polymerase delta was shown to insert Ara-C opposite 8-oxo-dG, resulting in termination of DNA synthesis.	Cytarabine	143-148	DNA polymerase delta 1, catalytic subunit	Homo sapiens	102-122
33747637-7	2021	Moderate knockdown of BAFF-R in MCL cells did not affect its viability, but sensitized them to cytarabine treatment in vitro and in vivo, with prolonged mice survival.	Cytarabine	95-105	TNF receptor superfamily member 13C	Homo sapiens	22-28
33747637-9	2021	Conversely, the addition of recombinant BAFF (rhBAFF) to MCL cells protected them from cytarabine-induced apoptosis.	Cytarabine	87-97	TNF superfamily member 13b	Homo sapiens	40-44
33658491-7	2021	Notably, the GLI1 inhibitor GANT61 and the CDK4/6 inhibitor PD 0332991 had synergistic effects in promoting Ara-c sensitivity in AML cell lines and patient samples.	Cytarabine	108-113	GLI family zinc finger 1	Homo sapiens	13-17
33658491-7	2021	Notably, the GLI1 inhibitor GANT61 and the CDK4/6 inhibitor PD 0332991 had synergistic effects in promoting Ara-c sensitivity in AML cell lines and patient samples.	Cytarabine	108-113	cyclin dependent kinase 4	Homo sapiens	43-49
33393145-0	2021	BACH2-mediated FOS confers cytarabine resistance via stromal microenvironment alterations in pediatric ALL.	Cytarabine	27-37	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	15-18
33393145-6	2021	BACH2 blockade also promoted cell adhesion to bone marrow stromal cells and conferred cytarabine (Ara-C) resistant properties to leukemia cells by altering stromal microenvironment.	Cytarabine	86-96	BTB domain and CNC homolog 2	Homo sapiens	0-5
33393145-6	2021	BACH2 blockade also promoted cell adhesion to bone marrow stromal cells and conferred cytarabine (Ara-C) resistant properties to leukemia cells by altering stromal microenvironment.	Cytarabine	98-103	BTB domain and CNC homolog 2	Homo sapiens	0-5
33393145-8	2021	Blocking FOS by chemical compounds enhanced the effect of Ara-C treatment in both primary p-ALL cells and pre-B ALL-driven leukemia xenografts and prolonged survival of tumor-bearing mice.	Cytarabine	58-63	FBJ osteosarcoma oncogene	Mus musculus	9-12
33393145-9	2021	These data highlight an interconnected network of BACH2-FOS, disruption of which could render current chemotherapies more effective and offer a promising therapeutic strategy to overcome Ara-C resistance in p-ALL.	Cytarabine	187-192	BTB domain and CNC homolog 2	Homo sapiens	50-55
33393145-9	2021	These data highlight an interconnected network of BACH2-FOS, disruption of which could render current chemotherapies more effective and offer a promising therapeutic strategy to overcome Ara-C resistance in p-ALL.	Cytarabine	187-192	FBJ osteosarcoma oncogene	Mus musculus	56-59
33531064-6	2021	METHODS: By utilizing the unique nature of mass cytometry for single cell multiparameter analysis, we have explored the proteomic effect and intracellular signaling response in individual leukemic cells with internal tandem duplication of FLT3 (FLT3-ITD) after midostaurin treatment in combination with daunorubicin or cytarabine.	Cytarabine	319-329	fms related receptor tyrosine kinase 3	Homo sapiens	239-243
33626530-0	2021	Deoxycytidine Kinase (DCK) Mutations in Human Acute Myeloid Leukemia Resistant to Cytarabine.	Cytarabine	82-92	deoxycytidine kinase	Homo sapiens	0-20
33626530-0	2021	Deoxycytidine Kinase (DCK) Mutations in Human Acute Myeloid Leukemia Resistant to Cytarabine.	Cytarabine	82-92	deoxycytidine kinase	Homo sapiens	22-25
33626530-2	2021	Deoxycytidine kinase, encoded by DCK, catalyzes phosphorylation of cytarabine to cytarabine monophosphate, a necessary step for eventual incorporation of cytarabine triphosphate into DNA and for clinical efficacy.	Cytarabine	67-77	deoxycytidine kinase	Homo sapiens	0-20
33626530-2	2021	Deoxycytidine kinase, encoded by DCK, catalyzes phosphorylation of cytarabine to cytarabine monophosphate, a necessary step for eventual incorporation of cytarabine triphosphate into DNA and for clinical efficacy.	Cytarabine	67-77	deoxycytidine kinase	Homo sapiens	33-36
33626530-3	2021	Whether DCK mutations make AML cells resistant to cytarabine is controversial.	Cytarabine	50-60	deoxycytidine kinase	Homo sapiens	8-11
33626530-5	2021	DCK mutations were detected in 4 subjects with AML relapsing after achieving a complete remission and receiving high-dose cytarabine postremission therapy.	Cytarabine	122-132	deoxycytidine kinase	Homo sapiens	0-3
33626530-7	2021	DCK was also mutated in cytarabine-resistant but not parental AML cell lines.	Cytarabine	24-34	deoxycytidine kinase	Homo sapiens	0-3
33626530-8	2021	DCK mRNA concentrations were significantly decreased in cytarabine-resistant K562 and SHI-1 cells compared with cytarabine-sensitive parental cells.	Cytarabine	56-66	deoxycytidine kinase	Homo sapiens	0-3
33626530-8	2021	DCK mRNA concentrations were significantly decreased in cytarabine-resistant K562 and SHI-1 cells compared with cytarabine-sensitive parental cells.	Cytarabine	112-122	deoxycytidine kinase	Homo sapiens	0-3
33626530-10	2021	Overexpression of wild-type DCK restored cytarabine sensitivity to previously resistant leukemia cell lines.	Cytarabine	41-51	deoxycytidine kinase	Homo sapiens	28-31
33592119-10	2021	Patients treated with cytarabine had the highest yield of CD34+ cells (median 7.5 x 106 /kg vs 5.8 and 2.4 for etoposide and cyclophosphamide, P = .001).	Cytarabine	22-32	CD34 molecule	Homo sapiens	58-62
33592119-11	2021	Higher percentage of patients was able to collect >=2 x 106 CD34+ cells/kg during one leukapheresis after cytarabine (76% vs 21% for cyclophosphamide vs 36% for etoposide, P = .001).	Cytarabine	106-116	CD34 molecule	Homo sapiens	60-64
33592119-16	2021	Cytarabine is associated with the highest rate of successful mobilization and the highest yield of mobilized CD34+ cells.	Cytarabine	0-10	CD34 molecule	Homo sapiens	109-113
32911532-10	2021	Treatment with cytarabine (AraC) further induced BCL6 expression, and the levels of BCL6 induction were correlated with resistance to AraC.	Cytarabine	15-25	B cell leukemia/lymphoma 6	Mus musculus	49-53
32911532-10	2021	Treatment with cytarabine (AraC) further induced BCL6 expression, and the levels of BCL6 induction were correlated with resistance to AraC.	Cytarabine	15-25	B cell leukemia/lymphoma 6	Mus musculus	84-88
32911532-10	2021	Treatment with cytarabine (AraC) further induced BCL6 expression, and the levels of BCL6 induction were correlated with resistance to AraC.	Cytarabine	27-31	B cell leukemia/lymphoma 6	Mus musculus	49-53
32911532-10	2021	Treatment with cytarabine (AraC) further induced BCL6 expression, and the levels of BCL6 induction were correlated with resistance to AraC.	Cytarabine	134-138	B cell leukemia/lymphoma 6	Mus musculus	84-88
33531064-6	2021	METHODS: By utilizing the unique nature of mass cytometry for single cell multiparameter analysis, we have explored the proteomic effect and intracellular signaling response in individual leukemic cells with internal tandem duplication of FLT3 (FLT3-ITD) after midostaurin treatment in combination with daunorubicin or cytarabine.	Cytarabine	319-329	fms related receptor tyrosine kinase 3	Homo sapiens	245-249
33531064-9	2021	Moreover, we found elevated levels of FLT3 surface expression after cytarabine treatment.	Cytarabine	68-78	fms related receptor tyrosine kinase 3	Homo sapiens	38-42
33531064-10	2021	Interestingly, the surface localization of FLT3 receptor increased in vivo on the blast cell population of two AML patients during day 3 of induction therapy (daunorubicin; once/day from day 1-3 and cytarabine; twice/day from day 1-7).	Cytarabine	199-209	fms related receptor tyrosine kinase 3	Homo sapiens	43-47
33531064-11	2021	We found FLT3 receptor expression to correlate with intracellular cytarabine (AraC) response.	Cytarabine	66-76	fms related receptor tyrosine kinase 3	Homo sapiens	9-13
33531064-11	2021	We found FLT3 receptor expression to correlate with intracellular cytarabine (AraC) response.	Cytarabine	78-82	fms related receptor tyrosine kinase 3	Homo sapiens	9-13
33531064-12	2021	AML cell line cultured with AraC with or without PKC412 had an antagonizing phosphorylation inhibition of pAKT (p = 0.042 and 0.0261, respectively) and pERK1/2 (0.0134 and 0.0096, respectively) in FLT3high compared to FLT3low expressing cell populations.	Cytarabine	28-32	fms related receptor tyrosine kinase 3	Homo sapiens	197-201
33531064-12	2021	AML cell line cultured with AraC with or without PKC412 had an antagonizing phosphorylation inhibition of pAKT (p = 0.042 and 0.0261, respectively) and pERK1/2 (0.0134 and 0.0096, respectively) in FLT3high compared to FLT3low expressing cell populations.	Cytarabine	28-32	fms related receptor tyrosine kinase 3	Homo sapiens	218-222
33017025-11	2021	CONCLUSION: Cytarabine administration reduces the viability of human chordoma cells.	Cytarabine	12-22	CHDM	Homo sapiens	69-77
33453340-5	2021	Drebrin1 downregulation impeded cell adhesion to bone marrow stromal cells, resulting in improvement of sensitivity to cytarabine.	Cytarabine	119-129	drebrin 1	Homo sapiens	0-8
32564393-8	2021	Our findings demonstrate the anti-leukemia activity of fentanyl and synergistic effects between fentanyl and cytarabine in AML, via opioid receptor-independent suppression of Ras and STAT5 pathways.	Cytarabine	109-119	signal transducer and activator of transcription 5A	Homo sapiens	183-188
32447346-4	2021	Transcriptomic dataset analyses reveal that a USP7 gene signature is highly enriched in cells from AML patients at relapse, as well as in residual blasts from patient-derived xenograft (PDX) models treated with clinically relevant doses of cytarabine, which indicates a relationship between USP7 expression and resistance to therapy.	Cytarabine	240-250	ubiquitin specific peptidase 7	Homo sapiens	46-50
32447346-4	2021	Transcriptomic dataset analyses reveal that a USP7 gene signature is highly enriched in cells from AML patients at relapse, as well as in residual blasts from patient-derived xenograft (PDX) models treated with clinically relevant doses of cytarabine, which indicates a relationship between USP7 expression and resistance to therapy.	Cytarabine	240-250	ubiquitin specific peptidase 7	Homo sapiens	291-295
32447346-7	2021	Finally, we demonstrated that USP7 inhibition acts in synergy with cytarabine to kill AML cell lines and primary cells of patients with high USP7 levels.	Cytarabine	67-77	ubiquitin specific peptidase 7	Homo sapiens	141-145
33075425-0	2021	A Novel cytarabine analog evokes synthetic lethality by targeting MK2 in p53-deficient cancer cells.	Cytarabine	8-18	MAPK activated protein kinase 2	Homo sapiens	66-69
33075425-0	2021	A Novel cytarabine analog evokes synthetic lethality by targeting MK2 in p53-deficient cancer cells.	Cytarabine	8-18	tumor protein p53	Homo sapiens	73-76
33075425-2	2021	However, 2"-fluoro-4"-seleno-ara-C (F-Se-Ara-C), a new generation of cytarabine (Ara-C) analogs, exhibited potent antitumor activity against the p53-deficient prostate cancer cell line PC-3.	Cytarabine	69-79	tumor protein p53	Homo sapiens	145-148
33075425-2	2021	However, 2"-fluoro-4"-seleno-ara-C (F-Se-Ara-C), a new generation of cytarabine (Ara-C) analogs, exhibited potent antitumor activity against the p53-deficient prostate cancer cell line PC-3.	Cytarabine	41-46	tumor protein p53	Homo sapiens	145-148
33462236-3	2021	CALCRL knockdown impairs leukemic growth, decreases LSC frequency, and sensitizes to cytarabine in patient-derived xenograft models.	Cytarabine	85-95	calcitonin receptor like receptor	Homo sapiens	0-6
33416165-4	2021	Subsequently, the protective effect of FAPalpha on Cytosine arabinoside (Ara-C)-induced apoptosis in Kasumi-1 cells was investigated via small interfering (si)RNA, and its underlying mechanism was examined by western blotting.	Cytarabine	51-71	fibroblast activation protein alpha	Homo sapiens	39-47
33416165-4	2021	Subsequently, the protective effect of FAPalpha on Cytosine arabinoside (Ara-C)-induced apoptosis in Kasumi-1 cells was investigated via small interfering (si)RNA, and its underlying mechanism was examined by western blotting.	Cytarabine	73-78	fibroblast activation protein alpha	Homo sapiens	39-47
33416165-7	2021	It was found that Kasumi-1 cells expressed beta-catenin, which could be inhibited by Ara-C, and beta-catenin expression was significantly activated when co-cultured with BMMSCs, even in the presence of Ara-C.	Cytarabine	85-90	catenin beta 1	Homo sapiens	43-55
33513156-9	2021	We also examined the therapeutic efficacy of these drugs in combination with cytosine arabinoside and the effects of SLFN11 on the efficacy of cytosine arabinoside in SLFN11-overexpressing cells.	Cytarabine	143-163	schlafen family member 11	Homo sapiens	117-123
33513156-9	2021	We also examined the therapeutic efficacy of these drugs in combination with cytosine arabinoside and the effects of SLFN11 on the efficacy of cytosine arabinoside in SLFN11-overexpressing cells.	Cytarabine	143-163	schlafen family member 11	Homo sapiens	167-173
33513156-12	2021	The EZH2 and HDAC epigenetic modifiers upregulated SLFN11 expression in GCB-derived lymphoma cells and made them more susceptible to cytosine arabinoside.	Cytarabine	133-153	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	4-8
33513156-12	2021	The EZH2 and HDAC epigenetic modifiers upregulated SLFN11 expression in GCB-derived lymphoma cells and made them more susceptible to cytosine arabinoside.	Cytarabine	133-153	histone deacetylase 9	Homo sapiens	13-17
33513156-12	2021	The EZH2 and HDAC epigenetic modifiers upregulated SLFN11 expression in GCB-derived lymphoma cells and made them more susceptible to cytosine arabinoside.	Cytarabine	133-153	schlafen family member 11	Homo sapiens	51-57
33513156-13	2021	SLFN11 overexpression further sensitized GCB-derived lymphoma cells to cytosine arabinoside.	Cytarabine	71-91	schlafen family member 11	Homo sapiens	0-6
33513156-15	2021	GCB-derived lymphomas with low SLFN11 expression can be treated by the combination of epigenetic modifiers and cytosine arabinoside.	Cytarabine	111-131	schlafen family member 11	Homo sapiens	31-37
33436370-5	2021	Moreover, pharmacological inhibition of PHGDH sensitised FLT3-ITD AMLs to the standard of care chemotherapeutic cytarabine.	Cytarabine	112-122	phosphoglycerate dehydrogenase	Homo sapiens	40-45
33473264-4	2021	Here, we present an AML patient resembling APL with a novel cleavage and polyadenylation specific factor 6 (CPSF6)-RARG fusion, showing resistance to ATRA and poor response to chemotherapy with homoharringtonine and cytarabine.	Cytarabine	216-226	cleavage and polyadenylation specific factor 6	Homo sapiens	60-106
33473264-4	2021	Here, we present an AML patient resembling APL with a novel cleavage and polyadenylation specific factor 6 (CPSF6)-RARG fusion, showing resistance to ATRA and poor response to chemotherapy with homoharringtonine and cytarabine.	Cytarabine	216-226	cleavage and polyadenylation specific factor 6	Homo sapiens	108-113
33473264-4	2021	Here, we present an AML patient resembling APL with a novel cleavage and polyadenylation specific factor 6 (CPSF6)-RARG fusion, showing resistance to ATRA and poor response to chemotherapy with homoharringtonine and cytarabine.	Cytarabine	216-226	retinoic acid receptor gamma	Homo sapiens	115-119
33017025-13	2021	Based on our findings, we recommend the evaluation of cytarabine and tretinoin in an expanded set of human chordoma cell lines and animal models.	Cytarabine	54-64	CHDM	Homo sapiens	107-115
33414469-5	2021	Nrf2 overexpression protected the AML cells from apoptosis induced by cytarabine in vitro and increased the risk of drug resistance associated with a gene mutation in vivo.	Cytarabine	70-80	NFE2 like bZIP transcription factor 2	Homo sapiens	0-4
33071214-0	2021	Selective dysregulation of ABC transporters in methotrexate-resistant leukemia T-cells can confer cross-resistance to cytarabine, vincristine and dexamethasone, but not doxorubicin.	Cytarabine	118-128	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	27-30
32905646-0	2021	DNA Methylation-Based Epigenetic Repression of SLC22A4 Promotes Resistance to Cytarabine in Acute Myeloid Leukemia.	Cytarabine	78-88	solute carrier family 22 member 4	Homo sapiens	47-54
32905646-1	2021	Reduced expression of the uptake transporter, OCTN1 (SLC22A4), has been reported as a strong predictor of poor event-free and overall survival in multiple cohorts of patients with acute myeloid leukemia (AML) receiving the cytidine nucleoside analog, cytarabine (Ara-C).	Cytarabine	251-261	solute carrier family 22 member 4	Homo sapiens	46-51
32905646-1	2021	Reduced expression of the uptake transporter, OCTN1 (SLC22A4), has been reported as a strong predictor of poor event-free and overall survival in multiple cohorts of patients with acute myeloid leukemia (AML) receiving the cytidine nucleoside analog, cytarabine (Ara-C).	Cytarabine	251-261	solute carrier family 22 member 4	Homo sapiens	53-60
32905646-1	2021	Reduced expression of the uptake transporter, OCTN1 (SLC22A4), has been reported as a strong predictor of poor event-free and overall survival in multiple cohorts of patients with acute myeloid leukemia (AML) receiving the cytidine nucleoside analog, cytarabine (Ara-C).	Cytarabine	263-268	solute carrier family 22 member 4	Homo sapiens	46-51
32905646-1	2021	Reduced expression of the uptake transporter, OCTN1 (SLC22A4), has been reported as a strong predictor of poor event-free and overall survival in multiple cohorts of patients with acute myeloid leukemia (AML) receiving the cytidine nucleoside analog, cytarabine (Ara-C).	Cytarabine	263-268	solute carrier family 22 member 4	Homo sapiens	53-60
32905646-3	2021	We found increased basal SLC22A4 methylation was associated with decreased Ara-C uptake in AML cell lines.	Cytarabine	75-80	solute carrier family 22 member 4	Homo sapiens	25-32
33356802-0	2021	JAK-STAT inhibitor as a potential therapeutic opportunity in AML patients resistant to cytarabine and epigenetic therapy.	Cytarabine	87-97	signal transducer and activator of transcription 3	Homo sapiens	4-8
32950042-0	2020	Post-remission Therapy with Repeated Courses of High Dose Cytarabine, Idarubicin and Limited Autologous Stem Cell Support Achieves a Very Good Long-Term Outcome in ELN Favorable and Intermediate-Risk AML.	Cytarabine	58-68	elastin	Homo sapiens	164-167
33189657-0	2021	Corrigendum to "AC220 and AraC cause differential inhibitory dynamics in patient-derived M5-AML with FLT3-ITD and, thus, ultimately distinct therapeutic outcomes" [Experimental Hematology 2017;45:36-44].	Cytarabine	26-30	fms related receptor tyrosine kinase 3	Homo sapiens	101-105
32638373-1	2021	The sterile alpha motif and histidine-aspartic domain-containing protein 1 (SAMHD1) has been demonstrated to predict the response to high-dose cytarabine consolidation treatment in acute myeloid leukemia patients.	Cytarabine	143-153	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	76-82
32638373-2	2021	Here, we evaluated SAMHD1 as potential biomarker for the response to high-dose cytarabine in mantle cell lymphoma (MCL) patients.	Cytarabine	79-89	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	19-25
32638373-6	2021	In patients treated with high-dose cytarabine- or fludarabine-containing regimes, SAMHD1 expression was not significantly associated with FFS or complete remission rate.	Cytarabine	35-45	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	82-88
32638373-7	2021	SAMHD1 expression in B cell lymphoma cell lines, however, inversely correlated with their in vitro response to cytarabine as single agent (R = 0.65, p = 0.0065).	Cytarabine	111-121	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	0-6
33270982-8	2021	We showed that miR-15a-5p and miR-21-5p overexpression decreased apoptosis induced by cytarabine and/or daunorubicin.	Cytarabine	86-96	microRNA 215	Homo sapiens	30-39
33374216-0	2020	Fludarabine, High-Dose Cytarabine and Idarubicin-Based Induction May Overcome the Negative Prognostic Impact of FLT3-ITD in NPM1 Mutated AML, Irrespectively of FLT3-ITD Allelic Burden.	Cytarabine	23-33	fms related receptor tyrosine kinase 3	Homo sapiens	112-116
33276759-10	2020	In brief, combined radotinib and Ara-C significantly induced Annexin V-positive cells, cytosolic cytochrome C, and the pro-apoptotic protein Bax in AML cells including HL60, HEL92.1.7, and THP-1.	Cytarabine	33-38	annexin A5	Homo sapiens	61-70
33276759-10	2020	In brief, combined radotinib and Ara-C significantly induced Annexin V-positive cells, cytosolic cytochrome C, and the pro-apoptotic protein Bax in AML cells including HL60, HEL92.1.7, and THP-1.	Cytarabine	33-38	BCL2 associated X, apoptosis regulator	Homo sapiens	141-144
33276759-11	2020	In addition, mitochondrial membrane potential and Bcl-xl protein were markedly decreased by radotinib and Ara-C.	Cytarabine	106-111	BCL2 like 1	Homo sapiens	50-56
33276759-14	2020	Additionally, radotinib and Ara-C co-treatment induced G0/G1 arrest via the induction of CDKIs such as p21 and p27 and the inhibition of CDK2 and cyclin E. Thus, radotinib/Ara-C induces mitochondrial-dependent apoptosis and G0/G1 arrest via the regulation of the CDKI-CDK-cyclin cascade in AML cells.	Cytarabine	28-33	H3 histone pseudogene 16	Homo sapiens	103-106
33276759-14	2020	Additionally, radotinib and Ara-C co-treatment induced G0/G1 arrest via the induction of CDKIs such as p21 and p27 and the inhibition of CDK2 and cyclin E. Thus, radotinib/Ara-C induces mitochondrial-dependent apoptosis and G0/G1 arrest via the regulation of the CDKI-CDK-cyclin cascade in AML cells.	Cytarabine	28-33	dynactin subunit 6	Homo sapiens	111-114
33276759-14	2020	Additionally, radotinib and Ara-C co-treatment induced G0/G1 arrest via the induction of CDKIs such as p21 and p27 and the inhibition of CDK2 and cyclin E. Thus, radotinib/Ara-C induces mitochondrial-dependent apoptosis and G0/G1 arrest via the regulation of the CDKI-CDK-cyclin cascade in AML cells.	Cytarabine	28-33	cyclin dependent kinase 2	Homo sapiens	137-141
33276759-14	2020	Additionally, radotinib and Ara-C co-treatment induced G0/G1 arrest via the induction of CDKIs such as p21 and p27 and the inhibition of CDK2 and cyclin E. Thus, radotinib/Ara-C induces mitochondrial-dependent apoptosis and G0/G1 arrest via the regulation of the CDKI-CDK-cyclin cascade in AML cells.	Cytarabine	28-33	cyclin dependent kinase 2	Homo sapiens	89-92
33276759-14	2020	Additionally, radotinib and Ara-C co-treatment induced G0/G1 arrest via the induction of CDKIs such as p21 and p27 and the inhibition of CDK2 and cyclin E. Thus, radotinib/Ara-C induces mitochondrial-dependent apoptosis and G0/G1 arrest via the regulation of the CDKI-CDK-cyclin cascade in AML cells.	Cytarabine	28-33	proliferating cell nuclear antigen	Homo sapiens	146-152
33096154-3	2020	Accordingly, several studies on combining glucose transporter (GLUT) inhibitors with chemotherapeutic agents, such as doxorubicin, paclitaxel, and cytarabine, showed synergistic or additive anticancer effects, reduced chemo-, radio-, and immuno-resistance, and reduced toxicity due to lowering the therapeutic doses required for desired chemotherapeutic effects, as compared with monotherapy.	Cytarabine	147-157	solute carrier family 2 member 1	Homo sapiens	42-61
33096154-3	2020	Accordingly, several studies on combining glucose transporter (GLUT) inhibitors with chemotherapeutic agents, such as doxorubicin, paclitaxel, and cytarabine, showed synergistic or additive anticancer effects, reduced chemo-, radio-, and immuno-resistance, and reduced toxicity due to lowering the therapeutic doses required for desired chemotherapeutic effects, as compared with monotherapy.	Cytarabine	147-157	solute carrier family 2 member 1	Homo sapiens	63-67
33290798-0	2021	Cytosine arabinoside induces phosphorylation of histone H2AX in hippocampal neurons via a noncanonical pathway.	Cytarabine	0-20	H2A.X variant histone	Homo sapiens	48-60
33290798-3	2021	To identify the mechanism by which Ara-C kills neurons, we assessed the levels of phosphorylated histone H2AX (gamma-H2AX), a marker for DNA double-strand breaks (DSBs), in hippocampal neurons cultured for 48 h with Ara-C.	Cytarabine	35-40	H2A.X variant histone	Homo sapiens	97-109
33290798-7	2021	Furthermore, Ara-C-induced gamma-H2AX formation appeared to utilize cyclin-dependent kinase 7, but not ataxia telangiectasia mutated (ATM) or ATM and Rad3 related, which are well-known kinases in gamma-H2AX formation.	Cytarabine	13-18	cyclin dependent kinase 7	Homo sapiens	68-93
33967147-8	2021	After the standard induction therapy with daunorubicin and cytarabine, the number of myeloblasts in the bone marrow decreased, and the amplified MYC signals disappeared.	Cytarabine	59-69	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	145-148
33276759-14	2020	Additionally, radotinib and Ara-C co-treatment induced G0/G1 arrest via the induction of CDKIs such as p21 and p27 and the inhibition of CDK2 and cyclin E. Thus, radotinib/Ara-C induces mitochondrial-dependent apoptosis and G0/G1 arrest via the regulation of the CDKI-CDK-cyclin cascade in AML cells.	Cytarabine	172-177	H3 histone pseudogene 16	Homo sapiens	103-106
33276759-14	2020	Additionally, radotinib and Ara-C co-treatment induced G0/G1 arrest via the induction of CDKIs such as p21 and p27 and the inhibition of CDK2 and cyclin E. Thus, radotinib/Ara-C induces mitochondrial-dependent apoptosis and G0/G1 arrest via the regulation of the CDKI-CDK-cyclin cascade in AML cells.	Cytarabine	172-177	dynactin subunit 6	Homo sapiens	111-114
33276759-14	2020	Additionally, radotinib and Ara-C co-treatment induced G0/G1 arrest via the induction of CDKIs such as p21 and p27 and the inhibition of CDK2 and cyclin E. Thus, radotinib/Ara-C induces mitochondrial-dependent apoptosis and G0/G1 arrest via the regulation of the CDKI-CDK-cyclin cascade in AML cells.	Cytarabine	172-177	cyclin dependent kinase 2	Homo sapiens	89-92
33276759-14	2020	Additionally, radotinib and Ara-C co-treatment induced G0/G1 arrest via the induction of CDKIs such as p21 and p27 and the inhibition of CDK2 and cyclin E. Thus, radotinib/Ara-C induces mitochondrial-dependent apoptosis and G0/G1 arrest via the regulation of the CDKI-CDK-cyclin cascade in AML cells.	Cytarabine	172-177	proliferating cell nuclear antigen	Homo sapiens	146-152
33211826-5	2020	The impact of TP53mut VAF on clinical outcomes was driven by patients treated with a cytarabine-based regimen (median OS, 4.7 vs 7.3 months for VAF >40% vs <=40%; P = .006), whereas VAF did not significantly affect OS in patients treated with HMA.	Cytarabine	85-95	tumor protein p53	Homo sapiens	14-21
33262524-4	2021	The expression of both miR-10a and its downstream targets were strongly predictive of MDM2 inhibitor sensitivity in cell lines, primary AML specimens, and correlated to response in patients treated with both MDM2 inhibitors and cytarabine.	Cytarabine	228-238	microRNA 10a	Homo sapiens	23-30
33262524-5	2021	Furthermore, miR-10a inhibition induced synergy between MDM2 inhibitor Nutlin-3a and cytarabine in both in vitro and in vivo AML models.	Cytarabine	85-95	microRNA 10a	Homo sapiens	13-20
33262524-7	2021	Together these findings demonstrate that miR-10a may be useful as both a biomarker to identify patients most likely to respond to cytarabine+MDM2 inhibition and also a druggable target to increase their efficacy.	Cytarabine	130-140	microRNA 10a	Homo sapiens	41-48
33211826-8	2020	The best long-term outcomes were observed in those with 1 TP53 mutation with VAF <=40% who received a frontline cytarabine-based regimen (2-year OS, 38% vs 6% for all others; P < .001).	Cytarabine	112-122	tumor protein p53	Homo sapiens	58-62
33077697-0	2020	MicroRNA-143 sensitizes acute myeloid leukemia cells to cytarabine via targeting ATG7- and ATG2B-dependent autophagy.	Cytarabine	56-66	microRNA 143	Homo sapiens	0-12
33159047-9	2020	In addition, inhibition of SYK increases the sensitivity of LSCs to cytarabine (AraC), a standard of AML induction therapy.	Cytarabine	68-78	spleen tyrosine kinase	Mus musculus	27-30
33159047-9	2020	In addition, inhibition of SYK increases the sensitivity of LSCs to cytarabine (AraC), a standard of AML induction therapy.	Cytarabine	80-84	spleen tyrosine kinase	Mus musculus	27-30
32152464-0	2020	UGT1A1 genotype influences clinical outcome in patients with intermediate-risk acute myeloid leukemia treated with cytarabine-based chemotherapy.	Cytarabine	115-125	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
32152464-4	2020	Here we report the association between the UGT1A1 rs8175347 genotype and the clinical outcome of 455 intermediate-risk cytogenetic AML patients receiving cytarabine-based chemotherapy.	Cytarabine	154-164	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	43-49
33120845-13	2020	LESSONS: APL patients with STAT5B-RARa is not only resistant to ATRA, but also to conventional combination chemotherapy such as daunorubicin and cytarabine/idarubicin and cytarabine or other regimens.	Cytarabine	145-155	signal transducer and activator of transcription 5B	Homo sapiens	27-33
33120845-13	2020	LESSONS: APL patients with STAT5B-RARa is not only resistant to ATRA, but also to conventional combination chemotherapy such as daunorubicin and cytarabine/idarubicin and cytarabine or other regimens.	Cytarabine	145-155	retinoic acid receptor alpha	Homo sapiens	34-38
33120845-13	2020	LESSONS: APL patients with STAT5B-RARa is not only resistant to ATRA, but also to conventional combination chemotherapy such as daunorubicin and cytarabine/idarubicin and cytarabine or other regimens.	Cytarabine	171-181	signal transducer and activator of transcription 5B	Homo sapiens	27-33
33120845-13	2020	LESSONS: APL patients with STAT5B-RARa is not only resistant to ATRA, but also to conventional combination chemotherapy such as daunorubicin and cytarabine/idarubicin and cytarabine or other regimens.	Cytarabine	171-181	retinoic acid receptor alpha	Homo sapiens	34-38
33077697-3	2020	Here, we report that cytarabine treatment reduces miR-143 expression in AML cell lines and primary AML cells.	Cytarabine	21-31	microRNA 143	Homo sapiens	50-57
33077697-4	2020	Moreover, ectopic expression of miR-143 further decreases cell viability in cytarabine-treated AML cells.	Cytarabine	76-86	microRNA 143	Homo sapiens	32-39
33077697-5	2020	By contrast, miR-143 knockdown inhibits cytarabine-induced cytotoxicity, together indicating a role of miR-143 in enhancing cytarabine sensitivity in AML.	Cytarabine	40-50	microRNA 143	Homo sapiens	13-20
33077697-5	2020	By contrast, miR-143 knockdown inhibits cytarabine-induced cytotoxicity, together indicating a role of miR-143 in enhancing cytarabine sensitivity in AML.	Cytarabine	40-50	microRNA 143	Homo sapiens	103-110
32990804-1	2020	PURPOSE: Cytarabine, a key chemotherapy agent for acute myeloid leukemia (AML) treatment, is deaminated into inactive uracil-arabinoside by cytidine deaminase.	Cytarabine	9-19	cytidine deaminase	Homo sapiens	140-158
32687450-1	2020	PURPOSE: The B-cell lymphoma 2 (BCL-2) inhibitor venetoclax has an emerging role in acute myeloid leukemia (AML), with promising response rates in combination with hypomethylating agents or low-dose cytarabine in older patients.	Cytarabine	199-209	BCL2 apoptosis regulator	Homo sapiens	13-30
32687450-1	2020	PURPOSE: The B-cell lymphoma 2 (BCL-2) inhibitor venetoclax has an emerging role in acute myeloid leukemia (AML), with promising response rates in combination with hypomethylating agents or low-dose cytarabine in older patients.	Cytarabine	199-209	BCL2 apoptosis regulator	Homo sapiens	32-37
33077697-5	2020	By contrast, miR-143 knockdown inhibits cytarabine-induced cytotoxicity, together indicating a role of miR-143 in enhancing cytarabine sensitivity in AML.	Cytarabine	124-134	microRNA 143	Homo sapiens	13-20
33077697-0	2020	MicroRNA-143 sensitizes acute myeloid leukemia cells to cytarabine via targeting ATG7- and ATG2B-dependent autophagy.	Cytarabine	56-66	autophagy related 7	Homo sapiens	81-85
33077697-5	2020	By contrast, miR-143 knockdown inhibits cytarabine-induced cytotoxicity, together indicating a role of miR-143 in enhancing cytarabine sensitivity in AML.	Cytarabine	124-134	microRNA 143	Homo sapiens	103-110
33077697-6	2020	Subsequently, we show that miR-143 inhibits autophagy in cytarabine-treated AML cells by directly targeting autophagy-related proteins (ATG), ATG7 and ATG2B, two critical known components of autophagic machinery.	Cytarabine	57-67	microRNA 143	Homo sapiens	27-34
33077697-6	2020	Subsequently, we show that miR-143 inhibits autophagy in cytarabine-treated AML cells by directly targeting autophagy-related proteins (ATG), ATG7 and ATG2B, two critical known components of autophagic machinery.	Cytarabine	57-67	autophagy related 7	Homo sapiens	142-146
33077697-0	2020	MicroRNA-143 sensitizes acute myeloid leukemia cells to cytarabine via targeting ATG7- and ATG2B-dependent autophagy.	Cytarabine	56-66	autophagy related 2B	Homo sapiens	91-96
33077697-6	2020	Subsequently, we show that miR-143 inhibits autophagy in cytarabine-treated AML cells by directly targeting autophagy-related proteins (ATG), ATG7 and ATG2B, two critical known components of autophagic machinery.	Cytarabine	57-67	autophagy related 2B	Homo sapiens	151-156
33008453-2	2020	Here, we report a case of a 55-year-old female undergoing treatment for CD20+ B cell acute lymphoblastic leukemia who experienced a viral reactivation after receiving rituximab, cytarabine, and dasatinib.	Cytarabine	178-188	keratin 20	Homo sapiens	72-76
33077697-8	2020	Overall, this study demonstrates that targeting ATG7 and ATG2B-dependent autophagy is a critical mechanism by which miR-143 sensitizes AML to cytarabine, implicating it as a potential therapeutic target in AML treatment.	Cytarabine	142-152	autophagy related 7	Homo sapiens	48-52
33077697-8	2020	Overall, this study demonstrates that targeting ATG7 and ATG2B-dependent autophagy is a critical mechanism by which miR-143 sensitizes AML to cytarabine, implicating it as a potential therapeutic target in AML treatment.	Cytarabine	142-152	autophagy related 2B	Homo sapiens	57-62
33077697-8	2020	Overall, this study demonstrates that targeting ATG7 and ATG2B-dependent autophagy is a critical mechanism by which miR-143 sensitizes AML to cytarabine, implicating it as a potential therapeutic target in AML treatment.	Cytarabine	142-152	microRNA 143	Homo sapiens	116-123
33123543-7	2020	T-5224, the inhibitor of FosB, was administered to AML cell lines, which could inhibit cell proliferation, promote apoptosis, and restore the sensitivity of AML cells to cytarabine (Ara-C).	Cytarabine	170-180	FosB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	25-29
33123543-7	2020	T-5224, the inhibitor of FosB, was administered to AML cell lines, which could inhibit cell proliferation, promote apoptosis, and restore the sensitivity of AML cells to cytarabine (Ara-C).	Cytarabine	182-187	FosB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	25-29
33123543-8	2020	In summary, a higher level of hsa-miR-12462 in AML cells is associated with increased sensitivity to Ara-C via targeting FosB.	Cytarabine	101-106	FosB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	121-125
32641297-2	2020	Here, we show that the ectonucleotidase CD39 (ENTPD1) is upregulated in cytarabine (AraC)-resistant leukemic cells from both AML cell lines and patient samples in vivo and in vitro.	Cytarabine	84-88	ectonucleoside triphosphate diphosphohydrolase 1	Homo sapiens	40-44
32641297-0	2020	Extracellular ATP and CD39 activate cAMP-mediated mitochondrial stress response to promote cytarabine resistance in acute myeloid leukemia.	Cytarabine	91-101	ectonucleoside triphosphate diphosphohydrolase 1	Homo sapiens	22-26
32641297-2	2020	Here, we show that the ectonucleotidase CD39 (ENTPD1) is upregulated in cytarabine (AraC)-resistant leukemic cells from both AML cell lines and patient samples in vivo and in vitro.	Cytarabine	72-82	ectonucleoside triphosphate diphosphohydrolase 1	Homo sapiens	40-44
32641297-2	2020	Here, we show that the ectonucleotidase CD39 (ENTPD1) is upregulated in cytarabine (AraC)-resistant leukemic cells from both AML cell lines and patient samples in vivo and in vitro.	Cytarabine	84-88	ectonucleoside triphosphate diphosphohydrolase 1	Homo sapiens	46-52
32641297-2	2020	Here, we show that the ectonucleotidase CD39 (ENTPD1) is upregulated in cytarabine (AraC)-resistant leukemic cells from both AML cell lines and patient samples in vivo and in vitro.	Cytarabine	72-82	ectonucleoside triphosphate diphosphohydrolase 1	Homo sapiens	46-52
32641297-4	2020	High CD39 activity promotes AraC resistance by enhancing mitochondrial activity and biogenesis through activation of a cAMP-mediated adaptive mitochondrial stress response.	Cytarabine	28-32	ectonucleoside triphosphate diphosphohydrolase 1	Homo sapiens	5-9
32641297-5	2020	Finally, genetic and pharmacological inhibition of CD39 eATPase activity blocks the mitochondrial reprogramming triggered by AraC treatment and markedly enhances its cytotoxicity in AML cells in vitro and in vivo.	Cytarabine	125-129	ectonucleoside triphosphate diphosphohydrolase 1	Homo sapiens	51-55
32788570-0	2020	Expression of Fibroblast Growth Factor 4 in a Rat Model of Polydactyly of the Thumb Induced by Cytarabine.	Cytarabine	95-105	fibroblast growth factor 4	Rattus norvegicus	14-40
32543749-8	2020	Furthermore, overexpression of miR-582-5p can increase sensitivity of cells to Ara-C.	Cytarabine	79-84	microRNA 582	Homo sapiens	31-38
33499894-10	2020	CONCLUSION: These observations in 72 BCP-ALL cell lines suggested that the risk allele of the relapse-linked SNPs of ARID5B may be involved in a higher relapse rate because of resistance to chemotherapeutic agents such as VCR, CY, and AraC.	Cytarabine	235-239	AT-rich interaction domain 5B	Homo sapiens	117-123
32748108-1	2020	BACKGROUND: AML patients with FLT3/ITD mutations have poor response to cytarabine-based chemotherapy.	Cytarabine	71-81	fms related receptor tyrosine kinase 3	Homo sapiens	30-34
32748108-2	2020	FLT3 inhibitors (FLT3i) may resensitize cells to cytarabine (CYT).	Cytarabine	49-59	fms related receptor tyrosine kinase 3	Homo sapiens	0-4
32748108-2	2020	FLT3 inhibitors (FLT3i) may resensitize cells to cytarabine (CYT).	Cytarabine	61-64	fms related receptor tyrosine kinase 3	Homo sapiens	0-4
32748108-15	2020	CONCLUSION: Simultaneous administration of quizartinib and CYT every other day is a promising combination regimen for AML patients with FLT3 mutations.	Cytarabine	59-62	fms related receptor tyrosine kinase 3	Homo sapiens	136-140
32788570-1	2020	BACKGROUND The aim of this study was to assess the expression and mechanisms of fibroblast growth factor 4 in polydactyly of the thumb induced by cytarabine.	Cytarabine	146-156	fibroblast growth factor 4	Rattus norvegicus	80-106
32788570-11	2020	In this process, cytarabine can induce the expression of FGF4 on the tip of the embryonic limb bud, which further leads to abnormal development of the embryonic limb bud and eventually causes a congenital deformity.	Cytarabine	17-27	fibroblast growth factor 4	Rattus norvegicus	57-61
32298020-6	2020	RESULTS: The mean peak of CD34+ cells/ul in peripheral blood was 132 (range, 84-202) in Ara-C and 51 (range, 29-69) in Cy cohort (p < 0.001).	Cytarabine	88-93	CD34 molecule	Homo sapiens	26-30
32298020-9	2020	In the Ara-C group 98% of patients obtained more than 4x106 CD34+ cells/kg required for tandem transplantation.	Cytarabine	7-12	CD34 molecule	Homo sapiens	60-64
32708452-6	2020	Therefore, we generated GLI3-knockdown cell lines using small hairpin RNAs (shRNA) and evaluated their sensitivity to Ara-C in vitro.	Cytarabine	118-123	GLI family zinc finger 3	Homo sapiens	24-28
32686665-5	2020	We also demonstrate that Adenylate kinase isoenzyme 1 (AK1) inactivates antimetabolites like Cytarabine.	Cytarabine	93-103	adenylate kinase 1	Homo sapiens	25-53
32686665-5	2020	We also demonstrate that Adenylate kinase isoenzyme 1 (AK1) inactivates antimetabolites like Cytarabine.	Cytarabine	93-103	adenylate kinase 1	Homo sapiens	55-58
32686665-6	2020	Consequently, high AK1 levels correlate with poor survival of Cytarabine-treated acute myeloid leukemia patients, qualifying AK1 as a patient stratification marker and possibly as a drug target.	Cytarabine	62-72	adenylate kinase 1	Homo sapiens	19-22
32686665-6	2020	Consequently, high AK1 levels correlate with poor survival of Cytarabine-treated acute myeloid leukemia patients, qualifying AK1 as a patient stratification marker and possibly as a drug target.	Cytarabine	62-72	adenylate kinase 1	Homo sapiens	125-128
32703317-8	2020	In summary, a higher level of hsa-miR-12462 in AML cells is associated with increased sensitivity to cytarabine chemotherapy via downregulation of SLC9A1.	Cytarabine	101-111	solute carrier family 9 member A1	Homo sapiens	147-153
32708452-7	2020	The knockdown of GLI3 partly abolished the effect of Ara-C on colony formation and induction of apoptosis, indicating that GLI3 downregulation results in Ara-C resistance.	Cytarabine	53-58	GLI family zinc finger 3	Homo sapiens	17-21
32708452-7	2020	The knockdown of GLI3 partly abolished the effect of Ara-C on colony formation and induction of apoptosis, indicating that GLI3 downregulation results in Ara-C resistance.	Cytarabine	53-58	GLI family zinc finger 3	Homo sapiens	123-127
32708452-7	2020	The knockdown of GLI3 partly abolished the effect of Ara-C on colony formation and induction of apoptosis, indicating that GLI3 downregulation results in Ara-C resistance.	Cytarabine	154-159	GLI family zinc finger 3	Homo sapiens	17-21
32708452-7	2020	The knockdown of GLI3 partly abolished the effect of Ara-C on colony formation and induction of apoptosis, indicating that GLI3 downregulation results in Ara-C resistance.	Cytarabine	154-159	GLI family zinc finger 3	Homo sapiens	123-127
32708452-9	2020	Knockdown of GLI3 resulted in the upregulation of SAM and HD domain-containing protein 1 (SAMHD1), cytidine deaminase (CDA), and ATP-binding cassette C11 (ABCC11)/multidrug resistance-associated protein 8 (MRP8), each of which has been identified as a predictive marker for Ara-C response in acute myeloid leukemia.	Cytarabine	274-279	GLI family zinc finger 3	Homo sapiens	13-17
32029439-1	2020	PURPOSE: Cytarabine, 100-200 mg/mE+2/d, is commonly-used in induction therapy of acute myeloid leukaemia (AML).	Cytarabine	9-19	malic enzyme 2, NAD(+)-dependent, mitochondrial	Mus musculus	32-38
32665796-7	2020	RNA sequencing revealed that cytarabine treatment promoted MRTF-SRF pathway activation.	Cytarabine	29-39	serum response factor	Mus musculus	64-67
32145118-0	2020	Mec (mitoxantrone, etoposide, and cytarabine) induces complete remission and is an effective bridge to transplantat in acute myeloid leukemia.	Cytarabine	34-44	C-C motif chemokine ligand 28	Homo sapiens	0-3
32606608-5	2020	We, therefore, tested the hypothesis of the combination Ara-C with NK-1R antagonist could enhance the efficacy of Ara-C.	Cytarabine	114-119	tachykinin receptor 1	Homo sapiens	67-72
32581304-7	2020	SAMHD1 has a larger impact on nelarabine/AraG than on cytarabine in ALL cells.	Cytarabine	54-64	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	0-6
32429253-4	2020	Ex vivo response of primary AML blasts towards cytarabine (Ara C), daunorubicin (DNR), etoposide (VP16), and cladribine (2-CdA) was associated with the expression of 101, 345, 206, and 599 genes, respectively (p < 0.001, FDR 0.004-0.416).	Cytarabine	47-57	cytidine deaminase	Homo sapiens	123-126
32037927-3	2020	CPX-351 is a liposomal encapsulated formulation of cytarabine and daunorubicin in a 5:1 molar ratio that has been demonstrated to deliver synergistic ratiometric dosing of these drugs in pre-clinical studies.	Cytarabine	51-61	T-box transcription factor 22	Homo sapiens	0-3
32037927-4	2020	Early phase studies noted the encapsulated formulation of CPX-351 led to the extended duration of detectable cytarabine and daunorubicin levels compared to conventional chemotherapy, which may contribute to prolonged cytopenias.	Cytarabine	109-119	T-box transcription factor 22	Homo sapiens	58-61
32433559-5	2020	In-vitro, Kasumi-1 leukemic cell line, sorted by CD34 expression, showed increased apoptosis only in the CD34- subpopulation after exposure to cytosine arabinoside (Ara-C) or daunorubicin.	Cytarabine	143-163	CD34 molecule	Homo sapiens	49-53
32433559-5	2020	In-vitro, Kasumi-1 leukemic cell line, sorted by CD34 expression, showed increased apoptosis only in the CD34- subpopulation after exposure to cytosine arabinoside (Ara-C) or daunorubicin.	Cytarabine	143-163	CD34 molecule	Homo sapiens	105-109
32433559-7	2020	MEK1/2 inhibition elevated Ara-C ability to induce apoptosis in CD34+ cells, suggesting that MEK1/2-ERK1/2 is surviving signaling, which correlates to cell maturation levels and plays a role in chemoresistance.	Cytarabine	27-32	mitogen-activated protein kinase kinase 1	Homo sapiens	0-6
32433559-7	2020	MEK1/2 inhibition elevated Ara-C ability to induce apoptosis in CD34+ cells, suggesting that MEK1/2-ERK1/2 is surviving signaling, which correlates to cell maturation levels and plays a role in chemoresistance.	Cytarabine	27-32	CD34 molecule	Homo sapiens	64-68
32433559-7	2020	MEK1/2 inhibition elevated Ara-C ability to induce apoptosis in CD34+ cells, suggesting that MEK1/2-ERK1/2 is surviving signaling, which correlates to cell maturation levels and plays a role in chemoresistance.	Cytarabine	27-32	mitogen-activated protein kinase kinase 1	Homo sapiens	93-99
32433559-7	2020	MEK1/2 inhibition elevated Ara-C ability to induce apoptosis in CD34+ cells, suggesting that MEK1/2-ERK1/2 is surviving signaling, which correlates to cell maturation levels and plays a role in chemoresistance.	Cytarabine	27-32	mitogen-activated protein kinase 3	Homo sapiens	100-106
32509169-8	2020	In cellular experiments, circ-ANXA2 was upregulated in AML cell lines, and its knockdown suppressed proliferation, enhanced apoptosis of THP-1 and KG-1 cells and increased their chemosensitivity to cytarabine and daunorbicin.	Cytarabine	198-208	annexin A2	Homo sapiens	30-35
32429253-4	2020	Ex vivo response of primary AML blasts towards cytarabine (Ara C), daunorubicin (DNR), etoposide (VP16), and cladribine (2-CdA) was associated with the expression of 101, 345, 206, and 599 genes, respectively (p < 0.001, FDR 0.004-0.416).	Cytarabine	59-64	cytidine deaminase	Homo sapiens	123-126
32432757-0	2020	TUG1 weakens the sensitivity of acute myeloid leukemia cells to cytarabine by regulating miR-655-3p/CCND1 axis.	Cytarabine	64-74	taurine up-regulated 1	Homo sapiens	0-4
32432757-0	2020	TUG1 weakens the sensitivity of acute myeloid leukemia cells to cytarabine by regulating miR-655-3p/CCND1 axis.	Cytarabine	64-74	cyclin D1	Homo sapiens	100-105
32432757-10	2020	MiR-655-3p directly targeted CCND1, and CCND1 overexpression attenuated miR-655-3p restoration-mediated reinforcement of Ara-C sensitivity in AML cells.	Cytarabine	121-126	cyclin D1	Homo sapiens	40-45
32432757-12	2020	CONCLUSIONS: TUG1 weakened the sensitivity of AML cells to Ara-C by up-regulating CCND1 via miR-655-3p, suggesting a new insight into the chemotherapy of AML.	Cytarabine	59-64	taurine up-regulated 1	Homo sapiens	13-17
32432757-2	2020	However, the function and mechanism of TUG1 in cytarabine (Ara-C) sensitivity in AML remain unclear.	Cytarabine	47-57	taurine up-regulated 1	Homo sapiens	39-43
32432757-12	2020	CONCLUSIONS: TUG1 weakened the sensitivity of AML cells to Ara-C by up-regulating CCND1 via miR-655-3p, suggesting a new insight into the chemotherapy of AML.	Cytarabine	59-64	cyclin D1	Homo sapiens	82-87
32432757-2	2020	However, the function and mechanism of TUG1 in cytarabine (Ara-C) sensitivity in AML remain unclear.	Cytarabine	59-64	taurine up-regulated 1	Homo sapiens	39-43
32432757-8	2020	Higher expression levels of TUG1 or CCND1, and lower expression levels of miR-655-3p both notably reversed Ara-C-induced proliferation inhibition and apoptosis promotion in AML cells.	Cytarabine	107-112	taurine up-regulated 1	Homo sapiens	28-32
32432757-9	2020	TUG1 was a sponge of miR-655-3p, and TUG1 knockdown enhanced the sensitivity of AML cells to Ara-C by regulating miR-655-3p.	Cytarabine	93-98	taurine up-regulated 1	Homo sapiens	0-4
32432757-9	2020	TUG1 was a sponge of miR-655-3p, and TUG1 knockdown enhanced the sensitivity of AML cells to Ara-C by regulating miR-655-3p.	Cytarabine	93-98	taurine up-regulated 1	Homo sapiens	37-41
31860140-4	2020	In this phase 1 dose escalation study, the authors evaluated the safety of BV combined with mitoxantrone, etoposide, and cytarabine (MEC) re-induction chemotherapy for patients with CD30-expressing R/R AML.	Cytarabine	121-131	TNF receptor superfamily member 8	Homo sapiens	182-186
32171069-2	2020	The BCL-2 inhibitor, venetoclax, has shown promising activity in combination with hypomethylating agents and low-dose cytarabine in older adults for whom chemotherapy is not suitable with newly diagnosed acute myeloid leukaemia.	Cytarabine	118-128	BCL2 apoptosis regulator	Homo sapiens	4-9
32296637-6	2020	We demonstrated that ISC-4-mediated p-Akt inhibition caused apoptosis in primary AML (CD34+) stem cells and enhanced efficacy of cytarabine.	Cytarabine	129-139	AKT serine/threonine kinase 1	Homo sapiens	38-41
32296703-0	2020	Disrupting the LC3 Interaction Region (LIR) Binding of Selective Autophagy Receptors Sensitizes AML Cell Lines to Cytarabine.	Cytarabine	114-124	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	15-18
33742970-3	2021	Knockdown of JMJD3 can decrease the proliferation of AML cells and increase the chemosensitivity of daunorubicin (DNR) and cytarabine (Ara-C).	Cytarabine	123-133	lysine demethylase 6B	Homo sapiens	13-18
33742970-3	2021	Knockdown of JMJD3 can decrease the proliferation of AML cells and increase the chemosensitivity of daunorubicin (DNR) and cytarabine (Ara-C).	Cytarabine	135-140	lysine demethylase 6B	Homo sapiens	13-18
31850653-0	2020	Surge of serum interleukin-2 level in a Japanese patient with cytarabine syndrome.	Cytarabine	62-72	interleukin 2	Homo sapiens	15-28
31950591-0	2020	Ribonucleotide reductase inhibitors suppress SAMHD1 ara-CTPase activity enhancing cytarabine efficacy.	Cytarabine	82-92	SAM domain and HD domain, 1	Mus musculus	45-51
30940050-1	2020	INTRODUCTION: The aim of this study was to investigate the influence of high-dose cytosine arabinoside (HDAC)-containing treatments followed by autologous hematopoietic stem cell transplantation on the survival of patients with mantle cell lymphoma.	Cytarabine	82-102	histone deacetylase 9	Homo sapiens	104-108
32123152-3	2020	CASE REPORT Here we report a case of a 30-year-old male who presented with numb chin syndrome in the form of jaw pain, paresthesia, and hypoesthesia of the mental area as the presenting symptoms of acute of myeloid leukemia with t(8;21) treated with (3+7) protocol (3 days anthracycline+7 days cytarabine).	Cytarabine	294-304	NUMB endocytic adaptor protein	Homo sapiens	75-79
32093419-0	2020	Increased Expression of Micro-RNA-23a Mediates Chemoresistance to Cytarabine in Acute Myeloid Leukemia.	Cytarabine	66-76	microRNA 23a	Homo sapiens	24-37
32093419-6	2020	Analysis of clinical data revealed that high miR-23a expression correlated with relapsed/refractory (R/R) AML disease stages, the leukemic stem cell compartment, as well as with inferior overall survival (OS) and event-free survival (EFS) in AraC-treated patients.	Cytarabine	242-246	microRNA 23a	Homo sapiens	45-52
31926250-6	2020	KEY FINDINGS: We found that metformin could synergistically sensitize AML cells to Ara-C via inhibiting mTORC1/P70S6K pathway.	Cytarabine	83-88	CREB regulated transcription coactivator 1	Mus musculus	104-110
31904363-0	2020	HOTAIRM1 knockdown enhances cytarabine-induced cytotoxicity by suppression of glycolysis through the Wnt/beta-catenin/PFKP pathway in acute myeloid leukemia cells.	Cytarabine	28-38	HOXA transcript antisense RNA, myeloid-specific 1	Homo sapiens	0-8
31904363-0	2020	HOTAIRM1 knockdown enhances cytarabine-induced cytotoxicity by suppression of glycolysis through the Wnt/beta-catenin/PFKP pathway in acute myeloid leukemia cells.	Cytarabine	28-38	catenin beta 1	Homo sapiens	105-117
31904363-0	2020	HOTAIRM1 knockdown enhances cytarabine-induced cytotoxicity by suppression of glycolysis through the Wnt/beta-catenin/PFKP pathway in acute myeloid leukemia cells.	Cytarabine	28-38	phosphofructokinase, platelet	Homo sapiens	118-122
31904363-4	2020	The present study aimed to investigate the effect of HOTAIRM1 on the cytarabine (Ara-C) resistance in leukemia cell lines and to explore the underlying mechanism.	Cytarabine	69-79	HOXA transcript antisense RNA, myeloid-specific 1	Homo sapiens	53-61
31904363-4	2020	The present study aimed to investigate the effect of HOTAIRM1 on the cytarabine (Ara-C) resistance in leukemia cell lines and to explore the underlying mechanism.	Cytarabine	81-86	HOXA transcript antisense RNA, myeloid-specific 1	Homo sapiens	53-61
31904363-11	2020	The results showed that knockdown of HOTAIRM1 enhanced Ara-C-induced reduction of cell viability and increase of cell apoptosis.	Cytarabine	55-60	HOXA transcript antisense RNA, myeloid-specific 1	Homo sapiens	37-45
31926250-6	2020	KEY FINDINGS: We found that metformin could synergistically sensitize AML cells to Ara-C via inhibiting mTORC1/P70S6K pathway.	Cytarabine	83-88	ribosomal protein S6 kinase B1	Homo sapiens	111-117
31926250-0	2020	Inhibition of mTORC1/P70S6K pathway by Metformin synergistically sensitizes Acute Myeloid Leukemia to Ara-C.	Cytarabine	102-107	CREB regulated transcription coactivator 1	Mus musculus	14-20
31926250-0	2020	Inhibition of mTORC1/P70S6K pathway by Metformin synergistically sensitizes Acute Myeloid Leukemia to Ara-C.	Cytarabine	102-107	ribosomal protein S6 kinase B1	Homo sapiens	21-27
31926250-8	2020	SIGNIFICANCE: We firstly found the synergistic anti-tumor effect of Ara-C/metformin in AML through inhibiting mTORC1/P70S6K pathway.	Cytarabine	68-73	CREB regulated transcription coactivator 1	Mus musculus	110-116
31926250-8	2020	SIGNIFICANCE: We firstly found the synergistic anti-tumor effect of Ara-C/metformin in AML through inhibiting mTORC1/P70S6K pathway.	Cytarabine	68-73	ribosomal protein S6 kinase B1	Homo sapiens	117-123
31201358-6	2020	KDM6A-null myeloid leukemia cells were more resistant to treatment with the chemotherapeutic agents cytarabine (AraC) and daunorubicin.	Cytarabine	100-110	lysine demethylase 6A	Homo sapiens	0-5
31769058-0	2020	Acute myeloid leukemia with a novel CPSF6-RARG variant is sensitive to homoharringtonine and cytarabine chemotherapy.	Cytarabine	93-103	cleavage and polyadenylation specific factor 6	Homo sapiens	36-41
31769058-0	2020	Acute myeloid leukemia with a novel CPSF6-RARG variant is sensitive to homoharringtonine and cytarabine chemotherapy.	Cytarabine	93-103	retinoic acid receptor gamma	Homo sapiens	42-46
32062360-11	2020	FHL1-targeted intervention enhances the sensitivity of AML cells to cytarabine.	Cytarabine	68-78	four and a half LIM domains 1	Homo sapiens	0-4
31959790-0	2020	Clinical heterogeneity under induction with different dosages of cytarabine in core binding factor acute myeloid leukaemia.	Cytarabine	65-75	CCAAT enhancer binding protein zeta	Homo sapiens	79-98
31959790-1	2020	Repeated cycles of post-remission high-dose cytarabine (Ara-C) have been suggested to improve survival in core binding factor (CBF) acute myeloid leukaemia (AML).	Cytarabine	44-54	CCAAT enhancer binding protein zeta	Homo sapiens	106-125
31959790-1	2020	Repeated cycles of post-remission high-dose cytarabine (Ara-C) have been suggested to improve survival in core binding factor (CBF) acute myeloid leukaemia (AML).	Cytarabine	44-54	CCAAT enhancer binding protein zeta	Homo sapiens	127-130
31959790-1	2020	Repeated cycles of post-remission high-dose cytarabine (Ara-C) have been suggested to improve survival in core binding factor (CBF) acute myeloid leukaemia (AML).	Cytarabine	56-61	CCAAT enhancer binding protein zeta	Homo sapiens	106-125
31959790-1	2020	Repeated cycles of post-remission high-dose cytarabine (Ara-C) have been suggested to improve survival in core binding factor (CBF) acute myeloid leukaemia (AML).	Cytarabine	56-61	CCAAT enhancer binding protein zeta	Homo sapiens	127-130
32460231-10	2020	These experiments showed that TDP1-/-TDP2-/- cells were more sensitive to the agents Azidothymidine (zidovudine), Cytarabine, Abacavir, Gemcitabine, and Trifluridine than TDP1-/- or TDP2-/- cells.	Cytarabine	114-124	tyrosyl-DNA phosphodiesterase 1	Homo sapiens	30-34
32460231-10	2020	These experiments showed that TDP1-/-TDP2-/- cells were more sensitive to the agents Azidothymidine (zidovudine), Cytarabine, Abacavir, Gemcitabine, and Trifluridine than TDP1-/- or TDP2-/- cells.	Cytarabine	114-124	tyrosyl-DNA phosphodiesterase 2	Homo sapiens	37-41
31904363-16	2020	These findings suggested that HOTAIRM1 might be a therapeutic target for overcoming the Ara-C resistance in AML.	Cytarabine	88-93	HOXA transcript antisense RNA, myeloid-specific 1	Homo sapiens	30-38
32015759-2	2020	The AML with inv(16)(p13.1q22) or t (16;16)(p13.1;q22) is associated with a high rate of complete remission (CR) and favorable overall survival (OS) when treated with high-dose Cytarabine.	Cytarabine	177-187	inversin	Homo sapiens	13-16
31201358-6	2020	KDM6A-null myeloid leukemia cells were more resistant to treatment with the chemotherapeutic agents cytarabine (AraC) and daunorubicin.	Cytarabine	112-116	lysine demethylase 6A	Homo sapiens	0-5
31201358-7	2020	Inducible re-expression of KDM6A in KDM6A-null cell lines suppressed proliferation and sensitized cells again to AraC treatment.	Cytarabine	113-117	lysine demethylase 6A	Homo sapiens	27-32
31201358-7	2020	Inducible re-expression of KDM6A in KDM6A-null cell lines suppressed proliferation and sensitized cells again to AraC treatment.	Cytarabine	113-117	lysine demethylase 6A	Homo sapiens	36-41
31201358-8	2020	RNA expression analysis and functional studies revealed that resistance to AraC was conferred by downregulation of the nucleoside membrane transporter ENT1 (SLC29A1) by reduced H3K27 acetylation at the ENT1 locus.	Cytarabine	75-79	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	151-155
31201358-8	2020	RNA expression analysis and functional studies revealed that resistance to AraC was conferred by downregulation of the nucleoside membrane transporter ENT1 (SLC29A1) by reduced H3K27 acetylation at the ENT1 locus.	Cytarabine	75-79	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	157-164
31201358-8	2020	RNA expression analysis and functional studies revealed that resistance to AraC was conferred by downregulation of the nucleoside membrane transporter ENT1 (SLC29A1) by reduced H3K27 acetylation at the ENT1 locus.	Cytarabine	75-79	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	202-206
32189555-8	2020	However, araC and dFdC treatment led to increased dCK protein but decreased dCK activity.	Cytarabine	9-13	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	50-53
32189555-8	2020	However, araC and dFdC treatment led to increased dCK protein but decreased dCK activity.	Cytarabine	9-13	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	76-79
31778791-1	2020	Treatment of pediatric acute leukemia might involve combined therapies targeting the FMS-like tyrosine kinase 3 (FLT3) receptor (i.e. quizartinib - AC220) and nucleotide metabolism (cytarabine - AraC).	Cytarabine	195-199	fms related receptor tyrosine kinase 3	Homo sapiens	113-117
32727269-2	2020	Earlier we demonstrated that DEX decreased the activity of deoxycytidine kinase (dCK) which is essential for the activation of cytarabine (ara-C).	Cytarabine	127-137	deoxycytidine kinase	Rattus norvegicus	59-79
32727269-2	2020	Earlier we demonstrated that DEX decreased the activity of deoxycytidine kinase (dCK) which is essential for the activation of cytarabine (ara-C).	Cytarabine	127-137	sticky	Drosophila melanogaster	81-84
32727269-2	2020	Earlier we demonstrated that DEX decreased the activity of deoxycytidine kinase (dCK) which is essential for the activation of cytarabine (ara-C).	Cytarabine	139-144	deoxycytidine kinase	Rattus norvegicus	59-79
32727269-2	2020	Earlier we demonstrated that DEX decreased the activity of deoxycytidine kinase (dCK) which is essential for the activation of cytarabine (ara-C).	Cytarabine	139-144	sticky	Drosophila melanogaster	81-84
32727269-7	2020	In the liver of BNML bearing rats DEX decreased dCK activity 33%, while ara-C increased dCK activity slightly (to 129%), but in the combination of ara-C/DEX dCK activity was also decreased.	Cytarabine	72-77	sticky	Drosophila melanogaster	88-91
32727269-7	2020	In the liver of BNML bearing rats DEX decreased dCK activity 33%, while ara-C increased dCK activity slightly (to 129%), but in the combination of ara-C/DEX dCK activity was also decreased.	Cytarabine	72-77	sticky	Drosophila melanogaster	88-91
32727269-9	2020	In BNML leukemic spleens DEX decreased dCK activity 41% and gem/dex 46%, but ara-C increased dCK activity to 123%, but in the combination this effect was neutralized.	Cytarabine	77-82	sticky	Drosophila melanogaster	93-96
31778791-0	2020	FMS-like tyrosine kinase 3 (FLT3) modulates key enzymes of nucleotide metabolism implicated in cytarabine responsiveness in pediatric acute leukemia.	Cytarabine	95-105	fms related receptor tyrosine kinase 3	Homo sapiens	0-26
31778791-0	2020	FMS-like tyrosine kinase 3 (FLT3) modulates key enzymes of nucleotide metabolism implicated in cytarabine responsiveness in pediatric acute leukemia.	Cytarabine	95-105	fms related receptor tyrosine kinase 3	Homo sapiens	28-32
31778791-2	2020	This study addressed the possibility of FLT3 modulating nucleoside salvage processes and, eventually, cytarabine action.	Cytarabine	102-112	fms related receptor tyrosine kinase 3	Homo sapiens	40-44
31778791-6	2020	Indeed, inhibition of cN-II with anthraquinone-2,6-disulfonic acid (AdiS) further potentiated the synergistic action of AC220 and cytarabine, at low concentrations of this nucleoside analog.	Cytarabine	130-140	5'-nucleotidase, cytosolic II	Homo sapiens	22-27
31704958-0	2019	Structural insights into mutagenicity of anticancer nucleoside analog cytarabine during replication by DNA polymerase eta.	Cytarabine	70-80	DNA polymerase eta	Homo sapiens	103-121
31881855-17	2019	Treatment with both GQC-05 with a Bcl-2/Bcl-XL inhibitor Navitoclax results in increased cytotoxic activity, which is more pronounced than Navitoclax or GQC-05 alone, and more significant than Navitoclax in combination with cytarabine and doxorubicin that are currently being used clinically.	Cytarabine	224-234	BCL2 apoptosis regulator	Homo sapiens	34-39
31832201-0	2019	Role of equilibrative nucleoside transporter 1 (ENT1) in the disposition of cytarabine in mice.	Cytarabine	76-86	solute carrier family 29 (nucleoside transporters), member 1	Mus musculus	8-46
31832201-0	2019	Role of equilibrative nucleoside transporter 1 (ENT1) in the disposition of cytarabine in mice.	Cytarabine	76-86	solute carrier family 29 (nucleoside transporters), member 1	Mus musculus	48-52
31779969-4	2019	Core binding factor (CBF) AML is typically treated with post-remission high-dose cytarabine (HiDAC) without allogeneic hematopoietic stem cell transplantation (HSCT), whereas those with intermediate or adverse-risk cytogenetics are treated with post-remission cytarabine followed by allogeneic HSCT in CR1 when feasible.	Cytarabine	81-91	CCAAT enhancer binding protein zeta	Homo sapiens	0-19
31779969-4	2019	Core binding factor (CBF) AML is typically treated with post-remission high-dose cytarabine (HiDAC) without allogeneic hematopoietic stem cell transplantation (HSCT), whereas those with intermediate or adverse-risk cytogenetics are treated with post-remission cytarabine followed by allogeneic HSCT in CR1 when feasible.	Cytarabine	81-91	CCAAT enhancer binding protein zeta	Homo sapiens	21-24
31779969-4	2019	Core binding factor (CBF) AML is typically treated with post-remission high-dose cytarabine (HiDAC) without allogeneic hematopoietic stem cell transplantation (HSCT), whereas those with intermediate or adverse-risk cytogenetics are treated with post-remission cytarabine followed by allogeneic HSCT in CR1 when feasible.	Cytarabine	260-270	CCAAT enhancer binding protein zeta	Homo sapiens	0-19
31779969-4	2019	Core binding factor (CBF) AML is typically treated with post-remission high-dose cytarabine (HiDAC) without allogeneic hematopoietic stem cell transplantation (HSCT), whereas those with intermediate or adverse-risk cytogenetics are treated with post-remission cytarabine followed by allogeneic HSCT in CR1 when feasible.	Cytarabine	260-270	CCAAT enhancer binding protein zeta	Homo sapiens	21-24
31779969-6	2019	CBF AML benefits most from high-dose cytarabine (HiDAC), and dasatinib appears promising as an adjunct for those for KIT-mutated CBF AML.	Cytarabine	37-47	CCAAT enhancer binding protein zeta	Homo sapiens	0-3
30975911-5	2019	Exogenous expression of FLT3/ITD leads to increased Rac1 activity, reactive oxygen species, phosphorylated STAT5, DNA damage response factors and cytarabine resistance.	Cytarabine	146-156	fms related receptor tyrosine kinase 3	Homo sapiens	24-28
30975911-8	2019	Moreover, in a mouse model of FLT3/ITD acute myeloid leukemia, treatment with the CHK1 inhibitor MK8776 + cytarabine extended survival over cytarabine alone.	Cytarabine	106-116	FMS-like tyrosine kinase 3	Mus musculus	30-34
30975911-8	2019	Moreover, in a mouse model of FLT3/ITD acute myeloid leukemia, treatment with the CHK1 inhibitor MK8776 + cytarabine extended survival over cytarabine alone.	Cytarabine	106-116	checkpoint kinase 1	Mus musculus	82-86
30975911-8	2019	Moreover, in a mouse model of FLT3/ITD acute myeloid leukemia, treatment with the CHK1 inhibitor MK8776 + cytarabine extended survival over cytarabine alone.	Cytarabine	140-150	FMS-like tyrosine kinase 3	Mus musculus	30-34
30975911-8	2019	Moreover, in a mouse model of FLT3/ITD acute myeloid leukemia, treatment with the CHK1 inhibitor MK8776 + cytarabine extended survival over cytarabine alone.	Cytarabine	140-150	checkpoint kinase 1	Mus musculus	82-86
32009807-1	2019	Purpose: The addition of midostaurin to standard chemotherapy (cytarabine and daunorubicin) has shown significant improvements in the survival of patients with acute myeloid leukemia with the FLT3 mutation (FLT3-AML).	Cytarabine	63-73	fms related receptor tyrosine kinase 3	Homo sapiens	192-196
32009807-1	2019	Purpose: The addition of midostaurin to standard chemotherapy (cytarabine and daunorubicin) has shown significant improvements in the survival of patients with acute myeloid leukemia with the FLT3 mutation (FLT3-AML).	Cytarabine	63-73	fms related receptor tyrosine kinase 3	Homo sapiens	207-211
31817634-11	2019	In vivo experiments in an AML mouse model highlighted both improved survival and a significant reduction of leukemia cell burden in the bone marrow of mice treated with the combination of Notch pan-inhibitors (GSIs) plus chemotherapy (Ara-C).	Cytarabine	235-240	notch 1	Mus musculus	188-193
30967619-3	2019	Both alleles cooperated with Mll-Af9 to accelerate leukemia development that resulted in resistance to standard Cytarabine-based chemotherapy.	Cytarabine	112-122	lysine (K)-specific methyltransferase 2A	Mus musculus	29-32
30967619-3	2019	Both alleles cooperated with Mll-Af9 to accelerate leukemia development that resulted in resistance to standard Cytarabine-based chemotherapy.	Cytarabine	112-122	myeloid/lymphoid or mixed-lineage leukemia; translocated to, 3	Mus musculus	33-36
30967619-5	2019	Thus, after Cytarabine treatment, Setd2-mutant leukemic cells exit from the S phase and progress to the G2/M phase.	Cytarabine	12-22	SET domain containing 2	Mus musculus	34-39
31672129-4	2019	CASE PRESENTATION: A 28-years-old woman in the 26th week of gestation diagnosed with FLT3/ITD-mutated AML, complete remission was induced by Daunorubicin and Cytarabine, and subsequently with 5-azacytidine (75 mg/m2 daily for 7 days) with no fetal hematological or toxicity issues.	Cytarabine	158-168	fms related receptor tyrosine kinase 3	Homo sapiens	85-89
31545464-11	2019	Notably, AKT inhibition increased the susceptibility of KG1alpha cells to chemotherapy with idarubicin and AraC.	Cytarabine	107-111	AKT serine/threonine kinase 1	Homo sapiens	9-12
31501154-8	2019	We also demonstrated that AraC (but not VCR) - induced activation of MSC, mitochondrial transfer and mitochondrial mass increase in a murine NSG model of disseminated SEM-derived ALL wherein CD19+ cells closely associated with nestin+ MSC after AraC but not the other conditions.	Cytarabine	26-30	CD19 antigen	Mus musculus	191-195
31681584-7	2019	Both SCF and NGF exerted protective action against doxorubicin and cytarabine for t(8;21) AML and NB cells.	Cytarabine	67-77	KIT ligand	Homo sapiens	5-8
31358527-0	2019	Targeting Myeloperoxidase Disrupts Mitochondrial Redox Balance and Overcomes Cytarabine Resistance in Human Acute Myeloid Leukemia.	Cytarabine	77-87	myeloperoxidase	Homo sapiens	10-25
31236919-2	2019	We found that sensitivity of primary AML cells to cytarabine correlated with SOD2 acetylation and the ability of the drug to induce mitochondrial ROS.	Cytarabine	50-60	superoxide dismutase 2, mitochondrial	Mus musculus	77-81
31236919-5	2019	Furthermore, SIRT3 enhanced oxidative phosphorylation (OxPhos) in AML cells under both basic and cytarabine-treated conditions.	Cytarabine	97-107	sirtuin 3	Mus musculus	13-18
31236919-7	2019	SIRT3 inhibitor displayed synergy with cytarabine to ablate AML cells in vitro and in mouse models.	Cytarabine	39-49	sirtuin 3	Mus musculus	0-5
31322047-0	2019	Ara-c induces cell cycle G1/S arrest by inducing upregulation of the INK4 family gene or directly inhibiting the formation of the cell cycle-dependent complex CDK4/cyclin D1.	Cytarabine	0-5	cyclin D1	Homo sapiens	164-173
31575041-2	2019	We investigated the potential for high-resolution phenomic analysis in yeast to predict such genetic vulnerabilities by systematic, comprehensive, and quantitative assessment of drug-gene interaction for gemcitabine and cytarabine, substrates of deoxycytidine kinase that have similar molecular structures yet distinct antitumor efficacy.	Cytarabine	220-230	deoxycytidine kinase	Homo sapiens	246-266
31575041-3	2019	Human deoxycytidine kinase (dCK) was conditionally expressed in the Saccharomyces cerevisiae genomic library of knockout and knockdown (YKO/KD) strains, to globally and quantitatively characterize differential drug-gene interaction for gemcitabine and cytarabine.	Cytarabine	252-262	deoxycytidine kinase	Homo sapiens	6-26
31575041-3	2019	Human deoxycytidine kinase (dCK) was conditionally expressed in the Saccharomyces cerevisiae genomic library of knockout and knockdown (YKO/KD) strains, to globally and quantitatively characterize differential drug-gene interaction for gemcitabine and cytarabine.	Cytarabine	252-262	sticky	Drosophila melanogaster	28-31
31322047-0	2019	Ara-c induces cell cycle G1/S arrest by inducing upregulation of the INK4 family gene or directly inhibiting the formation of the cell cycle-dependent complex CDK4/cyclin D1.	Cytarabine	0-5	cyclin dependent kinase inhibitor 2A	Homo sapiens	69-73
30940905-3	2019	Here, we found that chemotherapeutic drugs (e.g., Ara-C, DNR, 6-MP) induced the expression of niche-protecting cytokines (GDF15, CCL3 and CCL4) in both ALL cell lines and primary cells in vitro.	Cytarabine	50-55	growth differentiation factor 15	Mus musculus	122-127
30940905-3	2019	Here, we found that chemotherapeutic drugs (e.g., Ara-C, DNR, 6-MP) induced the expression of niche-protecting cytokines (GDF15, CCL3 and CCL4) in both ALL cell lines and primary cells in vitro.	Cytarabine	50-55	chemokine (C-C motif) ligand 3	Mus musculus	129-133
30940905-3	2019	Here, we found that chemotherapeutic drugs (e.g., Ara-C, DNR, 6-MP) induced the expression of niche-protecting cytokines (GDF15, CCL3 and CCL4) in both ALL cell lines and primary cells in vitro.	Cytarabine	50-55	chemokine (C-C motif) ligand 4	Mus musculus	138-142
30940905-6	2019	Furthermore, we found that both pharmacological and genetic perturbation of ATM and p65 significantly decreased the residual ALL cells after Ara-C treatment in ALL xenograft mouse models.	Cytarabine	141-146	ataxia telangiectasia mutated	Mus musculus	76-79
30940905-6	2019	Furthermore, we found that both pharmacological and genetic perturbation of ATM and p65 significantly decreased the residual ALL cells after Ara-C treatment in ALL xenograft mouse models.	Cytarabine	141-146	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	84-87
31454720-3	2019	Large inter-patient pharmacokinetics variability has been reported, and genetic polymorphisms affecting cytidine deaminase (CDA), the liver enzyme responsible for the conversion of Ara-C to inactive uracil arabinoside (AraU) could be a culprit for either life-threatening toxicities or poor efficacy related to substantial changes in plasma exposure levels among patients.	Cytarabine	181-186	cytidine deaminase	Homo sapiens	104-122
31454720-3	2019	Large inter-patient pharmacokinetics variability has been reported, and genetic polymorphisms affecting cytidine deaminase (CDA), the liver enzyme responsible for the conversion of Ara-C to inactive uracil arabinoside (AraU) could be a culprit for either life-threatening toxicities or poor efficacy related to substantial changes in plasma exposure levels among patients.	Cytarabine	181-186	cytidine deaminase	Homo sapiens	124-127
31454720-7	2019	The performance and reliability of this method was tested as part of an investigational study in AML patients treated with low dose cytarabine and confirmed marked differences in drug exposure levels and metabolic ratio, depending on the CDA status of the patients.	Cytarabine	132-142	cytidine deaminase	Homo sapiens	238-241
31322047-0	2019	Ara-c induces cell cycle G1/S arrest by inducing upregulation of the INK4 family gene or directly inhibiting the formation of the cell cycle-dependent complex CDK4/cyclin D1.	Cytarabine	0-5	cyclin dependent kinase 4	Homo sapiens	159-163
31322047-5	2019	Finally, a potential association between Ara-c-induced cell cycle arrest and INK4-associated gene expression was evaluated.	Cytarabine	41-46	cyclin dependent kinase inhibitor 2A	Homo sapiens	77-81
31322047-8	2019	Moreover, Ara-c-induced cell cycle arrest was found to be associated with an Ara-c-induced upregulation of INK4 family gene expression, which ultimately inhibited the formation of the CDK4/cyclin D1 complex.	Cytarabine	10-15	cyclin dependent kinase inhibitor 2A	Homo sapiens	107-111
31322047-8	2019	Moreover, Ara-c-induced cell cycle arrest was found to be associated with an Ara-c-induced upregulation of INK4 family gene expression, which ultimately inhibited the formation of the CDK4/cyclin D1 complex.	Cytarabine	10-15	cyclin dependent kinase 4	Homo sapiens	184-188
31322047-8	2019	Moreover, Ara-c-induced cell cycle arrest was found to be associated with an Ara-c-induced upregulation of INK4 family gene expression, which ultimately inhibited the formation of the CDK4/cyclin D1 complex.	Cytarabine	10-15	cyclin D1	Homo sapiens	189-198
31322047-8	2019	Moreover, Ara-c-induced cell cycle arrest was found to be associated with an Ara-c-induced upregulation of INK4 family gene expression, which ultimately inhibited the formation of the CDK4/cyclin D1 complex.	Cytarabine	77-82	cyclin dependent kinase inhibitor 2A	Homo sapiens	107-111
31322047-8	2019	Moreover, Ara-c-induced cell cycle arrest was found to be associated with an Ara-c-induced upregulation of INK4 family gene expression, which ultimately inhibited the formation of the CDK4/cyclin D1 complex.	Cytarabine	77-82	cyclin dependent kinase 4	Homo sapiens	184-188
31322047-8	2019	Moreover, Ara-c-induced cell cycle arrest was found to be associated with an Ara-c-induced upregulation of INK4 family gene expression, which ultimately inhibited the formation of the CDK4/cyclin D1 complex.	Cytarabine	77-82	cyclin D1	Homo sapiens	189-198
31322047-10	2019	Moreover, Ara-c was shown to promote the upregulation of INK4 family genes, at the same time, Ara-c could directly regulate the cell cycle-dependent genes CDK4 and cyclin D1 (CCND1), independent of the INK4 family genes.	Cytarabine	10-15	cyclin dependent kinase inhibitor 2A	Homo sapiens	57-61
31322047-10	2019	Moreover, Ara-c was shown to promote the upregulation of INK4 family genes, at the same time, Ara-c could directly regulate the cell cycle-dependent genes CDK4 and cyclin D1 (CCND1), independent of the INK4 family genes.	Cytarabine	10-15	cyclin dependent kinase 4	Homo sapiens	155-159
31322047-10	2019	Moreover, Ara-c was shown to promote the upregulation of INK4 family genes, at the same time, Ara-c could directly regulate the cell cycle-dependent genes CDK4 and cyclin D1 (CCND1), independent of the INK4 family genes.	Cytarabine	10-15	cyclin D1	Homo sapiens	164-173
31322047-10	2019	Moreover, Ara-c was shown to promote the upregulation of INK4 family genes, at the same time, Ara-c could directly regulate the cell cycle-dependent genes CDK4 and cyclin D1 (CCND1), independent of the INK4 family genes.	Cytarabine	10-15	cyclin D1	Homo sapiens	175-180
31322047-10	2019	Moreover, Ara-c was shown to promote the upregulation of INK4 family genes, at the same time, Ara-c could directly regulate the cell cycle-dependent genes CDK4 and cyclin D1 (CCND1), independent of the INK4 family genes.	Cytarabine	94-99	cyclin dependent kinase inhibitor 2A	Homo sapiens	57-61
31322047-10	2019	Moreover, Ara-c was shown to promote the upregulation of INK4 family genes, at the same time, Ara-c could directly regulate the cell cycle-dependent genes CDK4 and cyclin D1 (CCND1), independent of the INK4 family genes.	Cytarabine	94-99	cyclin dependent kinase 4	Homo sapiens	155-159
31322047-10	2019	Moreover, Ara-c was shown to promote the upregulation of INK4 family genes, at the same time, Ara-c could directly regulate the cell cycle-dependent genes CDK4 and cyclin D1 (CCND1), independent of the INK4 family genes.	Cytarabine	94-99	cyclin D1	Homo sapiens	164-173
31322047-10	2019	Moreover, Ara-c was shown to promote the upregulation of INK4 family genes, at the same time, Ara-c could directly regulate the cell cycle-dependent genes CDK4 and cyclin D1 (CCND1), independent of the INK4 family genes.	Cytarabine	94-99	cyclin D1	Homo sapiens	175-180
31363040-7	2019	In summary, dnr and Ara-C selection pressure induces acute reductions in ceramide levels and large increases in S1P and C1P, concomitant with cell resilience bolstered by enhanced mitochondrial remodeling.	Cytarabine	20-25	membrane bound transcription factor peptidase, site 1	Homo sapiens	112-123
31299413-3	2019	We now show mechanistically that EC activation induces the secretion of interleukin-8 (IL-8) leading to significant expansion of non-adherent AML cells and resistance to cytarabine (Ara-C).	Cytarabine	182-187	C-X-C motif chemokine ligand 8	Homo sapiens	72-85
31363040-4	2019	Resistant cells, those selected for growth in Ara-C- and dnr-containing medium (HL-60/Ara-C and HL-60/dnr, respectively), demonstrated upregulated expression and activity of glucosylceramide synthase, acid ceramidase (AC), and sphingosine kinase 1 (SPHK1); were more resistant to ceramide than parental cells; and displayed sensitivity to inhibitors of SL metabolism.	Cytarabine	46-51	UDP-glucose ceramide glucosyltransferase	Homo sapiens	174-199
31363040-4	2019	Resistant cells, those selected for growth in Ara-C- and dnr-containing medium (HL-60/Ara-C and HL-60/dnr, respectively), demonstrated upregulated expression and activity of glucosylceramide synthase, acid ceramidase (AC), and sphingosine kinase 1 (SPHK1); were more resistant to ceramide than parental cells; and displayed sensitivity to inhibitors of SL metabolism.	Cytarabine	46-51	N-acylsphingosine amidohydrolase 1	Homo sapiens	201-216
31363040-4	2019	Resistant cells, those selected for growth in Ara-C- and dnr-containing medium (HL-60/Ara-C and HL-60/dnr, respectively), demonstrated upregulated expression and activity of glucosylceramide synthase, acid ceramidase (AC), and sphingosine kinase 1 (SPHK1); were more resistant to ceramide than parental cells; and displayed sensitivity to inhibitors of SL metabolism.	Cytarabine	46-51	N-acylsphingosine amidohydrolase 1	Homo sapiens	218-220
31363040-4	2019	Resistant cells, those selected for growth in Ara-C- and dnr-containing medium (HL-60/Ara-C and HL-60/dnr, respectively), demonstrated upregulated expression and activity of glucosylceramide synthase, acid ceramidase (AC), and sphingosine kinase 1 (SPHK1); were more resistant to ceramide than parental cells; and displayed sensitivity to inhibitors of SL metabolism.	Cytarabine	46-51	sphingosine kinase 1	Homo sapiens	227-247
31363040-4	2019	Resistant cells, those selected for growth in Ara-C- and dnr-containing medium (HL-60/Ara-C and HL-60/dnr, respectively), demonstrated upregulated expression and activity of glucosylceramide synthase, acid ceramidase (AC), and sphingosine kinase 1 (SPHK1); were more resistant to ceramide than parental cells; and displayed sensitivity to inhibitors of SL metabolism.	Cytarabine	46-51	sphingosine kinase 1	Homo sapiens	249-254
31299413-3	2019	We now show mechanistically that EC activation induces the secretion of interleukin-8 (IL-8) leading to significant expansion of non-adherent AML cells and resistance to cytarabine (Ara-C).	Cytarabine	170-180	C-X-C motif chemokine ligand 8	Homo sapiens	72-85
31299413-3	2019	We now show mechanistically that EC activation induces the secretion of interleukin-8 (IL-8) leading to significant expansion of non-adherent AML cells and resistance to cytarabine (Ara-C).	Cytarabine	170-180	C-X-C motif chemokine ligand 8	Homo sapiens	87-91
31299413-3	2019	We now show mechanistically that EC activation induces the secretion of interleukin-8 (IL-8) leading to significant expansion of non-adherent AML cells and resistance to cytarabine (Ara-C).	Cytarabine	182-187	C-X-C motif chemokine ligand 8	Homo sapiens	87-91
31273062-0	2019	Deletion of the Miz-1 POZ Domain Increases Efficacy of Cytarabine Treatment in T- and B-ALL/Lymphoma Mouse Models.	Cytarabine	55-65	zinc finger and BTB domain containing 17	Mus musculus	16-21
31152020-1	2019	PURPOSE: The histone deacetylase (HDAC) inhibitor panobinostat potentiates anthracycline and cytarabine cytotoxicity in acute myeloid leukemia (AML) cells.	Cytarabine	93-103	histone deacetylase 9	Homo sapiens	13-32
31152020-1	2019	PURPOSE: The histone deacetylase (HDAC) inhibitor panobinostat potentiates anthracycline and cytarabine cytotoxicity in acute myeloid leukemia (AML) cells.	Cytarabine	93-103	histone deacetylase 9	Homo sapiens	34-38
31273062-6	2019	Acute ablation of the Miz-1 POZ domain enhanced the effect of cytarabine treatment.	Cytarabine	62-72	zinc finger and BTB domain containing 17	Mus musculus	22-27
30679330-0	2019	Romidepsin enhances the efficacy of cytarabine in vivo, revealing histone deacetylase inhibition as a promising therapeutic strategy for KMT2A-rearranged infant acute lymphoblastic leukemia.	Cytarabine	36-46	lysine methyltransferase 2A	Homo sapiens	137-142
31115604-4	2019	When THP-1 and SHI-1 cells were primed with 20 ng/mL G-CSF or GM-CSF followed by Ara-C and ACR, cell proliferation rate in the CAGM (Ara-C, ACR, and GM-CSF) regimen was lower than in the CAG regimen (P &lt; 0.05).	Cytarabine	81-86	GLI family zinc finger 2	Homo sapiens	5-10
30992301-0	2019	A Phase I/II Trial of MEC (Mitoxantrone, Etoposide, Cytarabine) in Combination with Ixazomib for Relapsed Refractory Acute Myeloid Leukemia.	Cytarabine	52-62	C-C motif chemokine ligand 28	Homo sapiens	22-25
31311121-5	2019	In this study, we tested NK cell activity against KG1a (AML cell line) with and without two types of pretreatment-Ara-C treatment that induced NKG2D ligands (increased activating signal) and/or blocking of HLA-KIR (killer-immunoglobulin-like receptors) interaction (decreased inhibitory signal).	Cytarabine	114-119	killer cell lectin like receptor K1	Homo sapiens	143-148
30948162-3	2019	CBF AML is most common and as such, its treatment is more clearly established, consisting of intensive induction chemotherapy followed by cytarabine based consolidation.	Cytarabine	138-148	CCAAT enhancer binding protein zeta	Homo sapiens	0-3
31010844-3	2019	REH/Ara-C 1) was not crossresistant to vincristine or methotrexate; 2) showed a similar proliferation rate and cell surface marker expression as parental REH; 3) demonstrated decreased chemotaxis toward bone marrow stromal cells; and 4) expressed higher transcript levels of cytidine deaminase (CDA) and mitoNEET (CISD1) than the parental REH cell line.	Cytarabine	4-9	cytidine deaminase	Homo sapiens	275-293
31010844-3	2019	REH/Ara-C 1) was not crossresistant to vincristine or methotrexate; 2) showed a similar proliferation rate and cell surface marker expression as parental REH; 3) demonstrated decreased chemotaxis toward bone marrow stromal cells; and 4) expressed higher transcript levels of cytidine deaminase (CDA) and mitoNEET (CISD1) than the parental REH cell line.	Cytarabine	4-9	cytidine deaminase	Homo sapiens	295-298
31010844-3	2019	REH/Ara-C 1) was not crossresistant to vincristine or methotrexate; 2) showed a similar proliferation rate and cell surface marker expression as parental REH; 3) demonstrated decreased chemotaxis toward bone marrow stromal cells; and 4) expressed higher transcript levels of cytidine deaminase (CDA) and mitoNEET (CISD1) than the parental REH cell line.	Cytarabine	4-9	CDGSH iron sulfur domain 1	Homo sapiens	304-312
31010844-3	2019	REH/Ara-C 1) was not crossresistant to vincristine or methotrexate; 2) showed a similar proliferation rate and cell surface marker expression as parental REH; 3) demonstrated decreased chemotaxis toward bone marrow stromal cells; and 4) expressed higher transcript levels of cytidine deaminase (CDA) and mitoNEET (CISD1) than the parental REH cell line.	Cytarabine	4-9	CDGSH iron sulfur domain 1	Homo sapiens	314-319
31355227-8	2019	In addition, Ara-C further inhibited the growth and induced the apoptosis of miR-19a ASODN-transfected cells (P&lt;0.05) in a time dependent manner.	Cytarabine	13-18	microRNA 19a	Homo sapiens	77-84
31355227-10	2019	Conclusions: miRNA-19a ASODN can inhibit the proliferation and induce apoptosis of HL60 cells and may exert synergistic effects with Ara-C on HL60 cells.	Cytarabine	133-138	microRNA 19a	Homo sapiens	13-22
31069015-1	2019	Activating internal tandem duplication (ITD) and tyrosine kinase domain (TKD) point mutations in Fms-like tyrosine kinase 3 (FLT3) occur in approximately 30% of patients with acute myeloid leukemia (AML), and confer a poor prognosis with standard cytarabine/anthracycline or azacitidine-based chemotherapy regimens.	Cytarabine	247-257	fms related receptor tyrosine kinase 3	Homo sapiens	97-123
30920135-5	2019	We also observed that stromal CYP3A4 expression is up-regulated by drugs commonly used in AML induction therapy, cytarabine, etoposide and daunorubicin, resulting in cross-resistance.	Cytarabine	113-123	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	30-36
30808254-4	2019	TNT formation between MSCs and HUVECs could be induced by treating HUVECs with cytarabine (Ara-C), and human bone marrow mesenchymal stem cells (hBMMSCs) could transfer mitochondria to injured HUVECs through TNTs.	Cytarabine	79-89	chromosome 16 open reading frame 82	Homo sapiens	0-3
30808254-4	2019	TNT formation between MSCs and HUVECs could be induced by treating HUVECs with cytarabine (Ara-C), and human bone marrow mesenchymal stem cells (hBMMSCs) could transfer mitochondria to injured HUVECs through TNTs.	Cytarabine	91-96	chromosome 16 open reading frame 82	Homo sapiens	0-3
31022985-7	2019	Using correlation analysis and functional validation experiments, our data demonstrates that miR-34a-5p and miR-24-3p regulate DCK, an enzyme involved in activation of cytarabine and DCDT, an enzyme involved in metabolic inactivation of cytarabine expression, respectively.	Cytarabine	168-178	deoxycytidine kinase	Homo sapiens	127-130
31022985-7	2019	Using correlation analysis and functional validation experiments, our data demonstrates that miR-34a-5p and miR-24-3p regulate DCK, an enzyme involved in activation of cytarabine and DCDT, an enzyme involved in metabolic inactivation of cytarabine expression, respectively.	Cytarabine	237-247	deoxycytidine kinase	Homo sapiens	127-130
30920135-6	2019	Cytarabine also up-regulated CDA expression.	Cytarabine	0-10	cytidine deaminase	Homo sapiens	29-32
31101804-6	2019	All Cytarabine-resistant sublines lost deoxycytidine kinase (dCK) expression, rendering them refractory to Cytarabine.	Cytarabine	4-14	deoxycytidine kinase	Homo sapiens	39-59
31101804-6	2019	All Cytarabine-resistant sublines lost deoxycytidine kinase (dCK) expression, rendering them refractory to Cytarabine.	Cytarabine	4-14	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	61-64
31069015-1	2019	Activating internal tandem duplication (ITD) and tyrosine kinase domain (TKD) point mutations in Fms-like tyrosine kinase 3 (FLT3) occur in approximately 30% of patients with acute myeloid leukemia (AML), and confer a poor prognosis with standard cytarabine/anthracycline or azacitidine-based chemotherapy regimens.	Cytarabine	247-257	fms related receptor tyrosine kinase 3	Homo sapiens	125-129
30970520-3	2019	However, the function and molecular mechanism of MALAT1 in regulating cytarabine (Ara-C) resistance of AML are largely unknown.	Cytarabine	70-80	metastasis associated lung adenocarcinoma transcript 1	Homo sapiens	49-55
30970520-3	2019	However, the function and molecular mechanism of MALAT1 in regulating cytarabine (Ara-C) resistance of AML are largely unknown.	Cytarabine	82-87	metastasis associated lung adenocarcinoma transcript 1	Homo sapiens	49-55
30970520-0	2019	MALAT1 knockdown inhibits proliferation and enhances cytarabine chemosensitivity by upregulating miR-96 in acute myeloid leukemia cells.	Cytarabine	53-63	metastasis associated lung adenocarcinoma transcript 1	Homo sapiens	0-6
30970520-9	2019	Knockdown of MALAT1 inhibited the proliferation, induced apoptosis, and enhanced Ara-C sensitivity of AML cells.	Cytarabine	81-86	metastasis associated lung adenocarcinoma transcript 1	Homo sapiens	13-19
30970520-11	2019	miR-96 downregulation abolished the effects of MALAT1 knockdown on the proliferation, apoptosis, Ara-C sensitivity in AML cells.	Cytarabine	97-102	microRNA 96	Homo sapiens	0-6
30970520-11	2019	miR-96 downregulation abolished the effects of MALAT1 knockdown on the proliferation, apoptosis, Ara-C sensitivity in AML cells.	Cytarabine	97-102	metastasis associated lung adenocarcinoma transcript 1	Homo sapiens	47-53
30970520-12	2019	In conclusion, MALAT1 knockdown inhibited proliferation, promoted apoptosis and enhanced Ara-C sensitivity in AML cells by upregulating miR-96, providing novel insights into the critical role of MALAT1 as a miRNA sponge in AML.	Cytarabine	89-94	metastasis associated lung adenocarcinoma transcript 1	Homo sapiens	15-21
30970520-12	2019	In conclusion, MALAT1 knockdown inhibited proliferation, promoted apoptosis and enhanced Ara-C sensitivity in AML cells by upregulating miR-96, providing novel insights into the critical role of MALAT1 as a miRNA sponge in AML.	Cytarabine	89-94	microRNA 96	Homo sapiens	136-142
30291336-10	2019	More interestingly, Romidepsin preferentially targets CD123+ cells, while chemotherapy drug Ara-C mainly targeted fast-growing, CD123- cells.	Cytarabine	92-97	interleukin 3 receptor subunit alpha	Homo sapiens	128-133
30578743-6	2019	Among ND patients 18-64, the most common initial treatment was standard-to-intermediate dose cytarabine-based therapies (43.2% for FLT3mut and 55.9% for FLT3wt ); among ND patients >=65, the most common initial treatment was hypomethylating agent-based therapies (36.0% and 47.2%).	Cytarabine	93-103	fms related receptor tyrosine kinase 3	Homo sapiens	131-135
30578743-6	2019	Among ND patients 18-64, the most common initial treatment was standard-to-intermediate dose cytarabine-based therapies (43.2% for FLT3mut and 55.9% for FLT3wt ); among ND patients >=65, the most common initial treatment was hypomethylating agent-based therapies (36.0% and 47.2%).	Cytarabine	93-103	fms related receptor tyrosine kinase 3	Homo sapiens	153-157
30979482-0	2019	Significance of Granulocyte Colony-Stimulating Factor-Combined High-Dose Cytarabine, Cyclophosphamide, and Total Body Irradiation in Allogeneic Hematopoietic Cell Transplantation for Myeloid Malignant Neoplasms.	Cytarabine	73-83	colony stimulating factor 3	Homo sapiens	16-53
30816541-9	2019	PharmGkb analysis identified single nucleotide polymorphisms (SNPs) of rs5030743 and rs1130609 of RRM2, which can be treated with cladribine and cytarabine.	Cytarabine	145-155	ribonucleotide reductase regulatory subunit M2	Homo sapiens	98-102
30931006-2	2019	Diversely substituted indoles (Ar1) react with quinoline aldehydes, quinolone aldehydes, chromone aldehydes, and fluorene aldehydes (Ar2CHO) and coumarins (Ar3) in 1:1:1 ratio to form the corresponding tris(heteroaryl)methanes (Ar1Ar2Ar3)CH along with (Ar1Ar1Ar2)CH triads.	Cytarabine	156-159	transcription factor 20	Homo sapiens	31-34
30262569-3	2019	However, it is not yet known whether NRF2 can be used as a prognostic biomarker in MDS, or whether elevated NRF2 levels are associated with cytarabine resistance.	Cytarabine	140-150	NFE2 like bZIP transcription factor 2	Homo sapiens	108-112
30763062-2	2019	Previously, we discovered a novel form of cancer drug resistance where the Glioma-associated protein 1 (GLI1) elevates UGT1A glucuronidation enzymes, thereby glucuronidating cytarabine and ribavirin, leading to resistance in leukemia patients.	Cytarabine	174-184	GLI family zinc finger 1	Homo sapiens	75-102
30763062-2	2019	Previously, we discovered a novel form of cancer drug resistance where the Glioma-associated protein 1 (GLI1) elevates UGT1A glucuronidation enzymes, thereby glucuronidating cytarabine and ribavirin, leading to resistance in leukemia patients.	Cytarabine	174-184	GLI family zinc finger 1	Homo sapiens	104-108
30763062-2	2019	Previously, we discovered a novel form of cancer drug resistance where the Glioma-associated protein 1 (GLI1) elevates UGT1A glucuronidation enzymes, thereby glucuronidating cytarabine and ribavirin, leading to resistance in leukemia patients.	Cytarabine	174-184	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	119-124
30862120-0	2019	Cytarabine-Resistant FLT3-ITD Leukemia Cells are Associated with TP53 Mutation and Multiple Pathway Alterations-Possible Therapeutic Efficacy of Cabozantinib.	Cytarabine	0-10	transformation related protein 53	Mus musculus	65-69
30862120-2	2019	We aimed to establish a cytarabine-resistant line from FLT3-ITD-positive MV4-11 (MV4-11-P) cells and examine the development of resistance.	Cytarabine	24-34	fms related receptor tyrosine kinase 3	Homo sapiens	55-59
30862120-11	2019	Together, our findings suggest that Mcl-1 and Akt phosphorylation are potential therapeutic targets for p53 mutants and that cabozantinib is an effective treatment in cytarabine-resistant FLT3-ITD-positive AML.	Cytarabine	167-177	FMS-like tyrosine kinase 3	Mus musculus	188-192
30837643-2	2019	Checkpoint kinase 1 (CHK1), which is activated by DNA damage and replication stress, diminishes sensitivity to cytarabine and anthracyclines as single agents, suggesting that CHK1 inhibitors might increase the effectiveness of CPX-351.	Cytarabine	111-121	checkpoint kinase 1	Homo sapiens	0-19
30837643-2	2019	Checkpoint kinase 1 (CHK1), which is activated by DNA damage and replication stress, diminishes sensitivity to cytarabine and anthracyclines as single agents, suggesting that CHK1 inhibitors might increase the effectiveness of CPX-351.	Cytarabine	111-121	checkpoint kinase 1	Homo sapiens	21-25
30837643-2	2019	Checkpoint kinase 1 (CHK1), which is activated by DNA damage and replication stress, diminishes sensitivity to cytarabine and anthracyclines as single agents, suggesting that CHK1 inhibitors might increase the effectiveness of CPX-351.	Cytarabine	111-121	checkpoint kinase 1	Homo sapiens	175-179
30783426-6	2019	Inhibition of DDR1 activity by DDR1-specific inhibitor DDR-IN-1 accelerated cell death in the presence of Ara-C, DNR or their combination.	Cytarabine	106-111	discoidin domain receptor tyrosine kinase 1	Homo sapiens	14-18
30783426-6	2019	Inhibition of DDR1 activity by DDR1-specific inhibitor DDR-IN-1 accelerated cell death in the presence of Ara-C, DNR or their combination.	Cytarabine	106-111	discoidin domain receptor tyrosine kinase 1	Homo sapiens	31-35
30262569-6	2019	Downregulation of NRF2 by the inhibitor Luteolin, or lentiviral shRNA knockdown, enhanced the chemotherapeutic efficacy of cytarabine, while MDS cells treated by NRF2 agonist Sulforaphane showed increased resistance to cytarabine.	Cytarabine	123-133	NFE2 like bZIP transcription factor 2	Homo sapiens	18-22
30262569-6	2019	Downregulation of NRF2 by the inhibitor Luteolin, or lentiviral shRNA knockdown, enhanced the chemotherapeutic efficacy of cytarabine, while MDS cells treated by NRF2 agonist Sulforaphane showed increased resistance to cytarabine.	Cytarabine	219-229	NFE2 like bZIP transcription factor 2	Homo sapiens	18-22
30262569-7	2019	More importantly, pharmacological inhibition of NRF2 could sensitize primary high-risk MDS cells to cytarabine treatment.	Cytarabine	100-110	NFE2 like bZIP transcription factor 2	Homo sapiens	48-52
30262569-8	2019	Mechanistically, downregulation of dual specificity protein phosphatase 1, an NRF2 direct target gene, could abrogate cytarabine resistance in NRF2 elevated MDS cells.	Cytarabine	118-128	dual specificity phosphatase 1	Homo sapiens	35-73
30262569-8	2019	Mechanistically, downregulation of dual specificity protein phosphatase 1, an NRF2 direct target gene, could abrogate cytarabine resistance in NRF2 elevated MDS cells.	Cytarabine	118-128	NFE2 like bZIP transcription factor 2	Homo sapiens	78-82
30262569-8	2019	Mechanistically, downregulation of dual specificity protein phosphatase 1, an NRF2 direct target gene, could abrogate cytarabine resistance in NRF2 elevated MDS cells.	Cytarabine	118-128	NFE2 like bZIP transcription factor 2	Homo sapiens	143-147
30262569-9	2019	Silencing NRF2 or dual specificity protein phosphatase 1 also significantly sensitized cytarabine treatment and inhibited tumors in MDS cells transplanted mouse models in vivo Our study suggests that targeting NRF2 in combination with conventional chemotherapy could pave the way for future therapy for high-risk MDS.	Cytarabine	87-97	nuclear factor, erythroid derived 2, like 2	Mus musculus	10-14
30262569-9	2019	Silencing NRF2 or dual specificity protein phosphatase 1 also significantly sensitized cytarabine treatment and inhibited tumors in MDS cells transplanted mouse models in vivo Our study suggests that targeting NRF2 in combination with conventional chemotherapy could pave the way for future therapy for high-risk MDS.	Cytarabine	87-97	dual specificity phosphatase 1	Mus musculus	18-56
30262569-9	2019	Silencing NRF2 or dual specificity protein phosphatase 1 also significantly sensitized cytarabine treatment and inhibited tumors in MDS cells transplanted mouse models in vivo Our study suggests that targeting NRF2 in combination with conventional chemotherapy could pave the way for future therapy for high-risk MDS.	Cytarabine	87-97	nuclear factor, erythroid derived 2, like 2	Mus musculus	210-214
30593694-6	2019	Low-dose cytarabine can improve the outcomes of patients with TAM and high white blood cell count.	Cytarabine	9-19	Myeloproliferative syndrome, transient (transient abnormal myelopoiesis)	Homo sapiens	62-65
30325535-9	2019	FTH1 protein was also overexpressed in patient"s samples and correlated with the in vitro cytotoxic activity of cytarabine.	Cytarabine	112-122	ferritin heavy chain 1	Homo sapiens	0-4
30266677-10	2019	ID-AraC with G-CSF should be the preferred chemomobilization protocol for patients with MM scheduled to undergo tandem autoSCT.	Cytarabine	3-7	colony stimulating factor 3	Homo sapiens	13-18
30813354-4	2019	Clinical results deriving from studies using B-cell lymphoma 2 (BCL-2) inhibitors in combination with standard AML agents, such as azacytidine, decitabine, low-dose cytarabine, provided promising results and strongly support the use of these agents in the treatment of AML patients, particularly of elderly patients.	Cytarabine	165-175	BCL2 apoptosis regulator	Homo sapiens	45-62
30813354-4	2019	Clinical results deriving from studies using B-cell lymphoma 2 (BCL-2) inhibitors in combination with standard AML agents, such as azacytidine, decitabine, low-dose cytarabine, provided promising results and strongly support the use of these agents in the treatment of AML patients, particularly of elderly patients.	Cytarabine	165-175	BCL2 apoptosis regulator	Homo sapiens	64-69
29909708-0	2018	Recombinant human thrombopoietin (rh-TPO) for the prevention of severe thrombocytopenia induced by high-dose cytarabine: a prospective, randomized, self-controlled study.	Cytarabine	109-119	thrombopoietin	Homo sapiens	18-32
30431078-7	2019	The overexpression of SENP2 in the CLL cells decreased their invasive and proliferative ability, as well as their chemotactic response and enhanced their sensitivity to cytarabine and dexamethasone, while it promoted cell apoptosis.	Cytarabine	169-179	SUMO specific peptidase 2	Homo sapiens	22-27
30651113-0	2019	Memantine potentiates cytarabine-induced cell death of acute leukemia correlating with inhibition of Kv1.3 potassium channels, AKT and ERK1/2 signaling.	Cytarabine	22-32	potassium voltage-gated channel subfamily A member 3	Homo sapiens	101-106
30651113-0	2019	Memantine potentiates cytarabine-induced cell death of acute leukemia correlating with inhibition of Kv1.3 potassium channels, AKT and ERK1/2 signaling.	Cytarabine	22-32	AKT serine/threonine kinase 1	Homo sapiens	127-130
30651113-0	2019	Memantine potentiates cytarabine-induced cell death of acute leukemia correlating with inhibition of Kv1.3 potassium channels, AKT and ERK1/2 signaling.	Cytarabine	22-32	mitogen-activated protein kinase 3	Homo sapiens	135-141
30651113-5	2019	Here we evaluated whether pharmacological targeting of Kv1.3 channels by memantine promotes cell death of acute leukemia cells induced by chemotherapeutic cytarabine.	Cytarabine	155-165	potassium voltage-gated channel subfamily A member 3	Homo sapiens	55-60
30651113-14	2019	CONCLUSIONS: Our study underlines inhibition of Kv1.3 channels as a therapeutic strategy in acute leukemia and proposes co-treatment with memantine, a licensed and safe drug, as a potential approach to promote cytarabine-based cell death of various subtypes of acute leukemia.	Cytarabine	210-220	potassium voltage-gated channel subfamily A member 3	Homo sapiens	48-53
30535449-0	2019	Cyr61 decreases Cytarabine chemosensitivity in acute lymphoblastic leukemia cells via NF-kappaB pathway activation.	Cytarabine	16-26	cellular communication network factor 1	Homo sapiens	0-5
30535449-5	2019	The aim of the current study was to investigate the role of Cyr61 in regulating ALL cell chemosensitivity to Ara-C.	Cytarabine	109-114	cellular communication network factor 1	Homo sapiens	60-65
30535449-7	2019	Increased Cyr61 effectively decreased Ara-C-induced apoptosis of ALL cells, and its function was blocked by the use of the anti-Cyr61 monoclonal antibody 093G9.	Cytarabine	38-43	cellular communication network factor 1	Homo sapiens	10-15
30535449-7	2019	Increased Cyr61 effectively decreased Ara-C-induced apoptosis of ALL cells, and its function was blocked by the use of the anti-Cyr61 monoclonal antibody 093G9.	Cytarabine	38-43	cellular communication network factor 1	Homo sapiens	128-133
30535449-8	2019	Furthermore, Cyr61 increased the level of Bcl-2 in Ara-C-treated ALL cells.	Cytarabine	51-56	cellular communication network factor 1	Homo sapiens	13-18
30535449-8	2019	Furthermore, Cyr61 increased the level of Bcl-2 in Ara-C-treated ALL cells.	Cytarabine	51-56	BCL2 apoptosis regulator	Homo sapiens	42-47
30535449-9	2019	Mechanistically, it was shown that Cyr61 affected ALL cell resistance to Ara-C partially via the NF-kappaB pathway.	Cytarabine	73-78	cellular communication network factor 1	Homo sapiens	35-40
30204524-1	2019	Previously, we found that dual therapy by the CXCR4 inhibitor Plerixafor and cytosine arabinoside (Ara-C) effectively eradicated leukemia cells and concurrently activated immune cells in acute myeloid leukemia (AML).	Cytarabine	99-104	chemokine (C-X-C motif) receptor 4	Mus musculus	46-51
30598640-17	2018	Patients with RUNX1-RUNX1T1 gene fusion or without the ASXL1 gene mutation had a better chance of achieving CR when treated with cytarabine and daunorubicin induction chemotherapy.	Cytarabine	129-139	RUNX family transcription factor 1	Homo sapiens	14-19
30598640-17	2018	Patients with RUNX1-RUNX1T1 gene fusion or without the ASXL1 gene mutation had a better chance of achieving CR when treated with cytarabine and daunorubicin induction chemotherapy.	Cytarabine	129-139	RUNX1 partner transcriptional co-repressor 1	Homo sapiens	20-27
30598640-17	2018	Patients with RUNX1-RUNX1T1 gene fusion or without the ASXL1 gene mutation had a better chance of achieving CR when treated with cytarabine and daunorubicin induction chemotherapy.	Cytarabine	129-139	ASXL transcriptional regulator 1	Homo sapiens	55-60
30453100-4	2018	Because cytosine-arabinoside-induced apoptosis of MLL+ALL cells was inhibited by pretreatment with the CXCR4 inhibitor but rather accelerated by pretreatment with the CXCR7 inhibitor, an application of the CXCR7 inhibitor may become a good treatment option in future for MLL+ALL patients.	Cytarabine	8-28	lysine methyltransferase 2A	Homo sapiens	50-53
30453100-4	2018	Because cytosine-arabinoside-induced apoptosis of MLL+ALL cells was inhibited by pretreatment with the CXCR4 inhibitor but rather accelerated by pretreatment with the CXCR7 inhibitor, an application of the CXCR7 inhibitor may become a good treatment option in future for MLL+ALL patients.	Cytarabine	8-28	C-X-C motif chemokine receptor 4	Homo sapiens	103-108
30453100-4	2018	Because cytosine-arabinoside-induced apoptosis of MLL+ALL cells was inhibited by pretreatment with the CXCR4 inhibitor but rather accelerated by pretreatment with the CXCR7 inhibitor, an application of the CXCR7 inhibitor may become a good treatment option in future for MLL+ALL patients.	Cytarabine	8-28	atypical chemokine receptor 3	Homo sapiens	167-172
30453100-4	2018	Because cytosine-arabinoside-induced apoptosis of MLL+ALL cells was inhibited by pretreatment with the CXCR4 inhibitor but rather accelerated by pretreatment with the CXCR7 inhibitor, an application of the CXCR7 inhibitor may become a good treatment option in future for MLL+ALL patients.	Cytarabine	8-28	atypical chemokine receptor 3	Homo sapiens	206-211
30453100-4	2018	Because cytosine-arabinoside-induced apoptosis of MLL+ALL cells was inhibited by pretreatment with the CXCR4 inhibitor but rather accelerated by pretreatment with the CXCR7 inhibitor, an application of the CXCR7 inhibitor may become a good treatment option in future for MLL+ALL patients.	Cytarabine	8-28	lysine methyltransferase 2A	Homo sapiens	271-274
29909708-0	2018	Recombinant human thrombopoietin (rh-TPO) for the prevention of severe thrombocytopenia induced by high-dose cytarabine: a prospective, randomized, self-controlled study.	Cytarabine	109-119	thyroid peroxidase	Homo sapiens	37-40
29909708-1	2018	The aim of this randomized phase II study was to investigate the optimal timing of the administration of thrombopoietin to prevent cytarabine-induced thrombocytopenia.	Cytarabine	131-141	thrombopoietin	Homo sapiens	105-119
30519105-0	2018	Gene expression of hENT1, dCK, CDA, dCMPD and topoisomerase IIalpha as an indicator of chemotherapy response in AML treated with cytarabine and daunorubicin.	Cytarabine	129-139	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	19-24
30534052-7	2018	The proliferation inhibitor Ara-C completely suppressed the effect of RNase A on NPC counts, further supporting that RNase A increases NPC number mainly by promoting proliferation.	Cytarabine	28-33	ribonuclease, RNase A family, 1 (pancreatic)	Mus musculus	70-77
30534052-7	2018	The proliferation inhibitor Ara-C completely suppressed the effect of RNase A on NPC counts, further supporting that RNase A increases NPC number mainly by promoting proliferation.	Cytarabine	28-33	ribonuclease, RNase A family, 1 (pancreatic)	Mus musculus	117-124
30405880-6	2018	Consistent with association of rs1376041 and gene-expression in AML patients siRNA mediated knock-down of GPR56 increased cytarabine sensitivity of AML cell lines.	Cytarabine	122-132	adhesion G protein-coupled receptor G1	Homo sapiens	106-111
29994802-3	2018	Our findings indicated that ara-C induces autophagy (with alteration of LC3B, p62, and Beclin-1) in the cells; however, targeting autophagy by 3-methyladenine and chloroquine significantly increased caspase-dependent apoptosis and the sub-G1 compartment in ara-C-treated cells.	Cytarabine	28-33	microtubule associated protein 1 light chain 3 beta	Homo sapiens	72-76
29994802-3	2018	Our findings indicated that ara-C induces autophagy (with alteration of LC3B, p62, and Beclin-1) in the cells; however, targeting autophagy by 3-methyladenine and chloroquine significantly increased caspase-dependent apoptosis and the sub-G1 compartment in ara-C-treated cells.	Cytarabine	28-33	nucleoporin 62	Homo sapiens	78-81
29994802-3	2018	Our findings indicated that ara-C induces autophagy (with alteration of LC3B, p62, and Beclin-1) in the cells; however, targeting autophagy by 3-methyladenine and chloroquine significantly increased caspase-dependent apoptosis and the sub-G1 compartment in ara-C-treated cells.	Cytarabine	28-33	beclin 1	Homo sapiens	87-95
30341277-0	2018	Low-level expression of SAMHD1 in acute myeloid leukemia (AML) blasts correlates with improved outcome upon consolidation chemotherapy with high-dose cytarabine-based regimens.	Cytarabine	150-160	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	24-30
30341277-1	2018	Sterile alpha motif and histidine/aspartic acid domain containing protein 1 (SAMHD1) limits the efficacy of cytarabine (ara-C) used in AML by hydrolyzing its active metabolite ara-CTP and thus represents a promising therapeutic target.	Cytarabine	108-118	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	77-83
30341277-1	2018	Sterile alpha motif and histidine/aspartic acid domain containing protein 1 (SAMHD1) limits the efficacy of cytarabine (ara-C) used in AML by hydrolyzing its active metabolite ara-CTP and thus represents a promising therapeutic target.	Cytarabine	120-125	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	77-83
30341277-5	2018	A sizeable patient subset with low SAMHD1 expression (&lt;25% of positive blasts) was identified, which was significantly associated with longer event-free (EFS) and overall (OS) survival in patients receiving high-dose cytarabine (HDAC) during consolidation.	Cytarabine	220-230	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	35-41
30410347-6	2018	Conclusion: In brief, oVV-ING4 can increase the sensitivity of leukemia cells to cytarabine and induce cell apoptosis in vitro and in vivo.	Cytarabine	81-91	inhibitor of growth family member 4	Homo sapiens	26-30
30349319-3	2018	Low-dose decitabine, a hypomethylating drug, in combination with aclarubicin and cytarabine (DAC) has shown safety and efficacy in the treatment of AML; however, clinical data are limited for the treatment of RR-AML.	Cytarabine	81-91	arylacetamide deacetylase	Homo sapiens	93-96
30361682-6	2018	Furthermore, combined inhibition of Bcl-2/Bcl-XL and Mcl-1 could revert BMSC-mediated resistance against cytarabine + daunorubicin.	Cytarabine	105-115	BCL2 apoptosis regulator	Homo sapiens	36-41
30361682-6	2018	Furthermore, combined inhibition of Bcl-2/Bcl-XL and Mcl-1 could revert BMSC-mediated resistance against cytarabine + daunorubicin.	Cytarabine	105-115	BCL2 like 1	Homo sapiens	42-48
30361682-6	2018	Furthermore, combined inhibition of Bcl-2/Bcl-XL and Mcl-1 could revert BMSC-mediated resistance against cytarabine + daunorubicin.	Cytarabine	105-115	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	53-58
30405880-7	2018	Similarly for IGF1R, knockdown increased the cytarabine sensitivity of AML cell lines consistent with results in AML patients.	Cytarabine	45-55	insulin like growth factor 1 receptor	Homo sapiens	14-19
30405880-8	2018	Given both IGF1R and GPR56 are promising drug-targets in AML, our results on SNPs driving the expression/function of these genes will not only enhance our understanding of cytarabine resistance but also hold promise in personalizing AML for targeted therapies.	Cytarabine	172-182	insulin like growth factor 1 receptor	Homo sapiens	11-16
30405880-8	2018	Given both IGF1R and GPR56 are promising drug-targets in AML, our results on SNPs driving the expression/function of these genes will not only enhance our understanding of cytarabine resistance but also hold promise in personalizing AML for targeted therapies.	Cytarabine	172-182	adhesion G protein-coupled receptor G1	Homo sapiens	21-26
29748833-0	2018	Cytosine arabinoside prodrug designed to bind plasma serum albumin for drug delivery.	Cytarabine	0-20	albumin	Homo sapiens	53-66
30154068-7	2018	Care needs to be taken in interpreting CSF results in patients who have received intrathecal liposomal cytarabine.	Cytarabine	103-113	colony stimulating factor 2	Homo sapiens	39-42
30157922-4	2018	METHODS: We established an oncogenic N-MYC-driven B-ALL mouse model, which were subsequently treated with common chemotherapy drug cytarabine (Ara-C) and daunorubicin (DNR).	Cytarabine	131-141	v-myc avian myelocytomatosis viral related oncogene, neuroblastoma derived	Mus musculus	37-42
30127892-1	2018	The low-dose cytarabine, aclarubicin and granulocyte-colony stimulating factor (G-CSF) (CAG) priming regimen is an effective treatment for patients with relapsed or refractory acute myeloid leukemia (AML) and advanced myelodysplastic syndrome (MDS).	Cytarabine	13-23	colony stimulating factor 3	Homo sapiens	80-85
30088438-1	2018	AIM: Cytarabine (Ara-C), a mainstay of acute myeloid leukemia (AML) treatment, is a prodrug requiring activation to ara-CTP for its antileukemic activity.	Cytarabine	5-15	solute carrier family 25 member 1	Homo sapiens	120-123
30088438-1	2018	AIM: Cytarabine (Ara-C), a mainstay of acute myeloid leukemia (AML) treatment, is a prodrug requiring activation to ara-CTP for its antileukemic activity.	Cytarabine	17-22	solute carrier family 25 member 1	Homo sapiens	120-123
30088438-3	2018	METHOD: We investigated SNPs in 14 ara-C metabolic-pathway genes, for association with intracellular ara-CTP levels, in leukemic cells obtained post-initiation of cytarabine infusion in pediatric AML patients (n = 68).	Cytarabine	35-40	solute carrier family 25 member 1	Homo sapiens	105-108
30268834-9	2018	Drug screening of the two cell line subtypes yielded several potential candidates, such as cytarabine and enzastaurin for Cell-line-Subtype 1 (CS1) and a BTK inhibitor QL-XII-61 for Cell-line-Subtype 2 (CS2).	Cytarabine	91-101	ITPR interacting domain containing 2	Homo sapiens	143-146
30157922-4	2018	METHODS: We established an oncogenic N-MYC-driven B-ALL mouse model, which were subsequently treated with common chemotherapy drug cytarabine (Ara-C) and daunorubicin (DNR).	Cytarabine	143-148	v-myc avian myelocytomatosis viral related oncogene, neuroblastoma derived	Mus musculus	37-42
29559562-5	2018	In contrast, Pole-mutant cells displayed significantly increased sensitivity to cytarabine and fludarabine (IC50Pole P286R-mutant vs. wild-type: 0.05 vs. 0.17 mumol/L for cytarabine, 4.62 vs. 11.1 mumol/L for fludarabine; P < 0.001 for both comparisons).Conclusions: The favorable prognosis of POLE-mutant cancers cannot be explained by increased sensitivity to currently used adjuvant treatments.	Cytarabine	80-90	polymerase (DNA directed), epsilon	Mus musculus	13-17
30132679-8	2018	The CDK9 inhibitors alvocidib, atuveciclib, and TG02 have completed phase 1/2 clinical trials, with results available for the alvocidib trial showing improved complete remission rates (70% vs 46%; P = .003) for alvocidib in combination with cytarabine and mitoxantrone, versus cytarabine/daunorubicin, in patients with newly diagnosed AML.	Cytarabine	241-251	cyclin dependent kinase 9	Homo sapiens	4-8
30132679-8	2018	The CDK9 inhibitors alvocidib, atuveciclib, and TG02 have completed phase 1/2 clinical trials, with results available for the alvocidib trial showing improved complete remission rates (70% vs 46%; P = .003) for alvocidib in combination with cytarabine and mitoxantrone, versus cytarabine/daunorubicin, in patients with newly diagnosed AML.	Cytarabine	277-287	cyclin dependent kinase 9	Homo sapiens	4-8
29752949-5	2018	We found that treating AML cells with Ara-c or Sorafenib resulted in autophagy enhancement, and when autophagy was enhanced, nuclear LC3 moved into the cytoplasm.	Cytarabine	38-43	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	133-136
33168498-5	2018	Western blotting showed that treatment of the siRNA-transfected SHI-1 cells with 0-25 mumol/L curcumin or with 0-2.0 mumol/L Ara-C further increased the cell inhibition rate and obviously enhanced the expressions of p-P38 MAPK and p-JNK without significantly affecting p-ERK expression.	Cytarabine	125-130	mitogen-activated protein kinase 8	Homo sapiens	233-236
33168498-5	2018	Western blotting showed that treatment of the siRNA-transfected SHI-1 cells with 0-25 mumol/L curcumin or with 0-2.0 mumol/L Ara-C further increased the cell inhibition rate and obviously enhanced the expressions of p-P38 MAPK and p-JNK without significantly affecting p-ERK expression.	Cytarabine	125-130	mitogen-activated protein kinase 1	Homo sapiens	271-274
30016963-0	2018	Influence of UGT1A1 polymorphisms on the outcome of acute myeloid leukemia patients treated with cytarabine-base regimens.	Cytarabine	97-107	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-19
30016963-1	2018	BACKGROUNDS: UDP-glucuronosyltransferase 1A subfamily (UGT1A) enzymes can inactivate cytarabine (Ara-C) by glucuronidation, and thus serves as candidate genes for interindividual difference in Ara-C response.	Cytarabine	85-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-43
30016963-1	2018	BACKGROUNDS: UDP-glucuronosyltransferase 1A subfamily (UGT1A) enzymes can inactivate cytarabine (Ara-C) by glucuronidation, and thus serves as candidate genes for interindividual difference in Ara-C response.	Cytarabine	85-95	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	55-60
30016963-1	2018	BACKGROUNDS: UDP-glucuronosyltransferase 1A subfamily (UGT1A) enzymes can inactivate cytarabine (Ara-C) by glucuronidation, and thus serves as candidate genes for interindividual difference in Ara-C response.	Cytarabine	97-102	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-43
30016963-1	2018	BACKGROUNDS: UDP-glucuronosyltransferase 1A subfamily (UGT1A) enzymes can inactivate cytarabine (Ara-C) by glucuronidation, and thus serves as candidate genes for interindividual difference in Ara-C response.	Cytarabine	97-102	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	55-60
30016963-1	2018	BACKGROUNDS: UDP-glucuronosyltransferase 1A subfamily (UGT1A) enzymes can inactivate cytarabine (Ara-C) by glucuronidation, and thus serves as candidate genes for interindividual difference in Ara-C response.	Cytarabine	193-198	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	13-43
30016963-1	2018	BACKGROUNDS: UDP-glucuronosyltransferase 1A subfamily (UGT1A) enzymes can inactivate cytarabine (Ara-C) by glucuronidation, and thus serves as candidate genes for interindividual difference in Ara-C response.	Cytarabine	193-198	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	55-60
30016963-3	2018	METHODS: UGT1A1*6 and *28 polymorphisms resulting in reduced UGT1A1 activity were genotyped in 726 adult acute myeloid leukemia (AML) patients treated with Ara-C based regimens.	Cytarabine	156-161	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	61-67
30016963-5	2018	RESULTS: After one or two courses of Ara-C based induction chemotherapy, the complete remission (CR) rate was significantly higher in patients carrying the UGT1A1*6 (77.0%) or the UGT1A1*28 (76.4%) alleles as compared with corresponding wild-type homozygotes (66.9 and 68.5%, respectively).	Cytarabine	37-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	156-162
30016963-5	2018	RESULTS: After one or two courses of Ara-C based induction chemotherapy, the complete remission (CR) rate was significantly higher in patients carrying the UGT1A1*6 (77.0%) or the UGT1A1*28 (76.4%) alleles as compared with corresponding wild-type homozygotes (66.9 and 68.5%, respectively).	Cytarabine	37-42	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	180-186
30016963-7	2018	CONCLUSION: Our results suggest that UGT1A1*28 and UGT1A1*6 are associated with improved clinical outcomes in Chinese AML patients treated with Ara-C.	Cytarabine	144-149	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
30016963-7	2018	CONCLUSION: Our results suggest that UGT1A1*28 and UGT1A1*6 are associated with improved clinical outcomes in Chinese AML patients treated with Ara-C.	Cytarabine	144-149	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	51-57
29574276-3	2018	Our experiments show that activation of CXCR4 signaling in AML cells increases autophagic activity and decreases cytarabine-induced apoptosis.	Cytarabine	113-123	C-X-C motif chemokine receptor 4	Homo sapiens	40-45
29139328-9	2018	RESULTS: We found 5 muM CAPE sensitized all cell lines to cytarabine.	Cytarabine	58-68	structural maintenance of chromosomes 2	Homo sapiens	24-28
29559562-5	2018	In contrast, Pole-mutant cells displayed significantly increased sensitivity to cytarabine and fludarabine (IC50Pole P286R-mutant vs. wild-type: 0.05 vs. 0.17 mumol/L for cytarabine, 4.62 vs. 11.1 mumol/L for fludarabine; P < 0.001 for both comparisons).Conclusions: The favorable prognosis of POLE-mutant cancers cannot be explained by increased sensitivity to currently used adjuvant treatments.	Cytarabine	171-181	polymerase (DNA directed), epsilon	Mus musculus	13-17
29967774-8	2018	Overexpression of miR-652-3p using agomir increased the sensitivity to vincristine and cytarabine (all p&lt;0.05) and promoted apoptosis (both p&lt;0.05) in Reh and RS4:11 cells.	Cytarabine	87-97	microRNA 652	Homo sapiens	18-25
29645075-12	2018	Multivariate analysis identified the following as independent adverse factors for achievement of CR-CRp: platelets &lt; 50 x 109 /L (P &lt; .001), complex karyotype with &gt;=3 chromosomal abnormalities (P = .02), regimens that did not include cytarabine or hypomethylating agents (P = .014), and no prior CR lasting &gt;=12 months with frontline or salvage 1 therapies (P &lt; .001).	Cytarabine	244-254	C-reactive protein	Homo sapiens	97-99
29645075-12	2018	Multivariate analysis identified the following as independent adverse factors for achievement of CR-CRp: platelets &lt; 50 x 109 /L (P &lt; .001), complex karyotype with &gt;=3 chromosomal abnormalities (P = .02), regimens that did not include cytarabine or hypomethylating agents (P = .014), and no prior CR lasting &gt;=12 months with frontline or salvage 1 therapies (P &lt; .001).	Cytarabine	244-254	C-reactive protein	Homo sapiens	100-103
29645075-12	2018	Multivariate analysis identified the following as independent adverse factors for achievement of CR-CRp: platelets &lt; 50 x 109 /L (P &lt; .001), complex karyotype with &gt;=3 chromosomal abnormalities (P = .02), regimens that did not include cytarabine or hypomethylating agents (P = .014), and no prior CR lasting &gt;=12 months with frontline or salvage 1 therapies (P &lt; .001).	Cytarabine	244-254	C-reactive protein	Homo sapiens	100-102
29739902-5	2018	Furthermore, cytarabine inhibited viral DNA and RNA syntheses and induced the rapid degradation of KSHV major latent protein LANA (latency-associated nuclear antigen), leading to the suppression of KSHV latent replication.	Cytarabine	13-23	LANA	Human gammaherpesvirus 8	125-129
29567781-12	2018	Combination therapy with decitabine, vorinostat and cytarabine was tolerated in younger relapsed/refractory acute myeloid leukemia and should be explored further focusing on the KMT2A partial tandem duplication subset.	Cytarabine	52-62	lysine methyltransferase 2A	Homo sapiens	178-183
29759551-10	2018	Additionally, glucocorticoids, asparaginase, anthracycline, vincristine and cytarabine that trans-repress gene expression, deprives cells of asparagine, triggers cell cycle arrest, influences cytochrome-P450 polymorphism and inhibits DNA polymerase, respectively, have been used in chemotherapy in ALL patients.	Cytarabine	76-86	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	192-207
30148913-4	2018	The toxic effect should be mainly attributed to Cytarabine and not to methotrexate, since the central nervous system lacks Cytidine deaminase, the enzyme that degrades Cytarabine.	Cytarabine	168-178	cytidine deaminase	Homo sapiens	123-141
29872325-0	2018	miR-134 increases the antitumor effects of cytarabine by targeting Mnks in acute myeloid leukemia cells.	Cytarabine	43-53	microRNA 134	Homo sapiens	0-7
29872325-4	2018	Overexpression of miR-134 sensitized K562/A02 and HL-60/ADM cells to Ara-C, inhibited cell colony formation, and enhanced the ability of Ara-C to induce apoptosis.	Cytarabine	69-74	microRNA 134	Homo sapiens	18-25
29872325-4	2018	Overexpression of miR-134 sensitized K562/A02 and HL-60/ADM cells to Ara-C, inhibited cell colony formation, and enhanced the ability of Ara-C to induce apoptosis.	Cytarabine	137-142	microRNA 134	Homo sapiens	18-25
29872325-6	2018	Further investigation showed that miR-134 increased the anti-tumor effects of Ara-C through inhibiting phosphorylation of eukaryotic initiation factor 4E and downregulating Mcl-1 and bcl2, which was independent of p38 and Erk1/2 activation.	Cytarabine	78-83	microRNA 134	Homo sapiens	34-41
29872325-6	2018	Further investigation showed that miR-134 increased the anti-tumor effects of Ara-C through inhibiting phosphorylation of eukaryotic initiation factor 4E and downregulating Mcl-1 and bcl2, which was independent of p38 and Erk1/2 activation.	Cytarabine	78-83	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	173-178
29872325-6	2018	Further investigation showed that miR-134 increased the anti-tumor effects of Ara-C through inhibiting phosphorylation of eukaryotic initiation factor 4E and downregulating Mcl-1 and bcl2, which was independent of p38 and Erk1/2 activation.	Cytarabine	78-83	BCL2 apoptosis regulator	Homo sapiens	183-187
29872325-6	2018	Further investigation showed that miR-134 increased the anti-tumor effects of Ara-C through inhibiting phosphorylation of eukaryotic initiation factor 4E and downregulating Mcl-1 and bcl2, which was independent of p38 and Erk1/2 activation.	Cytarabine	78-83	mitogen-activated protein kinase 1	Homo sapiens	214-217
29872325-6	2018	Further investigation showed that miR-134 increased the anti-tumor effects of Ara-C through inhibiting phosphorylation of eukaryotic initiation factor 4E and downregulating Mcl-1 and bcl2, which was independent of p38 and Erk1/2 activation.	Cytarabine	78-83	mitogen-activated protein kinase 3	Homo sapiens	222-228
29872325-7	2018	Taken together, our results demonstrate that miR-134 plays a pivotal role in AML Ara-C resistance through increasing cell sensitivity to Ara-C and promoting apoptosis by targeting Mnks.	Cytarabine	81-86	microRNA 134	Homo sapiens	45-52
29872325-7	2018	Taken together, our results demonstrate that miR-134 plays a pivotal role in AML Ara-C resistance through increasing cell sensitivity to Ara-C and promoting apoptosis by targeting Mnks.	Cytarabine	137-142	microRNA 134	Homo sapiens	45-52
29761849-8	2018	Targeting MUC1-C was also associated with increased sensitivity of AML cells to Cytarabine (Ara-C) treatment by a survivin-dependent mechanism.	Cytarabine	80-90	mucin 1, cell surface associated	Homo sapiens	10-14
29761849-8	2018	Targeting MUC1-C was also associated with increased sensitivity of AML cells to Cytarabine (Ara-C) treatment by a survivin-dependent mechanism.	Cytarabine	92-97	mucin 1, cell surface associated	Homo sapiens	10-14
29739902-5	2018	Furthermore, cytarabine inhibited viral DNA and RNA syntheses and induced the rapid degradation of KSHV major latent protein LANA (latency-associated nuclear antigen), leading to the suppression of KSHV latent replication.	Cytarabine	13-23	LANA	Human gammaherpesvirus 8	131-165
29739902-13	2018	Of interest, cytarabine induced the degradation of KSHV major latent protein LANA, hence suppressing KSHV latent replication, which is required for PEL cell survival.	Cytarabine	13-23	LANA	Human gammaherpesvirus 8	77-81
29437791-3	2018	A phase I study of CPI-613 plus cytarabine and mitoxantrone was conducted in patients with relapsed or refractory AML.Results: Exposure to chemotherapy induced mitochondrial oxygen consumption that depended on PDH.	Cytarabine	32-42	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	210-213
29695239-0	2018	Bortezomib prevents cytarabine resistance in MCL, which is characterized by down-regulation of dCK and up-regulation of SPIB resulting in high NF-kappaB activity.	Cytarabine	20-30	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	95-98
29378418-3	2018	CPX-351, a novel liposomal formulation which encapsulates cytarabine and daunorubicin in 5:1 molar ratio, has shown promising efficacy, leading to recent US FDA approval for front-line therapy for patients with therapy-related AML and AML with myelodysplasia-related changes based on a large multicenter Phase III clinical trial.	Cytarabine	58-68	T-box transcription factor 22	Homo sapiens	0-3
29477371-7	2018	Surprisingly, positive results are being obtained in elderly acute myeloid leukemia patients, in whom inhibition of BCL2 is able to substantially increase the efficacy of low-dose cytarabine or hypomethylating agents.	Cytarabine	180-190	BCL2 apoptosis regulator	Homo sapiens	116-120
29695239-0	2018	Bortezomib prevents cytarabine resistance in MCL, which is characterized by down-regulation of dCK and up-regulation of SPIB resulting in high NF-kappaB activity.	Cytarabine	20-30	Spi-B transcription factor	Homo sapiens	120-124
29695239-0	2018	Bortezomib prevents cytarabine resistance in MCL, which is characterized by down-regulation of dCK and up-regulation of SPIB resulting in high NF-kappaB activity.	Cytarabine	20-30	nuclear factor kappa B subunit 1	Homo sapiens	143-152
29695239-10	2018	This was confirmed and show that the dCK levels are retained upon co-treatment, indicating a clinical use for bortezomib treatment in combination with cytarabine to avoid development of resistance.	Cytarabine	151-161	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	37-40
29695239-11	2018	The possibility to predict cytarabine resistance in diagnostic samples was assessed, but analysis show that a majority of patients have moderate to high expression of dCK at diagnosis, corresponding well to the initial clinical response to cytarabine treatment.	Cytarabine	27-37	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	167-170
29695239-11	2018	The possibility to predict cytarabine resistance in diagnostic samples was assessed, but analysis show that a majority of patients have moderate to high expression of dCK at diagnosis, corresponding well to the initial clinical response to cytarabine treatment.	Cytarabine	240-250	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	167-170
29695239-12	2018	CONCLUSION: We show that cytarabine resistance potentially can be avoided or at least delayed through co-treatment with bortezomib, and that down-regulation of dCK and up-regulation of SPIB and NF-kappaB are the main molecular events driving cytarabine resistance development.	Cytarabine	242-252	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	160-163
29695239-12	2018	CONCLUSION: We show that cytarabine resistance potentially can be avoided or at least delayed through co-treatment with bortezomib, and that down-regulation of dCK and up-regulation of SPIB and NF-kappaB are the main molecular events driving cytarabine resistance development.	Cytarabine	242-252	Spi-B transcription factor	Homo sapiens	185-189
29719594-8	2018	Heteronemin effectively down-regulated cytarabine-induced activation of MAPK, AP-1, NF-kappaB and c-myc, the down-stream targets of Ras signaling, which again validated the role of Ras in regulating the synergism.	Cytarabine	39-49	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	98-103
29473342-0	2018	Clofarabine exerts antileukemic activity against cytarabine-resistant B-cell precursor acute lymphoblastic leukemia with low deoxycytidine kinase expression.	Cytarabine	49-59	deoxycytidine kinase	Homo sapiens	125-145
29473342-8	2018	DCK knockout by genome editing with a CRISPR-Cas9 system in an Ara-C-sensitive-ALL cell line induced marked resistance to Ara-C, but not to vincristine and daunorubicin, indicating the involvement of DCK expression in the Ara-C sensitivity of BCP-ALL.	Cytarabine	122-127	deoxycytidine kinase	Homo sapiens	0-3
29473342-4	2018	In the first step of the metabolic pathway, Ara-C is phosphorylated to Ara-CMP by deoxycytidine kinase (DCK).	Cytarabine	44-49	deoxycytidine kinase	Homo sapiens	82-102
29473342-8	2018	DCK knockout by genome editing with a CRISPR-Cas9 system in an Ara-C-sensitive-ALL cell line induced marked resistance to Ara-C, but not to vincristine and daunorubicin, indicating the involvement of DCK expression in the Ara-C sensitivity of BCP-ALL.	Cytarabine	122-127	deoxycytidine kinase	Homo sapiens	0-3
29473342-4	2018	In the first step of the metabolic pathway, Ara-C is phosphorylated to Ara-CMP by deoxycytidine kinase (DCK).	Cytarabine	44-49	deoxycytidine kinase	Homo sapiens	104-107
29473342-12	2018	In contrast to Ara-C, although the knockout of DCK induced marked resistance to clofarabine, sensitivity to clofarabine was only marginally associated with DCK gene expression level, suggesting a possible efficacy of clofarabine for BCP-ALL that shows relative Ara-C resistance due to low DCK expression.	Cytarabine	261-266	deoxycytidine kinase	Homo sapiens	47-50
29473342-6	2018	We analyzed various cell lines for the possible involvement of DCK in the sensitivities of B-cell precursor ALL (BCP-ALL) to Ara-C.	Cytarabine	125-130	deoxycytidine kinase	Homo sapiens	63-66
29473342-7	2018	Higher DCK expression was associated with higher Ara-C sensitivity.	Cytarabine	49-54	deoxycytidine kinase	Homo sapiens	7-10
29473342-8	2018	DCK knockout by genome editing with a CRISPR-Cas9 system in an Ara-C-sensitive-ALL cell line induced marked resistance to Ara-C, but not to vincristine and daunorubicin, indicating the involvement of DCK expression in the Ara-C sensitivity of BCP-ALL.	Cytarabine	63-68	deoxycytidine kinase	Homo sapiens	0-3
29330206-4	2018	Alterations of epigenetic regulators were frequently gained at relapse with recurring alterations of KDM6A constituting a mechanism of cytarabine resistance.	Cytarabine	135-145	lysine demethylase 6A	Homo sapiens	101-106
29499095-1	2018	"Influence of genetic variants of IDH1, IDH2, TET2 and DNMT3A on cytarabine cytotoxicity in different populations" by Y. Wang &amp; J. K. Lamba1 The above article from the Journal of Clinical Pharmacy and Therapeutics, published online on 21 November 2017 in Wiley Online Library (wileyonlinelibrary.com), has been retracted following discussions with the authors, the Journal Editors and John Wiley &amp; Sons Ltd.	Cytarabine	65-75	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	34-38
29499095-1	2018	"Influence of genetic variants of IDH1, IDH2, TET2 and DNMT3A on cytarabine cytotoxicity in different populations" by Y. Wang &amp; J. K. Lamba1 The above article from the Journal of Clinical Pharmacy and Therapeutics, published online on 21 November 2017 in Wiley Online Library (wileyonlinelibrary.com), has been retracted following discussions with the authors, the Journal Editors and John Wiley &amp; Sons Ltd.	Cytarabine	65-75	isocitrate dehydrogenase (NADP(+)) 2	Homo sapiens	40-44
28751770-4	2018	We show that venetoclax synergizes with cytarabine and idarubicin to increase antileukemic efficacy in a TP53-dependent manner.	Cytarabine	40-50	tumor protein p53	Homo sapiens	105-109
29499095-1	2018	"Influence of genetic variants of IDH1, IDH2, TET2 and DNMT3A on cytarabine cytotoxicity in different populations" by Y. Wang &amp; J. K. Lamba1 The above article from the Journal of Clinical Pharmacy and Therapeutics, published online on 21 November 2017 in Wiley Online Library (wileyonlinelibrary.com), has been retracted following discussions with the authors, the Journal Editors and John Wiley &amp; Sons Ltd.	Cytarabine	65-75	tet methylcytosine dioxygenase 2	Homo sapiens	46-50
29499095-1	2018	"Influence of genetic variants of IDH1, IDH2, TET2 and DNMT3A on cytarabine cytotoxicity in different populations" by Y. Wang &amp; J. K. Lamba1 The above article from the Journal of Clinical Pharmacy and Therapeutics, published online on 21 November 2017 in Wiley Online Library (wileyonlinelibrary.com), has been retracted following discussions with the authors, the Journal Editors and John Wiley &amp; Sons Ltd.	Cytarabine	65-75	DNA methyltransferase 3 alpha	Homo sapiens	55-61
29499095-11	2018	Influence of genetic variants of IDH1, IDH2, TET2 and DNMT3A on cytarabine cytotoxicity in different populations.	Cytarabine	64-74	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	33-37
29499095-11	2018	Influence of genetic variants of IDH1, IDH2, TET2 and DNMT3A on cytarabine cytotoxicity in different populations.	Cytarabine	64-74	isocitrate dehydrogenase (NADP(+)) 2	Homo sapiens	39-43
29499095-11	2018	Influence of genetic variants of IDH1, IDH2, TET2 and DNMT3A on cytarabine cytotoxicity in different populations.	Cytarabine	64-74	tet methylcytosine dioxygenase 2	Homo sapiens	45-49
29499095-11	2018	Influence of genetic variants of IDH1, IDH2, TET2 and DNMT3A on cytarabine cytotoxicity in different populations.	Cytarabine	64-74	DNA methyltransferase 3 alpha	Homo sapiens	54-60
29496492-6	2018	Furthermore, significantly reduced IGFBP2, SERP1NC1, AMBP and GPX3, as well as dramatically increased CPE levels were observed in the CSF of NKTCL patients after cytarabine chemotherapy.	Cytarabine	162-172	carboxypeptidase E	Homo sapiens	102-105
29490977-0	2018	CDA as a predictive marker for life-threatening toxicities in patients with AML treated with cytarabine.	Cytarabine	93-103	cytidine deaminase	Homo sapiens	0-3
29490977-3	2018	Ara-C is detoxified in the liver by a single enzyme, cytidine deaminase (CDA), coded by a gene known to be highly polymorphic.	Cytarabine	0-5	cytidine deaminase	Homo sapiens	53-71
29490977-3	2018	Ara-C is detoxified in the liver by a single enzyme, cytidine deaminase (CDA), coded by a gene known to be highly polymorphic.	Cytarabine	0-5	cytidine deaminase	Homo sapiens	73-76
29490977-10	2018	Taken together, the results of this study strongly suggest that CDA is a predictive marker of life-threatening toxicities in patients with AML receiving induction therapy with standard Ara-C.	Cytarabine	185-190	cytidine deaminase	Homo sapiens	64-67
29274141-0	2018	Acquired resistance of phosphatase and tensin homolog-deficient cells to poly(ADP-ribose) polymerase inhibitor and Ara-C mediated by 53BP1 loss and SAMHD1 overexpression.	Cytarabine	115-120	tumor protein p53 binding protein 1	Homo sapiens	133-138
29274141-0	2018	Acquired resistance of phosphatase and tensin homolog-deficient cells to poly(ADP-ribose) polymerase inhibitor and Ara-C mediated by 53BP1 loss and SAMHD1 overexpression.	Cytarabine	115-120	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	148-154
29274141-13	2018	SAMHD1 was overexpressed in all the variants and its knockout completely restored their sensitivity to Ara-C but did not affect their PARPi sensitivity.	Cytarabine	103-108	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	0-6
29217775-6	2018	Cytarabine-induced G1-arrest can be converted to G2-arrest by doxorubicin treatment in certain B-cell lymphomas, which correlates with newly acquired sensitivity to the Wee1 inhibitor.	Cytarabine	0-10	WEE1 G2 checkpoint kinase	Homo sapiens	169-173
29139135-1	2018	Novel therapies have potential to improve outcomes in patients with acute myeloid leukemia (AML) harboring FLT3-ITD mutations that have high risk of relapse and poor survival following standard of care (SOC) cytarabine/anthracycline-based induction/consolidation chemotherapy.	Cytarabine	208-218	fms related receptor tyrosine kinase 3	Homo sapiens	107-111
30178381-3	2018	Previously, we found that altering the BMM by the CXCR4 antagonist led to enhanced cytotoxic activity of immune cells, which leads to increased susceptibility of leukemic cells to chemotherapeutic agents such as cytosine arabinoside (Ara-C) in leukemic BMM.	Cytarabine	212-232	C-X-C motif chemokine receptor 4	Homo sapiens	50-55
28592158-0	2018	Phase Ib study of the mTOR inhibitor everolimus with low dose cytarabine in elderly acute myeloid leukemia.	Cytarabine	62-72	mechanistic target of rapamycin kinase	Homo sapiens	22-26
29352124-4	2018	Interestingly, we found that DLBCL cells expressing hepatitis B virus X protein (HBX) did not exhibit enhanced cell growth but did show reduced sensitivity to methotrexate (MTX) and cytarabine (Ara-C), which induced S-phase arrest.	Cytarabine	182-192	X protein	Hepatitis B virus	81-84
29352124-4	2018	Interestingly, we found that DLBCL cells expressing hepatitis B virus X protein (HBX) did not exhibit enhanced cell growth but did show reduced sensitivity to methotrexate (MTX) and cytarabine (Ara-C), which induced S-phase arrest.	Cytarabine	194-199	X protein	Hepatitis B virus	81-84
30178381-3	2018	Previously, we found that altering the BMM by the CXCR4 antagonist led to enhanced cytotoxic activity of immune cells, which leads to increased susceptibility of leukemic cells to chemotherapeutic agents such as cytosine arabinoside (Ara-C) in leukemic BMM.	Cytarabine	234-239	C-X-C motif chemokine receptor 4	Homo sapiens	50-55
30178381-5	2018	Thus, we performed immunohistochemistry and observed that the capillary density of sinusoidal vessels was highly increased by CXCR4 antagonist with Ara-C in leukemia, showing the reconstruction of BMM with megakaryocytes in sinusoidal vessels by dual treatment.	Cytarabine	148-153	C-X-C motif chemokine receptor 4	Homo sapiens	126-131
30474474-1	2018	Sterile alpha motif and HD domain-containing protein 1 (SAMHD1) is a mammalian dNTP hydrolase (dNTPase) and functions as a negative regulator in the efficacy of cytarabine treatment of acute myeloid leukemia (AML).	Cytarabine	161-171	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	0-54
29911928-1	2018	Sterile alpha motif and HD domain-containing protein 1 (SAMHD1) is a mammalian dNTP hydrolase that acts as a negative regulator in the efficacy of cytarabine treatment against acute myeloid leukemia (AML).	Cytarabine	147-157	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	0-54
29911928-1	2018	Sterile alpha motif and HD domain-containing protein 1 (SAMHD1) is a mammalian dNTP hydrolase that acts as a negative regulator in the efficacy of cytarabine treatment against acute myeloid leukemia (AML).	Cytarabine	147-157	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	56-62
30474474-1	2018	Sterile alpha motif and HD domain-containing protein 1 (SAMHD1) is a mammalian dNTP hydrolase (dNTPase) and functions as a negative regulator in the efficacy of cytarabine treatment of acute myeloid leukemia (AML).	Cytarabine	161-171	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	56-62
30474474-1	2018	Sterile alpha motif and HD domain-containing protein 1 (SAMHD1) is a mammalian dNTP hydrolase (dNTPase) and functions as a negative regulator in the efficacy of cytarabine treatment of acute myeloid leukemia (AML).	Cytarabine	161-171	NTPase	Drosophila melanogaster	95-102
29025907-5	2018	As a result, SIRT6 depletion compromises the ability of leukemia cells to repair DNA double-strand breaks that, in turn, increases their sensitivity to daunorubicin and Ara-C, both in vitro and in vivo In contrast, low SIRT6 levels observed in normal CD34+ hematopoietic progenitors explain their weaker sensitivity to genotoxic stress.	Cytarabine	169-174	sirtuin 6	Homo sapiens	13-18
29312358-3	2017	In a cohort of AML patients, undergoing combined daunorubicin and cytarabine chemotherapy, a population of T regulatory cells (Tregs) with suppressive phenotype, expressing the immune checkpoint programmed cell death protein 1 (PD-1), was significantly increased.	Cytarabine	66-76	programmed cell death 1	Homo sapiens	195-226
29175378-0	2018	Increased activity of both CDK1 and CDK2 is necessary for the combinatorial activity of WEE1 inhibition and cytarabine.	Cytarabine	108-118	cyclin dependent kinase 1	Homo sapiens	27-31
29175378-0	2018	Increased activity of both CDK1 and CDK2 is necessary for the combinatorial activity of WEE1 inhibition and cytarabine.	Cytarabine	108-118	cyclin dependent kinase 2	Homo sapiens	36-40
29175378-2	2018	Our lab and others have demonstrated that a small-molecule inhibitor of WEE1, AZD1775, sensitizes acute leukemia cells to cytarabine; however, a mechanism of combinatorial activity has remained elusive.	Cytarabine	122-132	WEE1 G2 checkpoint kinase	Homo sapiens	72-76
29175378-3	2018	Thus, we sought to determine the relative contribution of WEE1 targets CDK1 and CDK2 to the combinatorial activity of AZD1775 and cytarabine.	Cytarabine	130-140	WEE1 G2 checkpoint kinase	Homo sapiens	58-62
29175378-5	2018	Expression of CDK1/2-AF together, but neither alone, enhanced the anti-proliferative effects, DNA damage and apoptosis induced by cytarabine.	Cytarabine	130-140	cyclin dependent kinase 1	Homo sapiens	14-18
29175378-6	2018	Furthermore, pharmacologic inhibition of CDK1 alone or CDK1 and CDK2 together reduced the combinatorial activity of AZD1775 and cytarabine.	Cytarabine	128-138	cyclin dependent kinase 1	Homo sapiens	41-45
29175378-6	2018	Furthermore, pharmacologic inhibition of CDK1 alone or CDK1 and CDK2 together reduced the combinatorial activity of AZD1775 and cytarabine.	Cytarabine	128-138	cyclin dependent kinase 1	Homo sapiens	55-59
29175378-6	2018	Furthermore, pharmacologic inhibition of CDK1 alone or CDK1 and CDK2 together reduced the combinatorial activity of AZD1775 and cytarabine.	Cytarabine	128-138	cyclin dependent kinase 2	Homo sapiens	64-68
29175378-7	2018	Thus, increased activity of both CDK1 and CDK2 in response to WEE1 inhibition is necessary for the combinatorial activity of AZD1775 and cytarabine.	Cytarabine	137-147	cyclin dependent kinase 1	Homo sapiens	33-37
29175378-7	2018	Thus, increased activity of both CDK1 and CDK2 in response to WEE1 inhibition is necessary for the combinatorial activity of AZD1775 and cytarabine.	Cytarabine	137-147	cyclin dependent kinase 2	Homo sapiens	42-46
29175378-7	2018	Thus, increased activity of both CDK1 and CDK2 in response to WEE1 inhibition is necessary for the combinatorial activity of AZD1775 and cytarabine.	Cytarabine	137-147	WEE1 G2 checkpoint kinase	Homo sapiens	62-66
29018079-6	2017	Heterozygous conditional inactivation of Setd2 in a murine model decreased the latency of MLL-AF9-induced leukemia and caused resistance to cytarabine treatment in vivo, whereas homozygous loss delayed leukemia formation.	Cytarabine	140-150	SET domain containing 2	Mus musculus	41-46
29055018-5	2017	Upregulation was also seen in primary human AML cells after treatment with cytarabine in vitro Upon overexpression, RUNX1 restricted proliferation, promoted apoptosis, and augmented the DNA damage response.	Cytarabine	75-85	RUNX family transcription factor 1	Homo sapiens	116-121
29018079-3	2017	SETD2 mutations led to resistance to DNA-damaging agents, cytarabine, 6-thioguanine, doxorubicin, and etoposide, but not to a non-DNA damaging agent, l-asparaginase.	Cytarabine	58-68	SET domain containing 2	Mus musculus	0-5
29018079-7	2017	Treatment with JIB-04, an inhibitor of the H3K9/36me3 demethylase KDM4A, restored H3K36me3 levels and sensitivity to cytarabine.	Cytarabine	117-127	lysine (K)-specific demethylase 4A	Mus musculus	66-71
29162833-0	2017	The combination of CHK1 inhibitor with G-CSF overrides cytarabine resistance in human acute myeloid leukemia.	Cytarabine	55-65	checkpoint kinase 1	Homo sapiens	19-23
29423065-7	2018	Finally, PRL-3 expression made Reh cells more resistance to cytarabine treatment.	Cytarabine	60-70	protein tyrosine phosphatase 4A3	Homo sapiens	9-14
29423065-9	2018	PRL-3 promoted adhesion, migration and resistance to cytarabine.	Cytarabine	53-63	protein tyrosine phosphatase 4A3	Homo sapiens	0-5
29312515-4	2017	In this study, the combination of chidamide (50 nM) with cytarabine (50 nM) showed synergistic inhibition on cell growth.The mean combination index values were 0.068, 0.158, and 0.226 in SKM-1, MUTZ-1, and KG-1 MDS cell lines, respectively.	Cytarabine	57-67	sodium voltage-gated channel alpha subunit 4	Homo sapiens	187-192
29312515-5	2017	The combination increased the acetylation levels of histone H3 and decreased HDAC activity in MDS cells.A low concentration (25 and 50 nM) of chidamide combined with low-dose cytarabine (50 nM) inhibited cell proliferation and arrested the cell cycle in the G0/G1 phasevia down-regulating CDK2 and up-regulating p21.	Cytarabine	175-185	cyclin dependent kinase 2	Homo sapiens	289-293
29312515-5	2017	The combination increased the acetylation levels of histone H3 and decreased HDAC activity in MDS cells.A low concentration (25 and 50 nM) of chidamide combined with low-dose cytarabine (50 nM) inhibited cell proliferation and arrested the cell cycle in the G0/G1 phasevia down-regulating CDK2 and up-regulating p21.	Cytarabine	175-185	H3 histone pseudogene 16	Homo sapiens	312-315
29101245-9	2017	Notch3 deletion also reduced the number of qNSCs activated after antimitotic cytosine beta-D-arabinofuranoside (Ara-C) treatment.	Cytarabine	77-110	notch 3	Mus musculus	0-6
29101245-9	2017	Notch3 deletion also reduced the number of qNSCs activated after antimitotic cytosine beta-D-arabinofuranoside (Ara-C) treatment.	Cytarabine	112-117	notch 3	Mus musculus	0-6
29174536-5	2017	Cytarabine and gemcitabine inhibited DAC monophosphate generation by the cytosolic proteins of HCT116 cells and recombinant human dCK protein, assessed using polyethylenimine cellulose thin-layered chromatography.	Cytarabine	0-10	arylacetamide deacetylase	Homo sapiens	37-40
29174536-5	2017	Cytarabine and gemcitabine inhibited DAC monophosphate generation by the cytosolic proteins of HCT116 cells and recombinant human dCK protein, assessed using polyethylenimine cellulose thin-layered chromatography.	Cytarabine	0-10	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	130-133
29162833-0	2017	The combination of CHK1 inhibitor with G-CSF overrides cytarabine resistance in human acute myeloid leukemia.	Cytarabine	55-65	colony stimulating factor 3	Homo sapiens	39-44
29162833-3	2017	Here we show that the CHK1 inhibitor (CHK1i) GDC-0575 enhances AraC-mediated killing of AML cells both in vitro and in vivo, thus abrogating any potential chemoresistance mechanisms involving DNA repair.	Cytarabine	63-67	checkpoint kinase 1	Homo sapiens	22-26
29081694-7	2017	Moreover, therapy with high dose cytarabine (HDAC) has significantly improved the prognosis of core binding factor (CBF) acute myeloid leukemia (AML) patients.	Cytarabine	33-43	CCAAT enhancer binding protein zeta	Homo sapiens	95-114
29164635-0	2017	Retracted: Influence of genetic variants of IDH1, IDH2, TET2 and DNMT3A on cytarabine cytotoxicity in different populations.	Cytarabine	75-85	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	44-48
29164635-0	2017	Retracted: Influence of genetic variants of IDH1, IDH2, TET2 and DNMT3A on cytarabine cytotoxicity in different populations.	Cytarabine	75-85	isocitrate dehydrogenase (NADP(+)) 2	Homo sapiens	50-54
29164635-0	2017	Retracted: Influence of genetic variants of IDH1, IDH2, TET2 and DNMT3A on cytarabine cytotoxicity in different populations.	Cytarabine	75-85	tet methylcytosine dioxygenase 2	Homo sapiens	56-60
29164635-0	2017	Retracted: Influence of genetic variants of IDH1, IDH2, TET2 and DNMT3A on cytarabine cytotoxicity in different populations.	Cytarabine	75-85	DNA methyltransferase 3 alpha	Homo sapiens	65-71
29164635-1	2017	"Influence of genetic variants of IDH1, IDH2, TET2 and DNMT3A on cytarabine cytotoxicity in different populations" by Y. Wang &amp; J. K. Lamba1 The above article from the Journal of Clinical Pharmacy and Therapeutics, published online on 21 November 2017 in Wiley Online Library (wileyonlinelibrary.com), has been retracted following discussions with the authors, the Journal Editors and John Wiley &amp; Sons Ltd.	Cytarabine	65-75	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	34-38
29164635-1	2017	"Influence of genetic variants of IDH1, IDH2, TET2 and DNMT3A on cytarabine cytotoxicity in different populations" by Y. Wang &amp; J. K. Lamba1 The above article from the Journal of Clinical Pharmacy and Therapeutics, published online on 21 November 2017 in Wiley Online Library (wileyonlinelibrary.com), has been retracted following discussions with the authors, the Journal Editors and John Wiley &amp; Sons Ltd.	Cytarabine	65-75	isocitrate dehydrogenase (NADP(+)) 2	Homo sapiens	40-44
29164635-1	2017	"Influence of genetic variants of IDH1, IDH2, TET2 and DNMT3A on cytarabine cytotoxicity in different populations" by Y. Wang &amp; J. K. Lamba1 The above article from the Journal of Clinical Pharmacy and Therapeutics, published online on 21 November 2017 in Wiley Online Library (wileyonlinelibrary.com), has been retracted following discussions with the authors, the Journal Editors and John Wiley &amp; Sons Ltd.	Cytarabine	65-75	tet methylcytosine dioxygenase 2	Homo sapiens	46-50
29164635-1	2017	"Influence of genetic variants of IDH1, IDH2, TET2 and DNMT3A on cytarabine cytotoxicity in different populations" by Y. Wang &amp; J. K. Lamba1 The above article from the Journal of Clinical Pharmacy and Therapeutics, published online on 21 November 2017 in Wiley Online Library (wileyonlinelibrary.com), has been retracted following discussions with the authors, the Journal Editors and John Wiley &amp; Sons Ltd.	Cytarabine	65-75	DNA methyltransferase 3 alpha	Homo sapiens	55-61
29164635-11	2017	Influence of genetic variants of IDH1, IDH2, TET2 and DNMT3A on cytarabine cytotoxicity in different populations.	Cytarabine	64-74	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	33-37
29164635-11	2017	Influence of genetic variants of IDH1, IDH2, TET2 and DNMT3A on cytarabine cytotoxicity in different populations.	Cytarabine	64-74	isocitrate dehydrogenase (NADP(+)) 2	Homo sapiens	39-43
29164635-11	2017	Influence of genetic variants of IDH1, IDH2, TET2 and DNMT3A on cytarabine cytotoxicity in different populations.	Cytarabine	64-74	tet methylcytosine dioxygenase 2	Homo sapiens	45-49
29164635-11	2017	Influence of genetic variants of IDH1, IDH2, TET2 and DNMT3A on cytarabine cytotoxicity in different populations.	Cytarabine	64-74	DNA methyltransferase 3 alpha	Homo sapiens	54-60
28982056-3	2017	In this study, we retrospectively evaluate safety and efficacy of a salvage regimen (CAGLP) consisting of G-CSF, low-dose cytarabine, aclarubicin, l-asparaginase and prednisone.	Cytarabine	122-132	calmodulin like 6	Homo sapiens	85-90
28819011-6	2017	In conclusion, we show that TP53 mutations identify a phenotypically distinct and highly aggressive form of MCL with poor or no response to regimens including cytarabine, rituximab, and autologous stem-cell transplant (ASCT).	Cytarabine	159-169	tumor protein p53	Homo sapiens	28-32
29057672-3	2017	A BRAF-V600E-mutated melanoma leptomeningeal metastases patient, treated by dabrafenib and liposomal cytarabine, presented after the first injection of liposomal cytarabine with hyperthermia and headaches.	Cytarabine	101-111	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	2-6
29057672-3	2017	A BRAF-V600E-mutated melanoma leptomeningeal metastases patient, treated by dabrafenib and liposomal cytarabine, presented after the first injection of liposomal cytarabine with hyperthermia and headaches.	Cytarabine	162-172	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	2-6
29081694-7	2017	Moreover, therapy with high dose cytarabine (HDAC) has significantly improved the prognosis of core binding factor (CBF) acute myeloid leukemia (AML) patients.	Cytarabine	33-43	CCAAT enhancer binding protein zeta	Homo sapiens	116-119
28957699-2	2017	Incorporation of AraC into DNA activates checkpoint kinase 1 (Chk1), leading to cell-cycle arrest and diminished AraC cytotoxicity, which can be reversed by the selective Chk1 inhibitor MK-8776.	Cytarabine	17-21	checkpoint kinase 1	Homo sapiens	41-60
28679652-11	2017	Transient transfection of GapmeR against XLOC_109948 in NPM1-mutated OCI-AML3 cell line treated with Ara-C or ATRA enhances apoptosis suggesting XLOC_109948 plays a role in drug sensitivity.	Cytarabine	101-106	nucleophosmin 1	Homo sapiens	56-60
28957699-2	2017	Incorporation of AraC into DNA activates checkpoint kinase 1 (Chk1), leading to cell-cycle arrest and diminished AraC cytotoxicity, which can be reversed by the selective Chk1 inhibitor MK-8776.	Cytarabine	17-21	checkpoint kinase 1	Homo sapiens	62-66
28957699-2	2017	Incorporation of AraC into DNA activates checkpoint kinase 1 (Chk1), leading to cell-cycle arrest and diminished AraC cytotoxicity, which can be reversed by the selective Chk1 inhibitor MK-8776.	Cytarabine	17-21	checkpoint kinase 1	Homo sapiens	171-175
28957699-2	2017	Incorporation of AraC into DNA activates checkpoint kinase 1 (Chk1), leading to cell-cycle arrest and diminished AraC cytotoxicity, which can be reversed by the selective Chk1 inhibitor MK-8776.	Cytarabine	113-117	checkpoint kinase 1	Homo sapiens	41-60
28957699-2	2017	Incorporation of AraC into DNA activates checkpoint kinase 1 (Chk1), leading to cell-cycle arrest and diminished AraC cytotoxicity, which can be reversed by the selective Chk1 inhibitor MK-8776.	Cytarabine	113-117	checkpoint kinase 1	Homo sapiens	62-66
28957699-2	2017	Incorporation of AraC into DNA activates checkpoint kinase 1 (Chk1), leading to cell-cycle arrest and diminished AraC cytotoxicity, which can be reversed by the selective Chk1 inhibitor MK-8776.	Cytarabine	113-117	checkpoint kinase 1	Homo sapiens	171-175
29469718-2	2017	We present a patient who developed ESS after induction of CLAG chemotherapy [2-Chlorodeoxyadenosine (2-CdA) with cytarabine (Ara-C) and (granulocyte-colony stimulating factor) G-CSF] for management of the blast crisis of his chronic myelogenous leukemia (CML).	Cytarabine	113-123	cytidine deaminase	Homo sapiens	103-106
28655785-2	2017	Inhibition of WEE1 with AZD1775 has been shown to sensitize cancer cells to genotoxic chemotherapies, including cytarabine in acute myeloid leukemia (AML) and T-ALL.	Cytarabine	112-122	WEE1 G2 checkpoint kinase	Homo sapiens	14-18
28952709-4	2017	Our data displaythat Ara-c (2muM and 1muM in KG-1 and U937 cell lines respectively), CUR (40muM in both cell lines), and also theircombination significantly increased the percentage of apoptotic cells.	Cytarabine	21-26	latexin	Homo sapiens	29-32
28952709-5	2017	Moreover, the mRNA level of OPN isoforms weredown regulated in the KG-1and U937 cell lines treated with Ara-c while, upregulated in KG-1and U937 cell lines treatedwith CUR and its combination.	Cytarabine	104-109	secreted phosphoprotein 1	Homo sapiens	28-31
28634224-2	2017	Here, it is demonstrated that untreated and cytarabine (AraC)-treated IGH/MYC-positive Burkitt lymphoma cells accumulate a high number of potentially lethal DNA double-strand breaks (DSB) and display low levels of the BRCA2 tumor suppressor protein, which is a key element of homologous recombination (HR)-mediated DSB repair.	Cytarabine	44-54	immunoglobulin heavy chain complex	Mus musculus	70-73
28610775-10	2017	Finally, chalcone A23 seems to have a synergic effect with the chemotherapy drugs cytarabine and vincristine.	Cytarabine	82-92	immunoglobulin kappa variable 2-24	Homo sapiens	18-21
27530244-5	2017	We speculate that posaconazole may inhibit the cytarabine efflux through P-glycoprotein inhibition leading to the patient"s palmar-plantar erythrodysesthesia and subsequent aplasia.	Cytarabine	47-57	ATP binding cassette subfamily B member 1	Homo sapiens	73-87
28502830-8	2017	Our time-dependent analyses of The Cancer Genome Atlas (TCGA) AML cohort indicate that high expression of SAMHD1, even though it critically limits the efficacy of high-dose ara-C therapy, might be associated with more favorable disease progression.	Cytarabine	173-178	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	106-112
28506695-6	2017	When Ara-C was added in the absence of growth factor, Annexin V assay revealed that TF-1 KITD816V was associated with a significantly lower proportion of apoptotic cells than TF-1 KITN822K (p &lt; 0.001).	Cytarabine	5-10	annexin A5	Homo sapiens	54-63
28810561-0	2017	Cytotoxic T lymphocytes promote cytarabine-induced acute myeloid leukemia cell apoptosis via inhibiting Bcl-2 expression.	Cytarabine	32-42	BCL2 apoptosis regulator	Homo sapiens	104-109
28810561-7	2017	Western blotting revealed that Bcl-2 expression was downregulated in AML cells following cytarabine and CTL treatment, indicating that the synergistic effect of this treatment on AML cell apoptosis is due to the downregulation of Bcl-2.	Cytarabine	89-99	BCL2 apoptosis regulator	Homo sapiens	31-36
28810561-7	2017	Western blotting revealed that Bcl-2 expression was downregulated in AML cells following cytarabine and CTL treatment, indicating that the synergistic effect of this treatment on AML cell apoptosis is due to the downregulation of Bcl-2.	Cytarabine	89-99	BCL2 apoptosis regulator	Homo sapiens	230-235
28595073-0	2017	Probing the binding reaction of cytarabine to human serum albumin using multispectroscopic techniques with the aid of molecular docking.	Cytarabine	32-42	albumin	Homo sapiens	52-65
28595073-2	2017	In the present study, the molecular interaction between cytarabine and human serum albumin (HSA) was investigated via fluorescence, UV-vis absorption, circular dichroism (CD) spectroscopy and molecular docking method under simulative physiological conditions.	Cytarabine	56-66	albumin	Homo sapiens	77-90
28634224-2	2017	Here, it is demonstrated that untreated and cytarabine (AraC)-treated IGH/MYC-positive Burkitt lymphoma cells accumulate a high number of potentially lethal DNA double-strand breaks (DSB) and display low levels of the BRCA2 tumor suppressor protein, which is a key element of homologous recombination (HR)-mediated DSB repair.	Cytarabine	44-54	myelocytomatosis oncogene	Mus musculus	74-77
28634224-2	2017	Here, it is demonstrated that untreated and cytarabine (AraC)-treated IGH/MYC-positive Burkitt lymphoma cells accumulate a high number of potentially lethal DNA double-strand breaks (DSB) and display low levels of the BRCA2 tumor suppressor protein, which is a key element of homologous recombination (HR)-mediated DSB repair.	Cytarabine	44-54	breast cancer 2, early onset	Mus musculus	218-223
28634224-2	2017	Here, it is demonstrated that untreated and cytarabine (AraC)-treated IGH/MYC-positive Burkitt lymphoma cells accumulate a high number of potentially lethal DNA double-strand breaks (DSB) and display low levels of the BRCA2 tumor suppressor protein, which is a key element of homologous recombination (HR)-mediated DSB repair.	Cytarabine	56-60	immunoglobulin heavy chain complex	Mus musculus	70-73
28634224-2	2017	Here, it is demonstrated that untreated and cytarabine (AraC)-treated IGH/MYC-positive Burkitt lymphoma cells accumulate a high number of potentially lethal DNA double-strand breaks (DSB) and display low levels of the BRCA2 tumor suppressor protein, which is a key element of homologous recombination (HR)-mediated DSB repair.	Cytarabine	56-60	myelocytomatosis oncogene	Mus musculus	74-77
28634224-2	2017	Here, it is demonstrated that untreated and cytarabine (AraC)-treated IGH/MYC-positive Burkitt lymphoma cells accumulate a high number of potentially lethal DNA double-strand breaks (DSB) and display low levels of the BRCA2 tumor suppressor protein, which is a key element of homologous recombination (HR)-mediated DSB repair.	Cytarabine	56-60	breast cancer 2, early onset	Mus musculus	218-223
28634224-3	2017	BRCA2 deficiency in IGH/MYC-positive cells was associated with diminished HR activity and hypersensitivity to PARP1 inhibitors (olaparib, talazoparib) used alone or in combination with cytarabine in vitro Moreover, talazoparib exerted a therapeutic effect in NGS mice bearing primary Burkitt lymphoma xenografts.	Cytarabine	185-195	immunoglobulin heavy chain complex	Mus musculus	20-23
28634224-3	2017	BRCA2 deficiency in IGH/MYC-positive cells was associated with diminished HR activity and hypersensitivity to PARP1 inhibitors (olaparib, talazoparib) used alone or in combination with cytarabine in vitro Moreover, talazoparib exerted a therapeutic effect in NGS mice bearing primary Burkitt lymphoma xenografts.	Cytarabine	185-195	myelocytomatosis oncogene	Mus musculus	24-27
28097942-7	2017	A regimen of low-dose cytarabine and aclarubicin combined with granulocyte-colony-stimulating factor (CAG) led to higher CR rates in the CD25-positive AML patients than intensive chemotherapies.	Cytarabine	22-32	interleukin 2 receptor subunit alpha	Homo sapiens	137-141
28712407-5	2017	Compared with control group without medication, the PML protein expression of APL cells in initial onset cases had larger fluorescent signals in the ATRA group, As2O3 group and As4S4 group, whereas there were no significant changes in the arabinoside cytosine group and the homoharringtonine group.	Cytarabine	239-259	PML nuclear body scaffold	Homo sapiens	52-55
28978059-6	2017	Targeting 6PGD and NADPH production was sufficient to block growth of AML cell lines resistant to the chemotherapeutics daunorubicin and cytarabine.	Cytarabine	137-147	phosphogluconate dehydrogenase	Homo sapiens	10-14
28978059-6	2017	Targeting 6PGD and NADPH production was sufficient to block growth of AML cell lines resistant to the chemotherapeutics daunorubicin and cytarabine.	Cytarabine	137-147	2,4-dienoyl-CoA reductase 1	Homo sapiens	19-24
28505160-5	2017	Primary AML samples with high ex-vivo IC50 to Ara-C, ATO, Dnr had significantly high NRF2 RNA expression.	Cytarabine	46-51	NFE2 like bZIP transcription factor 2	Homo sapiens	85-89
28672876-6	2017	2-Naphthyl-thiazolo[5,4-b]phenothiazine was identified as the most effective of the series by displaying against THP-1 cell lines a cytotoxicity close to cytarabine antineoplastic agent.	Cytarabine	154-164	GLI family zinc finger 2	Homo sapiens	113-118
28436707-1	2017	Recently, we demonstrated that sterile alpha motif and HD domain containing protein 1 (SAMHD1) is a major barrier in acute myelogenous leukemia (AML) cells to the cytotoxicity of cytarabine (ara-C), the most important drug in AML treatment.	Cytarabine	179-189	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	87-93
28436707-1	2017	Recently, we demonstrated that sterile alpha motif and HD domain containing protein 1 (SAMHD1) is a major barrier in acute myelogenous leukemia (AML) cells to the cytotoxicity of cytarabine (ara-C), the most important drug in AML treatment.	Cytarabine	191-196	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	87-93
27922189-2	2017	Here we assessed the role of ERK5 in AraC-induced cell death in AML cell lines HL60 and U937 using ERK5 inhibitors BIX02189 and XMD8-92.	Cytarabine	37-41	mitogen-activated protein kinase 7	Homo sapiens	29-33
27922189-3	2017	We report that inhibition of MEK5/ERK5 activity reduces AraC-induced cell death, DNA damage, the upregulated DNA damage biomarkers, and produced G2 phase cell cycle arrest.	Cytarabine	56-60	mitogen-activated protein kinase kinase 5	Homo sapiens	29-33
27922189-3	2017	We report that inhibition of MEK5/ERK5 activity reduces AraC-induced cell death, DNA damage, the upregulated DNA damage biomarkers, and produced G2 phase cell cycle arrest.	Cytarabine	56-60	mitogen-activated protein kinase 7	Homo sapiens	34-38
27922189-4	2017	In addition, the pro-survival protein P-Bcl2 Ser70 was found to be associated with decreased AraC-induced cell death following XMD8-92 treatment, suggesting a regulatory role of ERK5 on Bcl2 phosphorylation.	Cytarabine	93-97	BCL2 apoptosis regulator	Homo sapiens	40-44
27922189-4	2017	In addition, the pro-survival protein P-Bcl2 Ser70 was found to be associated with decreased AraC-induced cell death following XMD8-92 treatment, suggesting a regulatory role of ERK5 on Bcl2 phosphorylation.	Cytarabine	93-97	mitogen-activated protein kinase 7	Homo sapiens	178-182
27922189-4	2017	In addition, the pro-survival protein P-Bcl2 Ser70 was found to be associated with decreased AraC-induced cell death following XMD8-92 treatment, suggesting a regulatory role of ERK5 on Bcl2 phosphorylation.	Cytarabine	93-97	BCL2 apoptosis regulator	Homo sapiens	186-190
27922189-5	2017	Our study shows that the full potency of AraC cytotoxicity requires optimal ERK5 activity, suggesting a novel role of ERK5 in cancer chemotherapy.	Cytarabine	41-45	mitogen-activated protein kinase 7	Homo sapiens	76-80
27922189-5	2017	Our study shows that the full potency of AraC cytotoxicity requires optimal ERK5 activity, suggesting a novel role of ERK5 in cancer chemotherapy.	Cytarabine	41-45	mitogen-activated protein kinase 7	Homo sapiens	118-122
28500307-4	2017	Strikingly, leukemic cells with Alox5 overexpression showed a significantly higher sensitivity to the standard chemotherapeutic agents, i.e., doxorubicin (DOX) and cytarabine (Ara-C).	Cytarabine	164-174	arachidonate 5-lipoxygenase	Homo sapiens	32-37
28500307-4	2017	Strikingly, leukemic cells with Alox5 overexpression showed a significantly higher sensitivity to the standard chemotherapeutic agents, i.e., doxorubicin (DOX) and cytarabine (Ara-C).	Cytarabine	176-181	arachidonate 5-lipoxygenase	Homo sapiens	32-37
28721010-0	2017	Antiglioma effects of cytarabine on leptomeningeal metastasis of high-grade glioma by targeting the PI3K/Akt/mTOR pathway.	Cytarabine	22-32	AKT serine/threonine kinase 1	Homo sapiens	105-108
28721010-0	2017	Antiglioma effects of cytarabine on leptomeningeal metastasis of high-grade glioma by targeting the PI3K/Akt/mTOR pathway.	Cytarabine	22-32	mechanistic target of rapamycin kinase	Homo sapiens	109-113
28721010-10	2017	The present study confirmed that cytarabine inhibits proliferation and promotes apoptosis of U87 cells, and molecular analysis of this effect showed that cytarabine significantly reduces expression of phosphatidylinositol 3-kinase/serine/threonine kinase also known as the protein kinase B/mechanistic target of rapamycin (PI3K/Akt/mTOR) pathway, Ki-67, BCL2, and 4-1BB, and upregulates Bax and cleaved caspase-3.	Cytarabine	154-164	mechanistic target of rapamycin kinase	Homo sapiens	290-321
28721010-10	2017	The present study confirmed that cytarabine inhibits proliferation and promotes apoptosis of U87 cells, and molecular analysis of this effect showed that cytarabine significantly reduces expression of phosphatidylinositol 3-kinase/serine/threonine kinase also known as the protein kinase B/mechanistic target of rapamycin (PI3K/Akt/mTOR) pathway, Ki-67, BCL2, and 4-1BB, and upregulates Bax and cleaved caspase-3.	Cytarabine	154-164	AKT serine/threonine kinase 1	Homo sapiens	328-331
28721010-10	2017	The present study confirmed that cytarabine inhibits proliferation and promotes apoptosis of U87 cells, and molecular analysis of this effect showed that cytarabine significantly reduces expression of phosphatidylinositol 3-kinase/serine/threonine kinase also known as the protein kinase B/mechanistic target of rapamycin (PI3K/Akt/mTOR) pathway, Ki-67, BCL2, and 4-1BB, and upregulates Bax and cleaved caspase-3.	Cytarabine	154-164	mechanistic target of rapamycin kinase	Homo sapiens	332-336
28721010-10	2017	The present study confirmed that cytarabine inhibits proliferation and promotes apoptosis of U87 cells, and molecular analysis of this effect showed that cytarabine significantly reduces expression of phosphatidylinositol 3-kinase/serine/threonine kinase also known as the protein kinase B/mechanistic target of rapamycin (PI3K/Akt/mTOR) pathway, Ki-67, BCL2, and 4-1BB, and upregulates Bax and cleaved caspase-3.	Cytarabine	154-164	BCL2 apoptosis regulator	Homo sapiens	354-358
28721010-10	2017	The present study confirmed that cytarabine inhibits proliferation and promotes apoptosis of U87 cells, and molecular analysis of this effect showed that cytarabine significantly reduces expression of phosphatidylinositol 3-kinase/serine/threonine kinase also known as the protein kinase B/mechanistic target of rapamycin (PI3K/Akt/mTOR) pathway, Ki-67, BCL2, and 4-1BB, and upregulates Bax and cleaved caspase-3.	Cytarabine	154-164	TNF receptor superfamily member 9	Homo sapiens	364-369
28721010-10	2017	The present study confirmed that cytarabine inhibits proliferation and promotes apoptosis of U87 cells, and molecular analysis of this effect showed that cytarabine significantly reduces expression of phosphatidylinositol 3-kinase/serine/threonine kinase also known as the protein kinase B/mechanistic target of rapamycin (PI3K/Akt/mTOR) pathway, Ki-67, BCL2, and 4-1BB, and upregulates Bax and cleaved caspase-3.	Cytarabine	154-164	BCL2 associated X, apoptosis regulator	Homo sapiens	387-390
28586337-0	2017	Corrigendum: SAMHD1 is a biomarker for cytarabine response and a therapeutic target in acute myeloid leukemia.	Cytarabine	39-49	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	13-19
28419965-7	2017	Our results support chidamide alone or combine with cytarabine may be used as an alternative therapeutic choice for AML patients especially those with FLT3-ITD mutation or relapsed/refractory ones.	Cytarabine	52-62	fms related receptor tyrosine kinase 3	Homo sapiens	151-155
28505160-7	2017	Treatment with brusatol, a pharmacological inhibitor of Nrf2, improved sensitivity to Ara-C, ATO, and Dnr and reduced colony formation capacity.	Cytarabine	86-91	NFE2 like bZIP transcription factor 2	Homo sapiens	56-60
28505160-8	2017	AML cell lines stably overexpressing NRF2 showed increased resistance to ATO, Dnr and Ara-C and increased expression of downstream targets.	Cytarabine	86-91	NFE2 like bZIP transcription factor 2	Homo sapiens	37-41
28791810-3	2017	OBJECTIVES: The aim of the present study was to assess the effect of PJ-34 (PARP-1 inhibitor) on the cytotoxicity of different antileukemic drugs with different DNA damaging mechanisms and potency (doxorubicin, etoposide, cytarabine and chlorambucil) in human leukemic Jurkat and HL-60 cells.	Cytarabine	222-232	poly(ADP-ribose) polymerase 1	Homo sapiens	76-82
28339008-6	2017	We found that SNAP25 altered the morphology and the chemotherapeutic effects of arabinofuranosyl cytidine (Ara-C) on SNAP25-expressing MB cells.	Cytarabine	107-112	synaptosome associated protein 25	Homo sapiens	14-20
28536338-8	2017	After we started intrathecal infusion of methotrexate and Ara-C, referring to case reports clinical symptoms, including unconsciousness, headache, and left upper limb paralysis, improved and the CEA level in cerebrospinal fluid decreased.	Cytarabine	58-63	CEA cell adhesion molecule 3	Homo sapiens	195-198
28339008-6	2017	We found that SNAP25 altered the morphology and the chemotherapeutic effects of arabinofuranosyl cytidine (Ara-C) on SNAP25-expressing MB cells.	Cytarabine	107-112	synaptosome associated protein 25	Homo sapiens	117-123
28339008-8	2017	The detection of SNAP25 expression in MB cells may thus be essential for the chemotherapeutic application of Ara-C.	Cytarabine	109-114	synaptosome associated protein 25	Homo sapiens	17-23
26552712-12	2017	Finally, ABT-737 synergistically enhanced the cytotoxic effect of cytarabine and daunorubicin in CD34+ AML cells.	Cytarabine	66-76	CD34 molecule	Homo sapiens	97-101
27833094-8	2017	Our study shows that development of cytarabine resistance is associated with increased sensitivity to glucocorticoids in a subset of AML, suggesting a new therapeutic strategy that should be explored in a clinical trial of chemorefractory AML patients carrying wild-type FLT3.	Cytarabine	36-46	fms related receptor tyrosine kinase 3	Homo sapiens	271-275
28209616-3	2017	Through transcriptomic profiling, we determined that low expression of the ergothioneine transporter OCTN1 (SLC22A4; ETT) strongly predicts poor event-free survival and overall survival in multiple cohorts of AML patients receiving treatment with the cytidine nucleoside analogue cytarabine.	Cytarabine	280-290	solute carrier family 22 member 4	Homo sapiens	101-106
28209616-3	2017	Through transcriptomic profiling, we determined that low expression of the ergothioneine transporter OCTN1 (SLC22A4; ETT) strongly predicts poor event-free survival and overall survival in multiple cohorts of AML patients receiving treatment with the cytidine nucleoside analogue cytarabine.	Cytarabine	280-290	solute carrier family 22 member 4	Homo sapiens	108-115
27833094-4	2017	Genomic profiling uncovered deletion of the deoxycytidine kinase (DCK) gene in both MOLM-13- and SHI-1-derived cytarabine-resistant variants and in an AML patient sample.	Cytarabine	111-121	deoxycytidine kinase	Homo sapiens	44-64
27833094-4	2017	Genomic profiling uncovered deletion of the deoxycytidine kinase (DCK) gene in both MOLM-13- and SHI-1-derived cytarabine-resistant variants and in an AML patient sample.	Cytarabine	111-121	deoxycytidine kinase	Homo sapiens	66-69
27903745-6	2017	AraC treatment completely prevented the increase in number of activated microglia in the ARC, the expression of the proinflammatory cytokine tumor necrosis factor-alpha in microglia, and the recruitment of the nuclear factor-kappaB pathway while restoring hypothalamic leptin sensitivity.	Cytarabine	0-4	tumor necrosis factor	Mus musculus	141-168
28107581-3	2017	Downregulation of E-cadherin with an siRNA suppressed the adhesion of leukemia cells to bone marrow-derived mesenchymal stem cells and enhanced the anti-leukemia effect of cytarabine.	Cytarabine	172-182	cadherin 1	Homo sapiens	18-28
28107581-7	2017	Notably, short hairpin RNA-mediated IL-10 downregulation impaired engraftment of human AML cells and enhanced the anti-leukemia effect of cytarabine in conjunction with miR-9 upregulation and E-cadherin downregulation in a human AML xenograft model.	Cytarabine	138-148	interleukin 10	Homo sapiens	36-41
28089908-5	2017	This approach also allowed us to study the properties of distinct AML subclones, including differential drug susceptibilities of KRAS mutant and wild-type cells, and predict relapse based on increased cytarabine resistance of a KRAS wild-type subclone.	Cytarabine	201-211	KRAS proto-oncogene, GTPase	Homo sapiens	228-232
28335578-3	2017	The metabolic results revealed that four nucleotides (ATP, ADP, CDP, and dCTP) could be used as potential biomarkers indicating the benefit of high-dose Ara-C over lower dose Ara-C treatment.	Cytarabine	153-158	cut up	Drosophila melanogaster	73-77
28335578-3	2017	The metabolic results revealed that four nucleotides (ATP, ADP, CDP, and dCTP) could be used as potential biomarkers indicating the benefit of high-dose Ara-C over lower dose Ara-C treatment.	Cytarabine	175-180	cut up	Drosophila melanogaster	73-77
28614773-3	2017	Cytosine arabinoside, 5-fluorouracil, and hydroxyurea showed strong cytotoxicity (IC50 &lt; 10 muM), whereas indomethacin and dexamethasone had weaker cytotoxic effects.	Cytarabine	0-20	latexin	Homo sapiens	95-98
27991919-0	2017	SAMHD1 is a biomarker for cytarabine response and a therapeutic target in acute myeloid leukemia.	Cytarabine	26-36	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	0-6
27699652-3	2017	Inhibition of cell proliferation by DNA synthesis inhibitor cytosine arabinoside completely canceled the IGF-1"s cell differentiation promotion, suggesting the possibility that IGF-1"s differentiation-promotion effect is an indirect effect via IGF-1"s cell proliferation promotion.	Cytarabine	60-80	insulin like growth factor 1 L homeolog	Xenopus laevis	105-110
27699652-3	2017	Inhibition of cell proliferation by DNA synthesis inhibitor cytosine arabinoside completely canceled the IGF-1"s cell differentiation promotion, suggesting the possibility that IGF-1"s differentiation-promotion effect is an indirect effect via IGF-1"s cell proliferation promotion.	Cytarabine	60-80	insulin like growth factor 1 L homeolog	Xenopus laevis	177-182
27699652-3	2017	Inhibition of cell proliferation by DNA synthesis inhibitor cytosine arabinoside completely canceled the IGF-1"s cell differentiation promotion, suggesting the possibility that IGF-1"s differentiation-promotion effect is an indirect effect via IGF-1"s cell proliferation promotion.	Cytarabine	60-80	insulin like growth factor 1 L homeolog	Xenopus laevis	177-182
27338091-5	2017	Finally, in contrast to depletion or inhibition of cyclin-dependent kinase 4, CCND1 depletion increased chemosensitivity of MCL cells to replication inhibitors hydroxyurea and cytarabine.	Cytarabine	176-186	cyclin D1	Homo sapiens	78-83
28401188-2	2017	We identified sterile alpha motif and HD domain-containing protein 1 (SAMHD1) as an ara-CTPase that protects cancer cells from cytarabine-induced toxicity.	Cytarabine	127-137	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	14-68
28401188-2	2017	We identified sterile alpha motif and HD domain-containing protein 1 (SAMHD1) as an ara-CTPase that protects cancer cells from cytarabine-induced toxicity.	Cytarabine	127-137	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	70-76
28401188-3	2017	Therefore, we propose targeting SAMHD1 as a strategy to potentiate cytarabine and possibly other antimetabolite-based therapies.	Cytarabine	67-77	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	32-38
28013106-1	2017	PURPOSE: Identify AML patients most likely to respond to CPX-351, a nano-scale liposome formulation containing cytarabine and daunorubicin co-encapsulated at a 5:1 molar ratio.	Cytarabine	111-121	T-box transcription factor 22	Homo sapiens	57-60
27748370-6	2017	Knockdown (KD) of DOCK2 by shRNA selectively reduced cell proliferation and colony formation in leukemia cell lines with increased FLT3 activity, and greatly sensitized these cells to cytarabine treatment, alone and in combination with FLT3 tyrosine kinase inhibitors.	Cytarabine	184-194	dedicator of cytokinesis 2	Homo sapiens	18-23
27991919-5	2017	Although it has been postulated that SAMHD1 sensitizes cancer cells to nucleoside-analog derivatives through the depletion of competing dNTPs, we show here that SAMHD1 reduces Ara-C cytotoxicity in AML cells.	Cytarabine	176-181	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	161-167
27991919-7	2017	Loss of SAMHD1 activity-through genetic depletion, mutational inactivation of its triphosphohydrolase activity or proteasomal degradation using specialized, virus-like particles-potentiates the cytotoxicity of Ara-C in AML cells.	Cytarabine	210-215	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	8-14
27991919-8	2017	In mouse models of retroviral AML transplantation, as well as in retrospective analyses of adult patients with AML, the response to Ara-C-containing therapy was inversely correlated with SAMHD1 expression.	Cytarabine	132-137	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	187-193
27991919-9	2017	These results identify SAMHD1 as a potential biomarker for the stratification of patients with AML who might best respond to Ara-C-based therapy and as a target for treating Ara-C-refractory AML.	Cytarabine	125-130	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	23-29
27991919-9	2017	These results identify SAMHD1 as a potential biomarker for the stratification of patients with AML who might best respond to Ara-C-based therapy and as a target for treating Ara-C-refractory AML.	Cytarabine	174-179	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	23-29
28030834-7	2017	We found that inhibition of both HDAC1 and HDAC2 was necessary to decrease the expression of BRCA1, CHK1, and RAD51, enhance cytarabine- or daunorubicin-induced DNA damage and apoptosis, and abrogate cytarabine- or daunorubicin-induced cell cycle checkpoint activation in AML cells.	Cytarabine	125-135	histone deacetylase 1	Homo sapiens	33-38
28067901-0	2017	Targeting SAMHD1 with the Vpx protein to improve cytarabine therapy for hematological malignancies.	Cytarabine	49-59	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	10-16
28067901-0	2017	Targeting SAMHD1 with the Vpx protein to improve cytarabine therapy for hematological malignancies.	Cytarabine	49-59	vpx protein	Simian immunodeficiency virus	26-29
28067901-6	2017	Recombinant SAMHD1 exhibited ara-CTPase activity in vitro, and cells in which SAMHD1 expression was transiently reduced by treatment with the simian immunodeficiency virus (SIV) protein Vpx were dramatically more sensitive to ara-C-induced cytotoxicity.	Cytarabine	29-34	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	12-18
28067901-7	2017	CRISPR-Cas9-mediated disruption of the gene encoding SAMHD1 sensitized cells to ara-C, and this sensitivity could be abrogated by ectopic expression of wild-type (WT), but not dNTPase-deficient, SAMHD1.	Cytarabine	80-85	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	53-59
28067901-8	2017	Mouse models of AML lacking SAMHD1 were hypersensitive to ara-C, and treatment ex vivo with Vpx sensitized primary patient-derived AML blasts to ara-C.	Cytarabine	145-150	vpx protein	Simian immunodeficiency virus	92-95
28067901-9	2017	Finally, we identified SAMHD1 as a risk factor in cohorts of both pediatric and adult patients with de novo AML who received ara-C treatment.	Cytarabine	125-130	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	23-29
28067901-10	2017	Thus, SAMHD1 expression levels dictate patient sensitivity to ara-C, providing proof-of-concept that the targeting of SAMHD1 by Vpx could be an attractive therapeutic strategy for potentiating ara-C efficacy in hematological malignancies.	Cytarabine	62-67	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	6-12
28067901-10	2017	Thus, SAMHD1 expression levels dictate patient sensitivity to ara-C, providing proof-of-concept that the targeting of SAMHD1 by Vpx could be an attractive therapeutic strategy for potentiating ara-C efficacy in hematological malignancies.	Cytarabine	62-67	vpx protein	Simian immunodeficiency virus	128-131
28067901-10	2017	Thus, SAMHD1 expression levels dictate patient sensitivity to ara-C, providing proof-of-concept that the targeting of SAMHD1 by Vpx could be an attractive therapeutic strategy for potentiating ara-C efficacy in hematological malignancies.	Cytarabine	193-198	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	118-124
28067901-10	2017	Thus, SAMHD1 expression levels dictate patient sensitivity to ara-C, providing proof-of-concept that the targeting of SAMHD1 by Vpx could be an attractive therapeutic strategy for potentiating ara-C efficacy in hematological malignancies.	Cytarabine	193-198	vpx protein	Simian immunodeficiency virus	128-131
27974700-5	2017	Cytarabine downregulated TNTs and inhibited NF-kappaB alone and in combination with daunorubicin, providing additional support for involvement of the NF-kappaB pathway in TNT formation.	Cytarabine	0-10	nuclear factor kappa B subunit 1	Homo sapiens	44-53
27974700-5	2017	Cytarabine downregulated TNTs and inhibited NF-kappaB alone and in combination with daunorubicin, providing additional support for involvement of the NF-kappaB pathway in TNT formation.	Cytarabine	0-10	nuclear factor kappa B subunit 1	Homo sapiens	150-159
28030834-7	2017	We found that inhibition of both HDAC1 and HDAC2 was necessary to decrease the expression of BRCA1, CHK1, and RAD51, enhance cytarabine- or daunorubicin-induced DNA damage and apoptosis, and abrogate cytarabine- or daunorubicin-induced cell cycle checkpoint activation in AML cells.	Cytarabine	125-135	histone deacetylase 2	Homo sapiens	43-48
28030834-7	2017	We found that inhibition of both HDAC1 and HDAC2 was necessary to decrease the expression of BRCA1, CHK1, and RAD51, enhance cytarabine- or daunorubicin-induced DNA damage and apoptosis, and abrogate cytarabine- or daunorubicin-induced cell cycle checkpoint activation in AML cells.	Cytarabine	200-210	histone deacetylase 1	Homo sapiens	33-38
28030834-7	2017	We found that inhibition of both HDAC1 and HDAC2 was necessary to decrease the expression of BRCA1, CHK1, and RAD51, enhance cytarabine- or daunorubicin-induced DNA damage and apoptosis, and abrogate cytarabine- or daunorubicin-induced cell cycle checkpoint activation in AML cells.	Cytarabine	200-210	histone deacetylase 2	Homo sapiens	43-48
28030834-7	2017	We found that inhibition of both HDAC1 and HDAC2 was necessary to decrease the expression of BRCA1, CHK1, and RAD51, enhance cytarabine- or daunorubicin-induced DNA damage and apoptosis, and abrogate cytarabine- or daunorubicin-induced cell cycle checkpoint activation in AML cells.	Cytarabine	200-210	BRCA1 DNA repair associated	Homo sapiens	93-98
28030834-7	2017	We found that inhibition of both HDAC1 and HDAC2 was necessary to decrease the expression of BRCA1, CHK1, and RAD51, enhance cytarabine- or daunorubicin-induced DNA damage and apoptosis, and abrogate cytarabine- or daunorubicin-induced cell cycle checkpoint activation in AML cells.	Cytarabine	200-210	checkpoint kinase 1	Homo sapiens	100-104
28030834-7	2017	We found that inhibition of both HDAC1 and HDAC2 was necessary to decrease the expression of BRCA1, CHK1, and RAD51, enhance cytarabine- or daunorubicin-induced DNA damage and apoptosis, and abrogate cytarabine- or daunorubicin-induced cell cycle checkpoint activation in AML cells.	Cytarabine	200-210	RAD51 recombinase	Homo sapiens	110-115
27906612-1	2016	The 5"-nucleotidase cN-II has been shown to be associated with the sensitivity to nucleoside analogues, the survival of cytarabine treated leukemia patients and to cell proliferation.	Cytarabine	120-130	5'-nucleotidase ecto	Homo sapiens	4-19
27941792-10	2017	Finally, patients with reduced EZH2 levels at progression to standard therapy responded to the combination of bortezomib and cytarabine, concomitant with the re-establishment of EZH2 expression and blast clearance.	Cytarabine	125-135	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	31-35
27863389-6	2016	Combining cytarabine with NT1721 also attenuated the cytarabine-induced FLT3 ligand surge that has been linked to resistance to tyrosine kinase inhibitors.	Cytarabine	10-20	fms related receptor tyrosine kinase 3	Homo sapiens	72-76
27863389-6	2016	Combining cytarabine with NT1721 also attenuated the cytarabine-induced FLT3 ligand surge that has been linked to resistance to tyrosine kinase inhibitors.	Cytarabine	53-63	fms related receptor tyrosine kinase 3	Homo sapiens	72-76
27888802-6	2016	Co-treatment with TPL and araC or ADM upregulated pro-apoptotic caspase-9 protein, inhibited checkpoint kinase 1 (Chk1) and 2 (Chk2) phosphorylation, and induced gammaH2A.X (a DNA damage marker).	Cytarabine	26-30	caspase 9	Homo sapiens	64-73
27888802-6	2016	Co-treatment with TPL and araC or ADM upregulated pro-apoptotic caspase-9 protein, inhibited checkpoint kinase 1 (Chk1) and 2 (Chk2) phosphorylation, and induced gammaH2A.X (a DNA damage marker).	Cytarabine	26-30	checkpoint kinase 1	Homo sapiens	93-112
27888802-6	2016	Co-treatment with TPL and araC or ADM upregulated pro-apoptotic caspase-9 protein, inhibited checkpoint kinase 1 (Chk1) and 2 (Chk2) phosphorylation, and induced gammaH2A.X (a DNA damage marker).	Cytarabine	26-30	checkpoint kinase 1	Homo sapiens	114-118
27888802-6	2016	Co-treatment with TPL and araC or ADM upregulated pro-apoptotic caspase-9 protein, inhibited checkpoint kinase 1 (Chk1) and 2 (Chk2) phosphorylation, and induced gammaH2A.X (a DNA damage marker).	Cytarabine	26-30	checkpoint kinase 2	Homo sapiens	127-131
27906612-1	2016	The 5"-nucleotidase cN-II has been shown to be associated with the sensitivity to nucleoside analogues, the survival of cytarabine treated leukemia patients and to cell proliferation.	Cytarabine	120-130	5'-nucleotidase, cytosolic II	Homo sapiens	20-25
27160178-1	2016	Human cytidine deaminase (hCDA) is a biomedically important enzyme able to inactivate cytidine nucleoside analogs such as the antileukemic agent cytosine arabinoside (AraC) and thereby limit antineoplastic efficacy.	Cytarabine	145-165	cytidine deaminase	Homo sapiens	6-24
27160178-1	2016	Human cytidine deaminase (hCDA) is a biomedically important enzyme able to inactivate cytidine nucleoside analogs such as the antileukemic agent cytosine arabinoside (AraC) and thereby limit antineoplastic efficacy.	Cytarabine	145-165	cytidine deaminase	Homo sapiens	26-30
27160178-1	2016	Human cytidine deaminase (hCDA) is a biomedically important enzyme able to inactivate cytidine nucleoside analogs such as the antileukemic agent cytosine arabinoside (AraC) and thereby limit antineoplastic efficacy.	Cytarabine	167-171	cytidine deaminase	Homo sapiens	6-24
27160178-1	2016	Human cytidine deaminase (hCDA) is a biomedically important enzyme able to inactivate cytidine nucleoside analogs such as the antileukemic agent cytosine arabinoside (AraC) and thereby limit antineoplastic efficacy.	Cytarabine	167-171	cytidine deaminase	Homo sapiens	26-30
27160178-2	2016	Potent inhibitors of hCDA have been developed, e.g. zebularine, that when administered in combination with AraC enhance antineoplastic activity.	Cytarabine	107-111	cytidine deaminase	Homo sapiens	21-25
27160178-3	2016	Tandem hematopoietic stem cell (HSC) transplantation and combination chemotherapy (zebularine and AraC) could exhibit robust antineoplastic potency, but AraC-based chemotherapy regimens lead to pronounced myelosuppression due to relatively low hCDA activity in HSCs, and this approach could exacerbate this effect.	Cytarabine	153-157	cytidine deaminase	Homo sapiens	244-248
27994664-9	2016	In addition, restoration of NF-kappaB activity via TNF-alpha stimulation could attenuate the effect of NPM1mA overexpression on DNR-and Ara-C-induced apoptosis.	Cytarabine	136-141	nuclear factor kappa B subunit 1	Homo sapiens	28-37
27994664-9	2016	In addition, restoration of NF-kappaB activity via TNF-alpha stimulation could attenuate the effect of NPM1mA overexpression on DNR-and Ara-C-induced apoptosis.	Cytarabine	136-141	tumor necrosis factor	Homo sapiens	51-60
27994664-10	2016	Interestingly, expression of NPM1mA could upregulate Bax and downregulate Bcl-2 at mRNA and protein levels in THP-1 cells when treated with DNR or Ara-C.	Cytarabine	147-152	nucleophosmin 1	Homo sapiens	29-33
26917050-1	2016	The combination of mitoxantrone (MIT), etoposide (ETP), and cytarabine (Ara-C) (MEC) is a frequently used salvage therapy for acute leukemia, but has been associated with severe myelosuppression.	Cytarabine	60-70	C-C motif chemokine ligand 28	Homo sapiens	80-83
27603731-3	2016	Ara-C treatment increased neurite fragmentation and neuronal cell death in DRG explants and activated caspase-3 by cleaving it, which could induce apoptosis.	Cytarabine	0-5	caspase 3	Homo sapiens	102-111
27603731-6	2016	It was suggested that the neuroprotective effect of electrical stimulation is likely mediated by the inhibition of caspase-3 activation and therefore the inhibition of apoptosis following ara-C treatment.	Cytarabine	188-193	caspase 3	Homo sapiens	115-124
27709797-0	2016	Homoharringtonine combined with aclarubicin and cytarabine synergistically induces apoptosis in t(8;21) leukemia cells and triggers caspase-3-mediated cleavage of the AML1-ETO oncoprotein.	Cytarabine	48-58	caspase 3	Homo sapiens	132-141
27709797-0	2016	Homoharringtonine combined with aclarubicin and cytarabine synergistically induces apoptosis in t(8;21) leukemia cells and triggers caspase-3-mediated cleavage of the AML1-ETO oncoprotein.	Cytarabine	48-58	RUNX family transcription factor 1	Homo sapiens	167-171
27709797-0	2016	Homoharringtonine combined with aclarubicin and cytarabine synergistically induces apoptosis in t(8;21) leukemia cells and triggers caspase-3-mediated cleavage of the AML1-ETO oncoprotein.	Cytarabine	48-58	RUNX1 partner transcriptional co-repressor 1	Homo sapiens	172-175
26319201-6	2016	AraC-induced cell death, measured by annexin V/propidium iodide, was significantly (p&lt;0.01) increased by the 1-D2/CA combination in both cell lines, but not by 1-D2 or CA alone.	Cytarabine	0-4	annexin A5	Mus musculus	37-46
26917050-1	2016	The combination of mitoxantrone (MIT), etoposide (ETP), and cytarabine (Ara-C) (MEC) is a frequently used salvage therapy for acute leukemia, but has been associated with severe myelosuppression.	Cytarabine	72-77	C-C motif chemokine ligand 28	Homo sapiens	80-83
27801323-7	2016	Cox regression multifactor analysis showed genetics risk groups was the only risk factor for DFS(HR=0.258, 95% CI 0.100- 0.664, P=0.005), while genetics risk groups(HR=0.309, 95% CI 0.126- 0.756, P=0.010)and whether patients received more than one cycle of high dose of Ara-C as consolidation therapy(HR= 0.370, 95% CI 0.179- 0.765, P=0.007)were independent factors associated with OS.	Cytarabine	270-275	cytochrome c oxidase subunit 8A	Homo sapiens	0-3
27807322-8	2016	:  Results: Compared with the control group, the cell activity was significantly decreased and the level of serum HMGB1 was significantly increased in the chemotherapeutic (VCR, VP-16, Ara-C, ADM and As2O3) groups (all P&lt;0.05).	Cytarabine	185-190	high mobility group box 1	Homo sapiens	114-119
27980750-0	2016	All-trans retinoic acid (ATRA) in non-promyelocytic acute myeloid leukemia (AML): results of combination of ATRA with low-dose Ara-C in three elderly patients with NPM1-mutated AML unfit for intensive chemotherapy and review of the literature.	Cytarabine	127-132	nucleophosmin 1	Homo sapiens	164-168
27980750-1	2016	Based upon the clinical behavior of three patients, we suggest that the combination of low-dose Ara-C and all-trans retinoic acid may potentially be effective in some elderly patients, unfit for intensive chemotherapy, affected with NPM1-mutated acute myeloid leukemia without FLT3 mutations, warranting perspective clinical studies in these selected patients.	Cytarabine	96-101	nucleophosmin 1	Homo sapiens	233-237
27980750-1	2016	Based upon the clinical behavior of three patients, we suggest that the combination of low-dose Ara-C and all-trans retinoic acid may potentially be effective in some elderly patients, unfit for intensive chemotherapy, affected with NPM1-mutated acute myeloid leukemia without FLT3 mutations, warranting perspective clinical studies in these selected patients.	Cytarabine	96-101	fms related receptor tyrosine kinase 3	Homo sapiens	277-281
27762588-4	2016	The enzymatic release of cytarabine from the conjugate containing a GFLG spacer utilizing cathepsin B was verified.	Cytarabine	25-35	cathepsin B	Homo sapiens	90-101
27625304-5	2016	High abundance of CHK1 in AML patient cells correlated with higher clonogenic ability and more efficient DNA replication fork progression upon cytarabine treatment.	Cytarabine	143-153	checkpoint kinase 1	Homo sapiens	18-22
27556692-3	2016	We initially tested the potential of the highly specific Chk1 inhibitor SCH900776 to synergize with nucleoside analogs (NAs) fludarabine, cytarabine and gemcitabine in cell lines derived from B-cell malignancies.	Cytarabine	138-148	checkpoint kinase 1	Mus musculus	57-61
27622612-2	2016	We have previously demonstrated that a 22-mer peptide derived from fibronectin, FNIII14, can inhibit cell adhesion through the inactivation of beta1 integrin; when coadministered with cytarabine, FNIII14 completely eradicates acute myelogenous leukemia by suppressing CAM-DR.	Cytarabine	184-194	fibronectin 1	Homo sapiens	67-78
27625304-6	2016	Exposing the patient cells with the high abundance of CHK1 to SCH900776, an inhibitor of the kinase activity of CHK1, reduced clonogenic ability and progression of DNA replication in the presence of cytarabine.	Cytarabine	199-209	checkpoint kinase 1	Homo sapiens	54-58
27625304-6	2016	Exposing the patient cells with the high abundance of CHK1 to SCH900776, an inhibitor of the kinase activity of CHK1, reduced clonogenic ability and progression of DNA replication in the presence of cytarabine.	Cytarabine	199-209	checkpoint kinase 1	Homo sapiens	112-116
27625304-7	2016	These results indicated that some AML cells rely on an efficient CHK1-mediated replication stress response for viability and that therapeutic strategies that inhibit CHK1 could extend current cytarabine-based treatments and overcome drug resistance.	Cytarabine	192-202	checkpoint kinase 1	Homo sapiens	166-170
27432881-2	2016	BCR-ABL tyrosine kinase inhibitors (TKIs) imatinib and dasatinib inhibit fludarabine and cytarabine uptake.	Cytarabine	89-99	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
27377011-2	2016	Bile acid transporters are highly expressed both in enterocytes and hepatocytes and to increase the oral bioavailability and investigate the potential application of cytarabine for liver cancers, a transporter- recognizing prodrug strategy was applied to design and synthesize four conjugates of cytarabine with cholic acid (CA), chenodeoxycholic acid (CDCA), hyodeoxycholic acid (HDCA) and ursodeoxycholic acid (UDCA).	Cytarabine	166-176	UDP glucuronosyltransferase family 2 member B4	Homo sapiens	360-379
27611922-4	2016	Indeed, LSCs are highly enriched in CD34+CD38- leukemic cells that exhibit positive aldehyde dehydrogenase activity (ALDH+) on flow cytometry, these LSCs are resistant to currently existing treatments in AML such as cytarabine and anthracycline that, at the cost of great toxicity on normal cells, are highly active against the leukemic bulk, but spare the LSCs responsible for relapse.	Cytarabine	216-226	CD34 molecule	Homo sapiens	36-40
27611922-4	2016	Indeed, LSCs are highly enriched in CD34+CD38- leukemic cells that exhibit positive aldehyde dehydrogenase activity (ALDH+) on flow cytometry, these LSCs are resistant to currently existing treatments in AML such as cytarabine and anthracycline that, at the cost of great toxicity on normal cells, are highly active against the leukemic bulk, but spare the LSCs responsible for relapse.	Cytarabine	216-226	CD38 molecule	Homo sapiens	41-45
27422302-1	2016	PURPOSE: The solute carrier family 29 (equilibrative nucleoside transporter), member 1 (SLC29A1) is known to be involved in the transportation and resistance of the nucleoside analog cytosine arabinoside (AraC), one of the most effective drugs in the treatment of acute myeloid leukemia (AML).	Cytarabine	183-203	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	88-95
27268264-3	2016	Knockdown of Atg7 in AML cells using short hairpin RNA markedly increased apoptosis and DNA damage following treatment with cytarabine and idarubicin.	Cytarabine	124-134	autophagy related 7	Homo sapiens	13-17
27422302-1	2016	PURPOSE: The solute carrier family 29 (equilibrative nucleoside transporter), member 1 (SLC29A1) is known to be involved in the transportation and resistance of the nucleoside analog cytosine arabinoside (AraC), one of the most effective drugs in the treatment of acute myeloid leukemia (AML).	Cytarabine	205-209	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	88-95
26613208-0	2016	Deoxycytidine kinase is downregulated under hypoxic conditions and confers resistance against cytarabine in acute myeloid leukaemia.	Cytarabine	94-104	deoxycytidine kinase	Homo sapiens	0-20
27103402-0	2016	Binding of Released Bim to Mcl-1 is a Mechanism of Intrinsic Resistance to ABT-199 which can be Overcome by Combination with Daunorubicin or Cytarabine in AML Cells.	Cytarabine	141-151	BCL2 like 11	Homo sapiens	20-23
27103402-0	2016	Binding of Released Bim to Mcl-1 is a Mechanism of Intrinsic Resistance to ABT-199 which can be Overcome by Combination with Daunorubicin or Cytarabine in AML Cells.	Cytarabine	141-151	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	27-32
26613208-7	2016	CONCLUSIONS: In conclusion, our data reveal that hypoxia-induced downregulation of deoxycytidine kinase represents one stroma-cell-independent mechanism of drug resistance to cytarabine in acute myeloid leukaemia.	Cytarabine	175-185	deoxycytidine kinase	Homo sapiens	83-103
27548009-1	2016	AIM: DCK is a rate-limiting enzyme in cytarabine activation.	Cytarabine	38-48	deoxycytidine kinase	Homo sapiens	5-8
27103402-8	2016	Combining conventional chemotherapeutic agent cytarabine or daunorubicin with ABT-199 resulted in increased DNA damage along with decreased Mcl-1 protein levels, compared with ABT-199 alone, and synergistic induction of cell death in both AML cell lines and primary patient samples obtained from AML patients at diagnosis.	Cytarabine	46-56	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	140-145
27103402-9	2016	CONCLUSIONS: Our results demonstrate that sequestration of Bim by Mcl-1 is a mechanism of intrinsic ABT-199 resistance and supports the clinical development of ABT-199 in combination with cytarabine or daunorubicin for the treatment of AML.	Cytarabine	188-198	BCL2 like 11	Homo sapiens	59-62
27103402-9	2016	CONCLUSIONS: Our results demonstrate that sequestration of Bim by Mcl-1 is a mechanism of intrinsic ABT-199 resistance and supports the clinical development of ABT-199 in combination with cytarabine or daunorubicin for the treatment of AML.	Cytarabine	188-198	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	66-71
27342972-3	2016	We found that INPP4B-mediated resistance to genotoxic drug, cytarabine, was accompanied by lower p-H2AX accumulation in KG-1 cells, and INPP4B knockdown evidently sensitized KG-1 cells to cytarabine, meanwhile, p-H2AX expression was increased dramatically.	Cytarabine	60-70	inositol polyphosphate-4-phosphatase type II B	Homo sapiens	14-20
27342972-3	2016	We found that INPP4B-mediated resistance to genotoxic drug, cytarabine, was accompanied by lower p-H2AX accumulation in KG-1 cells, and INPP4B knockdown evidently sensitized KG-1 cells to cytarabine, meanwhile, p-H2AX expression was increased dramatically.	Cytarabine	60-70	H2A.X variant histone	Homo sapiens	99-103
27342972-3	2016	We found that INPP4B-mediated resistance to genotoxic drug, cytarabine, was accompanied by lower p-H2AX accumulation in KG-1 cells, and INPP4B knockdown evidently sensitized KG-1 cells to cytarabine, meanwhile, p-H2AX expression was increased dramatically.	Cytarabine	60-70	H2A.X variant histone	Homo sapiens	213-217
27342972-3	2016	We found that INPP4B-mediated resistance to genotoxic drug, cytarabine, was accompanied by lower p-H2AX accumulation in KG-1 cells, and INPP4B knockdown evidently sensitized KG-1 cells to cytarabine, meanwhile, p-H2AX expression was increased dramatically.	Cytarabine	188-198	inositol polyphosphate-4-phosphatase type II B	Homo sapiens	14-20
27342972-4	2016	Then, we observed that INPP4B knockdown inhibited the loss of p-H2AX expression after cytarabine removal in INPP4B-silenced KG-1 cells, whereas, in control KG-1 cells, the expression of p-H2AX was reduced in a time-dependent manner.	Cytarabine	86-96	inositol polyphosphate-4-phosphatase type II B	Homo sapiens	23-29
27342972-4	2016	Then, we observed that INPP4B knockdown inhibited the loss of p-H2AX expression after cytarabine removal in INPP4B-silenced KG-1 cells, whereas, in control KG-1 cells, the expression of p-H2AX was reduced in a time-dependent manner.	Cytarabine	86-96	H2A.X variant histone	Homo sapiens	64-68
27342972-4	2016	Then, we observed that INPP4B knockdown inhibited the loss of p-H2AX expression after cytarabine removal in INPP4B-silenced KG-1 cells, whereas, in control KG-1 cells, the expression of p-H2AX was reduced in a time-dependent manner.	Cytarabine	86-96	inositol polyphosphate-4-phosphatase type II B	Homo sapiens	108-114
27342972-7	2016	Finally, INPP4B expression was positively correlated with ATM expression in AML cells, both INPP4B knockdown and KU55933 can significantly sensitize primary myeloid leukemic cells to cytarabine treatment.Collectively, these data suggest that enhanced ATM-dependent DNA repair is involved in resistance to chemotherapy in INPP4Bhigh AML, which could be mediated by p65 nuclear translocation, combination chemotherapy with INPP4B or DNA repair pathway inhibition represents a promising strategy in INPP4Bhigh AML.	Cytarabine	183-193	inositol polyphosphate-4-phosphatase type II B	Homo sapiens	9-15
27342972-7	2016	Finally, INPP4B expression was positively correlated with ATM expression in AML cells, both INPP4B knockdown and KU55933 can significantly sensitize primary myeloid leukemic cells to cytarabine treatment.Collectively, these data suggest that enhanced ATM-dependent DNA repair is involved in resistance to chemotherapy in INPP4Bhigh AML, which could be mediated by p65 nuclear translocation, combination chemotherapy with INPP4B or DNA repair pathway inhibition represents a promising strategy in INPP4Bhigh AML.	Cytarabine	183-193	inositol polyphosphate-4-phosphatase type II B	Homo sapiens	92-98
27342972-7	2016	Finally, INPP4B expression was positively correlated with ATM expression in AML cells, both INPP4B knockdown and KU55933 can significantly sensitize primary myeloid leukemic cells to cytarabine treatment.Collectively, these data suggest that enhanced ATM-dependent DNA repair is involved in resistance to chemotherapy in INPP4Bhigh AML, which could be mediated by p65 nuclear translocation, combination chemotherapy with INPP4B or DNA repair pathway inhibition represents a promising strategy in INPP4Bhigh AML.	Cytarabine	183-193	ATM serine/threonine kinase	Homo sapiens	251-254
27342972-7	2016	Finally, INPP4B expression was positively correlated with ATM expression in AML cells, both INPP4B knockdown and KU55933 can significantly sensitize primary myeloid leukemic cells to cytarabine treatment.Collectively, these data suggest that enhanced ATM-dependent DNA repair is involved in resistance to chemotherapy in INPP4Bhigh AML, which could be mediated by p65 nuclear translocation, combination chemotherapy with INPP4B or DNA repair pathway inhibition represents a promising strategy in INPP4Bhigh AML.	Cytarabine	183-193	inositol polyphosphate-4-phosphatase type I A	Homo sapiens	9-14
27342972-7	2016	Finally, INPP4B expression was positively correlated with ATM expression in AML cells, both INPP4B knockdown and KU55933 can significantly sensitize primary myeloid leukemic cells to cytarabine treatment.Collectively, these data suggest that enhanced ATM-dependent DNA repair is involved in resistance to chemotherapy in INPP4Bhigh AML, which could be mediated by p65 nuclear translocation, combination chemotherapy with INPP4B or DNA repair pathway inhibition represents a promising strategy in INPP4Bhigh AML.	Cytarabine	183-193	RELA proto-oncogene, NF-kB subunit	Homo sapiens	364-367
27342972-7	2016	Finally, INPP4B expression was positively correlated with ATM expression in AML cells, both INPP4B knockdown and KU55933 can significantly sensitize primary myeloid leukemic cells to cytarabine treatment.Collectively, these data suggest that enhanced ATM-dependent DNA repair is involved in resistance to chemotherapy in INPP4Bhigh AML, which could be mediated by p65 nuclear translocation, combination chemotherapy with INPP4B or DNA repair pathway inhibition represents a promising strategy in INPP4Bhigh AML.	Cytarabine	183-193	inositol polyphosphate-4-phosphatase type II B	Homo sapiens	92-98
27342972-7	2016	Finally, INPP4B expression was positively correlated with ATM expression in AML cells, both INPP4B knockdown and KU55933 can significantly sensitize primary myeloid leukemic cells to cytarabine treatment.Collectively, these data suggest that enhanced ATM-dependent DNA repair is involved in resistance to chemotherapy in INPP4Bhigh AML, which could be mediated by p65 nuclear translocation, combination chemotherapy with INPP4B or DNA repair pathway inhibition represents a promising strategy in INPP4Bhigh AML.	Cytarabine	183-193	inositol polyphosphate-4-phosphatase type I A	Homo sapiens	92-97
27391351-0	2016	FLT3 is implicated in cytarabine transport by human equilibrative nucleoside transporter 1 in pediatric acute leukemia.	Cytarabine	22-32	fms related receptor tyrosine kinase 3	Homo sapiens	0-4
27391351-3	2016	Cytarabine is transported into cells by Human Equilibrative Nucleoside Transporter-1 (hENT1, SLC29A1), but the mechanisms that regulate hENT1 in acute leukemia have been scarcely studied.We explored the expression and functional link between FLT3 and main cytarabine transporters in 50 pediatric patients diagnosed with acute lymphoblastic leukemia and MLL rearrangement (ALL-MLL+) and other subtypes of leukemia, and in leukemia cell lines.A significant positive correlation was found between FLT3 and hENT1 expression in patients.	Cytarabine	0-10	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	46-84
27462781-0	2016	Inhibition of Mnk enhances apoptotic activity of cytarabine in acute myeloid leukemia cells.	Cytarabine	49-59	ATPase copper transporting alpha	Homo sapiens	14-17
27462781-4	2016	In this study, we showed a strong synergistic effect of Ara-C with either our Mnk inhibitor (MNKI-8e) or short hairpin RNA (shRNA) mediated knockdown of Mnks in MV4-11 AML cells.	Cytarabine	56-61	ATPase copper transporting alpha	Homo sapiens	78-81
27462781-6	2016	We showed that both MNKI-8e and Mnk shRNAs enhanced the ability of Ara-C to induce apoptosis.	Cytarabine	67-72	ATPase copper transporting alpha	Homo sapiens	32-35
27462781-7	2016	We found that Ara-C increased the phosphorylation of Erk1/2, p38 and eIF4E, which correlated with an enhanced level of anti-apoptotic Mcl-1 protein.	Cytarabine	14-19	mitogen-activated protein kinase 3	Homo sapiens	53-59
27462781-7	2016	We found that Ara-C increased the phosphorylation of Erk1/2, p38 and eIF4E, which correlated with an enhanced level of anti-apoptotic Mcl-1 protein.	Cytarabine	14-19	mitogen-activated protein kinase 1	Homo sapiens	61-64
27462781-7	2016	We found that Ara-C increased the phosphorylation of Erk1/2, p38 and eIF4E, which correlated with an enhanced level of anti-apoptotic Mcl-1 protein.	Cytarabine	14-19	eukaryotic translation initiation factor 4E	Homo sapiens	69-74
27462781-7	2016	We found that Ara-C increased the phosphorylation of Erk1/2, p38 and eIF4E, which correlated with an enhanced level of anti-apoptotic Mcl-1 protein.	Cytarabine	14-19	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	134-139
27462781-8	2016	Inhibition of Mnk activity suppressed the Ara-C-induced MAPK activity, and thus enhanced apoptosis in MV4-11 cells.	Cytarabine	42-47	ATPase copper transporting alpha	Homo sapiens	14-17
27462781-9	2016	Taken together, our study suggests that MAPK-Mnk-eIF4E pathway plays a critical role in Ara-C-treated MV4-11 cells and targeting Mnk may be a promising therapeutic strategy for sensitizing leukemic cells to Ara-C therapy.	Cytarabine	88-93	ATPase copper transporting alpha	Homo sapiens	45-48
27462781-9	2016	Taken together, our study suggests that MAPK-Mnk-eIF4E pathway plays a critical role in Ara-C-treated MV4-11 cells and targeting Mnk may be a promising therapeutic strategy for sensitizing leukemic cells to Ara-C therapy.	Cytarabine	88-93	eukaryotic translation initiation factor 4E	Homo sapiens	49-54
27462781-9	2016	Taken together, our study suggests that MAPK-Mnk-eIF4E pathway plays a critical role in Ara-C-treated MV4-11 cells and targeting Mnk may be a promising therapeutic strategy for sensitizing leukemic cells to Ara-C therapy.	Cytarabine	207-212	eukaryotic translation initiation factor 4E	Homo sapiens	49-54
27462781-9	2016	Taken together, our study suggests that MAPK-Mnk-eIF4E pathway plays a critical role in Ara-C-treated MV4-11 cells and targeting Mnk may be a promising therapeutic strategy for sensitizing leukemic cells to Ara-C therapy.	Cytarabine	207-212	ATPase copper transporting alpha	Homo sapiens	129-132
27391351-3	2016	Cytarabine is transported into cells by Human Equilibrative Nucleoside Transporter-1 (hENT1, SLC29A1), but the mechanisms that regulate hENT1 in acute leukemia have been scarcely studied.We explored the expression and functional link between FLT3 and main cytarabine transporters in 50 pediatric patients diagnosed with acute lymphoblastic leukemia and MLL rearrangement (ALL-MLL+) and other subtypes of leukemia, and in leukemia cell lines.A significant positive correlation was found between FLT3 and hENT1 expression in patients.	Cytarabine	0-10	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	86-91
27391351-3	2016	Cytarabine is transported into cells by Human Equilibrative Nucleoside Transporter-1 (hENT1, SLC29A1), but the mechanisms that regulate hENT1 in acute leukemia have been scarcely studied.We explored the expression and functional link between FLT3 and main cytarabine transporters in 50 pediatric patients diagnosed with acute lymphoblastic leukemia and MLL rearrangement (ALL-MLL+) and other subtypes of leukemia, and in leukemia cell lines.A significant positive correlation was found between FLT3 and hENT1 expression in patients.	Cytarabine	0-10	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	93-100
27391351-3	2016	Cytarabine is transported into cells by Human Equilibrative Nucleoside Transporter-1 (hENT1, SLC29A1), but the mechanisms that regulate hENT1 in acute leukemia have been scarcely studied.We explored the expression and functional link between FLT3 and main cytarabine transporters in 50 pediatric patients diagnosed with acute lymphoblastic leukemia and MLL rearrangement (ALL-MLL+) and other subtypes of leukemia, and in leukemia cell lines.A significant positive correlation was found between FLT3 and hENT1 expression in patients.	Cytarabine	0-10	fms related receptor tyrosine kinase 3	Homo sapiens	242-246
27391351-3	2016	Cytarabine is transported into cells by Human Equilibrative Nucleoside Transporter-1 (hENT1, SLC29A1), but the mechanisms that regulate hENT1 in acute leukemia have been scarcely studied.We explored the expression and functional link between FLT3 and main cytarabine transporters in 50 pediatric patients diagnosed with acute lymphoblastic leukemia and MLL rearrangement (ALL-MLL+) and other subtypes of leukemia, and in leukemia cell lines.A significant positive correlation was found between FLT3 and hENT1 expression in patients.	Cytarabine	0-10	lysine methyltransferase 2A	Homo sapiens	353-356
27391351-3	2016	Cytarabine is transported into cells by Human Equilibrative Nucleoside Transporter-1 (hENT1, SLC29A1), but the mechanisms that regulate hENT1 in acute leukemia have been scarcely studied.We explored the expression and functional link between FLT3 and main cytarabine transporters in 50 pediatric patients diagnosed with acute lymphoblastic leukemia and MLL rearrangement (ALL-MLL+) and other subtypes of leukemia, and in leukemia cell lines.A significant positive correlation was found between FLT3 and hENT1 expression in patients.	Cytarabine	0-10	lysine methyltransferase 2A	Homo sapiens	376-379
27391351-3	2016	Cytarabine is transported into cells by Human Equilibrative Nucleoside Transporter-1 (hENT1, SLC29A1), but the mechanisms that regulate hENT1 in acute leukemia have been scarcely studied.We explored the expression and functional link between FLT3 and main cytarabine transporters in 50 pediatric patients diagnosed with acute lymphoblastic leukemia and MLL rearrangement (ALL-MLL+) and other subtypes of leukemia, and in leukemia cell lines.A significant positive correlation was found between FLT3 and hENT1 expression in patients.	Cytarabine	0-10	fms related receptor tyrosine kinase 3	Homo sapiens	494-498
27349195-0	2016	Haematological cancer: Cytarabine - new standard of care for MCL.	Cytarabine	23-33	C-type lectin domain family 4 member D	Homo sapiens	61-64
27391351-4	2016	Cytarabine uptake into cells was mediated mainly by hENT1, hENT2 and hCNT1.	Cytarabine	0-10	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	52-57
27391351-4	2016	Cytarabine uptake into cells was mediated mainly by hENT1, hENT2 and hCNT1.	Cytarabine	0-10	solute carrier family 29 member 2	Homo sapiens	59-64
27391351-4	2016	Cytarabine uptake into cells was mediated mainly by hENT1, hENT2 and hCNT1.	Cytarabine	0-10	solute carrier family 28 member 1	Homo sapiens	69-74
27391351-5	2016	hENT1-mediated uptake of cytarabine was transiently abolished by the FLT3 inhibitor PKC412, and this effect was associated with decreased hENT1 mRNA and protein levels.	Cytarabine	25-35	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	0-5
27391351-5	2016	hENT1-mediated uptake of cytarabine was transiently abolished by the FLT3 inhibitor PKC412, and this effect was associated with decreased hENT1 mRNA and protein levels.	Cytarabine	25-35	fms related receptor tyrosine kinase 3	Homo sapiens	69-73
27391351-6	2016	Noticeably, the cytotoxicity of cytarabine was lower when cells were first exposed to FLT3 inhibitors (PKC412 or AC220), probably due to decreased hENT1 activity, but we observed a higher cytotoxic effect if FLT3 inhibitors were administered after cytarabine.FLT3 regulates hENT1 activity and thereby affects cytarabine cytotoxicity.	Cytarabine	32-42	fms related receptor tyrosine kinase 3	Homo sapiens	86-90
27391351-6	2016	Noticeably, the cytotoxicity of cytarabine was lower when cells were first exposed to FLT3 inhibitors (PKC412 or AC220), probably due to decreased hENT1 activity, but we observed a higher cytotoxic effect if FLT3 inhibitors were administered after cytarabine.FLT3 regulates hENT1 activity and thereby affects cytarabine cytotoxicity.	Cytarabine	32-42	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	147-152
27391351-6	2016	Noticeably, the cytotoxicity of cytarabine was lower when cells were first exposed to FLT3 inhibitors (PKC412 or AC220), probably due to decreased hENT1 activity, but we observed a higher cytotoxic effect if FLT3 inhibitors were administered after cytarabine.FLT3 regulates hENT1 activity and thereby affects cytarabine cytotoxicity.	Cytarabine	32-42	fms related receptor tyrosine kinase 3	Homo sapiens	208-212
27391351-6	2016	Noticeably, the cytotoxicity of cytarabine was lower when cells were first exposed to FLT3 inhibitors (PKC412 or AC220), probably due to decreased hENT1 activity, but we observed a higher cytotoxic effect if FLT3 inhibitors were administered after cytarabine.FLT3 regulates hENT1 activity and thereby affects cytarabine cytotoxicity.	Cytarabine	32-42	fms related receptor tyrosine kinase 3	Homo sapiens	208-212
27391351-6	2016	Noticeably, the cytotoxicity of cytarabine was lower when cells were first exposed to FLT3 inhibitors (PKC412 or AC220), probably due to decreased hENT1 activity, but we observed a higher cytotoxic effect if FLT3 inhibitors were administered after cytarabine.FLT3 regulates hENT1 activity and thereby affects cytarabine cytotoxicity.	Cytarabine	32-42	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	274-279
27391351-6	2016	Noticeably, the cytotoxicity of cytarabine was lower when cells were first exposed to FLT3 inhibitors (PKC412 or AC220), probably due to decreased hENT1 activity, but we observed a higher cytotoxic effect if FLT3 inhibitors were administered after cytarabine.FLT3 regulates hENT1 activity and thereby affects cytarabine cytotoxicity.	Cytarabine	248-258	fms related receptor tyrosine kinase 3	Homo sapiens	86-90
27391351-6	2016	Noticeably, the cytotoxicity of cytarabine was lower when cells were first exposed to FLT3 inhibitors (PKC412 or AC220), probably due to decreased hENT1 activity, but we observed a higher cytotoxic effect if FLT3 inhibitors were administered after cytarabine.FLT3 regulates hENT1 activity and thereby affects cytarabine cytotoxicity.	Cytarabine	248-258	fms related receptor tyrosine kinase 3	Homo sapiens	86-90
27481339-9	2016	Leukemia cell density was increased, especially in the endosteal region in FGF2/Ara-C -treated mice compared to mice treated with Ara-C only.	Cytarabine	80-85	fibroblast growth factor 2	Mus musculus	75-79
27481339-9	2016	Leukemia cell density was increased, especially in the endosteal region in FGF2/Ara-C -treated mice compared to mice treated with Ara-C only.	Cytarabine	130-135	fibroblast growth factor 2	Mus musculus	75-79
27387666-5	2016	The loss of p21 expression enhanced growth factor-independent proliferation and sensitivity to cytarabine as a consequence of concomitantly enriching the S+G2/M phase population and significantly increasing the expression of Pbx1, but not Evi-1, in FLT3-ITD+ cells.	Cytarabine	95-105	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	12-15
27374090-4	2016	Indeed, co-treatment with the pan-Pim kinase inhibitor AZD1208 or expression of a kinase-dead Pim-1 mutant sensitized FLT3-ITD cell lines to apoptosis triggered by chemotherapy drugs including the topoisomerase 2 inhibitors daunorubicin, etoposide and mitoxantrone, but not the nucleoside analog cytarabine.	Cytarabine	296-306	Pim-1 proto-oncogene, serine/threonine kinase	Homo sapiens	34-37
27374090-4	2016	Indeed, co-treatment with the pan-Pim kinase inhibitor AZD1208 or expression of a kinase-dead Pim-1 mutant sensitized FLT3-ITD cell lines to apoptosis triggered by chemotherapy drugs including the topoisomerase 2 inhibitors daunorubicin, etoposide and mitoxantrone, but not the nucleoside analog cytarabine.	Cytarabine	296-306	Pim-1 proto-oncogene, serine/threonine kinase	Homo sapiens	94-99
27374090-4	2016	Indeed, co-treatment with the pan-Pim kinase inhibitor AZD1208 or expression of a kinase-dead Pim-1 mutant sensitized FLT3-ITD cell lines to apoptosis triggered by chemotherapy drugs including the topoisomerase 2 inhibitors daunorubicin, etoposide and mitoxantrone, but not the nucleoside analog cytarabine.	Cytarabine	296-306	fms related receptor tyrosine kinase 3	Homo sapiens	118-122
27387666-5	2016	The loss of p21 expression enhanced growth factor-independent proliferation and sensitivity to cytarabine as a consequence of concomitantly enriching the S+G2/M phase population and significantly increasing the expression of Pbx1, but not Evi-1, in FLT3-ITD+ cells.	Cytarabine	95-105	pre B cell leukemia homeobox 1	Mus musculus	225-229
27387666-5	2016	The loss of p21 expression enhanced growth factor-independent proliferation and sensitivity to cytarabine as a consequence of concomitantly enriching the S+G2/M phase population and significantly increasing the expression of Pbx1, but not Evi-1, in FLT3-ITD+ cells.	Cytarabine	95-105	FMS-like tyrosine kinase 3	Mus musculus	249-253
27282562-10	2016	The combination of G-CSF and AMD3100 had stronger effects on killing the leukemia cells induced by Ara-C.	Cytarabine	99-104	colony stimulating factor 3	Homo sapiens	19-24
27347068-1	2016	Combining cytarabine, aclarubicin and granulocyte colony-stimulating factor (G-CSF) has demonstrated marked efficacy in the treatment of elderly and relapsed/refractory patients with acute myeloid leukemia (AML); however, the role of G-CSF remains poorly understood.	Cytarabine	10-20	colony stimulating factor 3	Homo sapiens	77-82
27347068-1	2016	Combining cytarabine, aclarubicin and granulocyte colony-stimulating factor (G-CSF) has demonstrated marked efficacy in the treatment of elderly and relapsed/refractory patients with acute myeloid leukemia (AML); however, the role of G-CSF remains poorly understood.	Cytarabine	10-20	colony stimulating factor 3	Homo sapiens	234-239
27144333-0	2016	The role of VDR and BIM in potentiation of cytarabine-induced cell death in human AML blasts.	Cytarabine	43-53	vitamin D receptor	Homo sapiens	12-15
26779634-8	2016	Variant homozygous XPF 673C &gt; T genotype was associated with higher dose of cytosine arabinoside treatment administrated to AML patients (p value = 0.04).	Cytarabine	79-99	ERCC excision repair 4, endonuclease catalytic subunit	Homo sapiens	19-22
27144333-0	2016	The role of VDR and BIM in potentiation of cytarabine-induced cell death in human AML blasts.	Cytarabine	43-53	BCL2 like 11	Homo sapiens	20-23
26663398-4	2016	Functional studies in vitro determined that four AML-directed chemotherapeutics (cytarabine, daunorubicin, etoposide, and mitoxantrone) are substrates for OATP1B1 and the mouse ortholog Oatp1b2.	Cytarabine	81-91	solute carrier organic anion transporter family member 1B1	Homo sapiens	155-162
27082496-6	2016	HIF-1alpha suppression by 2ME2 significantly induced apoptosis of AML cells, and it outperformed traditional chemotherapy drugs such as cytarabine.	Cytarabine	136-146	hypoxia inducible factor 1 subunit alpha	Homo sapiens	0-10
26663398-4	2016	Functional studies in vitro determined that four AML-directed chemotherapeutics (cytarabine, daunorubicin, etoposide, and mitoxantrone) are substrates for OATP1B1 and the mouse ortholog Oatp1b2.	Cytarabine	81-91	solute carrier organic anion transporter family, member 1b2	Mus musculus	186-193
27082972-5	2016	Using RT-qPCR, we noted that the combination of VPA and Ara-C significantly upregulated Bax expression and led to the arrest of leukemia cell proliferation, sub-G1 DNA accumulation and cell apoptosis, as demonstrated by flow cytometric analysis.	Cytarabine	56-61	BCL2 associated X, apoptosis regulator	Homo sapiens	88-91
27082972-6	2016	Significantly, further experiments revealed that knockdown of Bax expression prevented VPA and Ara-C-induced cell apoptosis in THP-1 cells.	Cytarabine	95-100	BCL2 associated X, apoptosis regulator	Homo sapiens	62-65
27119567-7	2016	IL-27 also decreased the responsiveness of the leukemic cells to chemotherapeutic drugs, cytarabine and daunorubicin.	Cytarabine	89-99	interleukin 27	Homo sapiens	0-5
27342487-4	2016	In addition, HL-60 cell line over-expressing Rheb was established, and the HL-60 cells and HL-60 cells with overexpression of Rheb were treated with Ara-C of different concentrations, the proliferation level was detected by CCK-8 method, and the IC50 was calculated.	Cytarabine	149-154	Ras homolog, mTORC1 binding	Homo sapiens	126-130
27342487-6	2016	Interestingly, higher expression of Rheb was associated with better survival and was sensitive to Ara-C treatment.	Cytarabine	98-103	Ras homolog, mTORC1 binding	Homo sapiens	36-40
27342487-9	2016	In vitro analysis of HL-60 line indicated that overexpression of Rheb could increased the cell sensitivity to Ara-C treatment (IC50=0.54 micromol/L) and caused HL-60 cell apoptosis.	Cytarabine	110-115	Ras homolog, mTORC1 binding	Homo sapiens	65-69
26842729-0	2016	ABCC4 Is a Determinant of Cytarabine-Induced Cytotoxicity and Myelosuppression.	Cytarabine	26-36	ATP-binding cassette, sub-family C (CFTR/MRP), member 4	Mus musculus	0-5
26718602-8	2016	Both markers were elevated in vitro and in vivo, and DEX and Ara-C were able to reduce IL-1beta and TGF-beta1 production.	Cytarabine	61-66	interleukin 1 beta	Rattus norvegicus	87-95
26718602-8	2016	Both markers were elevated in vitro and in vivo, and DEX and Ara-C were able to reduce IL-1beta and TGF-beta1 production.	Cytarabine	61-66	transforming growth factor, beta 1	Rattus norvegicus	100-109
26851026-4	2016	RESULTS: Pre-treatment with DAC restores cellular sensitivity in Ara-C-resistant AML cells.	Cytarabine	65-70	arylacetamide deacetylase	Homo sapiens	28-31
26851026-5	2016	In contrast, DAC/Ara-C combinations are antagonistic in other Ara-C-sensitive AML cells.	Cytarabine	62-67	arylacetamide deacetylase	Homo sapiens	13-16
27150998-0	2016	[Clinical Efficacy of Sorafenib Combined with Low Dose Cytarabine for Treating Patients with FLT3+ Relapsed and Refractory Acute Myeloid Leukemia].	Cytarabine	55-65	fms related receptor tyrosine kinase 3	Homo sapiens	93-97
27150998-1	2016	OBJECTIVE: To study the efficacy and safety of sorafenib combined with low dose cytarabine for treating patients with FLT3(+) relapsed and refractory acute myeloid leukemia (FLT3(+) RR-AML).	Cytarabine	80-90	fms related receptor tyrosine kinase 3	Homo sapiens	118-122
27150998-1	2016	OBJECTIVE: To study the efficacy and safety of sorafenib combined with low dose cytarabine for treating patients with FLT3(+) relapsed and refractory acute myeloid leukemia (FLT3(+) RR-AML).	Cytarabine	80-90	fms related receptor tyrosine kinase 3	Homo sapiens	174-178
27150998-2	2016	METHODS: Seven patients with FLT3(+) RR-AML were treated with sorafenib and low dose cytarabine.	Cytarabine	85-95	fms related receptor tyrosine kinase 3	Homo sapiens	29-33
27150998-6	2016	CONCLUSION: Sorafenib combined with low dose cytarabine can effectively induce the remission of FLT3(+) RR-AML patients, and is worth for further clinical trails to verify its safty and efficiency.	Cytarabine	45-55	fms related receptor tyrosine kinase 3	Homo sapiens	96-100
26842729-2	2016	Based on previous studies implicating ABCC4/MRP4 in the transport of nucleosides, we hypothesized that cytarabine is sensitive to ABCC4-mediated efflux, thereby decreasing its cytotoxic response against AML blasts.	Cytarabine	103-113	ATP-binding cassette, sub-family C (CFTR/MRP), member 4	Mus musculus	38-43
26842729-2	2016	Based on previous studies implicating ABCC4/MRP4 in the transport of nucleosides, we hypothesized that cytarabine is sensitive to ABCC4-mediated efflux, thereby decreasing its cytotoxic response against AML blasts.	Cytarabine	103-113	ATP-binding cassette, sub-family C (CFTR/MRP), member 4	Mus musculus	44-48
26842729-2	2016	Based on previous studies implicating ABCC4/MRP4 in the transport of nucleosides, we hypothesized that cytarabine is sensitive to ABCC4-mediated efflux, thereby decreasing its cytotoxic response against AML blasts.	Cytarabine	103-113	ATP-binding cassette, sub-family C (CFTR/MRP), member 4	Mus musculus	130-135
26842729-3	2016	The uptake of cytarabine and its monophosphate metabolite was found to be facilitated in ABCC4-expressing vesicles and intracellular retention was significantly impaired by overexpression of human ABCC4 or mouse Abcc4 (P &lt; 0.05).	Cytarabine	14-24	ATP binding cassette subfamily C member 4	Homo sapiens	89-94
26842729-3	2016	The uptake of cytarabine and its monophosphate metabolite was found to be facilitated in ABCC4-expressing vesicles and intracellular retention was significantly impaired by overexpression of human ABCC4 or mouse Abcc4 (P &lt; 0.05).	Cytarabine	14-24	ATP binding cassette subfamily C member 4	Homo sapiens	197-202
26842729-3	2016	The uptake of cytarabine and its monophosphate metabolite was found to be facilitated in ABCC4-expressing vesicles and intracellular retention was significantly impaired by overexpression of human ABCC4 or mouse Abcc4 (P &lt; 0.05).	Cytarabine	14-24	ATP-binding cassette, sub-family C (CFTR/MRP), member 4	Mus musculus	212-217
26284582-2	2016	We performed exon-array analysis and exon-specific PCR (ESPCR) to identify specific landscapes of exon expression that are associated with DEK and WT1 oncogene expression and the resistance of AML cells to AraC, doxorubicin or azacitidine.	Cytarabine	206-210	WT1 transcription factor	Homo sapiens	147-150
26842729-4	2016	ABCC4 was expressed highly in AML primary blasts and cell lines, and cytotoxicity of cytarabine in cells was increased in the presence of the ABCC4 inhibitors MK571 or sorafenib, as well as after ABCC4 siRNA.	Cytarabine	85-95	ATP-binding cassette, sub-family C (CFTR/MRP), member 4	Mus musculus	0-5
26842729-4	2016	ABCC4 was expressed highly in AML primary blasts and cell lines, and cytotoxicity of cytarabine in cells was increased in the presence of the ABCC4 inhibitors MK571 or sorafenib, as well as after ABCC4 siRNA.	Cytarabine	85-95	ATP-binding cassette, sub-family C (CFTR/MRP), member 4	Mus musculus	142-147
26842729-4	2016	ABCC4 was expressed highly in AML primary blasts and cell lines, and cytotoxicity of cytarabine in cells was increased in the presence of the ABCC4 inhibitors MK571 or sorafenib, as well as after ABCC4 siRNA.	Cytarabine	85-95	ATP-binding cassette, sub-family C (CFTR/MRP), member 4	Mus musculus	142-147
26842729-6	2016	Collectively, these studies demonstrate that ABCC4 plays a protective role against cytarabine-mediated insults in leukemic and host myeloid cells.	Cytarabine	83-93	ATP-binding cassette, sub-family C (CFTR/MRP), member 4	Mus musculus	45-50
26647771-10	2016	Thus, our findings collectively suggested that the expression level of SIRT2 has a positive relationship with DNR/Ara-C resistance and activity of ERK1/2 signaling pathway.	Cytarabine	114-119	sirtuin 2	Homo sapiens	71-76
26647771-11	2016	SIRT2 might regulate DNR/Ara-C sensitivity in AML cells at least partially through the ERK1/2 pathway.	Cytarabine	25-30	sirtuin 2	Homo sapiens	0-5
26647771-11	2016	SIRT2 might regulate DNR/Ara-C sensitivity in AML cells at least partially through the ERK1/2 pathway.	Cytarabine	25-30	mitogen-activated protein kinase 3	Homo sapiens	87-93
26551869-1	2015	In order to overcome the drawbacks of cytarabine (Ara-C), such as low lipophilicity as well as short plasma half-life and rapid inactivation, a new derivative of Ara-C was designed by incorporation into the non-toxic material, oleic acid (OA), obtaining an amphiphilic small molecular weight prodrug (OA-Ara).	Cytarabine	38-48	ATP binding cassette subfamily C member 6	Homo sapiens	50-53
26467917-7	2016	HDC was carmustine, etoposide, cytarabine, and melphalan (BEAM).	Cytarabine	31-41	histidine decarboxylase	Homo sapiens	0-3
27008269-11	2016	Furthermore, GANT61 enhanced the cytotoxicity of cytarabine (Ara-c) in primary CD34+ AML cells, indicating that inhibition of GLI1 could be a promising strategy to enhance chemosensitivity.	Cytarabine	49-59	CD34 molecule	Homo sapiens	79-83
27008269-11	2016	Furthermore, GANT61 enhanced the cytotoxicity of cytarabine (Ara-c) in primary CD34+ AML cells, indicating that inhibition of GLI1 could be a promising strategy to enhance chemosensitivity.	Cytarabine	49-59	GLI family zinc finger 1	Homo sapiens	126-130
27008269-11	2016	Furthermore, GANT61 enhanced the cytotoxicity of cytarabine (Ara-c) in primary CD34+ AML cells, indicating that inhibition of GLI1 could be a promising strategy to enhance chemosensitivity.	Cytarabine	61-66	CD34 molecule	Homo sapiens	79-83
27119162-0	2016	Expression Levels of Human Equilibrative Nucleoside Transporter 1 and Deoxycytidine Kinase Enzyme as Prognostic Factors in Patients with Acute Myeloid Leukemia Treated with Cytarabine.	Cytarabine	173-183	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	27-65
27119162-0	2016	Expression Levels of Human Equilibrative Nucleoside Transporter 1 and Deoxycytidine Kinase Enzyme as Prognostic Factors in Patients with Acute Myeloid Leukemia Treated with Cytarabine.	Cytarabine	173-183	deoxycytidine kinase	Homo sapiens	70-90
27119162-1	2016	BACKGROUND: Cytarabine (Ara-C) is the primary drug in different treatment schemas for acute myeloid leukemia (AML) and requires the human equilibrative nucleoside transporter (hENT1) to enter cells.	Cytarabine	12-22	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	176-181
27119162-1	2016	BACKGROUND: Cytarabine (Ara-C) is the primary drug in different treatment schemas for acute myeloid leukemia (AML) and requires the human equilibrative nucleoside transporter (hENT1) to enter cells.	Cytarabine	24-29	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	176-181
27321378-3	2016	High MN1 expression confers poor prognosis to AML patients and induces resistance to cytarabine and alltrans-retinoic acid (ATRA) induced differentiation.	Cytarabine	85-95	MN1 proto-oncogene, transcriptional regulator	Homo sapiens	5-8
26563595-0	2016	The hematopoietic tumor suppressor interferon regulatory factor 8 (IRF8) is upregulated by the antimetabolite cytarabine in leukemic cells involving the zinc finger protein ZNF224, acting as a cofactor of the Wilms" tumor gene 1 (WT1) protein.	Cytarabine	110-120	interferon regulatory factor 8	Homo sapiens	67-71
26563595-0	2016	The hematopoietic tumor suppressor interferon regulatory factor 8 (IRF8) is upregulated by the antimetabolite cytarabine in leukemic cells involving the zinc finger protein ZNF224, acting as a cofactor of the Wilms" tumor gene 1 (WT1) protein.	Cytarabine	110-120	zinc finger protein 224	Homo sapiens	173-179
26563595-0	2016	The hematopoietic tumor suppressor interferon regulatory factor 8 (IRF8) is upregulated by the antimetabolite cytarabine in leukemic cells involving the zinc finger protein ZNF224, acting as a cofactor of the Wilms" tumor gene 1 (WT1) protein.	Cytarabine	110-120	WT1 transcription factor	Homo sapiens	209-234
26563595-4	2016	The zinc finger protein ZNF224 can act as a transcriptional co-factor of WT1 and potentiate the cytotoxic response to the cytostatic drug cytarabine.	Cytarabine	138-148	zinc finger protein 224	Homo sapiens	24-30
26563595-4	2016	The zinc finger protein ZNF224 can act as a transcriptional co-factor of WT1 and potentiate the cytotoxic response to the cytostatic drug cytarabine.	Cytarabine	138-148	WT1 transcription factor	Homo sapiens	73-76
26563595-5	2016	We hypothesized that cytarabine upregulates IRF8 and that transcriptional control of IRF8 involves WT1 and ZNF224.	Cytarabine	21-31	interferon regulatory factor 8	Homo sapiens	44-48
26563595-6	2016	Treatment of leukemic K562 cells with cytarabine upregulated IRF8 protein and mRNA, which was correlated to increased expression of ZNF224.	Cytarabine	38-48	interferon regulatory factor 8	Homo sapiens	61-65
26563595-6	2016	Treatment of leukemic K562 cells with cytarabine upregulated IRF8 protein and mRNA, which was correlated to increased expression of ZNF224.	Cytarabine	38-48	zinc finger protein 224	Homo sapiens	132-138
26563595-7	2016	Knock down of ZNF224 with shRNA suppressed both basal and cytarabine-induced IRF8 expression.	Cytarabine	58-68	zinc finger protein 224	Homo sapiens	14-20
26563595-7	2016	Knock down of ZNF224 with shRNA suppressed both basal and cytarabine-induced IRF8 expression.	Cytarabine	58-68	interferon regulatory factor 8	Homo sapiens	77-81
26563595-10	2016	We conclude that cytarabine-induced upregulation of the IRF8 in leukemic cells involves increased levels of ZNF224, which can counteract the repressive activity of WT1 on the IRF8-promoter.	Cytarabine	17-27	interferon regulatory factor 8	Homo sapiens	56-60
26563595-10	2016	We conclude that cytarabine-induced upregulation of the IRF8 in leukemic cells involves increased levels of ZNF224, which can counteract the repressive activity of WT1 on the IRF8-promoter.	Cytarabine	17-27	zinc finger protein 224	Homo sapiens	108-114
26563595-10	2016	We conclude that cytarabine-induced upregulation of the IRF8 in leukemic cells involves increased levels of ZNF224, which can counteract the repressive activity of WT1 on the IRF8-promoter.	Cytarabine	17-27	WT1 transcription factor	Homo sapiens	164-167
26563595-10	2016	We conclude that cytarabine-induced upregulation of the IRF8 in leukemic cells involves increased levels of ZNF224, which can counteract the repressive activity of WT1 on the IRF8-promoter.	Cytarabine	17-27	interferon regulatory factor 8	Homo sapiens	175-179
26651614-3	2015	To apply this concept in the context of acute myeloid leukemia and myelodysplasia, we have investigated the overexpression of the multidrug resistance 1 (MDR1) and the cytidine deaminase (CDD) gene conferring resistance to anthracyclines and cytarabine (Ara-C), the two most important drugs in the treatment of these diseases.	Cytarabine	242-252	cytidine deaminase	Mus musculus	188-191
26748184-0	2016	The novel HSP90 inhibitor NVP-AUY922 shows synergistic anti-leukemic activity with cytarabine in vivo.	Cytarabine	83-93	heat shock protein 90 alpha family class A member 1	Homo sapiens	10-15
26278546-3	2016	These cells were then exposed to different concentration of cytarabine and curcumin to find out IC50 values and also its effect on MDR genes like MDR1, BCRP, LRP and FLT3 by RT-PCR method.	Cytarabine	60-70	ATP binding cassette subfamily B member 1	Homo sapiens	146-150
26278546-3	2016	These cells were then exposed to different concentration of cytarabine and curcumin to find out IC50 values and also its effect on MDR genes like MDR1, BCRP, LRP and FLT3 by RT-PCR method.	Cytarabine	60-70	BCR pseudogene 1	Homo sapiens	152-156
26278546-3	2016	These cells were then exposed to different concentration of cytarabine and curcumin to find out IC50 values and also its effect on MDR genes like MDR1, BCRP, LRP and FLT3 by RT-PCR method.	Cytarabine	60-70	LDL receptor related protein 1	Homo sapiens	158-161
26278546-3	2016	These cells were then exposed to different concentration of cytarabine and curcumin to find out IC50 values and also its effect on MDR genes like MDR1, BCRP, LRP and FLT3 by RT-PCR method.	Cytarabine	60-70	fms related receptor tyrosine kinase 3	Homo sapiens	166-170
26651614-3	2015	To apply this concept in the context of acute myeloid leukemia and myelodysplasia, we have investigated the overexpression of the multidrug resistance 1 (MDR1) and the cytidine deaminase (CDD) gene conferring resistance to anthracyclines and cytarabine (Ara-C), the two most important drugs in the treatment of these diseases.	Cytarabine	254-259	cytidine deaminase	Mus musculus	188-191
26651614-6	2015	RESULTS: Efficient chemoprotection of CDD and MDR1 transduced hematopoietic 32D as well as primary lin(-) cells was proven in the context of Ara-C and anthracycline application.	Cytarabine	141-146	cytidine deaminase	Mus musculus	38-41
26651614-6	2015	RESULTS: Efficient chemoprotection of CDD and MDR1 transduced hematopoietic 32D as well as primary lin(-) cells was proven in the context of Ara-C and anthracycline application.	Cytarabine	141-146	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	46-50
26551869-1	2015	In order to overcome the drawbacks of cytarabine (Ara-C), such as low lipophilicity as well as short plasma half-life and rapid inactivation, a new derivative of Ara-C was designed by incorporation into the non-toxic material, oleic acid (OA), obtaining an amphiphilic small molecular weight prodrug (OA-Ara).	Cytarabine	38-48	ATP binding cassette subfamily C member 6	Homo sapiens	162-165
26551869-1	2015	In order to overcome the drawbacks of cytarabine (Ara-C), such as low lipophilicity as well as short plasma half-life and rapid inactivation, a new derivative of Ara-C was designed by incorporation into the non-toxic material, oleic acid (OA), obtaining an amphiphilic small molecular weight prodrug (OA-Ara).	Cytarabine	38-48	ATP binding cassette subfamily C member 6	Homo sapiens	162-165
26708874-6	2015	When treated with cytarabine, the apoptosis rate and inhibitive rate of RYBP shRNA group were lower than those of NC group.	Cytarabine	18-28	RING1 and YY1 binding protein	Homo sapiens	72-76
26354033-1	2015	The cytidine deaminase (CDA) catalyzes the irreversible hydrolytic deamination of the cytarabine (AraC) into a 1-beta-D-arabinofuranosyluracil (AraU), an inactive metabolite that plays a crucial role in lowering the amount of AraC, a key chemotherapeutic drug, in the treatment of patients with acute myeloid leukemia (AML).	Cytarabine	86-96	cytidine deaminase	Homo sapiens	4-22
26354033-1	2015	The cytidine deaminase (CDA) catalyzes the irreversible hydrolytic deamination of the cytarabine (AraC) into a 1-beta-D-arabinofuranosyluracil (AraU), an inactive metabolite that plays a crucial role in lowering the amount of AraC, a key chemotherapeutic drug, in the treatment of patients with acute myeloid leukemia (AML).	Cytarabine	86-96	cytidine deaminase	Homo sapiens	24-27
26354033-1	2015	The cytidine deaminase (CDA) catalyzes the irreversible hydrolytic deamination of the cytarabine (AraC) into a 1-beta-D-arabinofuranosyluracil (AraU), an inactive metabolite that plays a crucial role in lowering the amount of AraC, a key chemotherapeutic drug, in the treatment of patients with acute myeloid leukemia (AML).	Cytarabine	98-102	cytidine deaminase	Homo sapiens	4-22
26354033-1	2015	The cytidine deaminase (CDA) catalyzes the irreversible hydrolytic deamination of the cytarabine (AraC) into a 1-beta-D-arabinofuranosyluracil (AraU), an inactive metabolite that plays a crucial role in lowering the amount of AraC, a key chemotherapeutic drug, in the treatment of patients with acute myeloid leukemia (AML).	Cytarabine	98-102	cytidine deaminase	Homo sapiens	24-27
26354033-1	2015	The cytidine deaminase (CDA) catalyzes the irreversible hydrolytic deamination of the cytarabine (AraC) into a 1-beta-D-arabinofuranosyluracil (AraU), an inactive metabolite that plays a crucial role in lowering the amount of AraC, a key chemotherapeutic drug, in the treatment of patients with acute myeloid leukemia (AML).	Cytarabine	226-230	cytidine deaminase	Homo sapiens	4-22
26354033-1	2015	The cytidine deaminase (CDA) catalyzes the irreversible hydrolytic deamination of the cytarabine (AraC) into a 1-beta-D-arabinofuranosyluracil (AraU), an inactive metabolite that plays a crucial role in lowering the amount of AraC, a key chemotherapeutic drug, in the treatment of patients with acute myeloid leukemia (AML).	Cytarabine	226-230	cytidine deaminase	Homo sapiens	24-27
26354033-2	2015	In this study, we hypothesized that CDA polymorphisms were associated with the AraC metabolism for AML treatment and/or related clinical phenotypes.	Cytarabine	79-83	cytidine deaminase	Homo sapiens	36-39
26617391-10	2015	Hypoxia-mediated down-regulation of FLT3 conferred resistance against cytarabine in vitro.	Cytarabine	70-80	fms related receptor tyrosine kinase 3	Homo sapiens	36-40
26475207-0	2015	FLT3-ITD drives Ara-C resistance in leukemic cells via the induction of RUNX3.	Cytarabine	16-21	fms related receptor tyrosine kinase 3	Homo sapiens	0-4
26475207-0	2015	FLT3-ITD drives Ara-C resistance in leukemic cells via the induction of RUNX3.	Cytarabine	16-21	RUNX family transcription factor 3	Homo sapiens	72-77
26475207-2	2015	We previously reported that FLT3-ITD confers resistance to cytosine arabinoside (Ara-C), a key cytotoxic agent in AML treatments.	Cytarabine	59-79	fms related receptor tyrosine kinase 3	Homo sapiens	28-32
26475207-2	2015	We previously reported that FLT3-ITD confers resistance to cytosine arabinoside (Ara-C), a key cytotoxic agent in AML treatments.	Cytarabine	81-86	fms related receptor tyrosine kinase 3	Homo sapiens	28-32
26475207-3	2015	In order to elucidate the detailed molecular mechanisms underlying the Ara-C resistance induced by FLT3-ITD, we performed a microarray gene expression analysis of the human leukemic cell line K562 transduced with FLT3-ITD (K562/FLT3-ITD) and identified RUNX3 as a downstream target of FLT3-ITD.	Cytarabine	71-76	fms related receptor tyrosine kinase 3	Homo sapiens	99-103
26475207-3	2015	In order to elucidate the detailed molecular mechanisms underlying the Ara-C resistance induced by FLT3-ITD, we performed a microarray gene expression analysis of the human leukemic cell line K562 transduced with FLT3-ITD (K562/FLT3-ITD) and identified RUNX3 as a downstream target of FLT3-ITD.	Cytarabine	71-76	fms related receptor tyrosine kinase 3	Homo sapiens	213-217
26475207-3	2015	In order to elucidate the detailed molecular mechanisms underlying the Ara-C resistance induced by FLT3-ITD, we performed a microarray gene expression analysis of the human leukemic cell line K562 transduced with FLT3-ITD (K562/FLT3-ITD) and identified RUNX3 as a downstream target of FLT3-ITD.	Cytarabine	71-76	fms related receptor tyrosine kinase 3	Homo sapiens	213-217
26475207-3	2015	In order to elucidate the detailed molecular mechanisms underlying the Ara-C resistance induced by FLT3-ITD, we performed a microarray gene expression analysis of the human leukemic cell line K562 transduced with FLT3-ITD (K562/FLT3-ITD) and identified RUNX3 as a downstream target of FLT3-ITD.	Cytarabine	71-76	fms related receptor tyrosine kinase 3	Homo sapiens	213-217
26475207-5	2015	The knockdown of the RUNX3 expression in the K562/FLT3-ITD cells increased the sensitivity to Ara-C, and the exogenous expression of RUNX3 per se resulted in the enhancement of Ara-C resistance in the K562 cells.	Cytarabine	94-99	RUNX family transcription factor 3	Homo sapiens	21-26
26475207-5	2015	The knockdown of the RUNX3 expression in the K562/FLT3-ITD cells increased the sensitivity to Ara-C, and the exogenous expression of RUNX3 per se resulted in the enhancement of Ara-C resistance in the K562 cells.	Cytarabine	94-99	fms related receptor tyrosine kinase 3	Homo sapiens	50-54
26475207-5	2015	The knockdown of the RUNX3 expression in the K562/FLT3-ITD cells increased the sensitivity to Ara-C, and the exogenous expression of RUNX3 per se resulted in the enhancement of Ara-C resistance in the K562 cells.	Cytarabine	177-182	RUNX family transcription factor 3	Homo sapiens	21-26
26475207-5	2015	The knockdown of the RUNX3 expression in the K562/FLT3-ITD cells increased the sensitivity to Ara-C, and the exogenous expression of RUNX3 per se resulted in the enhancement of Ara-C resistance in the K562 cells.	Cytarabine	177-182	RUNX family transcription factor 3	Homo sapiens	133-138
26475207-7	2015	Collectively, these findings demonstrate that RUNX3 is a prerequisite for Ara-C resistance via FLT3-ITD signaling.	Cytarabine	74-79	RUNX family transcription factor 3	Homo sapiens	46-51
26475207-7	2015	Collectively, these findings demonstrate that RUNX3 is a prerequisite for Ara-C resistance via FLT3-ITD signaling.	Cytarabine	74-79	fms related receptor tyrosine kinase 3	Homo sapiens	95-99
26708874-8	2015	CONCLUSIONS: RYBP gene silencing can inhibitive the apoptosis of HL-60 cells and significantly reduce the sensitivity to cytarabine, but this gene silencing can not affect the sensitivity to daunorubicin.	Cytarabine	121-131	RING1 and YY1 binding protein	Homo sapiens	13-17
25921248-0	2015	Deoxycytidine-kinase knockdown as a novel myeloprotective strategy in the context of fludarabine, cytarabine or cladribine therapy.	Cytarabine	98-108	deoxycytidine kinase	Homo sapiens	0-20
26125609-6	2015	Functionality of Dox-inducible hCDD expression was demonstrated by &gt;10-fold increase in cytosine arabinoside (1-beta-d-arabinofuranosylcytosine, Ara-C) resistance of Lv.TII.CDD-transduced K562 cells.	Cytarabine	91-111	natriuretic peptide A	Homo sapiens	32-35
26125609-6	2015	Functionality of Dox-inducible hCDD expression was demonstrated by &gt;10-fold increase in cytosine arabinoside (1-beta-d-arabinofuranosylcytosine, Ara-C) resistance of Lv.TII.CDD-transduced K562 cells.	Cytarabine	113-146	natriuretic peptide A	Homo sapiens	32-35
26125609-6	2015	Functionality of Dox-inducible hCDD expression was demonstrated by &gt;10-fold increase in cytosine arabinoside (1-beta-d-arabinofuranosylcytosine, Ara-C) resistance of Lv.TII.CDD-transduced K562 cells.	Cytarabine	148-153	natriuretic peptide A	Homo sapiens	32-35
26125609-7	2015	In addition, Lv.TII.CDD-transduced CD34(+)-derived myeloid cells were protected from up to 300 nm Ara-C (control affected from 50 nm onwards).	Cytarabine	98-103	natriuretic peptide A	Homo sapiens	20-23
26125609-7	2015	In addition, Lv.TII.CDD-transduced CD34(+)-derived myeloid cells were protected from up to 300 nm Ara-C (control affected from 50 nm onwards).	Cytarabine	98-103	CD34 molecule	Homo sapiens	35-39
26238482-3	2015	The aim of the present study was to determine whether the chemotherapeutic activity of Ara-C was enhanced by the overexpression of SPARC.	Cytarabine	87-92	secreted protein acidic and cysteine rich	Homo sapiens	131-136
26444983-0	2015	Redirection of CD4+ and CD8+ T lymphocytes via an anti-CD3 x anti-CD19 bi-specific antibody combined with cytosine arabinoside and the efficient lysis of patient-derived B-ALL cells.	Cytarabine	106-126	CD4 molecule	Homo sapiens	15-18
26444983-0	2015	Redirection of CD4+ and CD8+ T lymphocytes via an anti-CD3 x anti-CD19 bi-specific antibody combined with cytosine arabinoside and the efficient lysis of patient-derived B-ALL cells.	Cytarabine	106-126	CD8a molecule	Homo sapiens	24-27
26444983-0	2015	Redirection of CD4+ and CD8+ T lymphocytes via an anti-CD3 x anti-CD19 bi-specific antibody combined with cytosine arabinoside and the efficient lysis of patient-derived B-ALL cells.	Cytarabine	106-126	CD19 molecule	Homo sapiens	66-70
26444983-4	2015	The combination of the diabody or ds-diabody and Ara-C was highly effective in enhancing the cytotoxicity of T cells against the CD19+ human leukemia cell-line, Nalm-6, both in vitro and in vivo.	Cytarabine	49-54	CD19 molecule	Homo sapiens	129-133
26444983-6	2015	METHODS: This study aimed to detect the B7 family members B7.1 (CD80) and B7.2 (CD86) that were expressed in B-ALL patient-derived cells pre-treated by Ara-C (0.25 muM) and to determine the targeted killing ability of T cell subtypes induced by the diabody or ds-diabody combination with Ara-C both in vitro and in vivo.	Cytarabine	152-157	CD80 molecule	Homo sapiens	64-68
26444983-6	2015	METHODS: This study aimed to detect the B7 family members B7.1 (CD80) and B7.2 (CD86) that were expressed in B-ALL patient-derived cells pre-treated by Ara-C (0.25 muM) and to determine the targeted killing ability of T cell subtypes induced by the diabody or ds-diabody combination with Ara-C both in vitro and in vivo.	Cytarabine	152-157	CD86 molecule	Homo sapiens	80-84
26444983-6	2015	METHODS: This study aimed to detect the B7 family members B7.1 (CD80) and B7.2 (CD86) that were expressed in B-ALL patient-derived cells pre-treated by Ara-C (0.25 muM) and to determine the targeted killing ability of T cell subtypes induced by the diabody or ds-diabody combination with Ara-C both in vitro and in vivo.	Cytarabine	288-293	CD80 molecule	Homo sapiens	64-68
26444983-6	2015	METHODS: This study aimed to detect the B7 family members B7.1 (CD80) and B7.2 (CD86) that were expressed in B-ALL patient-derived cells pre-treated by Ara-C (0.25 muM) and to determine the targeted killing ability of T cell subtypes induced by the diabody or ds-diabody combination with Ara-C both in vitro and in vivo.	Cytarabine	288-293	CD86 molecule	Homo sapiens	80-84
26444983-8	2015	RESULT: Low-dose Ara-C enhanced CD80 and CD86 expression in nearly 50 % of specimens of B-ALL patient-derived cells.	Cytarabine	17-22	CD80 molecule	Homo sapiens	32-36
26444983-8	2015	RESULT: Low-dose Ara-C enhanced CD80 and CD86 expression in nearly 50 % of specimens of B-ALL patient-derived cells.	Cytarabine	17-22	CD86 molecule	Homo sapiens	41-45
26397212-0	2015	Knockdown of homeobox A5 by small hairpin RNA inhibits proliferation and enhances cytarabine chemosensitivity of acute myeloid leukemia cells.	Cytarabine	82-92	homeobox A5	Homo sapiens	13-24
26397212-10	2015	Furthermore, knockdown of HOXA5 in the U937 cells enhanced their chemosensitivity to cytarabine.	Cytarabine	85-95	homeobox A5	Homo sapiens	26-31
26174689-0	2015	The influence of cytidine deaminase -33delC polymorphism on treatment outcome with high-dose cytarabine in Chinese patients with relapsed acute myeloid leukaemia.	Cytarabine	93-103	cytidine deaminase	Homo sapiens	17-35
26174689-2	2015	The aim of our study was to evaluate the influence of cytidine deaminase (CDA) single nucleotide polymorphisms (SNPs) -451G&gt;A (rs532545), 435C&gt;T (rs1048977) and -33delC (rs3215400) on treatment outcome in patients with relapsed acute myeloid leukaemia (AML) after high-dose Ara-C chemotherapy.	Cytarabine	280-285	cytidine deaminase	Homo sapiens	54-72
26174689-2	2015	The aim of our study was to evaluate the influence of cytidine deaminase (CDA) single nucleotide polymorphisms (SNPs) -451G&gt;A (rs532545), 435C&gt;T (rs1048977) and -33delC (rs3215400) on treatment outcome in patients with relapsed acute myeloid leukaemia (AML) after high-dose Ara-C chemotherapy.	Cytarabine	280-285	cytidine deaminase	Homo sapiens	74-77
26375587-6	2015	By utilizing engineered cells with overexpression or knockdown of BCL-2 family proteins, Ara-C was found to be independent, while ABT-199 was dependent on BCL-XL.	Cytarabine	89-94	BCL2 apoptosis regulator	Homo sapiens	66-71
26320177-2	2015	We have previously shown that ZNF224 exerts a specific proapoptotic role in chronic myelogenous leukemia (CML) K562 cells and contributes to cytosine arabinoside-induced apoptosis, by modulating WT1-dependent transcription of apoptotic genes.	Cytarabine	141-161	zinc finger protein 224	Homo sapiens	30-36
26320177-2	2015	We have previously shown that ZNF224 exerts a specific proapoptotic role in chronic myelogenous leukemia (CML) K562 cells and contributes to cytosine arabinoside-induced apoptosis, by modulating WT1-dependent transcription of apoptotic genes.	Cytarabine	141-161	WT1 transcription factor	Homo sapiens	195-198
26334102-3	2015	Targeted inhibition of WEE1 with AZD1775 has emerged as a strategy to sensitize cancer cells to cytarabine and other chemotherapeutics.	Cytarabine	96-106	WEE1 G2 checkpoint kinase	Homo sapiens	23-27
26334102-8	2015	Inhibition of WEE1 with AZD1775 sensitizes T-ALL to several anti-leukemia agents, particularly cytarabine and that mechanistically, AZD1775 promotes apoptosis over DNA repair in cells treated with cytarabine.	Cytarabine	95-105	WEE1 G2 checkpoint kinase	Homo sapiens	14-18
26334102-8	2015	Inhibition of WEE1 with AZD1775 sensitizes T-ALL to several anti-leukemia agents, particularly cytarabine and that mechanistically, AZD1775 promotes apoptosis over DNA repair in cells treated with cytarabine.	Cytarabine	197-207	WEE1 G2 checkpoint kinase	Homo sapiens	14-18
26265695-3	2015	Furthermore, CHD4 depletion renders AML blasts more sensitive both in vitro and in vivo to genotoxic agents used in clinical therapy: daunorubicin (DNR) and cytarabine (ara-C).	Cytarabine	157-167	chromodomain helicase DNA binding protein 4	Mus musculus	13-17
26265695-3	2015	Furthermore, CHD4 depletion renders AML blasts more sensitive both in vitro and in vivo to genotoxic agents used in clinical therapy: daunorubicin (DNR) and cytarabine (ara-C).	Cytarabine	169-174	chromodomain helicase DNA binding protein 4	Mus musculus	13-17
26265695-4	2015	Sensitization to DNR and ara-C is mediated in part by activation of the ataxia-telangiectasia mutated pathway, which is preliminarily activated by a Tip60-dependent mechanism in response to chromatin relaxation and further activated by genotoxic agent-induced DSBs.	Cytarabine	25-30	K(lysine) acetyltransferase 5	Mus musculus	149-154
26139471-3	2015	The use of CD82 mAb in combination with cytarabine (AraC) significantly prolonged survival of immunodeficient mice-bearing human AML cells than did treatment with either AraC or CD82 mAb alone.	Cytarabine	170-174	CD82 antigen	Mus musculus	11-15
25985920-1	2015	Granulocyte colony-stimulating factor (G-CSF) increases the susceptibility of dormant malignant or nonmalignant hematopoietic cells to cytarabine arabinoside (Ara-C) through the induction of cell cycle entry.	Cytarabine	159-164	colony stimulating factor 3	Homo sapiens	0-37
25985920-1	2015	Granulocyte colony-stimulating factor (G-CSF) increases the susceptibility of dormant malignant or nonmalignant hematopoietic cells to cytarabine arabinoside (Ara-C) through the induction of cell cycle entry.	Cytarabine	159-164	colony stimulating factor 3	Homo sapiens	39-44
25985920-4	2015	The TBI &gt;= 8 Gy + Ara-C/G-CSF + CY regimen showed significantly higher incidence of neutrophil engraftment (hazard ratio, 1.52; 95% confidence interval [CI], 1.10 to 2.08; P = .009) and lower overall mortality (hazard ratio, .46; 95% CI, .26 to .82; P = .008) rates compared with those without a G-CSF regimen.	Cytarabine	21-26	colony stimulating factor 3	Homo sapiens	299-304
26165695-0	2015	SPARC ectopic overexpression inhibits growth and promotes programmed cell death in acute myeloid leukemia transformed from myelodysplastic syndrome cells, alone and in combination with Ara-C treatment.	Cytarabine	185-190	secreted protein acidic and cysteine rich	Homo sapiens	0-5
26188848-2	2015	MLL-rearranged infant ALL responds remarkably well to nucleoside analogue drugs in vitro, such as cytarabine and cladribine, and to the demethylating agents decitabine and zebularine as measured by cytotoxicity assays.	Cytarabine	98-108	lysine methyltransferase 2A	Homo sapiens	0-3
26189107-4	2015	Primary BMECs secreted significantly increased levels of VEGF-A and PDGF-AB after exposure to cytarabine.	Cytarabine	94-104	vascular endothelial growth factor A	Homo sapiens	57-63
26165695-6	2015	The microarray analysis results revealed that samples from SPARC-overexpressed cells compared to SPARC protein, in SKM-1 cells led to proliferation inhibition and promoted programmed cell death and these effects were greater when treated with Ara-C.	Cytarabine	243-248	secreted protein acidic and cysteine rich	Homo sapiens	59-64
26165695-6	2015	The microarray analysis results revealed that samples from SPARC-overexpressed cells compared to SPARC protein, in SKM-1 cells led to proliferation inhibition and promoted programmed cell death and these effects were greater when treated with Ara-C.	Cytarabine	243-248	secreted protein acidic and cysteine rich	Homo sapiens	97-102
26165695-7	2015	The mRNA and protein expression levels of SPARC were detected by SPARC overexpression in cells treated with Ara-C resulting in a significant upregulation of the mixed lineage kinase domain-like (MLKL) gene expression and five other genes.	Cytarabine	108-113	secreted protein acidic and cysteine rich	Homo sapiens	42-47
26165695-7	2015	The mRNA and protein expression levels of SPARC were detected by SPARC overexpression in cells treated with Ara-C resulting in a significant upregulation of the mixed lineage kinase domain-like (MLKL) gene expression and five other genes.	Cytarabine	108-113	secreted protein acidic and cysteine rich	Homo sapiens	65-70
26165695-7	2015	The mRNA and protein expression levels of SPARC were detected by SPARC overexpression in cells treated with Ara-C resulting in a significant upregulation of the mixed lineage kinase domain-like (MLKL) gene expression and five other genes.	Cytarabine	108-113	mixed lineage kinase domain like pseudokinase	Homo sapiens	161-193
26165695-7	2015	The mRNA and protein expression levels of SPARC were detected by SPARC overexpression in cells treated with Ara-C resulting in a significant upregulation of the mixed lineage kinase domain-like (MLKL) gene expression and five other genes.	Cytarabine	108-113	mixed lineage kinase domain like pseudokinase	Homo sapiens	195-199
26165695-9	2015	MLKL upregulation in SPARC overexpressed cells treated with Ara-C, indicates necrosis as a possible cell death process for the SKM-1 cells under these stringent conditions.	Cytarabine	60-65	mixed lineage kinase domain like pseudokinase	Homo sapiens	0-4
26165695-9	2015	MLKL upregulation in SPARC overexpressed cells treated with Ara-C, indicates necrosis as a possible cell death process for the SKM-1 cells under these stringent conditions.	Cytarabine	60-65	secreted protein acidic and cysteine rich	Homo sapiens	21-26
25672886-8	2015	Using SiRNA knockdown, and a cytosine arabinoside (araC) chemical inhibitor, we conclude that PCNA is important for viral replication and histone deposition.	Cytarabine	29-49	proliferating cell nuclear antigen	Homo sapiens	94-98
26832848-8	2015	In vitro studies confirmed that Twist1-overexpressing leukemic cells were more susceptible to cytarabine, but not daunorubicin, cytotoxicity.	Cytarabine	94-104	twist family bHLH transcription factor 1	Homo sapiens	32-38
25545165-6	2015	Functional analyses further showed that ALDH(+) cells from ALDH-numerous AML were quiescent, refractory to ARA-C treatment and capable of leukemic engraftment in a xenogenic mouse transplantation model.	Cytarabine	107-112	aldehyde dehydrogenase family 3, subfamily A1	Mus musculus	40-44
25545165-6	2015	Functional analyses further showed that ALDH(+) cells from ALDH-numerous AML were quiescent, refractory to ARA-C treatment and capable of leukemic engraftment in a xenogenic mouse transplantation model.	Cytarabine	107-112	aldehyde dehydrogenase family 3, subfamily A1	Mus musculus	59-63
25672886-8	2015	Using SiRNA knockdown, and a cytosine arabinoside (araC) chemical inhibitor, we conclude that PCNA is important for viral replication and histone deposition.	Cytarabine	51-55	proliferating cell nuclear antigen	Homo sapiens	94-98
26287405-1	2015	The aim of this study was to investigate the role of microRNA-335 (miR-335) in determining the treatment response and prognosis in adult acute myeloid leukemia (AML) patients receiving the cytarabine (Ara-C)-based chemotherapy.A total of 204 adult AML patients were collected.	Cytarabine	189-199	microRNA 335	Homo sapiens	53-65
26287405-1	2015	The aim of this study was to investigate the role of microRNA-335 (miR-335) in determining the treatment response and prognosis in adult acute myeloid leukemia (AML) patients receiving the cytarabine (Ara-C)-based chemotherapy.A total of 204 adult AML patients were collected.	Cytarabine	189-199	microRNA 335	Homo sapiens	67-74
26287405-1	2015	The aim of this study was to investigate the role of microRNA-335 (miR-335) in determining the treatment response and prognosis in adult acute myeloid leukemia (AML) patients receiving the cytarabine (Ara-C)-based chemotherapy.A total of 204 adult AML patients were collected.	Cytarabine	201-206	microRNA 335	Homo sapiens	53-65
26287405-1	2015	The aim of this study was to investigate the role of microRNA-335 (miR-335) in determining the treatment response and prognosis in adult acute myeloid leukemia (AML) patients receiving the cytarabine (Ara-C)-based chemotherapy.A total of 204 adult AML patients were collected.	Cytarabine	201-206	microRNA 335	Homo sapiens	67-74
26287405-7	2015	In contrast, high bone marrow miR-335 level was significantly associated with a poor treatment response and also predicted a worse prognosis indicated by the relapse-free survival and overall survival periods in adult AML patients receiving Ara-C-based chemotherapy.Our finding suggests that bone marrow miR-335 level may be used as a marker to predict the chemotherapy response and prognosis in adult AML patients.	Cytarabine	241-246	microRNA 335	Homo sapiens	30-37
26287405-7	2015	In contrast, high bone marrow miR-335 level was significantly associated with a poor treatment response and also predicted a worse prognosis indicated by the relapse-free survival and overall survival periods in adult AML patients receiving Ara-C-based chemotherapy.Our finding suggests that bone marrow miR-335 level may be used as a marker to predict the chemotherapy response and prognosis in adult AML patients.	Cytarabine	241-246	microRNA 335	Homo sapiens	304-311
26083014-7	2015	RNA expression of deoxycytidine kinase (DCK), human equilibrative nucleoside transporter-1 (ENT1) and ribonucleotide reductase M1 (RRM1) were significantly higher and cytidine deaminase (CDA) was significantly lower in ex vivo Ara-C sensitive samples.	Cytarabine	227-232	deoxycytidine kinase	Homo sapiens	18-38
25857773-2	2015	Recently, a number of papers demonstrated the involvement of cN-II in the mechanisms of resistance to antitumor drugs such as cytarabine, gemcitabine and fludarabine.	Cytarabine	126-136	5'-nucleotidase, cytosolic II	Homo sapiens	61-66
25857773-12	2015	SENTENCE: Resistance to fludarabine, gemcitabine and cytarabine can be determined by an increase of cN-II both through dephosphorylation of active drugs and perturbation of nucleotide pool.	Cytarabine	53-63	5'-nucleotidase, cytosolic II	Homo sapiens	100-105
25955569-0	2015	Concentrative nucleoside transporter 3 as a prognostic indicator for favorable outcome of t(8;21)-positive acute myeloid leukemia patients after cytarabine-based chemotherapy.	Cytarabine	145-155	solute carrier family 28 member 3	Homo sapiens	0-38
26314418-5	2015	Notch1 protein expression in L1210 cells were significantly decreased after treating with cytosine arabinoside of low and middle concentrations, but increased after treating with cytosine arabinoside of high concentration or prolonging time of cytosine arabinoside of middle con-centration.	Cytarabine	90-110	notch 1	Mus musculus	0-6
26314418-5	2015	Notch1 protein expression in L1210 cells were significantly decreased after treating with cytosine arabinoside of low and middle concentrations, but increased after treating with cytosine arabinoside of high concentration or prolonging time of cytosine arabinoside of middle con-centration.	Cytarabine	179-199	notch 1	Mus musculus	0-6
26314418-5	2015	Notch1 protein expression in L1210 cells were significantly decreased after treating with cytosine arabinoside of low and middle concentrations, but increased after treating with cytosine arabinoside of high concentration or prolonging time of cytosine arabinoside of middle con-centration.	Cytarabine	179-199	notch 1	Mus musculus	0-6
26314418-8	2015	The Notch1 protein expression is down-regulated in process of inhibiting L1210 cell proliferation by Ara-C and dexmethason.	Cytarabine	101-106	notch 1	Mus musculus	4-10
26177509-1	2015	Cytogenetically normal acute myeloid leukemia (CN-AML) patients harboring RUNX1 mutations have a dismal prognosis with anthracycline/cytarabine-based chemotherapy.	Cytarabine	133-143	RUNX family transcription factor 1	Homo sapiens	74-79
25888304-1	2015	Dormant leukemia cells, which might escape the cytotoxic effect of conditioning before hematopoietic stem cell transplantation (HSCT), could be induced to enter the cell cycle by granulocyte colony-stimulating factor (G-CSF) and become more susceptible to the cell-cycle-specific agent cytarabine arabinoside (Ara-C).	Cytarabine	310-315	colony stimulating factor 3	Homo sapiens	218-223
25896848-10	2015	Combination of C-1311 with cytarabine or doxorubicin again showed distinct synergistic activity in FLT3-ITD-positive cells.	Cytarabine	27-37	fms related receptor tyrosine kinase 3	Homo sapiens	99-103
25882550-0	2015	The HSP90 inhibitor ganetespib: A potential effective agent for Acute Myeloid Leukemia in combination with cytarabine.	Cytarabine	107-117	heat shock protein 90 alpha family class A member 1	Homo sapiens	4-9
25888304-2	2015	Based on this effect, we have utilized G-CSF-combined high-dose Ara-C in myeloablative conditioning for allogeneic bone marrow or peripheral blood stem cell transplantation from HLA-identical family donors since 1988.	Cytarabine	64-69	colony stimulating factor 3	Homo sapiens	39-44
25882550-5	2015	Combination treatment of primary blasts with ganetespib and cytarabine showed good synergistic interaction (combination index (CI): 0.47) across a range of drug effects with associated reduction in HSP70 feedback and AKT signaling levels.	Cytarabine	60-70	heat shock protein family A (Hsp70) member 4	Homo sapiens	198-203
25888304-3	2015	We report on the long-term outcomes of allogeneic HSCT using a conditioning regimen of 12Gy total body irradiation and G-CSF-combined high-dose Ara-C in 89 adult patients with acute myeloid leukemia, chronic myelogenous leukemia, or myelodysplastic syndrome.	Cytarabine	144-149	colony stimulating factor 3	Homo sapiens	119-124
25882550-5	2015	Combination treatment of primary blasts with ganetespib and cytarabine showed good synergistic interaction (combination index (CI): 0.47) across a range of drug effects with associated reduction in HSP70 feedback and AKT signaling levels.	Cytarabine	60-70	AKT serine/threonine kinase 1	Homo sapiens	217-220
26125761-0	2015	Ara-C and anti-CD47 antibody combination therapy eliminates acute monocytic leukemia THP-1 cells in vivo and in vitro.	Cytarabine	0-5	GLI family zinc finger 2	Homo sapiens	85-90
26125761-10	2015	Finally, single or combination treatment of THP-1 LSC-engrafted mice with cytarabine and anti-CD47 antibody resulted in targeting of LSCs and depletion of leukemia cells.	Cytarabine	74-84	GLI family zinc finger 2	Homo sapiens	44-49
25672398-1	2015	The antibody-based delivery of IL2 to extracellular targets expressed in the easily accessible tumor-associated vasculature has shown potent antileukemic activity in xenograft and immunocompetent murine models of acute myelogenous leukemia (AML), especially in combination with cytarabine.	Cytarabine	278-288	interleukin 2	Mus musculus	31-34
26028971-7	2015	Abrogation of Bcl2 activity by the Bcl2-specific inhibitor ABT 737 led to cell death in the presence of both cytarabine and daunorubicin, demonstrating that the cell adhesion-mediated drug resistance induced by Bcl2 and p27(Kip1) in the scaffold was similar to that seen in vivo.	Cytarabine	109-119	BCL2 apoptosis regulator	Homo sapiens	14-18
26028971-7	2015	Abrogation of Bcl2 activity by the Bcl2-specific inhibitor ABT 737 led to cell death in the presence of both cytarabine and daunorubicin, demonstrating that the cell adhesion-mediated drug resistance induced by Bcl2 and p27(Kip1) in the scaffold was similar to that seen in vivo.	Cytarabine	109-119	BCL2 apoptosis regulator	Homo sapiens	35-39
26028971-7	2015	Abrogation of Bcl2 activity by the Bcl2-specific inhibitor ABT 737 led to cell death in the presence of both cytarabine and daunorubicin, demonstrating that the cell adhesion-mediated drug resistance induced by Bcl2 and p27(Kip1) in the scaffold was similar to that seen in vivo.	Cytarabine	109-119	BCL2 apoptosis regulator	Homo sapiens	35-39
25810373-7	2015	Indeed, UGT levels in AML patients treated with ribavirin and/or cytarabine were elevated at relapse relative to diagnosis.	Cytarabine	65-75	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	8-11
25934555-8	2015	Effects on primary human AML cell viability and proliferation of low-dose cytarabine (0.01-0.5 muM) were also assessed.	Cytarabine	74-84	latexin	Homo sapiens	95-98
25934555-10	2015	RESULTS: Only cytarabine 44 muM had both antiproliferative and proapoptotic effects.	Cytarabine	14-24	latexin	Homo sapiens	28-31
25934555-15	2015	Cytarabine (0.01-0.05 muM) showed a dose-dependent antiproliferative effect on AML cells, and in contrast to the T cells this effect reached statistical significance even at 0.01 muM.	Cytarabine	0-10	latexin	Homo sapiens	22-25
25934555-15	2015	Cytarabine (0.01-0.05 muM) showed a dose-dependent antiproliferative effect on AML cells, and in contrast to the T cells this effect reached statistical significance even at 0.01 muM.	Cytarabine	0-10	latexin	Homo sapiens	179-182
25495470-4	2015	AREAS COVERED: Among the antimetabolites, a small but widely prescribed number of drugs (i.e., gemcitabine, capecitabine, cytarabine, azacytidine) share a same metabolic pattern driven by a liver enzyme, cytidine deaminase (CDA), coded by a gene displaying several genetic and epigenetic polymorphisms.	Cytarabine	122-132	cytidine deaminase	Homo sapiens	204-222
25744718-0	2015	CDK4/6 Inhibitor PD 0332991 Sensitizes Acute Myeloid Leukemia to Cytarabine-Mediated Cytotoxicity.	Cytarabine	65-75	cyclin dependent kinase 4	Homo sapiens	0-6
25744718-3	2015	By selective inhibition of CDK4/CDK6 with PD 0332991, which leads to early G1 arrest and synchronous S-phase entry upon release of the G1 block, we have developed a novel strategy to prime acute myeloid leukemia (AML) cells for cytotoxic killing by cytarabine (Ara-C).	Cytarabine	249-259	cyclin dependent kinase 4	Homo sapiens	27-31
25744718-3	2015	By selective inhibition of CDK4/CDK6 with PD 0332991, which leads to early G1 arrest and synchronous S-phase entry upon release of the G1 block, we have developed a novel strategy to prime acute myeloid leukemia (AML) cells for cytotoxic killing by cytarabine (Ara-C).	Cytarabine	249-259	cyclin dependent kinase 6	Homo sapiens	32-36
25744718-3	2015	By selective inhibition of CDK4/CDK6 with PD 0332991, which leads to early G1 arrest and synchronous S-phase entry upon release of the G1 block, we have developed a novel strategy to prime acute myeloid leukemia (AML) cells for cytotoxic killing by cytarabine (Ara-C).	Cytarabine	261-266	cyclin dependent kinase 4	Homo sapiens	27-31
25744718-3	2015	By selective inhibition of CDK4/CDK6 with PD 0332991, which leads to early G1 arrest and synchronous S-phase entry upon release of the G1 block, we have developed a novel strategy to prime acute myeloid leukemia (AML) cells for cytotoxic killing by cytarabine (Ara-C).	Cytarabine	261-266	cyclin dependent kinase 6	Homo sapiens	32-36
25744718-7	2015	In vivo, timely inhibition of CDK4/CDK6 by PD 0332991 and release profoundly suppresses tumor growth in response to reduced doses of Ara-C in a xenograft AML model.	Cytarabine	133-138	cyclin dependent kinase 4	Homo sapiens	30-34
25744718-7	2015	In vivo, timely inhibition of CDK4/CDK6 by PD 0332991 and release profoundly suppresses tumor growth in response to reduced doses of Ara-C in a xenograft AML model.	Cytarabine	133-138	cyclin dependent kinase 6	Homo sapiens	35-39
25744718-8	2015	Collectively, these data suggest selective and reversible inhibition of CDK4/CDK6 as an effective means to enhance Ara-C killing of AML cells at reduced doses, which has implications for the treatment of elderly AML patients who are unable to tolerate high-dose Ara-C therapy.	Cytarabine	115-120	cyclin dependent kinase 4	Homo sapiens	72-76
25744718-8	2015	Collectively, these data suggest selective and reversible inhibition of CDK4/CDK6 as an effective means to enhance Ara-C killing of AML cells at reduced doses, which has implications for the treatment of elderly AML patients who are unable to tolerate high-dose Ara-C therapy.	Cytarabine	115-120	cyclin dependent kinase 6	Homo sapiens	77-81
25744718-8	2015	Collectively, these data suggest selective and reversible inhibition of CDK4/CDK6 as an effective means to enhance Ara-C killing of AML cells at reduced doses, which has implications for the treatment of elderly AML patients who are unable to tolerate high-dose Ara-C therapy.	Cytarabine	262-267	cyclin dependent kinase 4	Homo sapiens	72-76
25744718-8	2015	Collectively, these data suggest selective and reversible inhibition of CDK4/CDK6 as an effective means to enhance Ara-C killing of AML cells at reduced doses, which has implications for the treatment of elderly AML patients who are unable to tolerate high-dose Ara-C therapy.	Cytarabine	262-267	cyclin dependent kinase 6	Homo sapiens	77-81
25495470-4	2015	AREAS COVERED: Among the antimetabolites, a small but widely prescribed number of drugs (i.e., gemcitabine, capecitabine, cytarabine, azacytidine) share a same metabolic pattern driven by a liver enzyme, cytidine deaminase (CDA), coded by a gene displaying several genetic and epigenetic polymorphisms.	Cytarabine	122-132	cytidine deaminase	Homo sapiens	224-227
25964636-3	2015	In the present report, the use of sorafenib in combination with cytarabine and idarubicin resulted in disease control for 7 months in an older patient with relapsed FLT3-positive AML.	Cytarabine	64-74	fms related receptor tyrosine kinase 3	Homo sapiens	165-169
26136865-5	2015	Furthermore, following knockdown GAPDH expression via siRNA transient transfection, HepG2 cells exhibited enhanced resistance to cytosine arabinoside (IC50, 308.28 microM vs. 67.68 microM in the control; P=0.01).	Cytarabine	129-149	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	33-38
25736313-7	2015	Ectopic overexpression of INPP4B conferred leukemic resistance to cytosine arabinoside (ara-C), daunorubicin, and etoposide.	Cytarabine	66-86	inositol polyphosphate-4-phosphatase type II B	Homo sapiens	26-32
25759982-8	2015	Transfection of the mimic miR-126-5p into the AML cell line, KG-1, resulted in a decrease in the sensitivity to cytarabin and the expression level of Klotho mRNA as well as the elevation in the phosphorylation of Akt.	Cytarabine	112-121	microRNA 1265	Homo sapiens	26-36
25736313-7	2015	Ectopic overexpression of INPP4B conferred leukemic resistance to cytosine arabinoside (ara-C), daunorubicin, and etoposide.	Cytarabine	88-93	inositol polyphosphate-4-phosphatase type II B	Homo sapiens	26-32
26131272-0	2015	Inhibition of ERK5 enhances cytarabine-induced apoptosis in acute myeloid leukemia cells.	Cytarabine	28-38	mitogen-activated protein kinase 7	Homo sapiens	14-18
25901794-6	2015	In addition, in vitro cell culture experiments with established cell lines and a second set of primary AML cells showed that oncogenic NRAS mutations predisposed cells to cytarabine (AraC) driven differentiation.	Cytarabine	171-181	NRAS proto-oncogene, GTPase	Homo sapiens	135-139
25901794-7	2015	Taken together, our findings show that AML with inv(16) and NRAS mutation have a differentiation gene signature, supporting the notion that NRAS mutation may predispose leukemic cells to AraC induced differentiation.	Cytarabine	187-191	NRAS proto-oncogene, GTPase	Homo sapiens	60-64
25901794-7	2015	Taken together, our findings show that AML with inv(16) and NRAS mutation have a differentiation gene signature, supporting the notion that NRAS mutation may predispose leukemic cells to AraC induced differentiation.	Cytarabine	187-191	NRAS proto-oncogene, GTPase	Homo sapiens	140-144
26131272-3	2015	The aim of this study was to investigate the effect of a specific ERK5 small interference RNA (siRNA) on proliferation and the sensitivity of HL-60 acute myeloid leukemia (AML) cells to the chemotherapeutic drug cytarabine.	Cytarabine	212-222	mitogen-activated protein kinase 7	Homo sapiens	66-70
26131272-9	2015	Surprisingly, ERK5 siRNA synergistically increased the cell toxic effects of cytarabine.	Cytarabine	77-87	mitogen-activated protein kinase 7	Homo sapiens	14-18
25242459-8	2015	We found that a 7-day infusion of Ara-C significantly reduced the total number of BrdU(+) and DCX(+) cells in the dentate gyrus (DG) in both hemispheres.	Cytarabine	34-39	doublecortin	Homo sapiens	94-97
25758781-7	2015	Depletion and complementation experiments validated the causal relationship between SLX4 defects and sensitivity to raltitrexed and cytarabine in addition to camptothecin.	Cytarabine	132-142	SLX4 structure-specific endonuclease subunit	Homo sapiens	84-88
25557962-7	2015	CONCLUSIONS: Our results indicate that DCK polymorphisms might be important genetic risk factors for hematologic toxicity during ALL treatment with ara-C.	Cytarabine	148-153	deoxycytidine kinase	Homo sapiens	39-42
25625234-0	2015	Ara-C increases gastric cancer cell invasion by upregulating CD-147-MMP-2/MMP-9 via the ERK signaling pathway.	Cytarabine	0-5	basigin (Ok blood group)	Homo sapiens	61-67
25625234-0	2015	Ara-C increases gastric cancer cell invasion by upregulating CD-147-MMP-2/MMP-9 via the ERK signaling pathway.	Cytarabine	0-5	matrix metallopeptidase 2	Homo sapiens	68-73
25625234-0	2015	Ara-C increases gastric cancer cell invasion by upregulating CD-147-MMP-2/MMP-9 via the ERK signaling pathway.	Cytarabine	0-5	matrix metallopeptidase 9	Homo sapiens	74-79
25625234-0	2015	Ara-C increases gastric cancer cell invasion by upregulating CD-147-MMP-2/MMP-9 via the ERK signaling pathway.	Cytarabine	0-5	mitogen-activated protein kinase 1	Homo sapiens	88-91
25625234-8	2015	Although low-dose Ara-C had no obvious effect on cell proliferation, it upregulated the expression of MMP-2, MMP-9 and CD-147 and ERK activation.	Cytarabine	18-23	matrix metallopeptidase 2	Homo sapiens	102-107
25625234-8	2015	Although low-dose Ara-C had no obvious effect on cell proliferation, it upregulated the expression of MMP-2, MMP-9 and CD-147 and ERK activation.	Cytarabine	18-23	matrix metallopeptidase 9	Homo sapiens	109-114
25625234-8	2015	Although low-dose Ara-C had no obvious effect on cell proliferation, it upregulated the expression of MMP-2, MMP-9 and CD-147 and ERK activation.	Cytarabine	18-23	basigin (Ok blood group)	Homo sapiens	119-125
25625234-8	2015	Although low-dose Ara-C had no obvious effect on cell proliferation, it upregulated the expression of MMP-2, MMP-9 and CD-147 and ERK activation.	Cytarabine	18-23	mitogen-activated protein kinase 1	Homo sapiens	130-133
25625234-10	2015	U-0126 and siRNA-CD-147 inhibited the induction of Ara-C in gastric cancer cell invasion.	Cytarabine	51-56	basigin (Ok blood group)	Homo sapiens	17-23
25625234-11	2015	Therefore, Ara-C enhances the invasiveness of gastric cancer cells by expression of CD-147 /MMP-2 and MMP-9 via the ERK signaling pathway.	Cytarabine	11-16	basigin (Ok blood group)	Homo sapiens	84-90
25625234-11	2015	Therefore, Ara-C enhances the invasiveness of gastric cancer cells by expression of CD-147 /MMP-2 and MMP-9 via the ERK signaling pathway.	Cytarabine	11-16	matrix metallopeptidase 2	Homo sapiens	92-97
25625234-11	2015	Therefore, Ara-C enhances the invasiveness of gastric cancer cells by expression of CD-147 /MMP-2 and MMP-9 via the ERK signaling pathway.	Cytarabine	11-16	matrix metallopeptidase 9	Homo sapiens	102-107
25625234-11	2015	Therefore, Ara-C enhances the invasiveness of gastric cancer cells by expression of CD-147 /MMP-2 and MMP-9 via the ERK signaling pathway.	Cytarabine	11-16	mitogen-activated protein kinase 1	Homo sapiens	116-119
25567217-0	2015	Association of ABCB1 polymorphisms with prognostic outcomes of anthracycline and cytarabine in Chinese patients with acute myeloid leukemia.	Cytarabine	81-91	ATP binding cassette subfamily B member 1	Homo sapiens	15-20
25768922-8	2015	The elevated ROS levels induced by Ara-C were caused by both over-generation of mitochondrial ROS and reduction of antioxidant enzymes (Cu/Zn Superoxide dismutase and catalase).	Cytarabine	35-40	catalase	Homo sapiens	167-175
25354577-3	2015	STUDY DESIGN AND METHODS: We report on 33 patients diagnosed with lymphoma who had at least one prior mobilization failure and received cytarabine at a dose of 400 mg/m(2) /day intravenously x 3 days plus granulocyte-colony-stimulating factor (G-CSF) 10 to 12 mug/kg/day as mobilization regimen.	Cytarabine	136-146	colony stimulating factor 3	Homo sapiens	205-242
25354577-3	2015	STUDY DESIGN AND METHODS: We report on 33 patients diagnosed with lymphoma who had at least one prior mobilization failure and received cytarabine at a dose of 400 mg/m(2) /day intravenously x 3 days plus granulocyte-colony-stimulating factor (G-CSF) 10 to 12 mug/kg/day as mobilization regimen.	Cytarabine	136-146	colony stimulating factor 3	Homo sapiens	244-249
25591760-0	2015	The OPN gene polymorphism confers the susceptibility and response to Ara-C based chemotherapy in Chinese AML patients.	Cytarabine	69-74	secreted phosphoprotein 1	Homo sapiens	4-7
25388161-0	2015	The NEDD8-activating enzyme inhibitor MLN4924 disrupts nucleotide metabolism and augments the efficacy of cytarabine.	Cytarabine	106-116	NEDD8 ubiquitin like modifier	Homo sapiens	4-9
25388161-0	2015	The NEDD8-activating enzyme inhibitor MLN4924 disrupts nucleotide metabolism and augments the efficacy of cytarabine.	Cytarabine	106-116	motilin	Homo sapiens	38-41
25591760-10	2015	Cellular assay indicated that the leukemic cell lines receiving the OPN -443C transfection have a significantly lower apoptosis rate to Ara-C treatment compared to cell lines transfected with -443T.	Cytarabine	136-141	secreted phosphoprotein 1	Homo sapiens	68-71
25425688-0	2015	A phase I trial of ribavirin and low-dose cytarabine for the treatment of relapsed and refractory acute myeloid leukemia with elevated eIF4E.	Cytarabine	42-52	eukaryotic translation initiation factor 4E	Homo sapiens	135-140
25674464-0	2014	Overexpression of MRP4 (ABCC4) and MRP5 (ABCC5) confer resistance to the nucleoside analogs cytarabine and troxacitabine, but not gemcitabine.	Cytarabine	92-102	ATP binding cassette subfamily C member 4	Homo sapiens	18-22
26637766-3	2015	A mutation in GATA1, common in AML of Down syndrome (ML-DS), renders cells more susceptible to cytarabine and anthracyclines, thus permitting targeted dose reductions to preserve high survival rates while reducing toxicity.	Cytarabine	95-105	GATA binding protein 1	Homo sapiens	14-19
25674464-1	2014	UNLABELLED: We aimed to determine whether the multidrug-resistance-proteins MRP4 (ABCC4) and MRP5 (ABCC5) confer resistance to the antimetabolites cytarabine (Ara-C), gemcitabine (GEM), and the L-nucleoside analog troxacitabine.	Cytarabine	147-157	ATP binding cassette subfamily C member 4	Homo sapiens	76-80
25674464-1	2014	UNLABELLED: We aimed to determine whether the multidrug-resistance-proteins MRP4 (ABCC4) and MRP5 (ABCC5) confer resistance to the antimetabolites cytarabine (Ara-C), gemcitabine (GEM), and the L-nucleoside analog troxacitabine.	Cytarabine	147-157	ATP binding cassette subfamily C member 4	Homo sapiens	82-87
25477336-10	2014	Inhibition of Gli1 reduced UGT1As, eliminated drug glucuronides, and renewed sensitivity to ribavirin and Ara-C.	Cytarabine	106-111	GLI family zinc finger 1	Homo sapiens	14-18
25674464-0	2014	Overexpression of MRP4 (ABCC4) and MRP5 (ABCC5) confer resistance to the nucleoside analogs cytarabine and troxacitabine, but not gemcitabine.	Cytarabine	92-102	ATP binding cassette subfamily C member 4	Homo sapiens	24-29
25674464-0	2014	Overexpression of MRP4 (ABCC4) and MRP5 (ABCC5) confer resistance to the nucleoside analogs cytarabine and troxacitabine, but not gemcitabine.	Cytarabine	92-102	ATP binding cassette subfamily C member 5	Homo sapiens	35-39
25674464-1	2014	UNLABELLED: We aimed to determine whether the multidrug-resistance-proteins MRP4 (ABCC4) and MRP5 (ABCC5) confer resistance to the antimetabolites cytarabine (Ara-C), gemcitabine (GEM), and the L-nucleoside analog troxacitabine.	Cytarabine	147-157	ATP binding cassette subfamily C member 5	Homo sapiens	93-97
25674464-1	2014	UNLABELLED: We aimed to determine whether the multidrug-resistance-proteins MRP4 (ABCC4) and MRP5 (ABCC5) confer resistance to the antimetabolites cytarabine (Ara-C), gemcitabine (GEM), and the L-nucleoside analog troxacitabine.	Cytarabine	147-157	ATP binding cassette subfamily C member 5	Homo sapiens	99-104
25674464-1	2014	UNLABELLED: We aimed to determine whether the multidrug-resistance-proteins MRP4 (ABCC4) and MRP5 (ABCC5) confer resistance to the antimetabolites cytarabine (Ara-C), gemcitabine (GEM), and the L-nucleoside analog troxacitabine.	Cytarabine	159-164	ATP binding cassette subfamily C member 4	Homo sapiens	76-80
25674464-1	2014	UNLABELLED: We aimed to determine whether the multidrug-resistance-proteins MRP4 (ABCC4) and MRP5 (ABCC5) confer resistance to the antimetabolites cytarabine (Ara-C), gemcitabine (GEM), and the L-nucleoside analog troxacitabine.	Cytarabine	159-164	ATP binding cassette subfamily C member 4	Homo sapiens	82-87
25674464-0	2014	Overexpression of MRP4 (ABCC4) and MRP5 (ABCC5) confer resistance to the nucleoside analogs cytarabine and troxacitabine, but not gemcitabine.	Cytarabine	92-102	ATP binding cassette subfamily C member 5	Homo sapiens	41-46
25674464-1	2014	UNLABELLED: We aimed to determine whether the multidrug-resistance-proteins MRP4 (ABCC4) and MRP5 (ABCC5) confer resistance to the antimetabolites cytarabine (Ara-C), gemcitabine (GEM), and the L-nucleoside analog troxacitabine.	Cytarabine	159-164	ATP binding cassette subfamily C member 5	Homo sapiens	93-97
25674464-1	2014	UNLABELLED: We aimed to determine whether the multidrug-resistance-proteins MRP4 (ABCC4) and MRP5 (ABCC5) confer resistance to the antimetabolites cytarabine (Ara-C), gemcitabine (GEM), and the L-nucleoside analog troxacitabine.	Cytarabine	159-164	ATP binding cassette subfamily C member 5	Homo sapiens	99-104
25469211-3	2014	Elacytarabine, a lipophilic 5"-elaidic acid ester or nucleoside analogue of cytosine arabinoside, was created with the intent of overcoming resistance mechanisms including reduced expression of the human equilibrative nucleoside transporter 1 (hENT1) required for cytarabine entry into cells, as well as increased activity of cytidine deaminase (CDA) which breaks down the active metabolite of cytarabine, ara-CTP.	Cytarabine	3-13	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	204-242
25674464-4	2014	At 4-hr exposure HEK/MRP4 cells were 2-4-fold resistant to troxacitabine, ara-C and 9-(2-phosphonylmethoxyethyl)adenine (PMEA), and HEK/MRP5i to ara-C and PMEA, but none to GEM.	Cytarabine	74-79	ATP binding cassette subfamily C member 4	Homo sapiens	21-25
25674464-4	2014	At 4-hr exposure HEK/MRP4 cells were 2-4-fold resistant to troxacitabine, ara-C and 9-(2-phosphonylmethoxyethyl)adenine (PMEA), and HEK/MRP5i to ara-C and PMEA, but none to GEM.	Cytarabine	145-150	ATP binding cassette subfamily C member 4	Homo sapiens	21-25
25674464-10	2014	IN CONCLUSION: MRP4 and MRP5 overexpression confer resistance to troxacitabine and ara-C, but not to GEM, which was associated with a rapid decline of the ara-C and troxacitabine-nucleotides in HEK/MRP4-5 cells.	Cytarabine	83-88	ATP binding cassette subfamily C member 4	Homo sapiens	15-19
25674464-10	2014	IN CONCLUSION: MRP4 and MRP5 overexpression confer resistance to troxacitabine and ara-C, but not to GEM, which was associated with a rapid decline of the ara-C and troxacitabine-nucleotides in HEK/MRP4-5 cells.	Cytarabine	83-88	ATP binding cassette subfamily C member 5	Homo sapiens	24-28
25674464-10	2014	IN CONCLUSION: MRP4 and MRP5 overexpression confer resistance to troxacitabine and ara-C, but not to GEM, which was associated with a rapid decline of the ara-C and troxacitabine-nucleotides in HEK/MRP4-5 cells.	Cytarabine	83-88	ATP binding cassette subfamily C member 4	Homo sapiens	198-202
25674464-10	2014	IN CONCLUSION: MRP4 and MRP5 overexpression confer resistance to troxacitabine and ara-C, but not to GEM, which was associated with a rapid decline of the ara-C and troxacitabine-nucleotides in HEK/MRP4-5 cells.	Cytarabine	155-160	ATP binding cassette subfamily C member 4	Homo sapiens	15-19
25674464-10	2014	IN CONCLUSION: MRP4 and MRP5 overexpression confer resistance to troxacitabine and ara-C, but not to GEM, which was associated with a rapid decline of the ara-C and troxacitabine-nucleotides in HEK/MRP4-5 cells.	Cytarabine	155-160	ATP binding cassette subfamily C member 5	Homo sapiens	24-28
25674464-10	2014	IN CONCLUSION: MRP4 and MRP5 overexpression confer resistance to troxacitabine and ara-C, but not to GEM, which was associated with a rapid decline of the ara-C and troxacitabine-nucleotides in HEK/MRP4-5 cells.	Cytarabine	155-160	ATP binding cassette subfamily C member 4	Homo sapiens	198-202
25485965-3	2014	We found that ZNF300 upregulation in K562 cells coincided with megakaryocytic differentiation induced by phorbol-12-myristate-13-acetate (PMA) or erythrocytic differentiation induced by cytosine arabinoside (Ara-C), respectively.	Cytarabine	186-206	zinc finger protein 300	Homo sapiens	14-20
25485965-3	2014	We found that ZNF300 upregulation in K562 cells coincided with megakaryocytic differentiation induced by phorbol-12-myristate-13-acetate (PMA) or erythrocytic differentiation induced by cytosine arabinoside (Ara-C), respectively.	Cytarabine	208-213	zinc finger protein 300	Homo sapiens	14-20
25485965-5	2014	Furthermore, Ara-C-induced erythrocytic differentiation was also suppressed in ZNF300 knockdown cells with decreased gamma-globin expression and CD235a expression.	Cytarabine	13-18	zinc finger protein 300	Homo sapiens	79-85
25485965-5	2014	Furthermore, Ara-C-induced erythrocytic differentiation was also suppressed in ZNF300 knockdown cells with decreased gamma-globin expression and CD235a expression.	Cytarabine	13-18	glycophorin A (MNS blood group)	Homo sapiens	145-151
25469211-7	2014	Use of hENT1 expression as a predictive marker for cytarabine or elacytarabine response has been studied with no conclusive validation to date.	Cytarabine	51-61	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	7-12
25469211-3	2014	Elacytarabine, a lipophilic 5"-elaidic acid ester or nucleoside analogue of cytosine arabinoside, was created with the intent of overcoming resistance mechanisms including reduced expression of the human equilibrative nucleoside transporter 1 (hENT1) required for cytarabine entry into cells, as well as increased activity of cytidine deaminase (CDA) which breaks down the active metabolite of cytarabine, ara-CTP.	Cytarabine	3-13	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	244-249
25469211-3	2014	Elacytarabine, a lipophilic 5"-elaidic acid ester or nucleoside analogue of cytosine arabinoside, was created with the intent of overcoming resistance mechanisms including reduced expression of the human equilibrative nucleoside transporter 1 (hENT1) required for cytarabine entry into cells, as well as increased activity of cytidine deaminase (CDA) which breaks down the active metabolite of cytarabine, ara-CTP.	Cytarabine	3-13	cytidine deaminase	Homo sapiens	326-344
25469211-3	2014	Elacytarabine, a lipophilic 5"-elaidic acid ester or nucleoside analogue of cytosine arabinoside, was created with the intent of overcoming resistance mechanisms including reduced expression of the human equilibrative nucleoside transporter 1 (hENT1) required for cytarabine entry into cells, as well as increased activity of cytidine deaminase (CDA) which breaks down the active metabolite of cytarabine, ara-CTP.	Cytarabine	3-13	cytidine deaminase	Homo sapiens	346-349
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.	Cytarabine	91-101	interleukin 1 beta	Homo sapiens	128-136
25398670-11	2014	CONCLUSIONS: AML patients with low activity of SLC29A1 genotype have shorter DFS and OS in Ara-C based therapy.	Cytarabine	91-96	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	47-54
25417874-1	2014	OBJECTIVE: To observe the efficacy and adverse reaction of the improvement program of cladribine combined with cytarabine (2-CdA+Ara-C) in treatment of children with refractory high-risk Langerhans cell histiocytosis (LCH).	Cytarabine	111-121	cytidine deaminase	Homo sapiens	125-128
24255981-6	2014	There is a trend suggesting that hENT1 expression influences response to cytarabine, but not sufficient to support it as a biomarker for guiding treatment.	Cytarabine	73-83	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	33-38
24962331-3	2014	One new therapeutic approach is preventing cell cycle checkpoint activation by inhibiting the upstream kinase wee1 with the first-in-class inhibitor MK-1775 in combination with the standard genotoxic agent cytarabine (AraC).	Cytarabine	206-216	WEE1 G2 checkpoint kinase	Homo sapiens	110-114
24962331-3	2014	One new therapeutic approach is preventing cell cycle checkpoint activation by inhibiting the upstream kinase wee1 with the first-in-class inhibitor MK-1775 in combination with the standard genotoxic agent cytarabine (AraC).	Cytarabine	218-222	WEE1 G2 checkpoint kinase	Homo sapiens	110-114
25003625-2	2014	Because of impaired transplantation, a study of cytidine deaminase (CDA), the liver enzyme responsible for cytarabine detoxification, was conducted before initiating treatment to evaluate the risk for toxicity in this patient.	Cytarabine	107-117	cytidine deaminase	Homo sapiens	48-66
25003625-2	2014	Because of impaired transplantation, a study of cytidine deaminase (CDA), the liver enzyme responsible for cytarabine detoxification, was conducted before initiating treatment to evaluate the risk for toxicity in this patient.	Cytarabine	107-117	cytidine deaminase	Homo sapiens	68-71
25138052-5	2014	TFC and TNC display enhanced effects with anticancer drugs cytarabine vincristine, andmethotrexate on inhibition of lung cancer cell growth and no toxicity to the normal human embryonic lung fibroblast and peripheral blood lymphocytes.	Cytarabine	59-69	tenascin C	Homo sapiens	8-11
24687871-8	2014	Gene expression profiling of the ICE-T treated tumorgrafts identified cytarabine (SLC29A1) as a potential therapy, which was shown, along with BGJ398, to be highly active in vivo.	Cytarabine	70-80	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	82-89
24956556-1	2014	Based on the potent anticancer activity of the D-arabino-configured cytosine nucleoside ara-C, novel 2"-substituted-4"-selenoarabinofuranosyl pyrimidines 3a-3u, comprising azido, fluoro, and hydroxyl substituents at C-2" were designed, synthesized, and evaluated for anticancer activity.	Cytarabine	88-93	complement C2	Homo sapiens	216-219
25000516-1	2014	AIMS: The cytosolic 5"-nucleotidase-III (NT5C3) is involved in the metabolism of the nucleoside analog, cytosine arabinose (AraC), and the expression level of NT5C3 is correlated with sensitivity to AraC in acute myeloid leukemia (AML) patients.	Cytarabine	124-128	5'-nucleotidase, cytosolic IIIA	Homo sapiens	41-46
25000516-1	2014	AIMS: The cytosolic 5"-nucleotidase-III (NT5C3) is involved in the metabolism of the nucleoside analog, cytosine arabinose (AraC), and the expression level of NT5C3 is correlated with sensitivity to AraC in acute myeloid leukemia (AML) patients.	Cytarabine	124-128	5'-nucleotidase, cytosolic IIIA	Homo sapiens	159-164
25000516-7	2014	CONCLUSIONS: The data suggest that genotyping the NT5C3 polymorphism may have the potential to identify patients more likely to respond to AraC-based chemotherapy.	Cytarabine	139-143	5'-nucleotidase, cytosolic IIIA	Homo sapiens	50-55
25187756-6	2014	siRNA-mediated down-regulation of CCN1 inhibited the proliferation and colony formation of U937 and Kasumi-1 cells and increased cytarabine-induced apoptosis.	Cytarabine	129-139	cellular communication network factor 1	Homo sapiens	34-38
24870236-8	2014	GLI1 alone is sufficient to drive UGT1A-dependent glucuronidation of ribavirin and Ara-C, and thus drug resistance.	Cytarabine	83-88	GLI family zinc finger 1	Homo sapiens	0-4
25116387-3	2014	We found protein modifying loss-of-function mutations in Dck in both Ara-C resistant cell lines.	Cytarabine	69-74	deoxycytidine kinase	Homo sapiens	57-60
25116387-4	2014	CRISPR and TALEN-based KO of Dck dramatically increased the IC50 of Ara-C and introduction of a DCK overexpression vector into Dck KO clones resulted in a significant increase in Ara-C sensitivity.	Cytarabine	68-73	deoxycytidine kinase	Homo sapiens	29-32
25116387-4	2014	CRISPR and TALEN-based KO of Dck dramatically increased the IC50 of Ara-C and introduction of a DCK overexpression vector into Dck KO clones resulted in a significant increase in Ara-C sensitivity.	Cytarabine	179-184	deoxycytidine kinase	Homo sapiens	29-32
25116387-4	2014	CRISPR and TALEN-based KO of Dck dramatically increased the IC50 of Ara-C and introduction of a DCK overexpression vector into Dck KO clones resulted in a significant increase in Ara-C sensitivity.	Cytarabine	179-184	deoxycytidine kinase	Homo sapiens	96-99
25116387-4	2014	CRISPR and TALEN-based KO of Dck dramatically increased the IC50 of Ara-C and introduction of a DCK overexpression vector into Dck KO clones resulted in a significant increase in Ara-C sensitivity.	Cytarabine	179-184	deoxycytidine kinase	Homo sapiens	127-130
25012726-13	2014	IMPLICATIONS: These findings suggest that ABCB1 gene polymorphisms are associated with antiemetic efficacy of ondansetron in the acute phase after high-dose cytarabine chemotherapy in AML patients.	Cytarabine	157-167	ATP binding cassette subfamily B member 1	Homo sapiens	42-47
24870236-8	2014	GLI1 alone is sufficient to drive UGT1A-dependent glucuronidation of ribavirin and Ara-C, and thus drug resistance.	Cytarabine	83-88	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	34-39
24944809-0	2014	The differentiation effect of low-dose cytosine arabinoside is disturbed in PU.1-knockdown K562 cells.	Cytarabine	39-59	Spi-1 proto-oncogene	Homo sapiens	76-80
24799523-3	2014	EXPERIMENTAL DESIGN: We treated B-cell lymphoma cells with the TLR1/2 agonist Pam3CSK4 and the genotoxic anticancer agent 1-beta-D-arabinofuranosylcytosine (Ara-C).	Cytarabine	157-162	toll-like receptor 12	Mus musculus	63-69
24799523-5	2014	RESULTS: The treatment of B-cell lymphoma cells with the TLR1/2 agonist Pam3CSK4 enhanced the anticancer effects of the genotoxic agent Ara-C.	Cytarabine	136-141	toll-like receptor 12	Mus musculus	57-63
24944809-2	2014	In this study, we investigated whether the effects of low-dose cytosine arabinoside (Ara-C), which is another erythroid differentiation inducer in K562 cells, is associated with the expression level of PU.1 in these cells.	Cytarabine	63-83	Spi-1 proto-oncogene	Homo sapiens	202-206
24944809-2	2014	In this study, we investigated whether the effects of low-dose cytosine arabinoside (Ara-C), which is another erythroid differentiation inducer in K562 cells, is associated with the expression level of PU.1 in these cells.	Cytarabine	85-90	Spi-1 proto-oncogene	Homo sapiens	202-206
24675086-0	2014	Chromosome breakage induced by the genotoxic agents mitomycin C and cytosine arabinoside is concentration and p53 dependent.	Cytarabine	68-88	tumor protein p53	Homo sapiens	110-113
24675086-8	2014	On the other hand, higher levels of micronucleus and p53 induction were shown in TK6 cells treated with araC and a G1/S arrest was observed after araC treatment.	Cytarabine	104-108	tumor protein p53	Homo sapiens	53-56
24675086-9	2014	p53 deficient NH32 cells showed an increased sensitivity of micronucleus (MN) induction after araC treatment compared with TK6 cells and less of an active G1/S phase checkpoint.	Cytarabine	94-98	tumor protein p53	Homo sapiens	0-3
24714637-0	2014	Inhibition of mTOR-dependent autophagy sensitizes leukemic cells to cytarabine-induced apoptotic death.	Cytarabine	68-78	mechanistic target of rapamycin kinase	Homo sapiens	14-18
24682933-10	2014	Importantly, silencing miR-200c expression sensitized the therapeutic effect of Ara-C (Cytarabine).	Cytarabine	80-85	microRNA 200c	Homo sapiens	23-31
24682933-10	2014	Importantly, silencing miR-200c expression sensitized the therapeutic effect of Ara-C (Cytarabine).	Cytarabine	87-97	microRNA 200c	Homo sapiens	23-31
24103790-4	2014	ABCC10 is a broad-specificity transporter of xenobiotics, including antitumor drugs, such as taxanes, epothilone B, vinca alkaloids, and cytarabine, as well as modulators of the estrogen pathway, such as tamoxifen.	Cytarabine	137-147	ATP binding cassette subfamily C member 10	Homo sapiens	0-6
24342948-0	2014	BCL2-specific inhibitor ABT-199 synergizes strongly with cytarabine against the early immature LOUCY cell line but not more-differentiated T-ALL cell lines.	Cytarabine	57-67	BCL2 apoptosis regulator	Homo sapiens	0-4
24972933-0	2014	Downregulation of deoxycytidine kinase in cytarabine-resistant mantle cell lymphoma cells confers cross-resistance to nucleoside analogs gemcitabine, fludarabine and cladribine, but not to other classes of anti-lymphoma agents.	Cytarabine	42-52	deoxycytidine kinase	Homo sapiens	18-38
24972933-9	2014	RESULTS: Marked downregulation of deoxycytidine-kinase (DCK) mRNA and protein expression was identified as the single most important molecular event associated with araC-resistance in all tested MCL cell lines and in 50% primary MCL samples.	Cytarabine	165-169	deoxycytidine kinase	Homo sapiens	34-54
24972933-9	2014	RESULTS: Marked downregulation of deoxycytidine-kinase (DCK) mRNA and protein expression was identified as the single most important molecular event associated with araC-resistance in all tested MCL cell lines and in 50% primary MCL samples.	Cytarabine	165-169	deoxycytidine kinase	Homo sapiens	56-59
24858818-8	2014	Notably, SYC-522 treatment significantly increased the sensitivity of MLL-rearranged leukemia cells to chemotherapeutics, such as mitoxantrone, etoposide and cytarabine.	Cytarabine	158-168	lysine methyltransferase 2A	Homo sapiens	70-73
24769646-4	2014	Combining ATRA with cytarabine had a synergistic antileukemic effect in MLL-AF9-positive cells in vitro.	Cytarabine	20-30	lysine methyltransferase 2A	Homo sapiens	72-75
24769646-4	2014	Combining ATRA with cytarabine had a synergistic antileukemic effect in MLL-AF9-positive cells in vitro.	Cytarabine	20-30	MLLT3 super elongation complex subunit	Homo sapiens	76-79
24714637-3	2014	Moreover, the expression of autophagy-related genes Atg4, Atg5 and Atg7 was stimulated by cytarabine in REH cells.	Cytarabine	90-100	autophagy related 5	Homo sapiens	58-62
24714637-3	2014	Moreover, the expression of autophagy-related genes Atg4, Atg5 and Atg7 was stimulated by cytarabine in REH cells.	Cytarabine	90-100	autophagy related 7	Homo sapiens	67-71
24714637-4	2014	Cytarabine reduced the phosphorylation of the major negative regulator of autophagy, mammalian target of rapamycin (mTOR), and its downstream target p70S6 kinase in REH cells, which was associated with downregulation of mTOR activator Akt and activation of extracellular signal- regulated kinase.	Cytarabine	0-10	mechanistic target of rapamycin kinase	Homo sapiens	85-114
24714637-4	2014	Cytarabine reduced the phosphorylation of the major negative regulator of autophagy, mammalian target of rapamycin (mTOR), and its downstream target p70S6 kinase in REH cells, which was associated with downregulation of mTOR activator Akt and activation of extracellular signal- regulated kinase.	Cytarabine	0-10	mechanistic target of rapamycin kinase	Homo sapiens	116-120
24714637-4	2014	Cytarabine reduced the phosphorylation of the major negative regulator of autophagy, mammalian target of rapamycin (mTOR), and its downstream target p70S6 kinase in REH cells, which was associated with downregulation of mTOR activator Akt and activation of extracellular signal- regulated kinase.	Cytarabine	0-10	mechanistic target of rapamycin kinase	Homo sapiens	220-224
24714637-4	2014	Cytarabine reduced the phosphorylation of the major negative regulator of autophagy, mammalian target of rapamycin (mTOR), and its downstream target p70S6 kinase in REH cells, which was associated with downregulation of mTOR activator Akt and activation of extracellular signal- regulated kinase.	Cytarabine	0-10	AKT serine/threonine kinase 1	Homo sapiens	235-238
24714637-6	2014	Leucine, an mTOR activator, reduced both cytarabine-induced autophagy and cytotoxicity.	Cytarabine	41-51	mechanistic target of rapamycin kinase	Homo sapiens	12-16
24714637-8	2014	Cytarabine also induced mTOR-dependent cytoprotective autophagy in HL-60 and MOLT-4 leukemic cell lines, as well as primary leukemic cells, but not normal leukocytes.	Cytarabine	0-10	mechanistic target of rapamycin kinase	Homo sapiens	24-28
24714637-9	2014	These data suggest that the therapeutic efficiency of cytarabine in leukemic patients could be increased by the inhibition of the mTOR-dependent autophagic response.	Cytarabine	54-64	mechanistic target of rapamycin kinase	Homo sapiens	130-134
24692694-2	2014	Cytarabine uses hENT1 and dCK for its activation.	Cytarabine	0-10	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	16-21
24413389-7	2014	After silencing HO-1 by siRNA transfection with lentivirus, the cells" proliferation induced by UA was increased as it was by Ara-C.	Cytarabine	126-131	heme oxygenase 1	Homo sapiens	16-20
24692694-2	2014	Cytarabine uses hENT1 and dCK for its activation.	Cytarabine	0-10	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	26-29
25011265-8	2014	The percentage of positive stained aging cells was dramatically increased, and could significantly up-regulate the expression of aging-related proteins P16 and RB, which were more obvious in the ASP + Ara-C group.	Cytarabine	201-206	cyclin dependent kinase inhibitor 2A	Homo sapiens	152-155
24474669-11	2014	CONCLUSIONS: We have developed a potent and selective pan-PIM inhibitor with single-agent antiproliferative activity and show that it synergizes with cytarabine in an AML xenograft model.	Cytarabine	150-160	Pim-1 proto-oncogene, serine/threonine kinase	Homo sapiens	58-61
24375249-0	2014	Knockdown of CD44 enhances chemosensitivity of acute myeloid leukemia cells to ADM and Ara-C.	Cytarabine	87-92	CD44 molecule (Indian blood group)	Homo sapiens	13-17
24375249-9	2014	siRNA/CD44 substantially induces cell apoptosis, inhibits cell proliferation, enhances susceptibility to ADM and Ara-C, and at the same time increases intracellular ADM accumulation even reverses chemoresistance to ADM and Ara-C.	Cytarabine	113-118	CD44 molecule (Indian blood group)	Homo sapiens	6-10
24375249-9	2014	siRNA/CD44 substantially induces cell apoptosis, inhibits cell proliferation, enhances susceptibility to ADM and Ara-C, and at the same time increases intracellular ADM accumulation even reverses chemoresistance to ADM and Ara-C.	Cytarabine	223-228	CD44 molecule (Indian blood group)	Homo sapiens	6-10
24375249-9	2014	siRNA/CD44 substantially induces cell apoptosis, inhibits cell proliferation, enhances susceptibility to ADM and Ara-C, and at the same time increases intracellular ADM accumulation even reverses chemoresistance to ADM and Ara-C.	Cytarabine	223-228	adrenomedullin	Homo sapiens	165-168
24375249-9	2014	siRNA/CD44 substantially induces cell apoptosis, inhibits cell proliferation, enhances susceptibility to ADM and Ara-C, and at the same time increases intracellular ADM accumulation even reverses chemoresistance to ADM and Ara-C.	Cytarabine	223-228	adrenomedullin	Homo sapiens	165-168
24375249-11	2014	Our study provides a novel clue that CD44 plays a significant role in the chemoresistance of AML cells to Ara-C and ADM.	Cytarabine	106-111	CD44 molecule (Indian blood group)	Homo sapiens	37-41
24184825-0	2014	Smac mimetic primes apoptosis-resistant acute myeloid leukaemia cells for cytarabine-induced cell death by triggering necroptosis.	Cytarabine	74-84	diablo IAP-binding mitochondrial protein	Homo sapiens	0-4
24184825-2	2014	Here, we report that the small-molecule Smac mimetic BV6, which antagonizes Inhibitor of Apoptosis (IAP) proteins, acts in concert with cytarabine (AraC) to trigger cell death in AML cells in a highly synergistic manner (combination index 0.02-0.27).	Cytarabine	136-146	diablo IAP-binding mitochondrial protein	Homo sapiens	40-44
23800093-9	2014	CONCLUSIONS: This preliminary result warrants further investigation of high-dose MTX and cytarabine plus G-CSF as a means to remobilize stem cells in those with prior failure to mobilize stem cells with chemotherapy and G-CSF.	Cytarabine	89-99	colony stimulating factor 3	Homo sapiens	220-225
23817178-7	2014	In contrast, only expression of the CXCR4-S339E mutant increased the BM retention of the cells and resistance to cytarabine treatment, and impaired detachment capacity and AMD3100-induced mobilization of engrafted leukemic cells.	Cytarabine	113-123	C-X-C motif chemokine receptor 4	Homo sapiens	36-41
24296429-0	2014	Facts about FCE (fludarabine, cytarabine, etoposide) in acute myeloid leukemia.	Cytarabine	30-40	ferrochelatase	Homo sapiens	12-15
24184161-10	2014	The depletion of COX-2 or ET-1 also suppressed VEGF-C-induced increases in the bcl-2/bax ratio and chemoresistance against etoposide and cytosine arabinoside in AML cells.	Cytarabine	137-157	prostaglandin-endoperoxide synthase 2	Homo sapiens	17-22
24184161-10	2014	The depletion of COX-2 or ET-1 also suppressed VEGF-C-induced increases in the bcl-2/bax ratio and chemoresistance against etoposide and cytosine arabinoside in AML cells.	Cytarabine	137-157	endothelin 1	Homo sapiens	26-30
24184161-10	2014	The depletion of COX-2 or ET-1 also suppressed VEGF-C-induced increases in the bcl-2/bax ratio and chemoresistance against etoposide and cytosine arabinoside in AML cells.	Cytarabine	137-157	vascular endothelial growth factor C	Homo sapiens	47-53
24013721-9	2014	Downregulation of ZEB1 by salinomycin increases the sensitivity of MCL cells to the cytotoxic effect of doxorubicin, cytarabine and gemcitabine.	Cytarabine	117-127	zinc finger E-box binding homeobox 1	Mus musculus	18-22
24183806-5	2014	Q27 variant is endowed with a greater catalytic efficiency toward the natural substrates and the antileukemic agent cytarabine (Ara-C), when compared to K27 variant.	Cytarabine	116-126	keratin 27	Homo sapiens	153-156
24080214-0	2014	Investigation and verification of a bioluminescent biosensor for the quantitation of ara-CTP generation: a biomarker for cytosine arabinoside sensitivity in acute myeloid leukaemia.	Cytarabine	121-141	solute carrier family 25 member 1	Homo sapiens	89-92
24080214-1	2014	A novel whole cell bacterial biosensor, which emits light in response to the active metabolite of cytosine arabinoside (ara-C, cytarabine), ara-CTP, has been investigated and verified.	Cytarabine	98-118	solute carrier family 25 member 1	Homo sapiens	144-147
24080214-1	2014	A novel whole cell bacterial biosensor, which emits light in response to the active metabolite of cytosine arabinoside (ara-C, cytarabine), ara-CTP, has been investigated and verified.	Cytarabine	120-125	solute carrier family 25 member 1	Homo sapiens	144-147
24080214-1	2014	A novel whole cell bacterial biosensor, which emits light in response to the active metabolite of cytosine arabinoside (ara-C, cytarabine), ara-CTP, has been investigated and verified.	Cytarabine	127-137	solute carrier family 25 member 1	Homo sapiens	144-147
24504051-8	2014	Furthermore, inhibitors modulating ERG druggable pathways WNT, PKC, and AKT, and chemotherapeutic agent cytarabine revealed ERG-induced drug resistance.	Cytarabine	104-114	ETS transcription factor ERG	Homo sapiens	124-127
25216956-5	2014	Transposition mutagenesis was used to create a cytidine deaminase (cdd)-deficient mutant of E. coli MG1655 that responded to ara-C.	Cytarabine	125-130	cytidine/deoxycytidine deaminase	Escherichia coli str. K-12 substr. MG1655	47-65
25216956-5	2014	Transposition mutagenesis was used to create a cytidine deaminase (cdd)-deficient mutant of E. coli MG1655 that responded to ara-C.	Cytarabine	125-130	cytidine/deoxycytidine deaminase	Escherichia coli str. K-12 substr. MG1655	67-70
25555870-0	2014	Knockdown of ERK/Slug signals sensitizes HL-60 Leukemia cells to Cytarabine via upregulation of PUMA.	Cytarabine	65-75	mitogen-activated protein kinase 1	Homo sapiens	13-16
25555870-0	2014	Knockdown of ERK/Slug signals sensitizes HL-60 Leukemia cells to Cytarabine via upregulation of PUMA.	Cytarabine	65-75	snail family transcriptional repressor 2	Homo sapiens	17-21
25555870-1	2014	OBJECTIVE: To study the mechanism of early chemosensitivity and later chemoresistance of Cytarabine (Cyt) to HL-60 cells to regulate ERK/Slug signal pathway.	Cytarabine	89-99	mitogen-activated protein kinase 1	Homo sapiens	133-136
25555870-1	2014	OBJECTIVE: To study the mechanism of early chemosensitivity and later chemoresistance of Cytarabine (Cyt) to HL-60 cells to regulate ERK/Slug signal pathway.	Cytarabine	89-99	snail family transcriptional repressor 2	Homo sapiens	137-141
25555870-1	2014	OBJECTIVE: To study the mechanism of early chemosensitivity and later chemoresistance of Cytarabine (Cyt) to HL-60 cells to regulate ERK/Slug signal pathway.	Cytarabine	89-92	mitogen-activated protein kinase 1	Homo sapiens	133-136
25555870-1	2014	OBJECTIVE: To study the mechanism of early chemosensitivity and later chemoresistance of Cytarabine (Cyt) to HL-60 cells to regulate ERK/Slug signal pathway.	Cytarabine	89-92	snail family transcriptional repressor 2	Homo sapiens	137-141
24940698-0	2014	Selection of the best blood compartment to measure cytidine deaminase activity to stratify for optimal gemcitabine or cytarabine treatment.	Cytarabine	118-128	cytidine deaminase	Homo sapiens	51-69
24940698-1	2014	Cytidine deaminase (CDA) plays a crucial role in the degradation of cytidine analogs, such as gemcitabine and cytarabine.	Cytarabine	110-120	cytidine deaminase	Homo sapiens	0-18
24940698-1	2014	Cytidine deaminase (CDA) plays a crucial role in the degradation of cytidine analogs, such as gemcitabine and cytarabine.	Cytarabine	110-120	cytidine deaminase	Homo sapiens	20-23
23686525-2	2013	We have also shown that CD34(+) /CD38(-) AML cells, one of compartments enriched for leukemia stem cells in most leukemia subgroups, were relatively resistant to cytarabine-mediated growth inhibition when compared to their CD34(+) /CD38(+) counterparts.	Cytarabine	162-172	CD34 molecule	Homo sapiens	24-28
24386436-3	2013	The mean values of GPA (CD235a) fluorescence intensity in the group of K562 cells pretreated by the toxin for 24 h and followed by cytosine arabinoside (Ara-C) treatment for 72 h were about 2-fold stronger than those of K562 cells induced by Ara-C alone.	Cytarabine	131-151	glycophorin A (MNS blood group)	Homo sapiens	24-30
24386436-3	2013	The mean values of GPA (CD235a) fluorescence intensity in the group of K562 cells pretreated by the toxin for 24 h and followed by cytosine arabinoside (Ara-C) treatment for 72 h were about 2-fold stronger than those of K562 cells induced by Ara-C alone.	Cytarabine	242-247	glycophorin A (MNS blood group)	Homo sapiens	24-30
24359526-1	2013	BACKGROUND: Chk1 inhibitors have emerged as promising anticancer therapeutic agents particularly when combined with antimetabolites such as gemcitabine, cytarabine or hydroxyurea.	Cytarabine	153-163	checkpoint kinase 1	Homo sapiens	12-16
24036285-11	2013	Interestingly, angiocidin+cytosine arabinoside (Ara-C) combination therapy reduced human AML in bone marrow by 79%.	Cytarabine	48-53	proteasome 26S subunit ubiquitin receptor, non-ATPase 4	Homo sapiens	15-25
24492044-0	2014	[Successful treatment with high-dose methotrexate/cytarabine regimen in a patient in SMILE regimen-resistant extranodal natural killer/T-cell lymphoma].	Cytarabine	50-60	transmembrane O-mannosyltransferase targeting cadherins 3	Homo sapiens	85-90
24754180-5	2014	Compared to the human leukemia NOD/SCID mouse model group with the treatments of APS, Ara-c and APS + Ara-c, We found that severe liver damage and pathological changes of the liver were able to alleviate: First, the number of white blood cells in the peripheral blood was significantly lower and with less transplanted K562 leukemia cells; Second, liver function damage was alleviated as liver function tests showed that alanine aminotransferase (ALT), aspartate aminotransferase (AST) and total bilirubin (TBiL) were significantly reduced, while the albumin (Alb) was notably increased; Third, liver antioxidant ability was improved as the activities of the antioxidant enzymes glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) were significantly increased, and the contents of GSH and malonaldehyde (MDA) were decreased significantly in the liver; Fourth, the inflammation of the liver was relieved as the level of IL-1beta and IL-6, the inflammatory cytokines, were decreased significantly in the liver.	Cytarabine	102-107	glutamic--pyruvic transaminase	Homo sapiens	421-445
24754180-5	2014	Compared to the human leukemia NOD/SCID mouse model group with the treatments of APS, Ara-c and APS + Ara-c, We found that severe liver damage and pathological changes of the liver were able to alleviate: First, the number of white blood cells in the peripheral blood was significantly lower and with less transplanted K562 leukemia cells; Second, liver function damage was alleviated as liver function tests showed that alanine aminotransferase (ALT), aspartate aminotransferase (AST) and total bilirubin (TBiL) were significantly reduced, while the albumin (Alb) was notably increased; Third, liver antioxidant ability was improved as the activities of the antioxidant enzymes glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) were significantly increased, and the contents of GSH and malonaldehyde (MDA) were decreased significantly in the liver; Fourth, the inflammation of the liver was relieved as the level of IL-1beta and IL-6, the inflammatory cytokines, were decreased significantly in the liver.	Cytarabine	102-107	solute carrier family 17 member 5	Homo sapiens	453-479
24754180-5	2014	Compared to the human leukemia NOD/SCID mouse model group with the treatments of APS, Ara-c and APS + Ara-c, We found that severe liver damage and pathological changes of the liver were able to alleviate: First, the number of white blood cells in the peripheral blood was significantly lower and with less transplanted K562 leukemia cells; Second, liver function damage was alleviated as liver function tests showed that alanine aminotransferase (ALT), aspartate aminotransferase (AST) and total bilirubin (TBiL) were significantly reduced, while the albumin (Alb) was notably increased; Third, liver antioxidant ability was improved as the activities of the antioxidant enzymes glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) were significantly increased, and the contents of GSH and malonaldehyde (MDA) were decreased significantly in the liver; Fourth, the inflammation of the liver was relieved as the level of IL-1beta and IL-6, the inflammatory cytokines, were decreased significantly in the liver.	Cytarabine	102-107	solute carrier family 17 member 5	Homo sapiens	481-484
24754180-5	2014	Compared to the human leukemia NOD/SCID mouse model group with the treatments of APS, Ara-c and APS + Ara-c, We found that severe liver damage and pathological changes of the liver were able to alleviate: First, the number of white blood cells in the peripheral blood was significantly lower and with less transplanted K562 leukemia cells; Second, liver function damage was alleviated as liver function tests showed that alanine aminotransferase (ALT), aspartate aminotransferase (AST) and total bilirubin (TBiL) were significantly reduced, while the albumin (Alb) was notably increased; Third, liver antioxidant ability was improved as the activities of the antioxidant enzymes glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) were significantly increased, and the contents of GSH and malonaldehyde (MDA) were decreased significantly in the liver; Fourth, the inflammation of the liver was relieved as the level of IL-1beta and IL-6, the inflammatory cytokines, were decreased significantly in the liver.	Cytarabine	102-107	albumin	Homo sapiens	560-563
24754180-5	2014	Compared to the human leukemia NOD/SCID mouse model group with the treatments of APS, Ara-c and APS + Ara-c, We found that severe liver damage and pathological changes of the liver were able to alleviate: First, the number of white blood cells in the peripheral blood was significantly lower and with less transplanted K562 leukemia cells; Second, liver function damage was alleviated as liver function tests showed that alanine aminotransferase (ALT), aspartate aminotransferase (AST) and total bilirubin (TBiL) were significantly reduced, while the albumin (Alb) was notably increased; Third, liver antioxidant ability was improved as the activities of the antioxidant enzymes glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) were significantly increased, and the contents of GSH and malonaldehyde (MDA) were decreased significantly in the liver; Fourth, the inflammation of the liver was relieved as the level of IL-1beta and IL-6, the inflammatory cytokines, were decreased significantly in the liver.	Cytarabine	102-107	interleukin 1 beta	Homo sapiens	930-938
24754180-5	2014	Compared to the human leukemia NOD/SCID mouse model group with the treatments of APS, Ara-c and APS + Ara-c, We found that severe liver damage and pathological changes of the liver were able to alleviate: First, the number of white blood cells in the peripheral blood was significantly lower and with less transplanted K562 leukemia cells; Second, liver function damage was alleviated as liver function tests showed that alanine aminotransferase (ALT), aspartate aminotransferase (AST) and total bilirubin (TBiL) were significantly reduced, while the albumin (Alb) was notably increased; Third, liver antioxidant ability was improved as the activities of the antioxidant enzymes glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) were significantly increased, and the contents of GSH and malonaldehyde (MDA) were decreased significantly in the liver; Fourth, the inflammation of the liver was relieved as the level of IL-1beta and IL-6, the inflammatory cytokines, were decreased significantly in the liver.	Cytarabine	102-107	interleukin 6	Homo sapiens	943-947
23686525-2	2013	We have also shown that CD34(+) /CD38(-) AML cells, one of compartments enriched for leukemia stem cells in most leukemia subgroups, were relatively resistant to cytarabine-mediated growth inhibition when compared to their CD34(+) /CD38(+) counterparts.	Cytarabine	162-172	CD38 molecule	Homo sapiens	33-37
24036158-5	2013	Cytarabine, vinblastine, vincristine, hydrocortisone, and mitoxantrone inhibited only OAT1, whereas tacrolimus, azathioprine, dexamethasone, cyclosporine, and 6-mercaptopurine had no effect on both transporters.	Cytarabine	0-10	solute carrier family 22 member 6	Homo sapiens	86-90
24121103-2	2013	We and others found that Wee1 inhibition sensitizes leukemia cells to cytarabine.	Cytarabine	70-80	WEE 1 homolog 1 (S. pombe)	Mus musculus	25-29
24121103-4	2013	Synergistic inhibition of proliferation with a Wee1 inhibitor in clinical development, MK1775, and cytarabine was observed in all acute myelogenous leukemia (AML) cell lines tested, regardless of p53 functionality.	Cytarabine	99-109	WEE 1 homolog 1 (S. pombe)	Mus musculus	47-51
24121103-5	2013	Mechanistic studies indicate that inhibition of Wee1 abrogates the S-phase checkpoint and augments apoptosis induced by cytarabine.	Cytarabine	120-130	WEE 1 homolog 1 (S. pombe)	Mus musculus	48-52
24044460-1	2013	This study showed that silencing BMP4 expression significantly activated caspase-2, 3, and 9, while decreasing Matrigel colony formation in Cytarabine (Ara-C)-treated leukemia HL-60 cells.	Cytarabine	140-150	bone morphogenetic protein 4	Homo sapiens	33-37
24370051-7	2013	The apoptosis of hBMMSC treated with salidroside were significantly higher as compared with control group (P &lt; 0.05); RT-PCR results demonstrated that the BCL-2 expression was significantly down regulated but BAX mRNA expressions was up-regulated in Ara- C group as compared with those in the control group.	Cytarabine	253-259	BCL2 apoptosis regulator	Homo sapiens	158-163
24044460-1	2013	This study showed that silencing BMP4 expression significantly activated caspase-2, 3, and 9, while decreasing Matrigel colony formation in Cytarabine (Ara-C)-treated leukemia HL-60 cells.	Cytarabine	152-157	bone morphogenetic protein 4	Homo sapiens	33-37
24044460-2	2013	In contrast, Ara-C significantly upregulated Atg5 and Beclin-1 expression, the ratio of LC3-II/LC3-I, and CDK1 and cyclin B1 expression in leukemia cells expressing BMP4.	Cytarabine	13-18	autophagy related 5	Homo sapiens	45-49
24044460-2	2013	In contrast, Ara-C significantly upregulated Atg5 and Beclin-1 expression, the ratio of LC3-II/LC3-I, and CDK1 and cyclin B1 expression in leukemia cells expressing BMP4.	Cytarabine	13-18	beclin 1	Homo sapiens	54-62
23830798-2	2013	A patient, with chemo- and trastuzumab-resistant HER2-overexpressing breast cancer, who presented concomitant acute promyelocytic leukemia, showed a response in her breast lesions to retinoic acid, arsenic, and aracytin.	Cytarabine	211-219	erb-b2 receptor tyrosine kinase 2	Homo sapiens	49-53
24044460-2	2013	In contrast, Ara-C significantly upregulated Atg5 and Beclin-1 expression, the ratio of LC3-II/LC3-I, and CDK1 and cyclin B1 expression in leukemia cells expressing BMP4.	Cytarabine	13-18	cyclin dependent kinase 1	Homo sapiens	106-110
24044460-2	2013	In contrast, Ara-C significantly upregulated Atg5 and Beclin-1 expression, the ratio of LC3-II/LC3-I, and CDK1 and cyclin B1 expression in leukemia cells expressing BMP4.	Cytarabine	13-18	cyclin B1	Homo sapiens	115-124
24044460-2	2013	In contrast, Ara-C significantly upregulated Atg5 and Beclin-1 expression, the ratio of LC3-II/LC3-I, and CDK1 and cyclin B1 expression in leukemia cells expressing BMP4.	Cytarabine	13-18	bone morphogenetic protein 4	Homo sapiens	165-169
24044460-4	2013	Injection of Ara-C significantly inhibited tumor growth in mice inoculated with leukemia cells with BMP4 silenced.	Cytarabine	13-18	bone morphogenetic protein 4	Mus musculus	100-104
24024897-8	2013	RRM1 SNPs rs1042919 (which occurs in linkage disequilbrium with multiple other SNPs) and promoter SNP rs1561876 were associated with intracellular 1-beta-D-arabinofuranosyl-CTP levels, response after remission induction therapy, risk of relapse and overall survival in AML patients receiving cytarabine and cladribine.	Cytarabine	292-302	ribonucleotide reductase catalytic subunit M1	Homo sapiens	0-4
24069261-8	2013	Incubation of BMP7 with MCL cell lines increased their resistance to bortezomib and cytarabine, while inhibition of BMP7 expression by siRNA correlated with increased cell death linked to drug application.	Cytarabine	84-94	bone morphogenetic protein 7	Homo sapiens	14-18
23775789-5	2013	We also show that Tdp1-/- cells are hypersensitive and accumulate more DNA damage when treated with ACV and Ara-C, implicating TDP1 in repairing CTNA-induced DNA damage.	Cytarabine	108-113	tyrosyl-DNA phosphodiesterase 1	Homo sapiens	18-22
23775789-5	2013	We also show that Tdp1-/- cells are hypersensitive and accumulate more DNA damage when treated with ACV and Ara-C, implicating TDP1 in repairing CTNA-induced DNA damage.	Cytarabine	108-113	tyrosyl-DNA phosphodiesterase 1	Homo sapiens	127-131
23902239-2	2013	Elacytarabine was rationally designed to circumvent cytarabine resistance related to decreased cellular uptake, due to the ability of the lipophilic drug moiety to enter the cell without the requirement of specialized nuclear transport proteins, including the hENT1.	Cytarabine	3-13	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	260-265
23919448-10	2013	Among the other factors that can lead to leukemic cell survival are the high levels in the liver and spleen of cytidine deaminase, the enzyme that inactivates cytarabine and drug resistance due to deficiency in deoxycytidine kinase, the enzyme that activates the prodrug, cytarabine.	Cytarabine	159-169	cytidine deaminase	Homo sapiens	111-129
23919448-10	2013	Among the other factors that can lead to leukemic cell survival are the high levels in the liver and spleen of cytidine deaminase, the enzyme that inactivates cytarabine and drug resistance due to deficiency in deoxycytidine kinase, the enzyme that activates the prodrug, cytarabine.	Cytarabine	272-282	cytidine deaminase	Homo sapiens	111-129
23919448-10	2013	Among the other factors that can lead to leukemic cell survival are the high levels in the liver and spleen of cytidine deaminase, the enzyme that inactivates cytarabine and drug resistance due to deficiency in deoxycytidine kinase, the enzyme that activates the prodrug, cytarabine.	Cytarabine	272-282	deoxycytidine kinase	Homo sapiens	211-231
22584460-0	2013	Profiling of drug-metabolizing enzymes/transporters in CD33+ acute myeloid leukemia patients treated with Gemtuzumab-Ozogamicin and Fludarabine, Cytarabine and Idarubicin.	Cytarabine	145-155	CD33 molecule	Homo sapiens	55-59
23879717-5	2013	In this study, we measured B7 family members B7.1 (CD80) and B7.2 (CD86) expressed on a CD19(+) human leukemia cell line, Nalm-6, stimulated by cytosine arabinoside (Ara-C).	Cytarabine	144-164	CD80 molecule	Homo sapiens	51-55
23879717-5	2013	In this study, we measured B7 family members B7.1 (CD80) and B7.2 (CD86) expressed on a CD19(+) human leukemia cell line, Nalm-6, stimulated by cytosine arabinoside (Ara-C).	Cytarabine	144-164	CD86 molecule	Homo sapiens	67-71
23879717-5	2013	In this study, we measured B7 family members B7.1 (CD80) and B7.2 (CD86) expressed on a CD19(+) human leukemia cell line, Nalm-6, stimulated by cytosine arabinoside (Ara-C).	Cytarabine	144-164	CD19 molecule	Homo sapiens	88-92
23879717-6	2013	We found that a low concentration of Ara-C could upregulate CD80 expressed on CD19(+) Nalm-6 cells.	Cytarabine	37-42	CD80 molecule	Homo sapiens	60-64
23879717-6	2013	We found that a low concentration of Ara-C could upregulate CD80 expressed on CD19(+) Nalm-6 cells.	Cytarabine	37-42	CD19 molecule	Homo sapiens	78-82
23879717-12	2013	It was noted that Ara-C could upregulate CD80 expressed on two of five specimens of acute B lymphoblastic leukemia patient-derived cells.	Cytarabine	18-23	CD80 molecule	Homo sapiens	41-45
23874683-5	2013	ShRNA knockdown of GATA1 in the megakaryocytic cell line Meg-01 resulted in significantly increased cytarabine (ara-C) and daunorubicin anti-proliferative sensitivities and decreased Bcl-xL transcript and protein levels.	Cytarabine	100-110	GATA binding protein 1	Homo sapiens	19-24
23570983-7	2013	Moreover, we also showed that the RRM1-overexpressing tumor cells were also cross-resistant to cytarabine, another nucleoside analog commonly used in cancer therapy, and 4-(N)-stearoyl cytarabine carried by solid lipid nanoparticles can also overcome the resistance.	Cytarabine	95-105	ribonucleotide reductase catalytic subunit M1	Homo sapiens	34-38
23874683-5	2013	ShRNA knockdown of GATA1 in the megakaryocytic cell line Meg-01 resulted in significantly increased cytarabine (ara-C) and daunorubicin anti-proliferative sensitivities and decreased Bcl-xL transcript and protein levels.	Cytarabine	100-110	protein tyrosine phosphatase non-receptor type 4	Homo sapiens	57-60
23874683-5	2013	ShRNA knockdown of GATA1 in the megakaryocytic cell line Meg-01 resulted in significantly increased cytarabine (ara-C) and daunorubicin anti-proliferative sensitivities and decreased Bcl-xL transcript and protein levels.	Cytarabine	112-117	GATA binding protein 1	Homo sapiens	19-24
23874683-5	2013	ShRNA knockdown of GATA1 in the megakaryocytic cell line Meg-01 resulted in significantly increased cytarabine (ara-C) and daunorubicin anti-proliferative sensitivities and decreased Bcl-xL transcript and protein levels.	Cytarabine	112-117	protein tyrosine phosphatase non-receptor type 4	Homo sapiens	57-60
23874683-7	2013	Treatment of the Meg-01 cells with the histone deacetylase inhibitor valproic acid resulted in down-regulation of both GATA1 and Bcl-xL and significantly enhanced ara-C sensitivity.	Cytarabine	163-168	protein tyrosine phosphatase non-receptor type 4	Homo sapiens	17-20
23866283-6	2013	The in vivo experiment showed that mice with AMoL had the most significant decrease in CD33(+)CD45(+) leukemia cells in peripheral blood and bone marrow and survived the longest after being treated with Ara-C (7 days) plus anti-CD47 monoclonal antibody (14 days) (P &lt; 0.01).	Cytarabine	203-208	CD33 antigen	Mus musculus	87-91
23292239-4	2013	The use of Ara-C was associated with significantly higher peak number of circulating CD34(+) cells compared with CY (P&lt;0.0001).	Cytarabine	11-16	CD34 molecule	Homo sapiens	85-89
23292239-5	2013	In the Ara-C group, 95% of patients with multiple myeloma (MM) collected at least 5 x 10(6) CD34(+) cells/kg required for tandem transplantation, and 97% of lymphoma patients collected at least 2 x 10(6) CD34(+) cells/kg, needed for a single autologous hematopoietic SCT (autoHSCT), which was achieved with a single leukapheresis in 91% of cases.	Cytarabine	7-12	CD34 molecule	Homo sapiens	92-96
23507523-8	2013	ALDH1A2 knock-down induced sensitivity to AraC treatment in K562AC cells, and ALDH1A2 overexpressed K562S cells acquired the AraC resistance.	Cytarabine	42-46	aldehyde dehydrogenase 1 family member A2	Homo sapiens	0-7
23866283-6	2013	The in vivo experiment showed that mice with AMoL had the most significant decrease in CD33(+)CD45(+) leukemia cells in peripheral blood and bone marrow and survived the longest after being treated with Ara-C (7 days) plus anti-CD47 monoclonal antibody (14 days) (P &lt; 0.01).	Cytarabine	203-208	protein tyrosine phosphatase, receptor type, C	Mus musculus	94-98
23512567-3	2013	For clinically fit patients younger than 60-65 years of age we recommend cytarabine-containing induction and conditioning regimens such as Rituximab (R)-CHOP alternating with R-DHAP followed by autologous SCT consolidation.	Cytarabine	73-83	DNA damage inducible transcript 3	Homo sapiens	153-157
23589674-7	2013	Moreover, using cell-cycle-dependent Ara-C chemotherapy to produce minimal residual disease (MRD) in leukemic mice, we show that OPN neutralization synergizes with Ara-C to reduce detectable BM MRD.	Cytarabine	37-42	secreted phosphoprotein 1	Mus musculus	129-132
23826077-0	2013	TGF-beta-Neutralizing Antibody 1D11 Enhances Cytarabine-Induced Apoptosis in AML Cells in the Bone Marrow Microenvironment.	Cytarabine	45-55	transforming growth factor beta 1	Homo sapiens	0-8
23826077-5	2013	Blocking TGFbeta with 1D11 further enhanced cytarabine (Ara-C)-induced apoptosis of AML cells in hypoxic and in normoxic conditions.	Cytarabine	44-54	transforming growth factor beta 1	Homo sapiens	9-16
23826077-5	2013	Blocking TGFbeta with 1D11 further enhanced cytarabine (Ara-C)-induced apoptosis of AML cells in hypoxic and in normoxic conditions.	Cytarabine	56-61	transforming growth factor beta 1	Homo sapiens	9-16
23538338-4	2013	MCC expression was induced by cytarabine treatment from 1.7- to 26.6-fold in LCLs.	Cytarabine	30-40	MCC regulator of WNT signaling pathway	Homo sapiens	0-3
23771655-8	2013	Moreover, in vivo cytarabine administration could extend survival of NOD/SCID mice, which was consistent with clinical observation.	Cytarabine	18-28	atrophin 1	Homo sapiens	69-72
23509154-5	2013	Such suppression of Mnk kinase activity and eIF4E phosphorylation by cercosporamide resulted in dose-dependent suppressive effects on primitive leukemic progenitors (CFU-L) from AML patients and enhanced the antileukemic properties of cytarabine (Ara-C) or mammalian target of rapamycin (mTOR) complex 1 inhibition.	Cytarabine	235-245	ATPase copper transporting alpha	Homo sapiens	20-23
23509154-5	2013	Such suppression of Mnk kinase activity and eIF4E phosphorylation by cercosporamide resulted in dose-dependent suppressive effects on primitive leukemic progenitors (CFU-L) from AML patients and enhanced the antileukemic properties of cytarabine (Ara-C) or mammalian target of rapamycin (mTOR) complex 1 inhibition.	Cytarabine	235-245	eukaryotic translation initiation factor 4E	Homo sapiens	44-49
23509154-5	2013	Such suppression of Mnk kinase activity and eIF4E phosphorylation by cercosporamide resulted in dose-dependent suppressive effects on primitive leukemic progenitors (CFU-L) from AML patients and enhanced the antileukemic properties of cytarabine (Ara-C) or mammalian target of rapamycin (mTOR) complex 1 inhibition.	Cytarabine	235-245	mechanistic target of rapamycin kinase	Homo sapiens	257-286
23509154-5	2013	Such suppression of Mnk kinase activity and eIF4E phosphorylation by cercosporamide resulted in dose-dependent suppressive effects on primitive leukemic progenitors (CFU-L) from AML patients and enhanced the antileukemic properties of cytarabine (Ara-C) or mammalian target of rapamycin (mTOR) complex 1 inhibition.	Cytarabine	235-245	mechanistic target of rapamycin kinase	Homo sapiens	288-292
23509154-5	2013	Such suppression of Mnk kinase activity and eIF4E phosphorylation by cercosporamide resulted in dose-dependent suppressive effects on primitive leukemic progenitors (CFU-L) from AML patients and enhanced the antileukemic properties of cytarabine (Ara-C) or mammalian target of rapamycin (mTOR) complex 1 inhibition.	Cytarabine	247-252	ATPase copper transporting alpha	Homo sapiens	20-23
23509154-7	2013	Altogether, this work demonstrates that the unique Mnk inhibitor cercosporamide suppresses phosphorylation of eIF4E and exhibits antileukemic effects, in support of future clinical-translational efforts involving combinations of Mnk inhibitors with cytarabine and/or mTOR inhibitors for the treatment of AML.	Cytarabine	249-259	ATPase copper transporting alpha	Homo sapiens	51-54
23362234-6	2013	Moreover, the DNA damaging drug cytosine arabinoside (ara-C) induces expression of ZNF224 in K562 cells and this induction enhances cell apoptotic response to ara-C.	Cytarabine	32-52	zinc finger protein 224	Homo sapiens	83-89
23362234-6	2013	Moreover, the DNA damaging drug cytosine arabinoside (ara-C) induces expression of ZNF224 in K562 cells and this induction enhances cell apoptotic response to ara-C.	Cytarabine	54-59	zinc finger protein 224	Homo sapiens	83-89
23362234-6	2013	Moreover, the DNA damaging drug cytosine arabinoside (ara-C) induces expression of ZNF224 in K562 cells and this induction enhances cell apoptotic response to ara-C.	Cytarabine	159-164	zinc finger protein 224	Homo sapiens	83-89
23320492-0	2013	Combination of guanine arabinoside and Bcl-2 inhibitor YC137 overcomes the cytarabine resistance in HL-60 leukemia cell line.	Cytarabine	75-85	BCL2 apoptosis regulator	Homo sapiens	39-44
23450319-1	2013	The objective of the present study was to examine and determine whether the human acute monocytic leukemia cell line THP-1 contains side population (SP) cells, and, if so, to increase the proportion of SP cells using arabinosylcytosine (Ara-C).	Cytarabine	217-235	GLI family zinc finger 2	Homo sapiens	117-122
23450319-1	2013	The objective of the present study was to examine and determine whether the human acute monocytic leukemia cell line THP-1 contains side population (SP) cells, and, if so, to increase the proportion of SP cells using arabinosylcytosine (Ara-C).	Cytarabine	237-242	GLI family zinc finger 2	Homo sapiens	117-122
23450319-4	2013	THP-1 cells were incubated with different concentrations of Ara-C for 24 h and the proportion of SP cells was detected.	Cytarabine	60-65	GLI family zinc finger 2	Homo sapiens	0-5
23450436-2	2013	The combination of bendamustine and cytarabine has demonstrated distinct and synergistic mechanisms of action in preclinical studies on cell lines and primary tumor cells of several B-cell lymphomas, including 17p deleted or TP53 mutated CLL.	Cytarabine	36-46	tumor protein p53	Homo sapiens	225-229
23356405-0	2013	The HSP90 inhibitor NVP-AUY922-AG inhibits the PI3K and IKK signalling pathways and synergizes with cytarabine in acute myeloid leukaemia cells.	Cytarabine	100-110	heat shock protein 90 alpha family class A member 1	Homo sapiens	4-9
23356405-11	2013	This study shows that the novel HSP90 inhibitor NVP-AUY922-AG has significant single agent activity in AML cells and is synergistic with Ara-C.	Cytarabine	137-142	heat shock protein 90 alpha family class A member 1	Homo sapiens	32-37
23320492-9	2013	HL-60/ara-C60 cells were also refractory to ara-C-induced apoptosis due to overexpression of Bcl-2 and Bcl-XL.	Cytarabine	6-11	BCL2 apoptosis regulator	Homo sapiens	93-98
23320492-9	2013	HL-60/ara-C60 cells were also refractory to ara-C-induced apoptosis due to overexpression of Bcl-2 and Bcl-XL.	Cytarabine	6-11	BCL2 like 1	Homo sapiens	103-109
23320492-10	2013	Combination treatment of ara-C with ara-G augmented the dCK protein level, thereby increasing ara-CTP production and subsequent cytotoxicity.	Cytarabine	25-30	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	56-59
23320492-2	2013	After being transported into leukemic cells, ara-C is phosphorylated, by several enzymes including deoxycytidine kinase (dCK), to ara-C triphosphate (ara-CTP), an active metabolite, and then incorporated into DNA, thereby inhibiting DNA synthesis.	Cytarabine	45-50	deoxycytidine kinase	Homo sapiens	99-119
23320492-2	2013	After being transported into leukemic cells, ara-C is phosphorylated, by several enzymes including deoxycytidine kinase (dCK), to ara-C triphosphate (ara-CTP), an active metabolite, and then incorporated into DNA, thereby inhibiting DNA synthesis.	Cytarabine	45-50	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	121-124
23320492-4	2013	Here, we established a new ara-C-resistant acute myeloid leukemia cell line (HL-60/ara-C60) with dual resistance characteristics of the anti-antimetabolic character of decreased ara-CTP production and an increase in the antiapoptotic factors Bcl-2 and Bcl-XL.	Cytarabine	27-32	BCL2 apoptosis regulator	Homo sapiens	242-247
23320492-4	2013	Here, we established a new ara-C-resistant acute myeloid leukemia cell line (HL-60/ara-C60) with dual resistance characteristics of the anti-antimetabolic character of decreased ara-CTP production and an increase in the antiapoptotic factors Bcl-2 and Bcl-XL.	Cytarabine	27-32	BCL2 like 1	Homo sapiens	252-258
23547862-0	2013	Prophylactic use of granulocyte colony-stimulating factor after consolidation therapy with high-dose cytarabine for acute myeloid leukemia.	Cytarabine	101-111	colony stimulating factor 3	Homo sapiens	20-57
23547862-4	2013	reported that granulocyte colony-stimulating factor administration following consolidation therapy with high-dose cytarabine is associated with decreased hospitalization rate and improved survival.	Cytarabine	114-124	colony stimulating factor 3	Homo sapiens	14-51
22313860-5	2012	Embedded in this study was peripheral blood sampling for TMPRSS2-ERG and SPINK1, two genes that are believed to define prostate cancer genotypes, to assess their utility as biomarkers This study suggests that at the delivered doses, cytarabine has limited efficacy and significant myelotoxicity suggesting, it does not have a role in the treatment of docetaxel-refractory CRPC.	Cytarabine	233-243	serine peptidase inhibitor Kazal type 1	Homo sapiens	73-79
23348613-7	2013	To study the functional relevance of prolyl oligopeptidase-glyceraldehyde-3-phosphate dehydrogenase interactions, we investigated whether this interaction was involved in cytosine arabinoside-induced glyceraldehyde-3-phosphate dehydrogenase nuclear translocation and cell death.	Cytarabine	171-191	prolyl endopeptidase	Homo sapiens	37-58
23348613-7	2013	To study the functional relevance of prolyl oligopeptidase-glyceraldehyde-3-phosphate dehydrogenase interactions, we investigated whether this interaction was involved in cytosine arabinoside-induced glyceraldehyde-3-phosphate dehydrogenase nuclear translocation and cell death.	Cytarabine	171-191	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	59-99
23348613-7	2013	To study the functional relevance of prolyl oligopeptidase-glyceraldehyde-3-phosphate dehydrogenase interactions, we investigated whether this interaction was involved in cytosine arabinoside-induced glyceraldehyde-3-phosphate dehydrogenase nuclear translocation and cell death.	Cytarabine	171-191	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	200-240
23348613-8	2013	Prolyl oligopeptidase inhibitor, SUAM-14746, and prolyl oligopeptidase knockdown successfully inhibited glyceraldehyde-3-phosphate dehydrogenase translocation and promoted the survival of cytosine arabinoside-treated NB-1 cells.	Cytarabine	188-208	prolyl endopeptidase	Homo sapiens	0-21
23348613-8	2013	Prolyl oligopeptidase inhibitor, SUAM-14746, and prolyl oligopeptidase knockdown successfully inhibited glyceraldehyde-3-phosphate dehydrogenase translocation and promoted the survival of cytosine arabinoside-treated NB-1 cells.	Cytarabine	188-208	prolyl endopeptidase	Homo sapiens	49-70
23348613-10	2013	These results indicate that the interaction between prolyl oligopeptidase and glyceraldehyde-3-phosphate dehydrogenase is required for cytosine arabinoside-induced glyceraldehyde-3-phosphate dehydrogenase nuclear translocation and cell death.	Cytarabine	135-155	prolyl endopeptidase	Homo sapiens	52-73
23348613-10	2013	These results indicate that the interaction between prolyl oligopeptidase and glyceraldehyde-3-phosphate dehydrogenase is required for cytosine arabinoside-induced glyceraldehyde-3-phosphate dehydrogenase nuclear translocation and cell death.	Cytarabine	135-155	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	78-118
23348613-10	2013	These results indicate that the interaction between prolyl oligopeptidase and glyceraldehyde-3-phosphate dehydrogenase is required for cytosine arabinoside-induced glyceraldehyde-3-phosphate dehydrogenase nuclear translocation and cell death.	Cytarabine	135-155	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	164-204
23263202-11	2013	In addition, the concentration-dependent induction of apoptosis in response to treatment with the cytostatic drugs cytarabine or daunorubicin was significantly reduced in TRAF6-depleted MV4-11 cells.	Cytarabine	115-125	TNF receptor associated factor 6	Homo sapiens	171-176
23361057-4	2013	RESULTS: We identified cytarabine and other related cytosine-based nucleoside analogues as being selectively toxic to MLH1 and MSH2-deficient tumour cells.	Cytarabine	23-33	mutL homolog 1	Mus musculus	118-122
23230131-2	2013	Wild-type enzymes and variants of CDA (Lys27Gln and Ala70Thr) and DCK (Ile24Val, Ala119Gly, and Pro122Ser) were expressed in and purified from Escherichia coli, and enzyme kinetic parameters were estimated for cytarabine (Ara-C), dFdC, and its metabolite 2",2"-difluorodeoxyuridine (dFdU) as substrates.	Cytarabine	210-220	cytidine deaminase	Homo sapiens	34-37
23230131-2	2013	Wild-type enzymes and variants of CDA (Lys27Gln and Ala70Thr) and DCK (Ile24Val, Ala119Gly, and Pro122Ser) were expressed in and purified from Escherichia coli, and enzyme kinetic parameters were estimated for cytarabine (Ara-C), dFdC, and its metabolite 2",2"-difluorodeoxyuridine (dFdU) as substrates.	Cytarabine	222-227	cytidine deaminase	Homo sapiens	34-37
24596527-4	2013	He was on G-CSF after cessation of high-dose and low-dose cytarabine chemotherapy.	Cytarabine	58-68	colony stimulating factor 3	Homo sapiens	10-15
23087055-6	2012	In addition, a number of cytotoxic substrates, including docetaxel, paclitaxel, and Ara-C, increased the ABCC10 basal ATPase activity.	Cytarabine	84-89	ATP-binding cassette, sub-family C (CFTR/MRP), member 10	Mus musculus	105-111
23087055-6	2012	In addition, a number of cytotoxic substrates, including docetaxel, paclitaxel, and Ara-C, increased the ABCC10 basal ATPase activity.	Cytarabine	84-89	dynein, axonemal, heavy chain 8	Mus musculus	118-124
22488249-0	2012	Targeting Aurora A kinase activity with the investigational agent alisertib increases the efficacy of cytarabine through a FOXO-dependent mechanism.	Cytarabine	102-112	aurora kinase A	Homo sapiens	10-18
22488249-5	2012	A link between Aurora A expression and sensitivity to ara-C was established, suggesting that Aurora A inhibition may be a promising strategy to increase the efficacy of ara-C.	Cytarabine	54-59	aurora kinase A	Homo sapiens	15-23
22488249-5	2012	A link between Aurora A expression and sensitivity to ara-C was established, suggesting that Aurora A inhibition may be a promising strategy to increase the efficacy of ara-C.	Cytarabine	54-59	aurora kinase A	Homo sapiens	93-101
22488249-5	2012	A link between Aurora A expression and sensitivity to ara-C was established, suggesting that Aurora A inhibition may be a promising strategy to increase the efficacy of ara-C.	Cytarabine	169-174	aurora kinase A	Homo sapiens	15-23
22488249-5	2012	A link between Aurora A expression and sensitivity to ara-C was established, suggesting that Aurora A inhibition may be a promising strategy to increase the efficacy of ara-C.	Cytarabine	169-174	aurora kinase A	Homo sapiens	93-101
22488249-7	2012	Targeted FOXO3a knockdown significantly blunted the pro-apoptotic effects of the alisertib/ara-C combination, indicating that it is an important regulator of sensitivity to these agents.	Cytarabine	91-96	forkhead box O3	Homo sapiens	9-15
22488249-9	2012	Our collective data indicate that targeting Aurora A with alisertib represents a novel approach to increase the efficacy of ara-C that warrants further investigation.	Cytarabine	124-129	aurora kinase A	Homo sapiens	44-52
23257432-7	2012	It is concluded that the apoptosis of U937 cells synergistically induced by bortezomib combined with low concentration Ara-C is possibly associated with up-regulation of phosphorylated form of JNK, P38 and down-regulation of phosphorylation of ERK induced by increase of ROS, resulting in decrease of mitochondrial potential.	Cytarabine	119-124	mitogen-activated protein kinase 8	Homo sapiens	193-196
23257432-7	2012	It is concluded that the apoptosis of U937 cells synergistically induced by bortezomib combined with low concentration Ara-C is possibly associated with up-regulation of phosphorylated form of JNK, P38 and down-regulation of phosphorylation of ERK induced by increase of ROS, resulting in decrease of mitochondrial potential.	Cytarabine	119-124	mitogen-activated protein kinase 14	Homo sapiens	198-201
23257432-7	2012	It is concluded that the apoptosis of U937 cells synergistically induced by bortezomib combined with low concentration Ara-C is possibly associated with up-regulation of phosphorylated form of JNK, P38 and down-regulation of phosphorylation of ERK induced by increase of ROS, resulting in decrease of mitochondrial potential.	Cytarabine	119-124	mitogen-activated protein kinase 1	Homo sapiens	244-247
22702906-1	2012	Elacytarabine is a novel cytotoxic nucleoside analogue, independent of nucleoside transporters (e.g. human Equilibrative Nucleoside Transporter 1 [hENT1]) for cell uptake, and mechanisms of action similar to those of cytarabine.	Cytarabine	3-13	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	147-152
23228943-7	2013	Moreover, AMPK inhibition in MLL-rearranged cell lines synergistically enhanced the antiproliferative effects of vincristine, daunorubicin, cytarabine, dexamethasone and L-asparaginase in most of the evaluated conditions.	Cytarabine	140-150	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	10-14
23228943-7	2013	Moreover, AMPK inhibition in MLL-rearranged cell lines synergistically enhanced the antiproliferative effects of vincristine, daunorubicin, cytarabine, dexamethasone and L-asparaginase in most of the evaluated conditions.	Cytarabine	140-150	lysine methyltransferase 2A	Homo sapiens	29-32
23230131-3	2013	All three CDA proteins showed similar K(m) and V(max) for Ara-C and dFdC deamination, except for CDA70Thr, which had a 2.5-fold lower K(m) and 6-fold lower V(max) for Ara-C deamination.	Cytarabine	58-63	cytidine deaminase	Homo sapiens	10-13
23230131-3	2013	All three CDA proteins showed similar K(m) and V(max) for Ara-C and dFdC deamination, except for CDA70Thr, which had a 2.5-fold lower K(m) and 6-fold lower V(max) for Ara-C deamination.	Cytarabine	167-172	cytidine deaminase	Homo sapiens	10-13
23230131-4	2013	All four DCK proteins yielded comparable metabolic activity for Ara-C and dFdC monophosphorylation, except for DCK24Val, which demonstrated an approximately 2-fold increase (P &lt; 0.05) in the intrinsic clearance of dFdC monophosphorylation due to a 40% decrease in K(m) (P &lt; 0.05).	Cytarabine	64-69	deoxycytidine kinase	Homo sapiens	9-12
23479503-3	2013	Clinically, CDD overexpression appears particularly suited to optimize treatment strategies for acute leukemias and myelodysplasias given the efficacy of ara-C (and to a lesser degree decitabine and azacytidine) in these disease entities.	Cytarabine	154-159	cytidine deaminase	Homo sapiens	12-15
23266733-3	2013	The mechanism of cytarabine that promotes MM cell escape is closely associated with the up-regulation of CXCR4.	Cytarabine	17-27	C-X-C motif chemokine receptor 4	Homo sapiens	105-110
23847416-2	2013	In this study, we followed events associated with cytosine arabinoside (Ara-C)-induced apoptosis in NB4 cells using DEP analysis.	Cytarabine	50-70	p21 (RAC1) activated kinase 3	Homo sapiens	72-75
23995115-5	2013	Multiple cycles of hyper-CVAD/MTX-Ara-C therapy with concomitant rituximab were administered, under which the patient was successfully maintained in complete remission.	Cytarabine	34-39	metaxin 1	Homo sapiens	30-33
23441221-13	2013	However, high doses of either vinblastine or cytarabine decreased MCL1 expression and induced dendritic cell death.	Cytarabine	45-55	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	66-70
23092873-1	2012	PURPOSE: Incorporation of cytarabine into DNA activates checkpoint kinase 1 (Chk1), which stabilizes stalled replication forks, induces S-phase slowing, and diminishes cytarabine cytotoxicity.	Cytarabine	26-36	checkpoint kinase 1	Homo sapiens	56-75
23092873-1	2012	PURPOSE: Incorporation of cytarabine into DNA activates checkpoint kinase 1 (Chk1), which stabilizes stalled replication forks, induces S-phase slowing, and diminishes cytarabine cytotoxicity.	Cytarabine	26-36	checkpoint kinase 1	Homo sapiens	77-81
23092873-1	2012	PURPOSE: Incorporation of cytarabine into DNA activates checkpoint kinase 1 (Chk1), which stabilizes stalled replication forks, induces S-phase slowing, and diminishes cytarabine cytotoxicity.	Cytarabine	168-178	checkpoint kinase 1	Homo sapiens	56-75
23092873-1	2012	PURPOSE: Incorporation of cytarabine into DNA activates checkpoint kinase 1 (Chk1), which stabilizes stalled replication forks, induces S-phase slowing, and diminishes cytarabine cytotoxicity.	Cytarabine	168-178	checkpoint kinase 1	Homo sapiens	77-81
23092873-2	2012	The selective Chk1 inhibitor SCH 900776 abrogates cytarabine-induced S-phase arrest and enhances cytarabine cytotoxicity in acute leukemia cell lines and leukemic blasts in vitro.	Cytarabine	50-60	checkpoint kinase 1	Homo sapiens	14-18
23092873-2	2012	The selective Chk1 inhibitor SCH 900776 abrogates cytarabine-induced S-phase arrest and enhances cytarabine cytotoxicity in acute leukemia cell lines and leukemic blasts in vitro.	Cytarabine	97-107	checkpoint kinase 1	Homo sapiens	14-18
22922207-8	2012	In contrast, arabinofuranosylcytosine-induced erythroid differentiation of K562 cells was significantly reduced with PDCD2 knockdown, with no effect on cell proliferation.	Cytarabine	13-37	programmed cell death 2	Homo sapiens	117-122
23189085-5	2012	However, there are additional genes that are relevant for the metabolism, activity, and/or transport of other chemotherapy drugs that are widely use in ALL, such as methotrexate, cyclophosphamide, vincristine, L-asparaginase, etoposide, cytarabine, or cytotoxic antibiotics.	Cytarabine	237-247	asparaginase and isoaspartyl peptidase 1	Homo sapiens	210-224
22869869-0	2012	Effects of selective checkpoint kinase 1 inhibition on cytarabine cytotoxicity in acute myelogenous leukemia cells in vitro.	Cytarabine	55-65	checkpoint kinase 1	Homo sapiens	21-40
22869869-1	2012	PURPOSE: Previous studies have shown that the replication checkpoint, which involves the kinases ataxia telangiectasia mutated and Rad3 related (ATR) and Chk1, contributes to cytarabine resistance in cell lines.	Cytarabine	175-185	ATR serine/threonine kinase	Homo sapiens	145-148
22869869-1	2012	PURPOSE: Previous studies have shown that the replication checkpoint, which involves the kinases ataxia telangiectasia mutated and Rad3 related (ATR) and Chk1, contributes to cytarabine resistance in cell lines.	Cytarabine	175-185	checkpoint kinase 1	Homo sapiens	154-158
22869869-6	2012	RESULTS: Immunoblotting revealed increased Chk1 phosphorylation, a marker of checkpoint activation, in more than half of Chk1-containing AMLs after 48 hours of cytarabine infusion.	Cytarabine	160-170	checkpoint kinase 1	Homo sapiens	43-47
22869869-6	2012	RESULTS: Immunoblotting revealed increased Chk1 phosphorylation, a marker of checkpoint activation, in more than half of Chk1-containing AMLs after 48 hours of cytarabine infusion.	Cytarabine	160-170	checkpoint kinase 1	Homo sapiens	121-125
22869869-7	2012	In human AML lines, SCH 900776 not only disrupted cytarabine-induced Chk1 activation and S-phase arrest but also markedly increased cytarabine-induced apoptosis.	Cytarabine	50-60	checkpoint kinase 1	Homo sapiens	69-73
22869869-9	2012	CONCLUSIONS: These results not only provide evidence for cytarabine-induced S-phase checkpoint activation in AML in the clinical setting, but also show that a selective Chk1 inhibitor can overcome the S-phase checkpoint and enhance the cytotoxicity of cytarabine.	Cytarabine	57-67	checkpoint kinase 1	Homo sapiens	169-173
22869869-9	2012	CONCLUSIONS: These results not only provide evidence for cytarabine-induced S-phase checkpoint activation in AML in the clinical setting, but also show that a selective Chk1 inhibitor can overcome the S-phase checkpoint and enhance the cytotoxicity of cytarabine.	Cytarabine	252-262	checkpoint kinase 1	Homo sapiens	169-173
22313860-5	2012	Embedded in this study was peripheral blood sampling for TMPRSS2-ERG and SPINK1, two genes that are believed to define prostate cancer genotypes, to assess their utility as biomarkers This study suggests that at the delivered doses, cytarabine has limited efficacy and significant myelotoxicity suggesting, it does not have a role in the treatment of docetaxel-refractory CRPC.	Cytarabine	233-243	transmembrane serine protease 2	Homo sapiens	57-64
22762562-4	2012	Male rats exposed to Ara-C (30 mg/kg/day) at embryonic days 19.5 and 20.5 show reduced cell numbers and heterotopias in hippocampal CA1 and CA2/3 regions, respectively, as well as cell loss in the superficial layers of the pre- and infralimbic cortex.	Cytarabine	21-26	carbonic anhydrase 1	Rattus norvegicus	132-135
22762562-4	2012	Male rats exposed to Ara-C (30 mg/kg/day) at embryonic days 19.5 and 20.5 show reduced cell numbers and heterotopias in hippocampal CA1 and CA2/3 regions, respectively, as well as cell loss in the superficial layers of the pre- and infralimbic cortex.	Cytarabine	21-26	carbonic anhydrase 3	Rattus norvegicus	140-145
22970056-3	2012	We found increased expression levels of deoxycytidine kinase (dCK) and human equilibrative nucleoside transporter 1 (hENT1) and decreased levels of multidrug resistance protein 5 (ABCC5) and ribonucleoside reductase subunit M1 (RRM1) expression in Ara-C-sensitive HL60 cells.	Cytarabine	248-253	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	62-65
23071472-0	2012	Aurora A kinase expression is increased in leukemia stem cells, and a selective Aurora A kinase inhibitor enhances Ara-C-induced apoptosis in acute myeloid leukemia stem cells.	Cytarabine	115-120	aurora kinase A	Homo sapiens	0-15
23071472-0	2012	Aurora A kinase expression is increased in leukemia stem cells, and a selective Aurora A kinase inhibitor enhances Ara-C-induced apoptosis in acute myeloid leukemia stem cells.	Cytarabine	115-120	aurora kinase A	Homo sapiens	80-95
23071472-8	2012	Inhibition of AurA plus cytarabine treatment in LSCs resulted in increased cytotoxicity compared to cytarabine treatment alone.	Cytarabine	100-110	aurora kinase A	Homo sapiens	14-18
23071472-9	2012	Additional stimulation with granulocyte-colony stimulating factor (G-CSF) increased the cell death caused by AurA inhibition plus cytarabine treatment.	Cytarabine	130-140	colony stimulating factor 3	Homo sapiens	28-65
23071472-9	2012	Additional stimulation with granulocyte-colony stimulating factor (G-CSF) increased the cell death caused by AurA inhibition plus cytarabine treatment.	Cytarabine	130-140	colony stimulating factor 3	Homo sapiens	67-72
22970056-5	2012	We examined the molecular markers for GEM and Ara-C sensitivity in MTA-resistant cells and found increased gene expression of dCK and hENT1.	Cytarabine	46-51	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	134-139
22970056-3	2012	We found increased expression levels of deoxycytidine kinase (dCK) and human equilibrative nucleoside transporter 1 (hENT1) and decreased levels of multidrug resistance protein 5 (ABCC5) and ribonucleoside reductase subunit M1 (RRM1) expression in Ara-C-sensitive HL60 cells.	Cytarabine	248-253	ATP binding cassette subfamily C member 5	Homo sapiens	180-185
22970056-5	2012	We examined the molecular markers for GEM and Ara-C sensitivity in MTA-resistant cells and found increased gene expression of dCK and hENT1.	Cytarabine	46-51	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	126-129
22539243-0	2012	Neurotoxicity of intra-CSF liposomal cytarabine (DepoCyt) administered for the treatment of leptomeningeal metastases: a retrospective case series.	Cytarabine	37-47	colony stimulating factor 2	Homo sapiens	23-26
23134856-9	2012	5 of 6 patients who failed to mobilize before got successful stem cell mobilization, 1/6 patient with AML-M(5) got a second failure after the mobilization of VP16 whose first time"s mobilization using Ara-C did not succeed.	Cytarabine	201-206	host cell factor C1	Homo sapiens	158-162
22839530-10	2012	In pre-B-cell lines, both SRSF1 and PRMT1 expression could be efficiently attenuated by the clinical chemotherapy agents arabinoside cytosine (Ara-c) or vincristine (VCR).	Cytarabine	121-141	serine and arginine rich splicing factor 1	Homo sapiens	26-31
22839530-10	2012	In pre-B-cell lines, both SRSF1 and PRMT1 expression could be efficiently attenuated by the clinical chemotherapy agents arabinoside cytosine (Ara-c) or vincristine (VCR).	Cytarabine	121-141	protein arginine methyltransferase 1	Homo sapiens	36-41
22839530-10	2012	In pre-B-cell lines, both SRSF1 and PRMT1 expression could be efficiently attenuated by the clinical chemotherapy agents arabinoside cytosine (Ara-c) or vincristine (VCR).	Cytarabine	143-148	serine and arginine rich splicing factor 1	Homo sapiens	26-31
22839530-10	2012	In pre-B-cell lines, both SRSF1 and PRMT1 expression could be efficiently attenuated by the clinical chemotherapy agents arabinoside cytosine (Ara-c) or vincristine (VCR).	Cytarabine	143-148	protein arginine methyltransferase 1	Homo sapiens	36-41
22884143-2	2012	Deoxycytidine kinase (DCK) and cytidine deaminase (CDA) are the key enzymes in the metabolism of Ara-C.	Cytarabine	97-102	deoxycytidine kinase	Homo sapiens	0-20
22185283-11	2012	The drug resistance reversal index of adriamycin, cytarabine and arsenic trioxide was 3.8-fold, 2.65-fold and 2.64-fold, respectively, after PTEN gene transfection.	Cytarabine	50-60	phosphatase and tensin homolog	Homo sapiens	141-145
22422824-7	2012	However, patients treated with the escalated-dose cytarabine regimen benefited from G-CSF priming, with improved event-free survival (P = .01) and overall survival (P = .003), compared with patients without G-CSF undergoing escalated-dose cytarabine treatment.	Cytarabine	50-60	colony stimulating factor 3	Homo sapiens	84-89
22422824-7	2012	However, patients treated with the escalated-dose cytarabine regimen benefited from G-CSF priming, with improved event-free survival (P = .01) and overall survival (P = .003), compared with patients without G-CSF undergoing escalated-dose cytarabine treatment.	Cytarabine	239-249	colony stimulating factor 3	Homo sapiens	84-89
22422824-8	2012	A significant survival advantage of sensitizing AML for chemotherapy with G-CSF was not apparent in the entire study group, but it was seen in patients treated with escalated-dose cytarabine during remission induction.	Cytarabine	180-190	colony stimulating factor 3	Homo sapiens	74-79
22884143-2	2012	Deoxycytidine kinase (DCK) and cytidine deaminase (CDA) are the key enzymes in the metabolism of Ara-C.	Cytarabine	97-102	deoxycytidine kinase	Homo sapiens	22-25
22884143-2	2012	Deoxycytidine kinase (DCK) and cytidine deaminase (CDA) are the key enzymes in the metabolism of Ara-C.	Cytarabine	97-102	cytidine deaminase	Homo sapiens	31-49
22884143-2	2012	Deoxycytidine kinase (DCK) and cytidine deaminase (CDA) are the key enzymes in the metabolism of Ara-C.	Cytarabine	97-102	cytidine deaminase	Homo sapiens	51-54
22884143-3	2012	Many single nucleotide polymorphisms (SNPs) and haplotypes of DCK and CDA, which contribute to susceptibility to Ara-C, have been identified in Africans and Europeans.	Cytarabine	113-118	deoxycytidine kinase	Homo sapiens	62-65
22884143-3	2012	Many single nucleotide polymorphisms (SNPs) and haplotypes of DCK and CDA, which contribute to susceptibility to Ara-C, have been identified in Africans and Europeans.	Cytarabine	113-118	cytidine deaminase	Homo sapiens	70-73
22739154-7	2012	Bortezomib and Ara-C also synergistically induced activation of caspase-9, caspase-8 and caspase-3.	Cytarabine	15-20	caspase 9	Homo sapiens	64-73
22687457-3	2012	The efficacy of CHOP as induction therapy before ASCT in MCL is questioned and there is now evidence that as pretreatment before ASCT, AraC + rituximab leads to deeper remission and prolongs progression-free survival compared to rituximab + CHOP.	Cytarabine	135-139	DNA damage inducible transcript 3	Homo sapiens	16-20
22687457-3	2012	The efficacy of CHOP as induction therapy before ASCT in MCL is questioned and there is now evidence that as pretreatment before ASCT, AraC + rituximab leads to deeper remission and prolongs progression-free survival compared to rituximab + CHOP.	Cytarabine	135-139	DNA damage inducible transcript 3	Homo sapiens	241-245
22289989-4	2012	Integration of these independent analyses strongly implicates cell-cycle checkpoint proteins, particularly WEE1, as critical mediators of AML cell survival after cytarabine exposure.	Cytarabine	162-172	WEE1 G2 checkpoint kinase	Homo sapiens	107-111
22289989-6	2012	Pharmacologic inhibition of WEE1 in AML cell lines and primary cells is synergistic with cytarabine.	Cytarabine	89-99	WEE1 G2 checkpoint kinase	Homo sapiens	28-32
22289989-7	2012	Further experiments demonstrate that inhibition of WEE1 prevents S-phase arrest induced by cytarabine, broadening the functions of WEE1 that may be exploited therapeutically.	Cytarabine	91-101	WEE1 G2 checkpoint kinase	Homo sapiens	51-55
22289989-7	2012	Further experiments demonstrate that inhibition of WEE1 prevents S-phase arrest induced by cytarabine, broadening the functions of WEE1 that may be exploited therapeutically.	Cytarabine	91-101	WEE1 G2 checkpoint kinase	Homo sapiens	131-135
22739154-7	2012	Bortezomib and Ara-C also synergistically induced activation of caspase-9, caspase-8 and caspase-3.	Cytarabine	15-20	caspase 8	Homo sapiens	75-84
22739154-7	2012	Bortezomib and Ara-C also synergistically induced activation of caspase-9, caspase-8 and caspase-3.	Cytarabine	15-20	caspase 3	Homo sapiens	89-98
22035418-9	2012	Ara-C causes neuronal cell death by introduction of apoptosis with reactive oxygen species, causing oxidative DNA damage and initiating the p53-dependent apoptotic program.	Cytarabine	0-5	tumor protein p53	Homo sapiens	140-143
22414310-12	2012	Ara-C infusion significantly abolished neurogenesis and spatial learning recovery after TBI and EPO treatment.	Cytarabine	0-5	erythropoietin	Rattus norvegicus	96-99
22474250-5	2012	The cell cycle-inhibiting effect of the prophylactic administration of Mig protected hematopoietic progenitor cells (HPCs) from 1-beta-d-arabinofuranosylcytosine in spleen colony assays and enhanced the irradiated recipients" survival.	Cytarabine	128-161	chemokine (C-X-C motif) ligand 9	Mus musculus	71-74
22020636-0	2012	Prognostic significance of alterations in IDH enzyme isoforms in patients with AML treated with high-dose cytarabine and idarubicin.	Cytarabine	106-116	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	42-45
22285911-5	2012	In addition to the ABCC subfamily members, ABCG2 has been shown to transport nucleoside drugs and nucleoside-monophosphate derivatives of clinically relevant nucleoside drugs such as cytarabine, cladribine, and clofarabine to name a few.	Cytarabine	183-193	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	43-48
22374841-6	2012	Furthermore, disease-stabilizing therapy altered the serum-cytokine profile, but the correlations between HSP70/HSP90/IL-1ra/HGF were maintained only when ATRA + valproic acid were combined with theophyllin but not when combined with cytarabine.	Cytarabine	234-244	heat shock protein family A (Hsp70) member 4	Homo sapiens	106-111
22209977-14	2012	CONCLUSIONS: This study for the first time demonstrated that downregulation of miR-181a and upregulation of Bcl-2 in leukaemia cells confer resistance to Ara-C-based therapy.	Cytarabine	154-159	BCL2 apoptosis regulator	Homo sapiens	108-113
22242831-0	2012	In vivo enrichment of cytidine deaminase gene-modified hematopoietic cells by prolonged cytosine-arabinoside application.	Cytarabine	88-108	cytidine deaminase	Mus musculus	22-40
22242831-1	2012	BACKGROUND AIMS: Drug-resistance genes have been explored as powerful in vivo selection markers in hematopoietic cell gene therapy, and cytidine deaminase (CDD) represents a particularly attractive candidate given the virtual absence of non-hematopoietic side-effects after low/intermediate dose application of the associated drug cytosine-arabinoside (Ara-C).	Cytarabine	331-351	cytidine deaminase	Mus musculus	136-154
22242831-1	2012	BACKGROUND AIMS: Drug-resistance genes have been explored as powerful in vivo selection markers in hematopoietic cell gene therapy, and cytidine deaminase (CDD) represents a particularly attractive candidate given the virtual absence of non-hematopoietic side-effects after low/intermediate dose application of the associated drug cytosine-arabinoside (Ara-C).	Cytarabine	331-351	cytidine deaminase	Mus musculus	156-159
22242831-1	2012	BACKGROUND AIMS: Drug-resistance genes have been explored as powerful in vivo selection markers in hematopoietic cell gene therapy, and cytidine deaminase (CDD) represents a particularly attractive candidate given the virtual absence of non-hematopoietic side-effects after low/intermediate dose application of the associated drug cytosine-arabinoside (Ara-C).	Cytarabine	353-358	cytidine deaminase	Mus musculus	136-154
22242831-1	2012	BACKGROUND AIMS: Drug-resistance genes have been explored as powerful in vivo selection markers in hematopoietic cell gene therapy, and cytidine deaminase (CDD) represents a particularly attractive candidate given the virtual absence of non-hematopoietic side-effects after low/intermediate dose application of the associated drug cytosine-arabinoside (Ara-C).	Cytarabine	353-358	cytidine deaminase	Mus musculus	156-159
22212197-10	2012	Moreover, Ara-C treatment significantly increased the oxidative stress, DNA damage, TUNEL positive cells, p53 and caspase-3 positive cells in the rat cerebellum.	Cytarabine	10-15	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	106-109
22167413-3	2012	The mTOR signaling pathway is frequently activated in acute myelogenous leukemia (AML) and we previously showed the safety of combining the mTOR inhibitor, sirolimus, with mitoxantrone, etoposide, and cytarabine (MEC) chemotherapy.	Cytarabine	201-211	mechanistic target of rapamycin kinase	Homo sapiens	4-8
22212197-10	2012	Moreover, Ara-C treatment significantly increased the oxidative stress, DNA damage, TUNEL positive cells, p53 and caspase-3 positive cells in the rat cerebellum.	Cytarabine	10-15	caspase 3	Rattus norvegicus	114-123
22212197-11	2012	Unlike short-term treatment, long-term Ara-C treatment significantly reduced calbindin expression in the cerebellum.	Cytarabine	39-44	calbindin 1	Rattus norvegicus	77-86
22212197-13	2012	Present results indicated that Ara-C, by inducing oxidative stress mediated DNA damage, executes neuronal apoptosis which is accompanied by an increase in the p53 and caspase-3, but decrease in the calbindin expression.	Cytarabine	31-36	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	159-162
22212197-13	2012	Present results indicated that Ara-C, by inducing oxidative stress mediated DNA damage, executes neuronal apoptosis which is accompanied by an increase in the p53 and caspase-3, but decrease in the calbindin expression.	Cytarabine	31-36	caspase 3	Rattus norvegicus	167-176
22212197-13	2012	Present results indicated that Ara-C, by inducing oxidative stress mediated DNA damage, executes neuronal apoptosis which is accompanied by an increase in the p53 and caspase-3, but decrease in the calbindin expression.	Cytarabine	31-36	calbindin 1	Rattus norvegicus	198-207
22399596-4	2012	RESULTS: Azacitidine and decitabine induced hypomethylation of the tumor suppressor gene cyclin-dependent kinase 4 inhibitor B (CDKN2B) in SKM-1 cells, whereas the deoxycytidine analog cytarabine did not.	Cytarabine	185-195	cyclin dependent kinase inhibitor 2B	Homo sapiens	128-134
22829255-1	2012	Patients suffering from acute myeloid leukemias (AML) bearing FMS-like tyrosine kinase-3-internal tandem duplications (FLT3-ITD) have poor outcomes following cytarabine- and anthracyclin-based induction therapy.	Cytarabine	158-168	fms related receptor tyrosine kinase 3	Homo sapiens	62-88
22829255-1	2012	Patients suffering from acute myeloid leukemias (AML) bearing FMS-like tyrosine kinase-3-internal tandem duplications (FLT3-ITD) have poor outcomes following cytarabine- and anthracyclin-based induction therapy.	Cytarabine	158-168	fms related receptor tyrosine kinase 3	Homo sapiens	119-123
22829255-6	2012	Heterologously expressed MCL-1 substituted for FLT3 signaling by conferring resistance of hematopoietic cells to antileukemia drugs such as cytarabine and daunorubicin, and to the proapoptotic BH3 mimetic ABT-737.	Cytarabine	140-150	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	25-30
22829255-6	2012	Heterologously expressed MCL-1 substituted for FLT3 signaling by conferring resistance of hematopoietic cells to antileukemia drugs such as cytarabine and daunorubicin, and to the proapoptotic BH3 mimetic ABT-737.	Cytarabine	140-150	fms related receptor tyrosine kinase 3	Homo sapiens	47-51
22265744-6	2012	Furthermore, CDy::UPRT-MSCs were significantly more sensitive to 5-fluorouracil (5FU), cisplatin, cyclophosphamide and cytosine arabinoside as determined by increased Caspase 3/7 activation and/or decreased relative proliferation.	Cytarabine	119-139	chromodomain Y-linked 1B	Homo sapiens	13-16
22265744-6	2012	Furthermore, CDy::UPRT-MSCs were significantly more sensitive to 5-fluorouracil (5FU), cisplatin, cyclophosphamide and cytosine arabinoside as determined by increased Caspase 3/7 activation and/or decreased relative proliferation.	Cytarabine	119-139	caspase 3	Homo sapiens	167-176
21689092-0	2012	Targeting PIM kinase activity significantly augments the efficacy of cytarabine.	Cytarabine	69-79	Pim-1 proto-oncogene, serine/threonine kinase	Homo sapiens	10-13
22304580-0	2012	Cytidine deaminase genetic variants influence RNA expression and cytarabine cytotoxicity in acute myeloid leukemia.	Cytarabine	65-75	cytidine deaminase	Homo sapiens	0-18
22304580-1	2012	AIM: Cytidine deaminase (CDA) irreversibly deaminates cytarabine (Ara-C), a key component of acute myeloid leukemia (AML) induction and consolidation therapy.	Cytarabine	54-64	cytidine deaminase	Homo sapiens	5-23
22304580-1	2012	AIM: Cytidine deaminase (CDA) irreversibly deaminates cytarabine (Ara-C), a key component of acute myeloid leukemia (AML) induction and consolidation therapy.	Cytarabine	54-64	cytidine deaminase	Homo sapiens	25-28
22304580-1	2012	AIM: Cytidine deaminase (CDA) irreversibly deaminates cytarabine (Ara-C), a key component of acute myeloid leukemia (AML) induction and consolidation therapy.	Cytarabine	66-71	cytidine deaminase	Homo sapiens	5-23
22304580-1	2012	AIM: Cytidine deaminase (CDA) irreversibly deaminates cytarabine (Ara-C), a key component of acute myeloid leukemia (AML) induction and consolidation therapy.	Cytarabine	66-71	cytidine deaminase	Homo sapiens	25-28
22304580-2	2012	CDA overexpression results in Ara-C resistance, while decreased expression is associated with toxicity.	Cytarabine	30-35	cytidine deaminase	Homo sapiens	0-3
21937694-6	2012	In agreement with PI3K/AKT as an effector for cytosine arabinoside resistance in acute myeloid leukemia, overexpression of GRP78 renders human leukemic cells more resistant to cytosine arabinoside-induced apoptosis, whereas knockdown of GRP78 sensitizes them.	Cytarabine	46-66	heat shock protein family A (Hsp70) member 5	Homo sapiens	123-128
21937694-6	2012	In agreement with PI3K/AKT as an effector for cytosine arabinoside resistance in acute myeloid leukemia, overexpression of GRP78 renders human leukemic cells more resistant to cytosine arabinoside-induced apoptosis, whereas knockdown of GRP78 sensitizes them.	Cytarabine	176-196	heat shock protein family A (Hsp70) member 5	Homo sapiens	123-128
21937694-6	2012	In agreement with PI3K/AKT as an effector for cytosine arabinoside resistance in acute myeloid leukemia, overexpression of GRP78 renders human leukemic cells more resistant to cytosine arabinoside-induced apoptosis, whereas knockdown of GRP78 sensitizes them.	Cytarabine	176-196	heat shock protein family A (Hsp70) member 5	Homo sapiens	237-242
23049558-6	2012	CNDAC is more effective at reducing viability and inducing apoptosis than ara-C at equivalent concentrations in the THP-1 cell line, which is defined as displaying resistance to ara-C.	Cytarabine	178-183	GLI family zinc finger 2	Homo sapiens	116-121
22232668-5	2012	BTC-null mice are less able to regenerate neuroblast numbers compared with WT littermates following depletion of proliferating cells using cytosine-beta-d-arabinofuranoside.	Cytarabine	139-172	betacellulin, epidermal growth factor family member	Mus musculus	0-3
22905229-5	2012	In vitro murine AML cells that overexpressed MN1 became resistant to treatment with cytarabine and highly resistant to doxorubicin.	Cytarabine	84-94	meningioma 1	Mus musculus	45-48
22201761-0	2012	Long term cultured HL-60 cells are intrinsically resistant to Ara-C through high CDA activity.	Cytarabine	62-67	cytidine deaminase	Homo sapiens	81-84
22201761-8	2012	In conclusion, the long term cultured cells are intrinsically resistant to ara-C through high CDA activity, but not low DCK activity.	Cytarabine	75-80	cytidine deaminase	Homo sapiens	94-97
22420547-7	2012	A decrease in Il-6 level after application of Cisplatin and Methotrexate and a 5-10 fold increase in the level of Il-6 after application of Etoposide, Carboplatin, Cytarabine, and Gemcitabine were registered in the medium with ganglioneuroblastoma.	Cytarabine	164-174	interleukin 6	Homo sapiens	114-118
22362285-3	2012	In the present study, the effect of PML targeting therapy with As(2)O(3) and cytarabine (Ara-C) on Daoy medulloblastoma cell proliferation was investigated.	Cytarabine	77-87	PML nuclear body scaffold	Homo sapiens	36-39
22362285-3	2012	In the present study, the effect of PML targeting therapy with As(2)O(3) and cytarabine (Ara-C) on Daoy medulloblastoma cell proliferation was investigated.	Cytarabine	89-94	PML nuclear body scaffold	Homo sapiens	36-39
23127884-10	2012	After ablation of adult neurogenesis with Ara-c infusion,  the beneficial effect of LBP treatment in reducing immobility time was not affected in 40 and 50 mg/kg CORT stressed rats.	Cytarabine	42-47	lipopolysaccharide binding protein	Rattus norvegicus	84-87
22905229-6	2012	This resistant phenotype was also seen in vivo, where treatment with the combination of cytarabine and doxorubicin selected for cells expressing MN1.	Cytarabine	88-98	MN1 proto-oncogene, transcriptional regulator	Homo sapiens	145-148
22629369-7	2012	The activity of the equilibrative nucleoside transporter 1 (ENT1), responsible for cytarabine cell incorporation, was investigated by measuring transport and intracellular accumulation of (3)H-adenosine.	Cytarabine	83-93	solute carrier family 29 (nucleoside transporters), member 1	Mus musculus	20-58
22629369-7	2012	The activity of the equilibrative nucleoside transporter 1 (ENT1), responsible for cytarabine cell incorporation, was investigated by measuring transport and intracellular accumulation of (3)H-adenosine.	Cytarabine	83-93	solute carrier family 29 (nucleoside transporters), member 1	Mus musculus	60-64
22629369-8	2012	RESULTS: Leukemia cell mobilization from the bone marrow into peripheral blood in vivo using a CXCR4 inhibitor induced chemo-sensitization of leukemia cells to cytarabine, which translated into a prolonged survival advantage in our mouse leukemia model.	Cytarabine	160-170	chemokine (C-X-C motif) receptor 4	Mus musculus	95-100
22629369-10	2012	Furthermore, the BM stromal cell supernatant induced a 50% reduction of the ENT1 activity in leukemia cells, reducing the incorporation of cytarabine.	Cytarabine	139-149	solute carrier family 29 (nucleoside transporters), member 1	Mus musculus	76-80
21964441-9	2011	Treatment with cytosine arabinoside decreased the expression of Bmp4.	Cytarabine	15-35	bone morphogenetic protein 4	Mus musculus	64-68
22523565-5	2012	delivery of Ara-C accelerated disease progression in SOD1(G93A) mouse model of ALS.	Cytarabine	12-17	superoxide dismutase 1, soluble	Mus musculus	53-57
22523565-6	2012	Ara-C treatment caused substantial decreases in the number of microglia, NG2+ progenitors, Olig2+ cells and CD3+ T cells in the lumbar spinal cord of symptomatic SOD1(G93A) transgenic mice.	Cytarabine	0-5	oligodendrocyte transcription factor 2	Mus musculus	91-96
22523565-6	2012	Ara-C treatment caused substantial decreases in the number of microglia, NG2+ progenitors, Olig2+ cells and CD3+ T cells in the lumbar spinal cord of symptomatic SOD1(G93A) transgenic mice.	Cytarabine	0-5	superoxide dismutase 1, soluble	Mus musculus	162-166
21880628-9	2011	Furthermore, our data showed that deregulated expression of tumor suppressor microRNAs, such as miR-29a and miR-30c, might contribute to sensitivity to cytarabine, which is observed in NPM1 mutated acute myeloid leukemia.	Cytarabine	152-162	microRNA 29a	Homo sapiens	96-103
21880628-9	2011	Furthermore, our data showed that deregulated expression of tumor suppressor microRNAs, such as miR-29a and miR-30c, might contribute to sensitivity to cytarabine, which is observed in NPM1 mutated acute myeloid leukemia.	Cytarabine	152-162	microRNA 30c-1	Homo sapiens	108-115
21880628-9	2011	Furthermore, our data showed that deregulated expression of tumor suppressor microRNAs, such as miR-29a and miR-30c, might contribute to sensitivity to cytarabine, which is observed in NPM1 mutated acute myeloid leukemia.	Cytarabine	152-162	nucleophosmin 1	Homo sapiens	185-189
21676437-7	2011	Because of the presumptive platelet-derived growth factor receptor alpha translocation and its sensitivity to tyrosine-kinase inhibitor, the patient was treated with imatinib mesylate, cytarabine, and idarubicin as induction and maintenance therapy; and she has remained free of disease for 5 months since the initial diagnosis.	Cytarabine	185-195	platelet derived growth factor receptor alpha	Homo sapiens	27-72
22132977-1	2011	Deoxycytidine kinase (dCK) is essential for phosphorylation of natural deoxynucleosides and analogs, such as gemcitabine and cytarabine, two widely used anticancer compounds.	Cytarabine	125-135	deoxycytidine kinase	Homo sapiens	0-20
20614162-6	2011	Furthermore, the Smac-mimetics synergize with Cytarabine, Etoposide and especially with TRAIL in combination treatments.	Cytarabine	46-56	diablo IAP-binding mitochondrial protein	Homo sapiens	17-21
21851218-7	2011	In the current study generation, the addition of high-dose Ara-C to a rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP)-like regimen followed by myeloablative consolidation achieved a significant improvement of progression-free survival.	Cytarabine	59-64	DNA damage inducible transcript 3	Homo sapiens	142-146
22132977-1	2011	Deoxycytidine kinase (dCK) is essential for phosphorylation of natural deoxynucleosides and analogs, such as gemcitabine and cytarabine, two widely used anticancer compounds.	Cytarabine	125-135	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	22-25
21791475-1	2011	BACKGROUND: In preclinical studies the heat shock protein 90 (Hsp90) inhibitor tanespimycin induced down-regulation of checkpoint kinase 1 (Chk1) and other client proteins as well as increased sensitivity of acute leukemia cells to cytarabine.	Cytarabine	232-242	heat shock protein 90 alpha family class A member 1	Homo sapiens	39-60
21456022-0	2011	Phase 1 study of arsenic trioxide, high-dose cytarabine, and idarubicin to down-regulate constitutive signal transducer and activator of transcription 3 activity in patients aged &lt;60 years with acute myeloid leukemia.	Cytarabine	45-55	signal transducer and activator of transcription 3	Homo sapiens	102-152
21791475-1	2011	BACKGROUND: In preclinical studies the heat shock protein 90 (Hsp90) inhibitor tanespimycin induced down-regulation of checkpoint kinase 1 (Chk1) and other client proteins as well as increased sensitivity of acute leukemia cells to cytarabine.	Cytarabine	232-242	heat shock protein 90 alpha family class A member 1	Homo sapiens	62-67
21791475-1	2011	BACKGROUND: In preclinical studies the heat shock protein 90 (Hsp90) inhibitor tanespimycin induced down-regulation of checkpoint kinase 1 (Chk1) and other client proteins as well as increased sensitivity of acute leukemia cells to cytarabine.	Cytarabine	232-242	checkpoint kinase 1	Homo sapiens	140-144
21719597-7	2011	Knockdown of NPM1 also sensitized OCI-AML3 to all-trans retinoic acid (ATRA) and cytarabine.	Cytarabine	81-91	nucleophosmin 1	Homo sapiens	13-17
21816906-7	2011	The positive effects of miR-32 on cell survival were confirmed by evidence of increased cell death in AML cells preexposed to antisense miR-32 before treatment with arabinocytosine, a chemotherapeutic drug used to treat human AML.	Cytarabine	165-180	microRNA 32	Homo sapiens	24-30
21712425-1	2011	Cytosolic 5"-nucleotidase II (NT5C2) is involved in the development of 1-beta-d-arabinofuranosylcytosine (ara-C) resistance and has been associated with clinical outcome in patients receiving ara-C-based chemotherapy.	Cytarabine	71-104	5'-nucleotidase, cytosolic II	Homo sapiens	30-35
21712425-1	2011	Cytosolic 5"-nucleotidase II (NT5C2) is involved in the development of 1-beta-d-arabinofuranosylcytosine (ara-C) resistance and has been associated with clinical outcome in patients receiving ara-C-based chemotherapy.	Cytarabine	106-111	5'-nucleotidase, cytosolic II	Homo sapiens	30-35
21712425-1	2011	Cytosolic 5"-nucleotidase II (NT5C2) is involved in the development of 1-beta-d-arabinofuranosylcytosine (ara-C) resistance and has been associated with clinical outcome in patients receiving ara-C-based chemotherapy.	Cytarabine	192-197	5'-nucleotidase, cytosolic II	Homo sapiens	30-35
21712425-2	2011	NT5C2 inactivates ara-C by dephosphorylating ara-C monophosphate to ara-C.	Cytarabine	18-23	5'-nucleotidase, cytosolic II	Homo sapiens	0-5
21712425-2	2011	NT5C2 inactivates ara-C by dephosphorylating ara-C monophosphate to ara-C.	Cytarabine	45-50	5'-nucleotidase, cytosolic II	Homo sapiens	0-5
21712425-7	2011	Furthermore, there was a correlation between NT5C2 mRNA expression and ara-C sensitivity in CEU but not in YRI cell lines.	Cytarabine	71-76	5'-nucleotidase, cytosolic II	Homo sapiens	45-50
21712425-10	2011	Of most interest, SNPs (linkage disequilibrium group CEU.12) in the 5"-untranslated region were associated with NT5C2 expression and ara-C sensitivity in HapMap cell lines and with NT5C2 mRNA expression and ara-C sensitivity in diagnostic leukemic blasts from pediatric patients with acute myeloid leukemia.	Cytarabine	133-138	5'-nucleotidase, cytosolic II	Homo sapiens	181-186
21712425-10	2011	Of most interest, SNPs (linkage disequilibrium group CEU.12) in the 5"-untranslated region were associated with NT5C2 expression and ara-C sensitivity in HapMap cell lines and with NT5C2 mRNA expression and ara-C sensitivity in diagnostic leukemic blasts from pediatric patients with acute myeloid leukemia.	Cytarabine	207-212	5'-nucleotidase, cytosolic II	Homo sapiens	112-117
21712425-10	2011	Of most interest, SNPs (linkage disequilibrium group CEU.12) in the 5"-untranslated region were associated with NT5C2 expression and ara-C sensitivity in HapMap cell lines and with NT5C2 mRNA expression and ara-C sensitivity in diagnostic leukemic blasts from pediatric patients with acute myeloid leukemia.	Cytarabine	207-212	5'-nucleotidase, cytosolic II	Homo sapiens	181-186
22338135-10	2011	Two or more courses of intermediate-dose Ara-C during consolidating chemotherapy can obviously prolong the OS and RFS of CBF AML patients.	Cytarabine	41-46	CCAAT enhancer binding protein zeta	Homo sapiens	121-124
21719597-7	2011	Knockdown of NPM1 also sensitized OCI-AML3 to all-trans retinoic acid (ATRA) and cytarabine.	Cytarabine	81-91	RUNX family transcription factor 2	Homo sapiens	38-42
21719597-10	2011	Thus, attenuating levels or oligomerization of NPM1 selectively induces apoptosis and sensitizes NPM1c+ expressing AML cells to treatment with ATRA and cytarabine.	Cytarabine	152-162	nucleophosmin 1	Homo sapiens	47-51
21694703-5	2011	Including the chemotherapeutic agent, Ara-C, from day 10 of induced differentiation enriched for cTnI/alpha-actinin double positive cells to 45%.	Cytarabine	38-43	troponin I3, cardiac type	Homo sapiens	97-101
21694703-5	2011	Including the chemotherapeutic agent, Ara-C, from day 10 of induced differentiation enriched for cTnI/alpha-actinin double positive cells to 45%.	Cytarabine	38-43	actinin alpha 1	Homo sapiens	102-115
22111065-2	2011	Therefore, the current trial attempted to evaluate the efficacy of granulocyte colony-stimulating factor (G-CSF) priming in remission induction chemotherapy with an intensified dose of Ara-C for newly diagnosed AML.	Cytarabine	185-190	colony stimulating factor 3	Homo sapiens	67-104
21911919-4	2011	This study aims to analyse the role of HO-1 in regulating apoptosis in AML cells in response to two front-line chemotherapeutic agents used for AML, cytarabine and daunorubicin.	Cytarabine	149-159	heme oxygenase 1	Homo sapiens	39-43
21911919-5	2011	Here we show that HO-1 expression in AML samples was increased in response to both cytarabine and daunorubicin treatment, and micro RNA (miRNA) silenced HO-1 expression in combination with either daunorubicin or cytarabine induced a greater apoptotic responses in AML cells.	Cytarabine	83-93	heme oxygenase 1	Homo sapiens	18-22
21911919-5	2011	Here we show that HO-1 expression in AML samples was increased in response to both cytarabine and daunorubicin treatment, and micro RNA (miRNA) silenced HO-1 expression in combination with either daunorubicin or cytarabine induced a greater apoptotic responses in AML cells.	Cytarabine	212-222	heme oxygenase 1	Homo sapiens	153-157
21911919-7	2011	However, ROS-dependent induction of HO-1 was limiting the apoptotic response that is seen in AML towards cytarabine and daunorubicin treatment.	Cytarabine	105-115	heme oxygenase 1	Homo sapiens	36-40
21824052-0	2011	A NME1 promoter SNP predicts Ara-C associated neurotoxicity in AML patients.	Cytarabine	29-34	NME/NM23 nucleoside diphosphate kinase 1	Homo sapiens	2-6
21598398-1	2011	Cytidine deaminase (EC 3.5.4.5, CDA), an enzyme of the pyrimidine salvage pathways, is responsible for the degradation and inactivation of several cytidine-based antitumor drugs such as cytarabine, gemcitabine, decitabine, and azacytidine.	Cytarabine	186-196	cytidine deaminase	Homo sapiens	0-18
22111065-2	2011	Therefore, the current trial attempted to evaluate the efficacy of granulocyte colony-stimulating factor (G-CSF) priming in remission induction chemotherapy with an intensified dose of Ara-C for newly diagnosed AML.	Cytarabine	185-190	colony stimulating factor 3	Homo sapiens	106-111
24648585-1	2011	OBJECTIVE: This article compares the effect of interferon alfa plus cytarabine (IFN-alfa + Ara-C) versus IFN-alfa alone on the chronic phase of chronic myelogenous leukemia.	Cytarabine	68-78	interferon alpha 1	Homo sapiens	80-83
22829167-1	2011	Retrospective analyses in non-randomised cohorts suggest that regimens containing fludarabine/Ara C and/or idarubicin/ara C may be more effective than daunorubicin/AraC (DA)-containing regimens in cases of acute myeloid leukaemia (AML) overexpressing p-glycoprotein (Pgp).	Cytarabine	94-99	ATP binding cassette subfamily B member 1	Homo sapiens	251-265
21816375-0	2011	Patterns of molecular response to and relapse after combination of sorafenib, idarubicin, and cytarabine in patients with FLT3 mutant acute myeloid leukemia.	Cytarabine	94-104	fms related receptor tyrosine kinase 3	Homo sapiens	122-126
21816375-4	2011	METHODS: We studied the patterns of molecular response and relapse in 18 patients with mutated FLT3 treated with the combination of sorafenib, idarubicin, and cytarabine.	Cytarabine	159-169	fms related receptor tyrosine kinase 3	Homo sapiens	95-99
21867639-0	2011	[In vitro effects of Wnt3a gene modification on mitigating damage of mouse bone marrow mesenchymal stem cells induced by Ara-C].	Cytarabine	121-126	wingless-type MMTV integration site family, member 3A	Mus musculus	21-26
21867639-12	2011	It is concluded that Wnt3a gene modification can significantly mitigate the damage of mouse bone marrow MSC induced by Ara-C.	Cytarabine	119-124	wingless-type MMTV integration site family, member 3A	Mus musculus	21-26
22829167-1	2011	Retrospective analyses in non-randomised cohorts suggest that regimens containing fludarabine/Ara C and/or idarubicin/ara C may be more effective than daunorubicin/AraC (DA)-containing regimens in cases of acute myeloid leukaemia (AML) overexpressing p-glycoprotein (Pgp).	Cytarabine	94-99	ATP binding cassette subfamily B member 1	Homo sapiens	267-270
22829167-1	2011	Retrospective analyses in non-randomised cohorts suggest that regimens containing fludarabine/Ara C and/or idarubicin/ara C may be more effective than daunorubicin/AraC (DA)-containing regimens in cases of acute myeloid leukaemia (AML) overexpressing p-glycoprotein (Pgp).	Cytarabine	118-123	ATP binding cassette subfamily B member 1	Homo sapiens	251-265
22829167-1	2011	Retrospective analyses in non-randomised cohorts suggest that regimens containing fludarabine/Ara C and/or idarubicin/ara C may be more effective than daunorubicin/AraC (DA)-containing regimens in cases of acute myeloid leukaemia (AML) overexpressing p-glycoprotein (Pgp).	Cytarabine	118-123	ATP binding cassette subfamily B member 1	Homo sapiens	267-270
21288478-3	2011	MATERIALS AND METHODS: A genetically defined mouse model of AML was used to examine the effects of the Flt3-ITD on response to cytarabine and doxorubicin in vitro and in vivo.	Cytarabine	127-137	FMS-like tyrosine kinase 3	Mus musculus	103-107
21781494-6	2011	CONCLUSION: hermap gene can stimulate erythroid differentiation of Ara-C induced K562 cells mainly through JAK/STAT5 signal transduction pathway.	Cytarabine	67-72	signal transducer and activator of transcription 5A	Homo sapiens	111-116
21128225-3	2011	In addition, we found that CD34(+) /CD38(-) cells were relatively resistant to cytarabine- and the inhibitor of the fms-like tyrosine kinase 3 (FLT3)-mediated growth inhibition, as measured by the clonogenic assay.	Cytarabine	79-89	CD34 molecule	Homo sapiens	27-31
21128225-3	2011	In addition, we found that CD34(+) /CD38(-) cells were relatively resistant to cytarabine- and the inhibitor of the fms-like tyrosine kinase 3 (FLT3)-mediated growth inhibition, as measured by the clonogenic assay.	Cytarabine	79-89	CD38 molecule	Homo sapiens	36-40
21128225-4	2011	Interestingly, blockade of JAK2/STAT5 signaling by the specific JAK2 inhibitor AZ960 stimulated cell cycling in CD34(+) /CD38(-) cells in conjunction with downregulation of cyclin-dependent kinase inhibitor p21(waf1) and sensitized these cells to the growth inhibition mediated by cytarabine and the FLT3 kinase inhibitor.	Cytarabine	281-291	Janus kinase 2	Homo sapiens	27-31
21128225-4	2011	Interestingly, blockade of JAK2/STAT5 signaling by the specific JAK2 inhibitor AZ960 stimulated cell cycling in CD34(+) /CD38(-) cells in conjunction with downregulation of cyclin-dependent kinase inhibitor p21(waf1) and sensitized these cells to the growth inhibition mediated by cytarabine and the FLT3 kinase inhibitor.	Cytarabine	281-291	signal transducer and activator of transcription 5A	Homo sapiens	32-37
21128225-4	2011	Interestingly, blockade of JAK2/STAT5 signaling by the specific JAK2 inhibitor AZ960 stimulated cell cycling in CD34(+) /CD38(-) cells in conjunction with downregulation of cyclin-dependent kinase inhibitor p21(waf1) and sensitized these cells to the growth inhibition mediated by cytarabine and the FLT3 kinase inhibitor.	Cytarabine	281-291	Janus kinase 2	Homo sapiens	64-68
21127859-2	2011	dCK phosphorylates and therefore activates nucleoside analogs such as cytarabine, gemcitabine, decitabine, cladribine, and clofarabine that are used routinely in cancer therapy.	Cytarabine	70-80	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	0-3
21576088-4	2011	Mouse embryo fibroblasts derived from Abcc10(-/-) mice were hypersensitive to docetaxel, paclitaxel, vincristine, and cytarabine (Ara-C) and exhibited increased cellular drug accumulation, relative to wild-type controls.	Cytarabine	118-128	ATP-binding cassette, sub-family C (CFTR/MRP), member 10	Mus musculus	38-44
21576088-4	2011	Mouse embryo fibroblasts derived from Abcc10(-/-) mice were hypersensitive to docetaxel, paclitaxel, vincristine, and cytarabine (Ara-C) and exhibited increased cellular drug accumulation, relative to wild-type controls.	Cytarabine	130-135	ATP-binding cassette, sub-family C (CFTR/MRP), member 10	Mus musculus	38-44
21216274-5	2011	RESULTS: Mad2(+/-) HPCs were protected from cytotoxic effects in vivo of a cell-cycle-specific agent, Ara-C, events consistent with Mad2(+/-) HPCs being in a slow or noncycling state, but not from recovery of functional HPC after treatment with non-cycle-specific cyclophosphamide or sublethal irradiation.	Cytarabine	102-107	MAD2 mitotic arrest deficient-like 1	Mus musculus	9-13
21216274-5	2011	RESULTS: Mad2(+/-) HPCs were protected from cytotoxic effects in vivo of a cell-cycle-specific agent, Ara-C, events consistent with Mad2(+/-) HPCs being in a slow or noncycling state, but not from recovery of functional HPC after treatment with non-cycle-specific cyclophosphamide or sublethal irradiation.	Cytarabine	102-107	MAD2 mitotic arrest deficient-like 1	Mus musculus	132-136
21288478-4	2011	RESULTS: In vitro, the Flt3-ITD conferred resistance to doxorubicin and doxorubicin plus Ara-C, but sensitivity to Ara-C alone.	Cytarabine	89-94	fms related receptor tyrosine kinase 3	Homo sapiens	23-27
21288478-4	2011	RESULTS: In vitro, the Flt3-ITD conferred resistance to doxorubicin and doxorubicin plus Ara-C, but sensitivity to Ara-C alone.	Cytarabine	115-120	fms related receptor tyrosine kinase 3	Homo sapiens	23-27
21288478-8	2011	In vivo, the Flt3-ITD accelerated engraftment that was partially reversible by Ara-C but not doxorubicin.	Cytarabine	79-84	fms related receptor tyrosine kinase 3	Homo sapiens	13-17
21288478-11	2011	CONCLUSIONS: These data demonstrate that the Flt3-ITD confers sensitivity to Ara-C, but resistance to doxorubicin in a manner that depends on p53.	Cytarabine	77-82	fms related receptor tyrosine kinase 3	Homo sapiens	45-49
21290089-9	2011	The DNA microarray analysis revealed eight genes (C19orf2, HSPA8, LGALS1, POU4F3, PSAP, AKT1, MBC2 and CACNA2D3) that were altered in all five ara-C-resistant lines compared to parental cells.	Cytarabine	143-148	URI1 prefoldin like chaperone	Homo sapiens	50-57
21290089-9	2011	The DNA microarray analysis revealed eight genes (C19orf2, HSPA8, LGALS1, POU4F3, PSAP, AKT1, MBC2 and CACNA2D3) that were altered in all five ara-C-resistant lines compared to parental cells.	Cytarabine	143-148	heat shock protein family A (Hsp70) member 8	Homo sapiens	59-64
21290089-5	2011	For this purpose, we newly established five ara-C-resistant leukemic clones from different blood cell lineage leukemic cell lines (HL-60, K562, CEM, THP1 and U937).	Cytarabine	44-49	GLI family zinc finger 2	Homo sapiens	149-153
21290089-9	2011	The DNA microarray analysis revealed eight genes (C19orf2, HSPA8, LGALS1, POU4F3, PSAP, AKT1, MBC2 and CACNA2D3) that were altered in all five ara-C-resistant lines compared to parental cells.	Cytarabine	143-148	galectin 1	Homo sapiens	66-72
21290089-9	2011	The DNA microarray analysis revealed eight genes (C19orf2, HSPA8, LGALS1, POU4F3, PSAP, AKT1, MBC2 and CACNA2D3) that were altered in all five ara-C-resistant lines compared to parental cells.	Cytarabine	143-148	POU class 4 homeobox 3	Homo sapiens	74-80
21290089-9	2011	The DNA microarray analysis revealed eight genes (C19orf2, HSPA8, LGALS1, POU4F3, PSAP, AKT1, MBC2 and CACNA2D3) that were altered in all five ara-C-resistant lines compared to parental cells.	Cytarabine	143-148	prosaposin	Homo sapiens	82-86
21290089-9	2011	The DNA microarray analysis revealed eight genes (C19orf2, HSPA8, LGALS1, POU4F3, PSAP, AKT1, MBC2 and CACNA2D3) that were altered in all five ara-C-resistant lines compared to parental cells.	Cytarabine	143-148	AKT serine/threonine kinase 1	Homo sapiens	88-92
21290089-9	2011	The DNA microarray analysis revealed eight genes (C19orf2, HSPA8, LGALS1, POU4F3, PSAP, AKT1, MBC2 and CACNA2D3) that were altered in all five ara-C-resistant lines compared to parental cells.	Cytarabine	143-148	extended synaptotagmin 1	Homo sapiens	94-98
21290089-9	2011	The DNA microarray analysis revealed eight genes (C19orf2, HSPA8, LGALS1, POU4F3, PSAP, AKT1, MBC2 and CACNA2D3) that were altered in all five ara-C-resistant lines compared to parental cells.	Cytarabine	143-148	calcium voltage-gated channel auxiliary subunit alpha2delta 3	Homo sapiens	103-111
21290089-10	2011	Both proteome and DNA microarray analyses further detected a reduced protein level of stathmin1 in the ara-C-resistant CEM subclone compared to its parental line.	Cytarabine	103-108	stathmin 1	Homo sapiens	86-95
21359182-11	2011	At clinically achievable concentrations, HDACIs that simultaneously inhibited both HDACs 1 and 6 showed the best anti-leukemic activities and significantly enhanced cytarabine-induced apoptosis.	Cytarabine	165-175	histone deacetylase 1	Homo sapiens	83-96
21521023-1	2011	AIM: To adopt an individualized approach to assess cytarabine (ara-C) hematotoxicity, we studied the relationship between pharmacogenetic variability in the cytidine deaminase gene (CDA) and ara-C toxicity in native peripheral blood mononuclear cells from 100 healthy volunteers.	Cytarabine	51-61	cytidine deaminase	Homo sapiens	182-185
21521023-5	2011	Inhibition of hENT1 reversed ara-C cytotoxicity.	Cytarabine	29-34	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	14-19
21521023-8	2011	CONCLUSION: Genetic polymorphisms within CDA may be risk factors for ara-C-induced hematotoxicity.	Cytarabine	69-74	cytidine deaminase	Homo sapiens	41-44
21168391-6	2011	We show here that CdA, but also fludarabine, gemcitabine, and cytarabine, strongly reduced the p21 protein level in EHEB cells as well as in JVM-2 cells, another CLL cell line.	Cytarabine	62-72	cyclin dependent kinase inhibitor 1A	Homo sapiens	95-98
21212792-6	2011	Furthermore, the combination of SNS-032 and Ara-C showed remarkable synergy that was associated with reduced mRNA levels of the antiapoptotic genes XIAP, BCL2 and MCL1.	Cytarabine	44-49	X-linked inhibitor of apoptosis	Homo sapiens	148-152
21212792-6	2011	Furthermore, the combination of SNS-032 and Ara-C showed remarkable synergy that was associated with reduced mRNA levels of the antiapoptotic genes XIAP, BCL2 and MCL1.	Cytarabine	44-49	BCL2 apoptosis regulator	Homo sapiens	154-158
21212792-6	2011	Furthermore, the combination of SNS-032 and Ara-C showed remarkable synergy that was associated with reduced mRNA levels of the antiapoptotic genes XIAP, BCL2 and MCL1.	Cytarabine	44-49	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	163-167
21212792-8	2011	Treatment with Ara-C alone significantly induced the transcription of the antiapoptotic genes BCL2 and XIAP.	Cytarabine	15-20	BCL2 apoptosis regulator	Homo sapiens	94-98
21212792-8	2011	Treatment with Ara-C alone significantly induced the transcription of the antiapoptotic genes BCL2 and XIAP.	Cytarabine	15-20	X-linked inhibitor of apoptosis	Homo sapiens	103-107
21212792-9	2011	In contrast, the combination of SNS-032 and Ara-C suppressed the transcription of BCL2, XIAP and MCL1.	Cytarabine	44-49	BCL2 apoptosis regulator	Homo sapiens	82-86
21212792-9	2011	In contrast, the combination of SNS-032 and Ara-C suppressed the transcription of BCL2, XIAP and MCL1.	Cytarabine	44-49	X-linked inhibitor of apoptosis	Homo sapiens	88-92
21212792-9	2011	In contrast, the combination of SNS-032 and Ara-C suppressed the transcription of BCL2, XIAP and MCL1.	Cytarabine	44-49	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	97-101
21359182-9	2011	RESULTS: Treatments with structurally diverse HDACIs and HDAC shRNA knockdown experiments revealed that down-regulation of both HDACs 1 and 6 is critical in enhancing cytarabine-induced apoptosis in pediatric AML, at least partly mediated by Bim.	Cytarabine	167-177	histone deacetylase 1	Homo sapiens	128-141
21359182-10	2011	However, down-regulation of HDAC2 may negatively impact cytarabine sensitivities in the disease.	Cytarabine	56-66	histone deacetylase 2	Homo sapiens	28-33
21980431-14	2011	Interestingly, FLT3 inhibitor resistance also correlated with resistance to cytosine arabinoside.	Cytarabine	76-96	fms related receptor tyrosine kinase 3	Homo sapiens	15-19
21792317-0	2011	The prognostic impact of K-RAS mutations in adult acute myeloid leukemia patients treated with high-dose cytarabine.	Cytarabine	105-115	KRAS proto-oncogene, GTPase	Homo sapiens	25-30
21792317-4	2011	OBJECTIVE: This study aimed to clarify the biologic and prognostic impact of K-RAS mutations in relation to the dose of cytarabine (ara-C) used in postinduction consolidation chemotherapy in adult AML patients.	Cytarabine	120-130	KRAS proto-oncogene, GTPase	Homo sapiens	77-82
21792317-4	2011	OBJECTIVE: This study aimed to clarify the biologic and prognostic impact of K-RAS mutations in relation to the dose of cytarabine (ara-C) used in postinduction consolidation chemotherapy in adult AML patients.	Cytarabine	132-137	KRAS proto-oncogene, GTPase	Homo sapiens	77-82
21792317-18	2011	CONCLUSION: It was concluded that adult AML patients carrying mutations in the K-RAS gene benefit from higher ara-C doses more than wtRAS patients, so pretreatment mutation detection could be an important predictor for treatment strategy and survival of adult AML patients.	Cytarabine	110-115	KRAS proto-oncogene, GTPase	Homo sapiens	79-84
22110660-10	2011	Increased basal apoptosis and sensitivities to ara-C, daunorubicin, and VP-16 accompanied by down-regulated Bcl-2 were also detected in the CMK GATA1 shRNA knockdown clones.	Cytarabine	47-52	cytidine/uridine monophosphate kinase 1	Homo sapiens	140-143
22110660-10	2011	Increased basal apoptosis and sensitivities to ara-C, daunorubicin, and VP-16 accompanied by down-regulated Bcl-2 were also detected in the CMK GATA1 shRNA knockdown clones.	Cytarabine	47-52	GATA binding protein 1	Homo sapiens	144-149
21131780-6	2010	We observed specific ablation of the mixed function DNA glycosylase/lyase Neil1 phenotypically enhanced several inhibitors of thymidine biosynthesis, as well as cellular phenotypes downstream of gemcitabine, cytarabine and clofarabine exposure.	Cytarabine	208-218	nei like DNA glycosylase 1	Homo sapiens	74-79
20979180-1	2010	Treatment with the nucleoside analog cytarabine has been shown to mimic changes in gene expression associated with downregulation of the EWS-FLI1 oncogene in Ewing sarcoma cell lines, selectively inhibit their growth in vitro, and cause tumor regression in athymic nude mice.	Cytarabine	37-47	Ewing sarcoma breakpoint region 1	Mus musculus	137-140
21368877-2	2010	Here, we determined whether CRT exposure at the cell surface (ecto-CRT) occurs in human cancer in response to anthracyclines in vivo, focusing on acute myeloid leukemia (AML), which is currently treated with a combination of aracytine and anthracyclines.	Cytarabine	225-234	calreticulin	Homo sapiens	28-31
20958082-0	2010	Translocator protein (TSPO) ligand-Ara-C (cytarabine) conjugates as a strategy to deliver antineoplastic drugs and to enhance drug clinical potential.	Cytarabine	35-40	translocator protein	Homo sapiens	0-20
20958082-0	2010	Translocator protein (TSPO) ligand-Ara-C (cytarabine) conjugates as a strategy to deliver antineoplastic drugs and to enhance drug clinical potential.	Cytarabine	35-40	translocator protein	Homo sapiens	22-26
20958082-0	2010	Translocator protein (TSPO) ligand-Ara-C (cytarabine) conjugates as a strategy to deliver antineoplastic drugs and to enhance drug clinical potential.	Cytarabine	42-52	translocator protein	Homo sapiens	0-20
20958082-0	2010	Translocator protein (TSPO) ligand-Ara-C (cytarabine) conjugates as a strategy to deliver antineoplastic drugs and to enhance drug clinical potential.	Cytarabine	42-52	translocator protein	Homo sapiens	22-26
20958082-1	2010	The aim of this work was to evaluate TSPO ligand-Ara-C conjugation as an approach for the selective delivery of the antineoplastic agent to brain tumors as well as for overcome P-gp resistance induction observed for the majority of cytotoxic agents, enhancing the drug clinical potential.	Cytarabine	49-54	translocator protein	Homo sapiens	37-41
21466125-9	2010	These effects were more evident in the late phase than in the early phase of co-culture with CD34-positive cells, suggesting that Ara-C-treated stromal cells preferably support very immature cells, rather than committed progenitor cells.	Cytarabine	130-135	CD34 molecule	Homo sapiens	93-97
20979180-1	2010	Treatment with the nucleoside analog cytarabine has been shown to mimic changes in gene expression associated with downregulation of the EWS-FLI1 oncogene in Ewing sarcoma cell lines, selectively inhibit their growth in vitro, and cause tumor regression in athymic nude mice.	Cytarabine	37-47	Friend leukemia integration 1	Mus musculus	141-145
21152064-3	2010	In chemotherapeutic sensitivity screening assays, cells overexpressing pp32 were selectively resistant to the nucleoside analogs gemcitabine and cytarabine (ARA-C), but were sensitized to 5-fluorouracil; conversely, silencing pp32 in pancreatic cancer cells enhanced gemcitabine sensitivity.	Cytarabine	145-155	acidic nuclear phosphoprotein 32 family member A	Homo sapiens	71-75
20547440-0	2010	Aurora-A kinase inhibition enhances the cytosine arabinoside-induced cell death in leukemia cells through apoptosis and mitotic catastrophe.	Cytarabine	40-60	aurora kinase A	Homo sapiens	0-8
20547440-2	2010	In the Ara-C-sensitive leukemia cell lines, silencing of Aur-A by small interfering RNA transfection led to a significant increase in the Ara-C-induced cell death rate through induction of mitochondria-mediated, caspase-dependent apoptosis.	Cytarabine	7-12	aurora kinase A	Homo sapiens	57-62
20547440-2	2010	In the Ara-C-sensitive leukemia cell lines, silencing of Aur-A by small interfering RNA transfection led to a significant increase in the Ara-C-induced cell death rate through induction of mitochondria-mediated, caspase-dependent apoptosis.	Cytarabine	138-143	aurora kinase A	Homo sapiens	57-62
20547440-3	2010	In contrast, combined treatment of the Ara-C-resistant leukemia cell lines with Aur-A siRNA and Ara-C remarkably enhanced the cell death rate via non-caspase-dependent mitotic catastrophe.	Cytarabine	39-44	aurora kinase A	Homo sapiens	80-85
21152064-3	2010	In chemotherapeutic sensitivity screening assays, cells overexpressing pp32 were selectively resistant to the nucleoside analogs gemcitabine and cytarabine (ARA-C), but were sensitized to 5-fluorouracil; conversely, silencing pp32 in pancreatic cancer cells enhanced gemcitabine sensitivity.	Cytarabine	157-162	acidic nuclear phosphoprotein 32 family member A	Homo sapiens	71-75
20547440-4	2010	Taken together, Aur-A inhibition was an effective treatment for both the Ara-C-sensitive and resistant leukemia cells by increasing apoptosis and mitotic catastrophe, respectively.	Cytarabine	73-78	aurora kinase A	Homo sapiens	16-21
20889917-7	2010	Cytarabine and VPA cooperatively induced DNA double-strand breaks, reflected in induction of gammaH2AX and apoptosis, accompanied by activation of caspase-9 and caspase-3.	Cytarabine	0-10	caspase 9	Homo sapiens	147-156
20889917-7	2010	Cytarabine and VPA cooperatively induced DNA double-strand breaks, reflected in induction of gammaH2AX and apoptosis, accompanied by activation of caspase-9 and caspase-3.	Cytarabine	0-10	caspase 3	Homo sapiens	161-170
20889917-8	2010	Further, VPA induced Bim expression and short hairpin RNA knockdown of Bim resulted in significantly decreased apoptosis induced by cytarabine and by cytarabine plus VPA.	Cytarabine	132-142	BCL2 like 11	Homo sapiens	71-74
20889917-8	2010	Further, VPA induced Bim expression and short hairpin RNA knockdown of Bim resulted in significantly decreased apoptosis induced by cytarabine and by cytarabine plus VPA.	Cytarabine	150-160	BCL2 like 11	Homo sapiens	71-74
20858843-11	2010	Biodistribution and pharmacokinetic studies suggested that saturation of available CD33 sites by (213)Bi-lintuzumab was achieved after partial cytoreduction with cytarabine.	Cytarabine	162-172	CD33 molecule	Homo sapiens	83-87
20587622-3	2010	We observed comparable reactivity for dFdC and Ara-C, and the substrate reactivity of CNDAC to recombinant human CDA was more than 10 times less efficient than those of Ara-C and dFdC.	Cytarabine	169-174	cytidine deaminase	Homo sapiens	113-116
21036735-5	2010	Exposure to either DNR or Ara-C resulted in modest increases in CRIM1 levels in HL60R0.5.	Cytarabine	26-31	cysteine rich transmembrane BMP regulator 1	Homo sapiens	64-69
20587622-4	2010	Next, we examined the in vitro chemosensitivity of TMK-1/CDA and observed a marked decrease in the sensitivity of TMK-1/CDA to Ara-C, dFdC, and CNDAC compared with mock-transfected cells.	Cytarabine	127-132	cytidine deaminase	Homo sapiens	51-60
20587622-4	2010	Next, we examined the in vitro chemosensitivity of TMK-1/CDA and observed a marked decrease in the sensitivity of TMK-1/CDA to Ara-C, dFdC, and CNDAC compared with mock-transfected cells.	Cytarabine	127-132	cytidine deaminase	Homo sapiens	114-123
20610036-11	2010	In contrast, this BDNF/EGF-associated functional recovery was abolished in mice receiving a co-infusion of 2% cytosine-b-d-arabinofuranoside (Ara-C), a mitotic inhibitor.	Cytarabine	142-147	brain derived neurotrophic factor	Mus musculus	18-22
19941076-2	2010	CDA also catalyzes the inactivation of some chemotherapeutic nucleoside analogues such as cytosine arabinoside and gemcitabine.	Cytarabine	90-110	cytidine deaminase	Homo sapiens	0-3
20664001-4	2010	Cytarabine induced phosphorylation/activation of Mnk and Mnk-mediated phosphorylation of eIF4E on Ser209, as evidenced by studies involving pharmacological inhibition of Mnk or experiments using cells with targeted disruption of Mnk1 and Mnk2 genes.	Cytarabine	0-10	ATPase copper transporting alpha	Homo sapiens	57-60
20664001-4	2010	Cytarabine induced phosphorylation/activation of Mnk and Mnk-mediated phosphorylation of eIF4E on Ser209, as evidenced by studies involving pharmacological inhibition of Mnk or experiments using cells with targeted disruption of Mnk1 and Mnk2 genes.	Cytarabine	0-10	MAPK interacting serine/threonine kinase 1	Homo sapiens	229-233
20664001-4	2010	Cytarabine induced phosphorylation/activation of Mnk and Mnk-mediated phosphorylation of eIF4E on Ser209, as evidenced by studies involving pharmacological inhibition of Mnk or experiments using cells with targeted disruption of Mnk1 and Mnk2 genes.	Cytarabine	0-10	MAPK interacting serine/threonine kinase 2	Homo sapiens	238-242
20664001-5	2010	To assess the functional relevance of cytarabine-inducible engagement of Mnk/eIF4E pathway, the effects of pharmacological inhibition of Mnk on cytarabine-mediated suppression of primitive leukemic progenitors [leukemic colony forming unit (CFU-L)] were examined.	Cytarabine	38-48	ATPase copper transporting alpha	Homo sapiens	73-76
20664001-5	2010	To assess the functional relevance of cytarabine-inducible engagement of Mnk/eIF4E pathway, the effects of pharmacological inhibition of Mnk on cytarabine-mediated suppression of primitive leukemic progenitors [leukemic colony forming unit (CFU-L)] were examined.	Cytarabine	144-154	ATPase copper transporting alpha	Homo sapiens	137-140
20664001-6	2010	Concomitant treatment of cells with a pharmacological inhibitor of Mnk or siRNA-mediated knockdown of Mnk1/2 strongly enhanced the suppressive effects of low cytarabine concentrations on CFU-L.	Cytarabine	158-168	ATPase copper transporting alpha	Homo sapiens	67-70
20664001-6	2010	Concomitant treatment of cells with a pharmacological inhibitor of Mnk or siRNA-mediated knockdown of Mnk1/2 strongly enhanced the suppressive effects of low cytarabine concentrations on CFU-L.	Cytarabine	158-168	MAPK interacting serine/threonine kinase 1	Homo sapiens	102-108
20610036-11	2010	In contrast, this BDNF/EGF-associated functional recovery was abolished in mice receiving a co-infusion of 2% cytosine-b-d-arabinofuranoside (Ara-C), a mitotic inhibitor.	Cytarabine	142-147	epidermal growth factor	Mus musculus	23-26
20664001-2	2010	We determined the effects of chemotherapy (cytarabine) on the activation status of Mnk in AML cells and its role in the generation of antileukemic responses.	Cytarabine	43-53	ATPase copper transporting alpha	Homo sapiens	83-86
20664001-4	2010	Cytarabine induced phosphorylation/activation of Mnk and Mnk-mediated phosphorylation of eIF4E on Ser209, as evidenced by studies involving pharmacological inhibition of Mnk or experiments using cells with targeted disruption of Mnk1 and Mnk2 genes.	Cytarabine	0-10	ATPase copper transporting alpha	Homo sapiens	49-52
20664001-4	2010	Cytarabine induced phosphorylation/activation of Mnk and Mnk-mediated phosphorylation of eIF4E on Ser209, as evidenced by studies involving pharmacological inhibition of Mnk or experiments using cells with targeted disruption of Mnk1 and Mnk2 genes.	Cytarabine	0-10	ATPase copper transporting alpha	Homo sapiens	57-60
20664001-4	2010	Cytarabine induced phosphorylation/activation of Mnk and Mnk-mediated phosphorylation of eIF4E on Ser209, as evidenced by studies involving pharmacological inhibition of Mnk or experiments using cells with targeted disruption of Mnk1 and Mnk2 genes.	Cytarabine	0-10	eukaryotic translation initiation factor 4E	Homo sapiens	89-94
21223722-14	2010	CONCLUSIONS: Lentivirus-mediated RNA interference targeting VEGFR1 gene reduces the proliferation, migration of U937 cell line and enhances its sensitivity to Ara-C.	Cytarabine	159-164	fms related receptor tyrosine kinase 1	Homo sapiens	60-66
20567819-2	2010	Twelve kinds of hydrolases were tested for the regioselective acylation reaction and the immobilized Candida antarctica lipase B (Novozym 435) showed the highest regioselectivity (&gt;99.9%) towards the 5"-OH of ara-C.	Cytarabine	212-217	PAN0_003d1715	Moesziomyces antarcticus	120-126
20736344-9	2010	JNJ-26854165 synergizes with 1-beta-arabinofuranosylcytosine or doxorubicin to induce p53-mediated apoptosis.	Cytarabine	29-60	tumor protein p53 L homeolog	Xenopus laevis	86-89
21513214-5	2010	No substantial increase of caspase-3 activation was observed in thymocytes treated with C60 fullerene plus irradiation, while antileukemic agent cytosine arabinoside was shown to induce caspase-3 activation both in Jurkat cells and thymocytes.	Cytarabine	145-165	caspase 3	Homo sapiens	186-195
20177738-9	2010	These observations indicate that Cbl-b promotes RBL-2H3 apoptosis induced by VP-16 or Ara-c, probably through inhibition of Akt and activation of ERK.	Cytarabine	86-91	Cbl proto-oncogene B	Rattus norvegicus	33-38
20670480-0	2010	Anti-miR-21 oligonucleotide enhances chemosensitivity of leukemic HL60 cells to arabinosylcytosine by inducing apoptosis.	Cytarabine	80-98	microRNA 21	Homo sapiens	5-11
20670480-4	2010	We used a specific anti-miR-21 oligonucleotide (AMO-miR-21) to sensitize leukemic HL60 cells to arabinosylcytosine (Ara-C) by down-regulating miR-21.	Cytarabine	96-114	microRNA 21	Homo sapiens	24-30
20670480-4	2010	We used a specific anti-miR-21 oligonucleotide (AMO-miR-21) to sensitize leukemic HL60 cells to arabinosylcytosine (Ara-C) by down-regulating miR-21.	Cytarabine	96-114	microRNA 21	Homo sapiens	52-58
20670480-4	2010	We used a specific anti-miR-21 oligonucleotide (AMO-miR-21) to sensitize leukemic HL60 cells to arabinosylcytosine (Ara-C) by down-regulating miR-21.	Cytarabine	96-114	microRNA 21	Homo sapiens	52-58
20670480-4	2010	We used a specific anti-miR-21 oligonucleotide (AMO-miR-21) to sensitize leukemic HL60 cells to arabinosylcytosine (Ara-C) by down-regulating miR-21.	Cytarabine	116-121	microRNA 21	Homo sapiens	24-30
20670480-4	2010	We used a specific anti-miR-21 oligonucleotide (AMO-miR-21) to sensitize leukemic HL60 cells to arabinosylcytosine (Ara-C) by down-regulating miR-21.	Cytarabine	116-121	microRNA 21	Homo sapiens	52-58
20670480-4	2010	We used a specific anti-miR-21 oligonucleotide (AMO-miR-21) to sensitize leukemic HL60 cells to arabinosylcytosine (Ara-C) by down-regulating miR-21.	Cytarabine	116-121	microRNA 21	Homo sapiens	52-58
20670480-5	2010	AMO-miR-21 alone effectively inhibited HL60 cell viability as measured by MTT assays and induced apoptosis as evaluated by flow cytometry, whereas AMO-miR-21 in combination with Ara-C enhanced HL60 cells to Ara-C-sensitivity and promoted Ara-C-induced apoptosis.	Cytarabine	207-212	microRNA 21	Homo sapiens	151-157
20670480-5	2010	AMO-miR-21 alone effectively inhibited HL60 cell viability as measured by MTT assays and induced apoptosis as evaluated by flow cytometry, whereas AMO-miR-21 in combination with Ara-C enhanced HL60 cells to Ara-C-sensitivity and promoted Ara-C-induced apoptosis.	Cytarabine	207-212	microRNA 21	Homo sapiens	151-157
20670480-8	2010	Our study suggests that AMO-miR-21 significantly sensitizes HL60 cells to Ara-C by inducing apoptosis and these effects of AMO-miR-21 may be partially due to its up-regulation of PDCD4.	Cytarabine	74-79	microRNA 21	Homo sapiens	28-34
20670480-8	2010	Our study suggests that AMO-miR-21 significantly sensitizes HL60 cells to Ara-C by inducing apoptosis and these effects of AMO-miR-21 may be partially due to its up-regulation of PDCD4.	Cytarabine	74-79	microRNA 21	Homo sapiens	127-133
20670480-8	2010	Our study suggests that AMO-miR-21 significantly sensitizes HL60 cells to Ara-C by inducing apoptosis and these effects of AMO-miR-21 may be partially due to its up-regulation of PDCD4.	Cytarabine	74-79	programmed cell death 4	Homo sapiens	179-184
20508618-0	2010	Deoxycytidine kinase is downregulated in Ara-C-resistant acute myeloid leukemia murine cell lines.	Cytarabine	41-46	deoxycytidine kinase	Mus musculus	0-20
20459144-0	2010	Incorporation of gemcitabine and cytarabine into DNA by DNA polymerase beta and ligase III/XRCC1.	Cytarabine	33-43	DNA polymerase beta	Homo sapiens	56-75
20459144-0	2010	Incorporation of gemcitabine and cytarabine into DNA by DNA polymerase beta and ligase III/XRCC1.	Cytarabine	33-43	X-ray repair cross complementing 1	Homo sapiens	91-96
20525348-14	2010	Those studies showed that knockdown of SMYD3, in pancreatic cancer cell lines increased gemcitabine and AraC resistance during cytotoxicity assay, consistent with the results of the association analysis.	Cytarabine	104-108	SET and MYND domain containing 3	Homo sapiens	39-44
20082300-2	2010	The human equilibrative nucleoside transporter 1 (hENT1) is a member of these proteins and mediates cellular entry of gemcitabine, cytarabine, and fludarabine.	Cytarabine	131-141	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	10-48
20544528-1	2010	Deoxycytidine kinase (dCK) is essential for phosphorylation of natural deoxynucleosides and analogs, such as gemcitabine and cytarabine, two widely used anticancer compounds.	Cytarabine	125-135	deoxycytidine kinase	Homo sapiens	0-20
20544528-1	2010	Deoxycytidine kinase (dCK) is essential for phosphorylation of natural deoxynucleosides and analogs, such as gemcitabine and cytarabine, two widely used anticancer compounds.	Cytarabine	125-135	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	22-25
20544528-6	2010	Methylation might therefore regulate transcription of dCK, and should be studied further to understand its role in influencing gemcitabine and cytarabine activity.	Cytarabine	143-153	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	54-57
20536350-3	2010	In this study, we aimed to investigate whether the synonymous genetic polymorphism A830G in the JAK2 gene is associated with the treatment outcomes of Ara-C-based chemotherapy regimens in patients with acute myeloid leukemia (AML).	Cytarabine	151-156	Janus kinase 2	Homo sapiens	96-100
20082300-2	2010	The human equilibrative nucleoside transporter 1 (hENT1) is a member of these proteins and mediates cellular entry of gemcitabine, cytarabine, and fludarabine.	Cytarabine	131-141	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	50-55
20159819-6	2010	RESULTS: At least 94% of patients receiving cytarabine-based therapy and surviving for more than 3 or 5 years achieved a CR with either initial or salvage therapy; limited data suggest the same for patients receiving initial therapies that did not contain cytarabine.	Cytarabine	44-54	C-reactive protein	Homo sapiens	121-123
19960516-9	2010	Infusing animals with the mitotic inhibitor cytosine arabinoside prevented the increase of beta-catenin signaling in the cortex, confirming that the majority of beta-catenin signaling after TBI occurs in newly born cells.	Cytarabine	44-64	catenin (cadherin associated protein), beta 1	Mus musculus	91-103
19960516-9	2010	Infusing animals with the mitotic inhibitor cytosine arabinoside prevented the increase of beta-catenin signaling in the cortex, confirming that the majority of beta-catenin signaling after TBI occurs in newly born cells.	Cytarabine	44-64	catenin (cadherin associated protein), beta 1	Mus musculus	161-173
20072158-1	2010	Core-binding factor (CBF) leukemias are characterized by a high degree of sensitivity to high-dose cytarabine (ARA-C) treatment and by a relatively favorable prognosis compared with most other forms of adult acute myeloid leukemia (AML).	Cytarabine	99-109	CCAAT enhancer binding protein zeta	Homo sapiens	0-19
20137150-14	2010	G-CSF can enhance cytotoxicity of drugs such as Ara-C and HHT by promoting G(0) phase cells into the reproductive cycle.	Cytarabine	48-53	colony stimulating factor 3	Homo sapiens	0-5
20072158-1	2010	Core-binding factor (CBF) leukemias are characterized by a high degree of sensitivity to high-dose cytarabine (ARA-C) treatment and by a relatively favorable prognosis compared with most other forms of adult acute myeloid leukemia (AML).	Cytarabine	99-109	CCAAT enhancer binding protein zeta	Homo sapiens	21-24
20072158-1	2010	Core-binding factor (CBF) leukemias are characterized by a high degree of sensitivity to high-dose cytarabine (ARA-C) treatment and by a relatively favorable prognosis compared with most other forms of adult acute myeloid leukemia (AML).	Cytarabine	111-116	CCAAT enhancer binding protein zeta	Homo sapiens	0-19
20072158-1	2010	Core-binding factor (CBF) leukemias are characterized by a high degree of sensitivity to high-dose cytarabine (ARA-C) treatment and by a relatively favorable prognosis compared with most other forms of adult acute myeloid leukemia (AML).	Cytarabine	111-116	CCAAT enhancer binding protein zeta	Homo sapiens	21-24
20072158-8	2010	The nuclear localization of PR3 is responsible for increased proliferation, apoptosis arrest and increased sensitivity to high-dose ARA-C.	Cytarabine	132-137	proteinase 3	Homo sapiens	28-31
20302779-9	2010	Pretreatment of K562 cells with Ara-C lead to the increased activity of NF-kappaB and the fraction of G(1) phase cells.	Cytarabine	32-37	nuclear factor kappa B subunit 1	Homo sapiens	72-81
19818205-10	2010	The Ara-C treatment on differentiating days 24-26 decreased Nanog and Oct3/4 expression in subsequent cultures.	Cytarabine	4-9	Nanog homeobox	Mus musculus	60-65
19818205-10	2010	The Ara-C treatment on differentiating days 24-26 decreased Nanog and Oct3/4 expression in subsequent cultures.	Cytarabine	4-9	POU domain, class 5, transcription factor 1	Mus musculus	70-76
20890066-1	2010	BACKGROUND: Single nucleotide polymorphisms (SNPs) of deoxycytidine kinase (dCK) and cytidine deaminase (CDA) are known to alter their enzymatic activities, which affect the metabolism of cytarabine.	Cytarabine	188-198	deoxycytidine kinase	Homo sapiens	54-74
20890066-1	2010	BACKGROUND: Single nucleotide polymorphisms (SNPs) of deoxycytidine kinase (dCK) and cytidine deaminase (CDA) are known to alter their enzymatic activities, which affect the metabolism of cytarabine.	Cytarabine	188-198	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	76-79
20890066-1	2010	BACKGROUND: Single nucleotide polymorphisms (SNPs) of deoxycytidine kinase (dCK) and cytidine deaminase (CDA) are known to alter their enzymatic activities, which affect the metabolism of cytarabine.	Cytarabine	188-198	cytidine deaminase	Homo sapiens	85-103
20890066-1	2010	BACKGROUND: Single nucleotide polymorphisms (SNPs) of deoxycytidine kinase (dCK) and cytidine deaminase (CDA) are known to alter their enzymatic activities, which affect the metabolism of cytarabine.	Cytarabine	188-198	cytidine deaminase	Homo sapiens	105-108
20890066-3	2010	Therefore, we hypothesized that a genetic variation of dCK and CDA genes may influence the risk of cytarabine-related toxicities and early response to treatment.	Cytarabine	99-109	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	55-58
20890066-3	2010	Therefore, we hypothesized that a genetic variation of dCK and CDA genes may influence the risk of cytarabine-related toxicities and early response to treatment.	Cytarabine	99-109	cytidine deaminase	Homo sapiens	63-66
20890066-13	2010	Children with dCK-360G allele were at risk of mucositis after receiving low-dose cytarabine (OR=3.7; 95%CI, 1.2--11.3).	Cytarabine	81-91	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	14-17
20890066-15	2010	CONCLUSION: The dCK-360G allele was found to increase the risk of mucositis after exposure to low-dose cytarabine in childhood ALL therapy.	Cytarabine	103-113	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	16-19
21123967-0	2010	Cell cycle-dependent priming action of granulocyte colony-stimulating factor (G-CSF) enhances in vitro apoptosis induction by cytarabine and etoposide in leukemia cell lines.	Cytarabine	126-136	colony stimulating factor 3	Homo sapiens	39-76
21123967-0	2010	Cell cycle-dependent priming action of granulocyte colony-stimulating factor (G-CSF) enhances in vitro apoptosis induction by cytarabine and etoposide in leukemia cell lines.	Cytarabine	126-136	colony stimulating factor 3	Homo sapiens	78-83
21123967-1	2010	We investigated the priming effect and mechanism of granulocyte colony-stimulating factor (G-CSF) in chemotherapy with low-dose Ara-C and VP-16 for acute myeloid leukemia.	Cytarabine	128-133	colony stimulating factor 3	Homo sapiens	52-89
21123967-1	2010	We investigated the priming effect and mechanism of granulocyte colony-stimulating factor (G-CSF) in chemotherapy with low-dose Ara-C and VP-16 for acute myeloid leukemia.	Cytarabine	128-133	colony stimulating factor 3	Homo sapiens	91-96
21123967-13	2010	G-CSF potentiates Ara-C- and VP-16-induced cytotoxicities through apoptosis induction by mobilizing resting G0-G1-phase cells into S phase.	Cytarabine	18-23	colony stimulating factor 3	Homo sapiens	0-5
20853604-5	2010	CD34+ cells were mobilized until molecular remission was achieved with high-dose Ara-C and granulocyte colony-stimulating factor.	Cytarabine	81-86	CD34 molecule	Homo sapiens	0-4
19959816-6	2010	Meanwhile, they also developed a novel cell-based assay that rests on the rescue of cells from dCK-dependent cytotoxic agents such as AraC.	Cytarabine	134-138	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	95-98
19853583-4	2009	The ENT1 promoter activity and the cellular uptake of ara-C were reduced in K562/FLT3-ITD cells, and rescued by pretreating the cells with PKC412, a FLT3 inhibitor.	Cytarabine	54-59	fms related receptor tyrosine kinase 3	Homo sapiens	81-85
19782724-6	2009	We reported that after UVN, immediate AraC infusion blocked the cell proliferation and decreased the number of GFAP-immunoreactive cells and GABAergic neurons observed in the vestibular nuclei of neurectomized cats.	Cytarabine	38-42	glial fibrillary acidic protein	Felis catus	111-115
19853583-0	2009	FLT3-ITD induces ara-C resistance in myeloid leukemic cells through the repression of the ENT1 expression.	Cytarabine	17-22	fms related receptor tyrosine kinase 3	Homo sapiens	0-4
19853583-0	2009	FLT3-ITD induces ara-C resistance in myeloid leukemic cells through the repression of the ENT1 expression.	Cytarabine	17-22	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	90-94
19853583-4	2009	The ENT1 promoter activity and the cellular uptake of ara-C were reduced in K562/FLT3-ITD cells, and rescued by pretreating the cells with PKC412, a FLT3 inhibitor.	Cytarabine	54-59	fms related receptor tyrosine kinase 3	Homo sapiens	149-153
19853583-3	2009	Both of these cell lines were specifically resistant to the pyrimidine analogue cytosine arabinoside (ara-C), an essential agent for AML, accompanied by the downregulation of equilibrative nucleoside transporter 1 (ENT1), a transporter responsible for the cellular uptake of ara-C.	Cytarabine	102-107	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	215-219
19853583-6	2009	Taken together, these findings suggest that FLT3-ITD specifically induces ara-C resistance in leukemic cells by the repression of ENT1 expression, possibly through the upregulation of HIF-1alpha, while also partially accounting for the poor prognosis of AML with FLT3-ITD due to resistance to the standard chemotherapy protocols which include ara-C.	Cytarabine	74-79	fms related receptor tyrosine kinase 3	Homo sapiens	44-48
19853583-3	2009	Both of these cell lines were specifically resistant to the pyrimidine analogue cytosine arabinoside (ara-C), an essential agent for AML, accompanied by the downregulation of equilibrative nucleoside transporter 1 (ENT1), a transporter responsible for the cellular uptake of ara-C.	Cytarabine	275-280	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	175-213
19853583-3	2009	Both of these cell lines were specifically resistant to the pyrimidine analogue cytosine arabinoside (ara-C), an essential agent for AML, accompanied by the downregulation of equilibrative nucleoside transporter 1 (ENT1), a transporter responsible for the cellular uptake of ara-C.	Cytarabine	275-280	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	215-219
19853583-6	2009	Taken together, these findings suggest that FLT3-ITD specifically induces ara-C resistance in leukemic cells by the repression of ENT1 expression, possibly through the upregulation of HIF-1alpha, while also partially accounting for the poor prognosis of AML with FLT3-ITD due to resistance to the standard chemotherapy protocols which include ara-C.	Cytarabine	74-79	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	130-134
19853583-6	2009	Taken together, these findings suggest that FLT3-ITD specifically induces ara-C resistance in leukemic cells by the repression of ENT1 expression, possibly through the upregulation of HIF-1alpha, while also partially accounting for the poor prognosis of AML with FLT3-ITD due to resistance to the standard chemotherapy protocols which include ara-C.	Cytarabine	74-79	hypoxia inducible factor 1 subunit alpha	Homo sapiens	184-194
19853583-6	2009	Taken together, these findings suggest that FLT3-ITD specifically induces ara-C resistance in leukemic cells by the repression of ENT1 expression, possibly through the upregulation of HIF-1alpha, while also partially accounting for the poor prognosis of AML with FLT3-ITD due to resistance to the standard chemotherapy protocols which include ara-C.	Cytarabine	74-79	fms related receptor tyrosine kinase 3	Homo sapiens	263-267
19853583-6	2009	Taken together, these findings suggest that FLT3-ITD specifically induces ara-C resistance in leukemic cells by the repression of ENT1 expression, possibly through the upregulation of HIF-1alpha, while also partially accounting for the poor prognosis of AML with FLT3-ITD due to resistance to the standard chemotherapy protocols which include ara-C.	Cytarabine	343-348	fms related receptor tyrosine kinase 3	Homo sapiens	44-48
19853583-6	2009	Taken together, these findings suggest that FLT3-ITD specifically induces ara-C resistance in leukemic cells by the repression of ENT1 expression, possibly through the upregulation of HIF-1alpha, while also partially accounting for the poor prognosis of AML with FLT3-ITD due to resistance to the standard chemotherapy protocols which include ara-C.	Cytarabine	343-348	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	130-134
19843865-4	2009	Moreover, we observe a beneficial effect of CHK1 inhibition in high-DNA damage level AML samples treated with 1-beta-d-arabinofuranosylcytosine.	Cytarabine	110-143	checkpoint kinase 1	Homo sapiens	44-48
21415871-0	2009	The Prognostic Impact of K-RAS Mutations in Adult Acute Myeloid Leukemia Patients Treated with High Dose Cytarabine.	Cytarabine	105-115	KRAS proto-oncogene, GTPase	Homo sapiens	25-30
21415871-4	2009	OBJECTIVE: This study aimed to clarify the biologic and prognostic impact of K-RAS mutations in relation to the dose of cytarabine (ara-C) used in post induction consolidation chemotherapy in adult AML patients.	Cytarabine	120-130	KRAS proto-oncogene, GTPase	Homo sapiens	77-82
21415871-4	2009	OBJECTIVE: This study aimed to clarify the biologic and prognostic impact of K-RAS mutations in relation to the dose of cytarabine (ara-C) used in post induction consolidation chemotherapy in adult AML patients.	Cytarabine	132-137	KRAS proto-oncogene, GTPase	Homo sapiens	77-82
21415871-20	2009	CONCLUSION: Adult AML patients carrying mutations in the K-RAS gene benefit from higher cytarabine doses more than wtRAS patients, so pretreatment mutation detection could be an important predictor for treatment strategy and survival of adult AML patients.	Cytarabine	88-98	KRAS proto-oncogene, GTPase	Homo sapiens	57-62
21415871-22	2009	KEY WORDS: K-RAS mutations - Acute myeloid leukemia - Cytarabine.	Cytarabine	54-64	KRAS proto-oncogene, GTPase	Homo sapiens	11-16
20193601-0	2009	[The influence of Ara-C on anti-CD3/anti-Pgp mediating T-lymphocytes activities against multi-drug resistant leukemia cells.].	Cytarabine	18-23	phosphoglycolate phosphatase	Homo sapiens	41-44
20193601-1	2009	OBJECTIVE: To investigate the role of Ara-C in regulating anti-CD3/anti-Pgp mediating T-lymphocytes activities against multi-drug resistant leukemia cells.	Cytarabine	38-43	phosphoglycolate phosphatase	Homo sapiens	72-75
20193601-6	2009	RESULTS: The expressions of B7-1 and B7-2 on K562 and K562/A02 cells treated by Ara-C was significantly higher than those untreated.	Cytarabine	80-85	CD80 molecule	Homo sapiens	28-41
20193601-9	2009	CONCLUSION: Ara-C may be an important adjuvant for improving anti-CD3/anti-Pgp mediating T-lymphocytes activities against multi-drug resistant leukemia cells.	Cytarabine	12-17	phosphoglycolate phosphatase	Homo sapiens	75-78
19890398-6	2009	We show that oncogenic RAS synergizes with cytotoxic agents such as cytarabine in activation of DNA damage checkpoints, resulting in a p53-dependent genetic program that reduces clonogenicity and increases myeloid differentiation.	Cytarabine	68-78	tumor protein p53	Homo sapiens	135-138
19898621-9	2009	One SNP in IQGAP2 (rs3797418) was significantly associated with variation in both the expression of multiple genes and gemcitabine and AraC IC(50).	Cytarabine	135-139	IQ motif containing GTPase activating protein 2	Homo sapiens	11-17
19446624-7	2009	Finally, the pH-sensitive ILs-CD33 formulation exhibited the highest cytotoxicity against HL60 cells, confirming the role of the NIPAM copolymer in promoting the escape of intact ara-C in the endosomes.	Cytarabine	179-184	CD33 molecule	Homo sapiens	30-34
19890398-7	2009	Our data can explain the beneficial effects observed for AML patients with oncogenic RAS treated with higher dosages of cytarabine and suggest that induction of p53-dependent differentiation, e.g. by interfering with Mdm2-mediated degradation, may be a rational approach to increase cure rate in response to chemotherapy.	Cytarabine	120-130	tumor protein p53	Homo sapiens	161-164
19890398-7	2009	Our data can explain the beneficial effects observed for AML patients with oncogenic RAS treated with higher dosages of cytarabine and suggest that induction of p53-dependent differentiation, e.g. by interfering with Mdm2-mediated degradation, may be a rational approach to increase cure rate in response to chemotherapy.	Cytarabine	120-130	MDM2 proto-oncogene	Homo sapiens	217-221
19523508-6	2009	A significant and selective reduction of NF-H isoform was observed in the cerebellum of AraC-treated animals, compared to the controls.	Cytarabine	88-92	neurofilament heavy chain	Rattus norvegicus	41-45
19283354-3	2009	The aim of our studies was to explore the utility of CYP3A-activated prodrugs of cytarabine and fludarabine monophosphate for the treatment of HCC.	Cytarabine	81-91	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	53-58
19458626-0	2009	SNP analyses in cytarabine metabolizing enzymes in AML patients and their impact on treatment response and patient survival: identification of CDA SNP C-451T as an independent prognostic parameter for survival.	Cytarabine	16-26	cytidine deaminase	Homo sapiens	143-146
19708031-0	2009	Expression of eukaryotic initiation factor 4E predicts clinical outcome in patients with mantle cell lymphoma treated with hyper-CVAD and rituximab, alternating with rituximab, high-dose methotrexate, and cytarabine.	Cytarabine	205-215	eukaryotic translation initiation factor 4E	Homo sapiens	14-45
19846953-0	2009	Rapid induction of P-glycoprotein mRNA and protein expression by cytarabine in HL-60 cells.	Cytarabine	65-75	ATP binding cassette subfamily B member 1	Homo sapiens	19-33
19846953-5	2009	RESULTS: After exposure to Ara-C, P-gp mRNA rapidly increased in all the cell lines.	Cytarabine	27-32	ATP binding cassette subfamily B member 1	Homo sapiens	34-38
19846953-6	2009	P-gp protein was detected in the sensitive cells after 8 h exposure to Ara-C.	Cytarabine	71-76	ATP binding cassette subfamily B member 1	Homo sapiens	0-4
19846953-9	2009	CONCLUSION: Ara-C rapidly increases P-gp mRNA and protein expression in sensitive and resistant cells, and GSTpi mRNA in resistant cells, in vitro.	Cytarabine	12-17	ATP binding cassette subfamily B member 1	Homo sapiens	36-40
19628630-2	2009	To elucidate the role of GAPDH in chemotherapy-induced stress, we analyzed its activity, protein level, intracellular distribution, and intranuclear mobility in human carcinoma cells A549 and UO31 after treatment with cytarabine, doxorubicin, and mercaptopurine.	Cytarabine	218-228	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	25-30
19628630-3	2009	After treatment with cytosine arabinoside (araC), enzymatically inactive GAPDH accumulated in the nucleus.	Cytarabine	21-41	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	73-78
19628630-3	2009	After treatment with cytosine arabinoside (araC), enzymatically inactive GAPDH accumulated in the nucleus.	Cytarabine	43-47	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	73-78
19628630-7	2009	GAPDH-depleted A549 cells were 50-fold more resistant to treatment with cytarabine (1.68 +/- 0.182 microM versus 0.03 +/- 0.015 microM in control).	Cytarabine	72-82	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	0-5
19548087-0	2009	Inhibition of MEK signaling enhances the ability of cytarabine to induce growth arrest and apoptosis of acute myelogenous leukemia cells.	Cytarabine	52-62	mitogen-activated protein kinase kinase 7	Homo sapiens	14-17
19638627-4	2009	Short hairpin RNA knockdown of RUNX1 in a non-DS AMkL cell line, Meg-01, resulted in significantly increased sensitivity to cytosine arabinoside, accompanied by significantly decreased expression of PIK3CD, which encodes the delta catalytic subunit of the survival kinase, phosphoinositide 3 (PI3)-kinase.	Cytarabine	124-144	RUNX family transcription factor 1	Homo sapiens	31-36
19638627-4	2009	Short hairpin RNA knockdown of RUNX1 in a non-DS AMkL cell line, Meg-01, resulted in significantly increased sensitivity to cytosine arabinoside, accompanied by significantly decreased expression of PIK3CD, which encodes the delta catalytic subunit of the survival kinase, phosphoinositide 3 (PI3)-kinase.	Cytarabine	124-144	protein tyrosine phosphatase non-receptor type 4	Homo sapiens	65-68
19638627-6	2009	Further, a PI3-kinase inhibitor, LY294002, and cytosine arabinoside synergized in antileukemia effects on Meg-01 and primary pediatric AMkL cells.	Cytarabine	47-67	protein tyrosine phosphatase non-receptor type 4	Homo sapiens	106-109
19584709-0	2009	Rapamycin, the mTOR kinase inhibitor, sensitizes acute myeloid leukemia cells, HL-60 cells, to the cytotoxic effect of arabinozide cytarabine.	Cytarabine	131-141	mechanistic target of rapamycin kinase	Homo sapiens	15-19
19548087-3	2009	AZD6244 effectively blocked AraC-induced MEK/ERK activation and enhanced its ability to induce growth arrest and apoptosis of NB4 and HL60 cells in parallel with induction of DNA damage as measured by detection of gamma-H2AX by Western Blot analysis, resulting in enhanced expression of p21( waf1 ) and downregulation of c-Myc and Bcl-xl in these cells.	Cytarabine	28-32	mitogen-activated protein kinase kinase 7	Homo sapiens	41-44
19548087-3	2009	AZD6244 effectively blocked AraC-induced MEK/ERK activation and enhanced its ability to induce growth arrest and apoptosis of NB4 and HL60 cells in parallel with induction of DNA damage as measured by detection of gamma-H2AX by Western Blot analysis, resulting in enhanced expression of p21( waf1 ) and downregulation of c-Myc and Bcl-xl in these cells.	Cytarabine	28-32	mitogen-activated protein kinase 1	Homo sapiens	45-48
19548087-3	2009	AZD6244 effectively blocked AraC-induced MEK/ERK activation and enhanced its ability to induce growth arrest and apoptosis of NB4 and HL60 cells in parallel with induction of DNA damage as measured by detection of gamma-H2AX by Western Blot analysis, resulting in enhanced expression of p21( waf1 ) and downregulation of c-Myc and Bcl-xl in these cells.	Cytarabine	28-32	cyclin dependent kinase inhibitor 1A	Homo sapiens	287-290
19548087-3	2009	AZD6244 effectively blocked AraC-induced MEK/ERK activation and enhanced its ability to induce growth arrest and apoptosis of NB4 and HL60 cells in parallel with induction of DNA damage as measured by detection of gamma-H2AX by Western Blot analysis, resulting in enhanced expression of p21( waf1 ) and downregulation of c-Myc and Bcl-xl in these cells.	Cytarabine	28-32	cyclin dependent kinase inhibitor 1A	Homo sapiens	292-296
19548087-3	2009	AZD6244 effectively blocked AraC-induced MEK/ERK activation and enhanced its ability to induce growth arrest and apoptosis of NB4 and HL60 cells in parallel with induction of DNA damage as measured by detection of gamma-H2AX by Western Blot analysis, resulting in enhanced expression of p21( waf1 ) and downregulation of c-Myc and Bcl-xl in these cells.	Cytarabine	28-32	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	321-326
19548087-3	2009	AZD6244 effectively blocked AraC-induced MEK/ERK activation and enhanced its ability to induce growth arrest and apoptosis of NB4 and HL60 cells in parallel with induction of DNA damage as measured by detection of gamma-H2AX by Western Blot analysis, resulting in enhanced expression of p21( waf1 ) and downregulation of c-Myc and Bcl-xl in these cells.	Cytarabine	28-32	BCL2 like 1	Homo sapiens	331-337
19625780-0	2009	The FLT3 inhibitor tandutinib (formerly MLN518) has sequence-independent synergistic effects with cytarabine and daunorubicin.	Cytarabine	98-108	fms related receptor tyrosine kinase 3	Homo sapiens	4-8
19428333-2	2009	After being transported into leukemic cells by human equilibrative nucleoside transporter 1 (hENT1), ara-C is phosphorylated to ara-C triphosphate (ara-CTP), an active metabolite, and then incorporated into DNA, thereby inhibiting DNA synthesis.	Cytarabine	101-106	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	53-91
19187960-0	2009	Twice daily fludarabine/Ara-C associated to idarubicin, G-CSF and ATRA is an effective salvage regimen in non-promyelocytic acute myeloid leukemia.	Cytarabine	24-29	colony stimulating factor 3	Homo sapiens	56-61
19657571-8	2009	HL-60/A cells showed multi-drug resistance phenotype characteristic by cross-resistance to adriamycin, daunorubicin, and arabinosylcytosine, due to the expression of MRP.	Cytarabine	121-139	ATP binding cassette subfamily C member 3	Homo sapiens	166-169
19657571-11	2009	Compared with the MRP expression level in the control group (nucleofected by control siRNA), the mRNA and protein expression levels of MRP in HL-60/A cells nucleofected by SKP2 siRNA were lower, and the latter cells were more sensitive to adriamycin, daunorubicin, and arabinosylcytosine.	Cytarabine	269-287	ATP binding cassette subfamily C member 3	Homo sapiens	135-138
19657571-11	2009	Compared with the MRP expression level in the control group (nucleofected by control siRNA), the mRNA and protein expression levels of MRP in HL-60/A cells nucleofected by SKP2 siRNA were lower, and the latter cells were more sensitive to adriamycin, daunorubicin, and arabinosylcytosine.	Cytarabine	269-287	S-phase kinase associated protein 2	Homo sapiens	172-176
19428333-10	2009	The dCK/cN-II ratio was again proportional to ara-CTP production and to ara-C sensitivity.	Cytarabine	46-51	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	4-7
19428333-10	2009	The dCK/cN-II ratio was again proportional to ara-CTP production and to ara-C sensitivity.	Cytarabine	46-51	5'-nucleotidase, cytosolic II	Homo sapiens	8-13
19428333-11	2009	The dCK/cN-II ratio may thus predict the capacity for ara-CTP production and ultimately, ara-C sensitivity in AML.	Cytarabine	54-59	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	4-7
19428333-11	2009	The dCK/cN-II ratio may thus predict the capacity for ara-CTP production and ultimately, ara-C sensitivity in AML.	Cytarabine	54-59	5'-nucleotidase, cytosolic II	Homo sapiens	8-13
19428333-2	2009	After being transported into leukemic cells by human equilibrative nucleoside transporter 1 (hENT1), ara-C is phosphorylated to ara-C triphosphate (ara-CTP), an active metabolite, and then incorporated into DNA, thereby inhibiting DNA synthesis.	Cytarabine	101-106	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	93-98
19379585-11	2009	Up-regulating expression of Ahi-1 protein with 140 kD in the nucleus was found in Jurkat cells after exposure to meisoindigo, cytarabine, homoharringtonine, methotrexate and etoposide, down-regulating expression of Ahi-1 with 140 kD in the cytoplasm was observed after treatment with meisoindigo.	Cytarabine	126-136	Abelson helper integration site 1	Homo sapiens	28-33
19292713-0	2009	Cytarabine-associated lymphoid dyscrasia with atypical T CD30+ infiltrate in a patient suffering from acute nonlymphoblastic leukaemia.	Cytarabine	0-10	TNF receptor superfamily member 8	Homo sapiens	57-61
19269175-2	2009	The SIMRA compounds containing ara-G, ara-C, ara-U or ara-A substitutions activated TLR8 in HEK293 cells.	Cytarabine	38-43	toll like receptor 8	Homo sapiens	84-88
19269175-3	2009	Interestingly, the SIMRA compound containing ara-C also activated TLR7 and stimulated immune responses in vivo in mice.	Cytarabine	45-50	toll-like receptor 7	Mus musculus	66-70
19287976-0	2009	Defective expression of deoxycytidine kinase in cytarabine-resistant acute myeloid leukemia cells.	Cytarabine	48-58	deoxycytidine kinase	Homo sapiens	24-44
19287976-2	2009	To elucidate mechanism responsible for the development of resistance to Ara-C, we established the Ara-C resistant AML-2/WT cell sublines, AML-2/IDAC and AML-2/ARC.	Cytarabine	72-77	RUNX family transcription factor 3	Homo sapiens	114-119
19287976-2	2009	To elucidate mechanism responsible for the development of resistance to Ara-C, we established the Ara-C resistant AML-2/WT cell sublines, AML-2/IDAC and AML-2/ARC.	Cytarabine	98-103	RUNX family transcription factor 3	Homo sapiens	114-119
19287976-2	2009	To elucidate mechanism responsible for the development of resistance to Ara-C, we established the Ara-C resistant AML-2/WT cell sublines, AML-2/IDAC and AML-2/ARC.	Cytarabine	98-103	RUNX family transcription factor 3	Homo sapiens	138-143
19287976-2	2009	To elucidate mechanism responsible for the development of resistance to Ara-C, we established the Ara-C resistant AML-2/WT cell sublines, AML-2/IDAC and AML-2/ARC.	Cytarabine	98-103	RUNX family transcription factor 3	Homo sapiens	138-143
19287976-4	2009	The results of the microarray analysis revealed a severe defect in the expression of deoxycytidine kinase (dCK), which plays a key role in the transformation of Ara-C to the active form in AML-2/IDAC cells.	Cytarabine	161-166	deoxycytidine kinase	Homo sapiens	85-105
19287976-4	2009	The results of the microarray analysis revealed a severe defect in the expression of deoxycytidine kinase (dCK), which plays a key role in the transformation of Ara-C to the active form in AML-2/IDAC cells.	Cytarabine	161-166	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	107-110
19287976-4	2009	The results of the microarray analysis revealed a severe defect in the expression of deoxycytidine kinase (dCK), which plays a key role in the transformation of Ara-C to the active form in AML-2/IDAC cells.	Cytarabine	161-166	RUNX family transcription factor 3	Homo sapiens	189-194
19287976-6	2009	The decreased expression of dCK also resulted in lower activity in both Ara-C resistant variants.	Cytarabine	72-77	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	28-31
19287976-7	2009	However, no significant difference in the intracellular concentration of Ara-C was observed among the cells tested, which indicates that the Ara-C resistant phenotype in our models occurred due to the lower expression and activity of dCK rather than a change in the ability to take up Ara-C.	Cytarabine	141-146	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	234-237
19287976-7	2009	However, no significant difference in the intracellular concentration of Ara-C was observed among the cells tested, which indicates that the Ara-C resistant phenotype in our models occurred due to the lower expression and activity of dCK rather than a change in the ability to take up Ara-C.	Cytarabine	141-146	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	234-237
19287976-8	2009	Additionally, in vitro assays using BM cells from AML patients revealed that the expression of dCK and the sensitivity to Ara-C were correlated.	Cytarabine	122-127	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	95-98
19287976-9	2009	Taken together, these findings demonstrate that dCK can regulate the in vitro cellular response to Ara-C in AML cells.	Cytarabine	99-104	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	48-51
19321614-6	2009	The PKR-dependent activation of MAPKs in DeltaE3L mutant-infected cells was abolished by treatment with cytosine beta-d-arabinoside.	Cytarabine	104-131	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	4-7
19245435-9	2009	Furthermore, combination with 10 microM cyclopamine significantly reduced drug resistance of CD34+ cell lines and primary CD34+ leukemic cells to Ara-C.	Cytarabine	146-151	CD34 molecule	Homo sapiens	122-126
19372559-4	2009	Using the cell proliferation assay, we found that knockdown of HMGB1-associated proteins resulted in 8-fold to 50-fold decreased chemosensitivity of A549 cells to cytarabine.	Cytarabine	163-173	high mobility group box 1	Homo sapiens	63-68
19372559-6	2009	Our results dissect the roles of HMGB1-associated proteins in DNA damage response: HMGB1 and HMGB2 facilitate p53 phosphorylation after exposure to genotoxic stress, and PDIA3 has been found essential for H2AX phosphorylation (no gamma-H2AX accumulated after 24-72 hours of incubation with 1 micromol/L of cytarabine in PDIA3 knockdown cells).	Cytarabine	306-316	high mobility group box 1	Homo sapiens	33-38
19372559-6	2009	Our results dissect the roles of HMGB1-associated proteins in DNA damage response: HMGB1 and HMGB2 facilitate p53 phosphorylation after exposure to genotoxic stress, and PDIA3 has been found essential for H2AX phosphorylation (no gamma-H2AX accumulated after 24-72 hours of incubation with 1 micromol/L of cytarabine in PDIA3 knockdown cells).	Cytarabine	306-316	protein disulfide isomerase family A member 3	Homo sapiens	170-175
19304516-10	2009	Valproic acid can inhibit the growth of HL-60/HT cells and enhance their Ara-C sensitivity possibly by increasing P27(Kip1) expression and causing cell cycle arrest in G(1) phase.	Cytarabine	73-78	zinc ribbon domain containing 2	Homo sapiens	114-117
19265549-5	2009	RESULTS: Significant differential modulation of 151 genes were found at 4 h after start of induction therapy with cytarabine and anthracycline, including significant overexpression of 31 genes associated with p53 regulation.	Cytarabine	114-124	tumor protein p53	Homo sapiens	209-212
19265549-7	2009	FLT3 mutations indicated that non-responders (5/7 patients, 8 versus 49 months survival) are characterized by a unique gene response profile before and at 4 h. At 18-24 h after chemotherapy, the gene expression of p53 target genes was attenuated, while genes involved in chemoresistance, cytarabine detoxification, chemokine networks and T cell receptor were prominent.	Cytarabine	288-298	fms related receptor tyrosine kinase 3	Homo sapiens	0-4
19265549-7	2009	FLT3 mutations indicated that non-responders (5/7 patients, 8 versus 49 months survival) are characterized by a unique gene response profile before and at 4 h. At 18-24 h after chemotherapy, the gene expression of p53 target genes was attenuated, while genes involved in chemoresistance, cytarabine detoxification, chemokine networks and T cell receptor were prominent.	Cytarabine	288-298	tumor protein p53	Homo sapiens	214-217
18677475-15	2009	CONCLUSIONS: HMW-MAA-specific mAb down-regulated P-Pyk2 expression and enhanced the anti-proliferative effect of cytarabine in vitro, but had no detectable effect on survival or growth of leukemia cells in vivo.	Cytarabine	113-123	chondroitin sulfate proteoglycan 4	Homo sapiens	13-20
19240178-8	2009	MRP8-transfected LLC-PK1 cells accumulated reduced intracellular levels of AraC (63% of the parental vector-transfected LLC-PK1 control cells) as well as AraC metabolites.	Cytarabine	75-79	ATP binding cassette subfamily C member 11	Homo sapiens	0-4
19240178-8	2009	MRP8-transfected LLC-PK1 cells accumulated reduced intracellular levels of AraC (63% of the parental vector-transfected LLC-PK1 control cells) as well as AraC metabolites.	Cytarabine	154-158	ATP binding cassette subfamily C member 11	Homo sapiens	0-4
19240178-10	2009	CONCLUSION: These data suggest that MRP8 is differentially expressed in AML blasts, that expression of MRP8 serves as a predictive marker for treatment outcome in AML, and that efflux of AraC metabolites by MRP8 is a mechanism that contributes to resistance of AML blasts.	Cytarabine	187-191	ATP binding cassette subfamily C member 11	Homo sapiens	36-40
19240178-10	2009	CONCLUSION: These data suggest that MRP8 is differentially expressed in AML blasts, that expression of MRP8 serves as a predictive marker for treatment outcome in AML, and that efflux of AraC metabolites by MRP8 is a mechanism that contributes to resistance of AML blasts.	Cytarabine	187-191	ATP binding cassette subfamily C member 11	Homo sapiens	103-107
19240178-10	2009	CONCLUSION: These data suggest that MRP8 is differentially expressed in AML blasts, that expression of MRP8 serves as a predictive marker for treatment outcome in AML, and that efflux of AraC metabolites by MRP8 is a mechanism that contributes to resistance of AML blasts.	Cytarabine	187-191	ATP binding cassette subfamily C member 11	Homo sapiens	103-107
19304516-10	2009	Valproic acid can inhibit the growth of HL-60/HT cells and enhance their Ara-C sensitivity possibly by increasing P27(Kip1) expression and causing cell cycle arrest in G(1) phase.	Cytarabine	73-78	cyclin dependent kinase inhibitor 1B	Homo sapiens	118-122
19204830-0	2009	Small hairpin RNA targeting at Bcl-2 increases cytarabine-induced apoptosis in Raji cells.	Cytarabine	47-57	BCL2 apoptosis regulator	Homo sapiens	31-36
18989890-2	2009	Cytarabine decreases EWS/FLI1 protein levels in Ewing sarcoma cells and has demonstrated preclinical activity against Ewing sarcoma in vitro and in vivo.	Cytarabine	0-10	EWS RNA binding protein 1	Homo sapiens	21-24
18989890-2	2009	Cytarabine decreases EWS/FLI1 protein levels in Ewing sarcoma cells and has demonstrated preclinical activity against Ewing sarcoma in vitro and in vivo.	Cytarabine	0-10	Fli-1 proto-oncogene, ETS transcription factor	Homo sapiens	25-29
19196993-3	2009	Deoxycytidine kinase (DCK) controls the rate-limiting step in the activation cascade of dFdC and ara-C.	Cytarabine	97-102	deoxycytidine kinase	Mus musculus	0-20
19196993-3	2009	Deoxycytidine kinase (DCK) controls the rate-limiting step in the activation cascade of dFdC and ara-C.	Cytarabine	97-102	deoxycytidine kinase	Mus musculus	22-25
19204830-2	2009	In this study, we investigated whether small hairpin RNA (shRNA) targeting at Bcl-2 mRNA could enhance cytarabine (Ara-C)-induced apoptosis in Raji cells.	Cytarabine	103-113	BCL2 apoptosis regulator	Homo sapiens	78-83
19204830-2	2009	In this study, we investigated whether small hairpin RNA (shRNA) targeting at Bcl-2 mRNA could enhance cytarabine (Ara-C)-induced apoptosis in Raji cells.	Cytarabine	115-120	BCL2 apoptosis regulator	Homo sapiens	78-83
19204830-11	2009	Apoptotic rates of Raji cells treated with Bcl-2 shRNA combined with Ara-C significantly increased (P &lt; 0.05), compared with either control shRNA/Ara-C combination or Ara-C-treated cells alone.	Cytarabine	69-74	BCL2 apoptosis regulator	Homo sapiens	43-48
19204830-11	2009	Apoptotic rates of Raji cells treated with Bcl-2 shRNA combined with Ara-C significantly increased (P &lt; 0.05), compared with either control shRNA/Ara-C combination or Ara-C-treated cells alone.	Cytarabine	149-154	BCL2 apoptosis regulator	Homo sapiens	43-48
19204830-11	2009	Apoptotic rates of Raji cells treated with Bcl-2 shRNA combined with Ara-C significantly increased (P &lt; 0.05), compared with either control shRNA/Ara-C combination or Ara-C-treated cells alone.	Cytarabine	149-154	BCL2 apoptosis regulator	Homo sapiens	43-48
19204830-12	2009	Our results suggest that the shRNA against Bcl-2 mRNA could increase Ara-C-induced apoptosis in Raji cells.	Cytarabine	69-74	BCL2 apoptosis regulator	Homo sapiens	43-48
19038561-0	2009	TRAIL-induced apoptosis of HL60 leukemia cells: two distinct phenotypes of acquired TRAIL resistance that are accompanied with resistance to TNFalpha but not to idarubicin and cytarabine.	Cytarabine	176-186	TNF superfamily member 10	Homo sapiens	84-89
19036079-5	2009	This was more notable in children who received idarubicin, fludarabine, ara-C, and granulocyte colony-stimulating factor (IDA-FLAG; ara-C = 7590 mg/m2) (5-year TRM 24 +/- 21% CC vs. 6 +/- 6% AA, 6 +/- 7% AC, P = 0.07) as consolidation therapy compared to idarubicin, dexamethasone, cytarabine, thioguanine, etoposide and daunomycin (IDA-DCTER; ara-C = 800 mg/m2) (5-year TRM 15 +/- 20% CC vs. 8 +/- 6% AA, 4 +/- 6% AC; P = 0.29).	Cytarabine	132-137	colony stimulating factor 3	Homo sapiens	83-120
19036079-5	2009	This was more notable in children who received idarubicin, fludarabine, ara-C, and granulocyte colony-stimulating factor (IDA-FLAG; ara-C = 7590 mg/m2) (5-year TRM 24 +/- 21% CC vs. 6 +/- 6% AA, 6 +/- 7% AC, P = 0.07) as consolidation therapy compared to idarubicin, dexamethasone, cytarabine, thioguanine, etoposide and daunomycin (IDA-DCTER; ara-C = 800 mg/m2) (5-year TRM 15 +/- 20% CC vs. 8 +/- 6% AA, 4 +/- 6% AC; P = 0.29).	Cytarabine	282-292	colony stimulating factor 3	Homo sapiens	83-120
19036079-5	2009	This was more notable in children who received idarubicin, fludarabine, ara-C, and granulocyte colony-stimulating factor (IDA-FLAG; ara-C = 7590 mg/m2) (5-year TRM 24 +/- 21% CC vs. 6 +/- 6% AA, 6 +/- 7% AC, P = 0.07) as consolidation therapy compared to idarubicin, dexamethasone, cytarabine, thioguanine, etoposide and daunomycin (IDA-DCTER; ara-C = 800 mg/m2) (5-year TRM 15 +/- 20% CC vs. 8 +/- 6% AA, 4 +/- 6% AC; P = 0.29).	Cytarabine	132-137	colony stimulating factor 3	Homo sapiens	83-120
19036079-7	2009	These data indicate that children with a low activity CDA genotype are at increased risk of TRM with ara-C based therapy for AML.	Cytarabine	101-106	cytidine deaminase	Homo sapiens	54-57
19036081-10	2009	In conclusion, high-dose Ara-C and BEAM with stem cell rescue in newly diagnosed MCL patients responsive to R-CHOP is a manageable treatment with respect to toxicity.	Cytarabine	25-30	DNA damage inducible transcript 3	Homo sapiens	110-114
19116148-0	2009	Identification of a novel point mutation in ENT1 that confers resistance to Ara-C in human T cell leukemia CCRF-CEM cells.	Cytarabine	76-81	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	44-48
18931345-4	2009	Sensitivity to DAC showed a low correlation (R = 0.44, P = .11) to that of 5-azacytidine (AZA), but a good correlation to that of cytarabine (Ara-C; R = 0.89, P &lt; .001).	Cytarabine	130-140	arylacetamide deacetylase	Homo sapiens	15-18
18931345-4	2009	Sensitivity to DAC showed a low correlation (R = 0.44, P = .11) to that of 5-azacytidine (AZA), but a good correlation to that of cytarabine (Ara-C; R = 0.89, P &lt; .001).	Cytarabine	142-147	arylacetamide deacetylase	Homo sapiens	15-18
19036079-0	2009	Cytidine deaminase genotype and toxicity of cytosine arabinoside therapy in children with acute myeloid leukemia.	Cytarabine	44-64	cytidine deaminase	Homo sapiens	0-18
19036079-1	2009	Cytosine arabinoside (ara-C) is irreversibly deaminated to a non-toxic metabolite by cytidine deaminase (CDA).	Cytarabine	0-20	cytidine deaminase	Homo sapiens	85-103
19036079-1	2009	Cytosine arabinoside (ara-C) is irreversibly deaminated to a non-toxic metabolite by cytidine deaminase (CDA).	Cytarabine	0-20	cytidine deaminase	Homo sapiens	105-108
19036079-1	2009	Cytosine arabinoside (ara-C) is irreversibly deaminated to a non-toxic metabolite by cytidine deaminase (CDA).	Cytarabine	22-27	cytidine deaminase	Homo sapiens	85-103
19036079-1	2009	Cytosine arabinoside (ara-C) is irreversibly deaminated to a non-toxic metabolite by cytidine deaminase (CDA).	Cytarabine	22-27	cytidine deaminase	Homo sapiens	105-108
19236746-0	2009	[Effects of human ERMAP-siRNA on erythroid differentiation of K562 cells induced by Ara-C].	Cytarabine	84-89	erythroblast membrane associated protein (Scianna blood group)	Homo sapiens	18-23
19236746-2	2009	Cell morphology, biphenylamine staining, expression of cell surface antigens as well as quantitative level of human ERMAP gene were observed during K562 cells differentiating toward erythroid lineage induced by Ara-C.	Cytarabine	211-216	erythroblast membrane associated protein (Scianna blood group)	Homo sapiens	116-121
19236746-3	2009	The results showed that at 72 hours after Ara-C treatment, ERMAP-shRNA/K562 cell size became large with increasing cytoplasm content.	Cytarabine	42-47	erythroblast membrane associated protein (Scianna blood group)	Homo sapiens	59-64
19236746-7	2009	It is concluded that the ERMAP-shRNA inhibits the Ara-C-induced erythroid differentiation of K562 cells, which further suggests that there is relationship between hERMAP and erythroid differentiation and development.	Cytarabine	50-55	erythroblast membrane associated protein (Scianna blood group)	Homo sapiens	25-30
19038561-3	2009	Prolonged exposure of TRAIL-sensitive leukemia cell line, wild-type (WT) HL60 cells to recombinant soluble TRAIL or to cytostatic agents, cytarabine and idarubicin, resulted in the establishment of resistant subclones with distinct phenotypic features.	Cytarabine	138-148	TNF superfamily member 10	Homo sapiens	22-27
19038561-3	2009	Prolonged exposure of TRAIL-sensitive leukemia cell line, wild-type (WT) HL60 cells to recombinant soluble TRAIL or to cytostatic agents, cytarabine and idarubicin, resulted in the establishment of resistant subclones with distinct phenotypic features.	Cytarabine	138-148	TNF superfamily member 10	Homo sapiens	107-112
20045991-1	2009	Cytidine deaminase, encoded by the CDA gene, catalyzes anti-cancer drugs gemcitabine and ara-C into their respective inactive metabolites.	Cytarabine	89-94	cytidine deaminase	Homo sapiens	0-18
19118001-4	2009	Consistent with the operation of an efflux pump, expression of MRP7 reduced the accumulation of Ara-C and PMEA.	Cytarabine	96-101	ATP binding cassette subfamily C member 10	Homo sapiens	63-67
19118001-3	2009	Here, it is shown by the analysis of MRP7-transfected HEK293 cells that, in addition to natural product agents, MRP7 is also able to confer resistance to nucleoside-based agents, such as the anticancer agents cytarabine (Ara-C) and gemcitabine, and the antiviral agents 2",3"-dideoxycytidine and PMEA.	Cytarabine	209-219	ATP binding cassette subfamily C member 10	Homo sapiens	37-41
19118001-3	2009	Here, it is shown by the analysis of MRP7-transfected HEK293 cells that, in addition to natural product agents, MRP7 is also able to confer resistance to nucleoside-based agents, such as the anticancer agents cytarabine (Ara-C) and gemcitabine, and the antiviral agents 2",3"-dideoxycytidine and PMEA.	Cytarabine	209-219	ATP binding cassette subfamily C member 10	Homo sapiens	112-116
19118001-3	2009	Here, it is shown by the analysis of MRP7-transfected HEK293 cells that, in addition to natural product agents, MRP7 is also able to confer resistance to nucleoside-based agents, such as the anticancer agents cytarabine (Ara-C) and gemcitabine, and the antiviral agents 2",3"-dideoxycytidine and PMEA.	Cytarabine	221-226	ATP binding cassette subfamily C member 10	Homo sapiens	37-41
19118001-3	2009	Here, it is shown by the analysis of MRP7-transfected HEK293 cells that, in addition to natural product agents, MRP7 is also able to confer resistance to nucleoside-based agents, such as the anticancer agents cytarabine (Ara-C) and gemcitabine, and the antiviral agents 2",3"-dideoxycytidine and PMEA.	Cytarabine	221-226	ATP binding cassette subfamily C member 10	Homo sapiens	112-116
18932257-0	2008	Treatment of core-binding-factor in acute myelogenous leukemia with fludarabine, cytarabine, and granulocyte colony-stimulating factor results in improved event-free survival.	Cytarabine	81-91	CCAAT enhancer binding protein zeta	Homo sapiens	13-32
18676016-4	2009	Liposome-encapsulated cytarabine:daunorubicin combinations exhibited drug ratio-dependent in vivo efficacy with the 5:1 molar drug ratio (designated CPX-351) having the greatest therapeutic index, despite using sub-MTD daunorubicin doses.	Cytarabine	22-32	metallothionein 1E	Homo sapiens	215-218
18927075-7	2008	The DeltaE3L virus-induced IRF-3 activation seen in PKR-sufficient cells was diminished by treatment with cytosine beta-D-arabinofuranoside.	Cytarabine	106-139	interferon regulatory factor 3	Homo sapiens	27-32
18927075-7	2008	The DeltaE3L virus-induced IRF-3 activation seen in PKR-sufficient cells was diminished by treatment with cytosine beta-D-arabinofuranoside.	Cytarabine	106-139	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	52-55
18932257-1	2008	BACKGROUND: Acute myelogenous leukemia (AML) associated with core-binding-factor (CBF) abnormalities is the type of leukemia most responsive to cytarabine (ara-C) therapy and is of relative favorable prognosis.	Cytarabine	144-154	CCAAT enhancer binding protein zeta	Homo sapiens	61-80
18932257-1	2008	BACKGROUND: Acute myelogenous leukemia (AML) associated with core-binding-factor (CBF) abnormalities is the type of leukemia most responsive to cytarabine (ara-C) therapy and is of relative favorable prognosis.	Cytarabine	144-154	CCAAT enhancer binding protein zeta	Homo sapiens	82-85
18932257-1	2008	BACKGROUND: Acute myelogenous leukemia (AML) associated with core-binding-factor (CBF) abnormalities is the type of leukemia most responsive to cytarabine (ara-C) therapy and is of relative favorable prognosis.	Cytarabine	156-161	CCAAT enhancer binding protein zeta	Homo sapiens	61-80
18932257-1	2008	BACKGROUND: Acute myelogenous leukemia (AML) associated with core-binding-factor (CBF) abnormalities is the type of leukemia most responsive to cytarabine (ara-C) therapy and is of relative favorable prognosis.	Cytarabine	156-161	CCAAT enhancer binding protein zeta	Homo sapiens	82-85
18932257-2	2008	In vitro and ex vivo observations suggest that increases in intracellular ara-C levels influenced by administration of fludarabine and granulocyte colony-stimulating factor (GCSF) increase the effect of ara-C, prompting us to clinically evaluate the efficacy of such combinations.	Cytarabine	74-79	colony stimulating factor 3	Homo sapiens	135-172
18932257-2	2008	In vitro and ex vivo observations suggest that increases in intracellular ara-C levels influenced by administration of fludarabine and granulocyte colony-stimulating factor (GCSF) increase the effect of ara-C, prompting us to clinically evaluate the efficacy of such combinations.	Cytarabine	74-79	colony stimulating factor 3	Homo sapiens	174-178
18932257-2	2008	In vitro and ex vivo observations suggest that increases in intracellular ara-C levels influenced by administration of fludarabine and granulocyte colony-stimulating factor (GCSF) increase the effect of ara-C, prompting us to clinically evaluate the efficacy of such combinations.	Cytarabine	203-208	colony stimulating factor 3	Homo sapiens	135-172
18932257-2	2008	In vitro and ex vivo observations suggest that increases in intracellular ara-C levels influenced by administration of fludarabine and granulocyte colony-stimulating factor (GCSF) increase the effect of ara-C, prompting us to clinically evaluate the efficacy of such combinations.	Cytarabine	203-208	colony stimulating factor 3	Homo sapiens	174-178
18932257-5	2008	CONCLUSIONS: Thus, our data lends clinical credence to the observed modulation of ara-C by fludarabine and GCSF.	Cytarabine	82-87	colony stimulating factor 3	Homo sapiens	107-111
18922616-6	2008	RESULTS: A synergistic effect was observed when triptolide was added to idarubicin or to AraC to induce apoptosis of THP-1 leukemic cells.	Cytarabine	89-93	GLI family zinc finger 2	Homo sapiens	117-122
18487954-6	2008	Most importantly, primitive leukemic progenitors present in the mononuclear cells (MNCs) that were isolated from the peripheral blood of freshly diagnosed untreated acute myeloid leukemic (AML) patients got more efficiently killed by cytosine arabinoside (AraC), when the cells were pre-treated with a pharmacological inhibitor of p38.	Cytarabine	234-254	mitogen-activated protein kinase 14	Homo sapiens	331-334
18854573-0	2008	Long-term disease-free survival after gemtuzumab, intermediate-dose cytarabine, and mitoxantrone in patients with CD33(+) primary resistant or relapsed acute myeloid leukemia.	Cytarabine	68-78	CD33 molecule	Homo sapiens	114-118
18756547-0	2008	Low dose interleukin-2 following intensification therapy with high dose cytarabine for acute myelogenous leukemia in first complete remission.	Cytarabine	72-82	interleukin 2	Homo sapiens	9-22
18928583-1	2008	This study was purposed to explore the clinical efficiency and side effects of GHA (G-CSF, homoharringtonine and low-dose cytarabine) priming chemotherapy for patients with refractory acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS), and its relationship with B7.1 expression.	Cytarabine	122-132	CD80 molecule	Homo sapiens	275-279
17960382-9	2008	In patient cells, incubations with ara-C and PKC412 resulted in synergistic effects in 17% of the FLT3/ITD positive samples compared to 0% synergistic in the FLT3/ITD negative samples (p &lt; 0.01).	Cytarabine	35-40	fms related receptor tyrosine kinase 3	Homo sapiens	98-102
17960382-9	2008	In patient cells, incubations with ara-C and PKC412 resulted in synergistic effects in 17% of the FLT3/ITD positive samples compared to 0% synergistic in the FLT3/ITD negative samples (p &lt; 0.01).	Cytarabine	35-40	fms related receptor tyrosine kinase 3	Homo sapiens	158-162
19048119-0	2008	Resistance to cytarabine induces the up-regulation of NKG2D ligands and enhances natural killer cell lysis of leukemic cells.	Cytarabine	14-24	killer cell lectin like receptor K1	Homo sapiens	54-59
19048119-7	2008	Constitutive phosphorylated extracellular signal-regulated kinase (ERK) but not pAKT was higher in araC-resistant cells than in parental cell lines.	Cytarabine	99-103	mitogen-activated protein kinase 1	Homo sapiens	28-65
19048119-7	2008	Constitutive phosphorylated extracellular signal-regulated kinase (ERK) but not pAKT was higher in araC-resistant cells than in parental cell lines.	Cytarabine	99-103	mitogen-activated protein kinase 1	Homo sapiens	67-70
19048119-10	2008	These results demonstrate that increased sensitivity of araC-resistant leukemic cells to NK cell lysis is caused by higher NKG2D ligand expression, resulting from more active ERK signaling pathway.	Cytarabine	56-60	killer cell lectin like receptor K1	Homo sapiens	123-128
19048119-10	2008	These results demonstrate that increased sensitivity of araC-resistant leukemic cells to NK cell lysis is caused by higher NKG2D ligand expression, resulting from more active ERK signaling pathway.	Cytarabine	56-60	mitogen-activated protein kinase 1	Homo sapiens	175-178
19099627-7	2008	After incubation with Ara-C and G-CSF for 48 hours, A3 cells were inhibited more obviously compared with incubation with Ara-C alone (p&lt;0.05, Ara-C 10(-5) mol/L and 10(-6) mol/L).	Cytarabine	121-126	colony stimulating factor 3	Homo sapiens	32-37
19099627-7	2008	After incubation with Ara-C and G-CSF for 48 hours, A3 cells were inhibited more obviously compared with incubation with Ara-C alone (p&lt;0.05, Ara-C 10(-5) mol/L and 10(-6) mol/L).	Cytarabine	121-126	colony stimulating factor 3	Homo sapiens	32-37
19099627-8	2008	After incubation with Ara-C, ACR and G-CSF for 48 hours, the apoptotic rate of A3 cells was much more than that after incubation with Ara-C and ACR.	Cytarabine	134-139	colony stimulating factor 3	Homo sapiens	37-42
18755251-4	2008	In the Ara-C treated rats, retraction of the apical dendrites was noted in the neurons in the ACC but not in the pyramidal neurons in the hippocampal region CA1.	Cytarabine	7-12	carbonic anhydrase 1	Rattus norvegicus	157-160
18790760-0	2008	hKSR-2, a vitamin D-regulated gene, inhibits apoptosis in arabinocytosine-treated HL60 leukemia cells.	Cytarabine	58-73	kinase suppressor of ras 2	Homo sapiens	0-6
18790760-4	2008	We found that whereas kinase suppressor of Ras-1 had no detectable effect on cell survival in the system studied here, 1,25-(OH)2D3-induced up-regulation of hKSR-2 enhanced the resistance of HL60 cells to arabinocytosine.	Cytarabine	205-220	kinase suppressor of ras 2	Homo sapiens	157-163
18790760-5	2008	Knockdown of hKSR-2 by either small interfering RNA or antisense oligonucleotides increased arabinocytosine-induced apoptosis, which was accompanied by reduced Bcl-2/Bax and Bcl-2/Bad ratios, and increased caspase-3 activating cleavage.	Cytarabine	92-107	kinase suppressor of ras 2	Homo sapiens	13-19
18418218-7	2008	Moreover, noncytotoxic concentrations of Bc2 or EqTx-II potentiated the cytotoxicity induced by low dose concentrations of all classical chemotherapeutics agents tested: cytosine arabinoside, doxorubicin, and vincristine.	Cytarabine	170-190	charged multivesicular body protein 2A	Homo sapiens	41-44
19967054-3	2008	Here, we report that the receptor interacting protein (RIP), a key adaptor protein of TNF signaling, was required to activate JNK in the cells treated with certain DNA damaging agents such as adriamycin (Adr) and 1-beta-D-arabinofuranosylcytosine (Ara-C) that cause slow and sustained activation, but it was not required when treated with N-methyl-N-nitro-N-nitrosoguanidine (MNNG) and short wavelength UV, which causes quick and transient activation.	Cytarabine	213-246	receptor interacting serine/threonine kinase 1	Homo sapiens	25-53
19967054-3	2008	Here, we report that the receptor interacting protein (RIP), a key adaptor protein of TNF signaling, was required to activate JNK in the cells treated with certain DNA damaging agents such as adriamycin (Adr) and 1-beta-D-arabinofuranosylcytosine (Ara-C) that cause slow and sustained activation, but it was not required when treated with N-methyl-N-nitro-N-nitrosoguanidine (MNNG) and short wavelength UV, which causes quick and transient activation.	Cytarabine	213-246	receptor interacting serine/threonine kinase 1	Homo sapiens	55-58
19967054-3	2008	Here, we report that the receptor interacting protein (RIP), a key adaptor protein of TNF signaling, was required to activate JNK in the cells treated with certain DNA damaging agents such as adriamycin (Adr) and 1-beta-D-arabinofuranosylcytosine (Ara-C) that cause slow and sustained activation, but it was not required when treated with N-methyl-N-nitro-N-nitrosoguanidine (MNNG) and short wavelength UV, which causes quick and transient activation.	Cytarabine	213-246	tumor necrosis factor	Homo sapiens	86-89
19967054-3	2008	Here, we report that the receptor interacting protein (RIP), a key adaptor protein of TNF signaling, was required to activate JNK in the cells treated with certain DNA damaging agents such as adriamycin (Adr) and 1-beta-D-arabinofuranosylcytosine (Ara-C) that cause slow and sustained activation, but it was not required when treated with N-methyl-N-nitro-N-nitrosoguanidine (MNNG) and short wavelength UV, which causes quick and transient activation.	Cytarabine	213-246	mitogen-activated protein kinase 8	Homo sapiens	126-129
19967054-3	2008	Here, we report that the receptor interacting protein (RIP), a key adaptor protein of TNF signaling, was required to activate JNK in the cells treated with certain DNA damaging agents such as adriamycin (Adr) and 1-beta-D-arabinofuranosylcytosine (Ara-C) that cause slow and sustained activation, but it was not required when treated with N-methyl-N-nitro-N-nitrosoguanidine (MNNG) and short wavelength UV, which causes quick and transient activation.	Cytarabine	248-253	receptor interacting serine/threonine kinase 1	Homo sapiens	25-53
19967054-3	2008	Here, we report that the receptor interacting protein (RIP), a key adaptor protein of TNF signaling, was required to activate JNK in the cells treated with certain DNA damaging agents such as adriamycin (Adr) and 1-beta-D-arabinofuranosylcytosine (Ara-C) that cause slow and sustained activation, but it was not required when treated with N-methyl-N-nitro-N-nitrosoguanidine (MNNG) and short wavelength UV, which causes quick and transient activation.	Cytarabine	248-253	receptor interacting serine/threonine kinase 1	Homo sapiens	55-58
19967054-3	2008	Here, we report that the receptor interacting protein (RIP), a key adaptor protein of TNF signaling, was required to activate JNK in the cells treated with certain DNA damaging agents such as adriamycin (Adr) and 1-beta-D-arabinofuranosylcytosine (Ara-C) that cause slow and sustained activation, but it was not required when treated with N-methyl-N-nitro-N-nitrosoguanidine (MNNG) and short wavelength UV, which causes quick and transient activation.	Cytarabine	248-253	tumor necrosis factor	Homo sapiens	86-89
19967054-3	2008	Here, we report that the receptor interacting protein (RIP), a key adaptor protein of TNF signaling, was required to activate JNK in the cells treated with certain DNA damaging agents such as adriamycin (Adr) and 1-beta-D-arabinofuranosylcytosine (Ara-C) that cause slow and sustained activation, but it was not required when treated with N-methyl-N-nitro-N-nitrosoguanidine (MNNG) and short wavelength UV, which causes quick and transient activation.	Cytarabine	248-253	mitogen-activated protein kinase 8	Homo sapiens	126-129
18414789-0	2008	Cytosine arabinoside affects the heat and capsaicin receptor TRPV1 localisation and sensitivity in human sensory neurons.	Cytarabine	0-20	transient receptor potential cation channel subfamily V member 1	Homo sapiens	61-66
18414789-3	2008	We studied the effects of Ara C on human dorsal root ganglion (DRG) neurons, especially the expression and sensitivity of the ion channel TRPV1, which responds to noxious heat and capsaicin and is a key mediator of neuropathic pain.	Cytarabine	26-31	transient receptor potential cation channel subfamily V member 1	Homo sapiens	138-143
18414789-5	2008	Double immunostaining for the regenerative neuronal marker Gap43 and the capsaicin receptor TRPV1 showed that the normal membrane-bound localisation of TRPV1 was absent in neurons with Ara C treatment, and as expected there was massive diminution of dividing non-neuronal cells.	Cytarabine	185-190	transient receptor potential cation channel subfamily V member 1	Homo sapiens	152-157
18414789-9	2008	CONCLUSIONS: It is postulated that Ara C treatment blocked insertion of TRPV1 in the cell membrane, resulting in accumulation of the receptors in the cytoplasm, loss of capsaicin sensitivity, and membrane-bound immunostaining, which was restored with a rebound on withdrawal of Ara C.	Cytarabine	35-40	transient receptor potential cation channel subfamily V member 1	Homo sapiens	72-77
18414789-9	2008	CONCLUSIONS: It is postulated that Ara C treatment blocked insertion of TRPV1 in the cell membrane, resulting in accumulation of the receptors in the cytoplasm, loss of capsaicin sensitivity, and membrane-bound immunostaining, which was restored with a rebound on withdrawal of Ara C.	Cytarabine	278-283	transient receptor potential cation channel subfamily V member 1	Homo sapiens	72-77
19035178-0	2008	[Study on the relationship between human cytidine deaminase gene polymorphisms and Ara-C sensitivity].	Cytarabine	83-88	cytidine deaminase	Homo sapiens	41-59
19035178-1	2008	OBJECTIVE: To study the relationship between coding single-nucleotide polymorphisms (cSNPs) in the human cytidine deaminase (CDA) gene and cytosine arabinoside (Ara-C) sensitivity in childhood acute leukemia (AL).	Cytarabine	139-159	cytidine deaminase	Homo sapiens	105-123
19035178-1	2008	OBJECTIVE: To study the relationship between coding single-nucleotide polymorphisms (cSNPs) in the human cytidine deaminase (CDA) gene and cytosine arabinoside (Ara-C) sensitivity in childhood acute leukemia (AL).	Cytarabine	139-159	cytidine deaminase	Homo sapiens	125-128
19035178-1	2008	OBJECTIVE: To study the relationship between coding single-nucleotide polymorphisms (cSNPs) in the human cytidine deaminase (CDA) gene and cytosine arabinoside (Ara-C) sensitivity in childhood acute leukemia (AL).	Cytarabine	161-166	cytidine deaminase	Homo sapiens	105-123
19035178-1	2008	OBJECTIVE: To study the relationship between coding single-nucleotide polymorphisms (cSNPs) in the human cytidine deaminase (CDA) gene and cytosine arabinoside (Ara-C) sensitivity in childhood acute leukemia (AL).	Cytarabine	161-166	cytidine deaminase	Homo sapiens	125-128
18549619-3	2008	The cytotoxic effect was measured by MTT assay; cell apoptosis rate was determined by flow cytometry after Annexin V/PI staining; the expression level of DR5 on surface of HL-60 cells treated with Ara-C at different concentrations for 24 hours was determined by flow cytometry.	Cytarabine	197-202	TNF receptor superfamily member 10b	Homo sapiens	154-157
18538080-0	2008	[Up-regulation of CD86 and cytokine expression in acute leukemia cells by Ara-C].	Cytarabine	74-79	CD86 molecule	Homo sapiens	18-22
18538080-1	2008	AIM: To observe the effects of Ara-c on the expression of CD86 molecule on acute leukemia cells and explore the possible mechanisms.	Cytarabine	31-36	CD86 molecule	Homo sapiens	58-62
18489990-0	2008	Long-term follow-up of allogeneic hematopoietic stem cell transplantation for de novo acute myelogenous leukemia with a conditioning regimen of total body irradiation and granulocyte colony-stimulating factor-combined high-dose cytarabine.	Cytarabine	228-238	colony stimulating factor 3	Homo sapiens	171-208
18489990-1	2008	We retrospectively evaluated the efficacy and safety of total body irradiation (TBI) and granulocyte colony-stimulating factor (G-CSF)-combined high-dose cytarabine as a conditioning regimen for allogeneic hematopoietic stem cell transplantation (HSCT) in patients with de novo acute myelogenous leukemia (AML).	Cytarabine	154-164	colony stimulating factor 3	Homo sapiens	89-126
18489990-1	2008	We retrospectively evaluated the efficacy and safety of total body irradiation (TBI) and granulocyte colony-stimulating factor (G-CSF)-combined high-dose cytarabine as a conditioning regimen for allogeneic hematopoietic stem cell transplantation (HSCT) in patients with de novo acute myelogenous leukemia (AML).	Cytarabine	154-164	colony stimulating factor 3	Homo sapiens	128-133
18489990-10	2008	These results suggest that G-CSF-combined high-dose cytarabine could be a promising component of the conditioning regimen for allogeneic HSCT for AML, providing a high DFS and low TRM.	Cytarabine	52-62	colony stimulating factor 3	Homo sapiens	27-32
18492113-4	2008	Treatment with recombinant human (rh)TGF-beta1 inhibited spontaneous and cytarabine-induced apoptosis in U937 cells, most prominently in U937 cells directly attached to MSCs.	Cytarabine	73-83	transforming growth factor beta 1	Homo sapiens	37-46
18600530-3	2008	SiRNA-transfected cells reduced in dCK activity were 3- to 6-fold less sensitive to CdA, AraC, and CAFdA.	Cytarabine	89-93	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	35-38
18600530-5	2008	dGK depletion in cells resulted in lower sensitivity to FaraA, dFdC, CAFdA, and AraG, but slightly higher sensitivity to CdA and AraC.	Cytarabine	129-133	Diacyl glycerol kinase	Drosophila melanogaster	0-3
18538080-2	2008	METHODS: The expression of CD86 on U937, HL-60 and NB4 cell lines treated with or without Ara-C wa assayed by flow cytometry.	Cytarabine	90-95	CD86 molecule	Homo sapiens	27-31
18538080-4	2008	RESULTS: UP-regulation of CD86 was observed on those cells treated by Ara-c.	Cytarabine	70-75	CD86 molecule	Homo sapiens	26-30
18549619-6	2008	The apoptosis rate of HL-60 cells in Ara-C + rsTRAIL tandem given group was higher than that in Ara-C + rsTRAIL simultaneously given group, the expression level of DR5 on surface of HL-60 cells and intracellular activity of caspase-8 in Ara-C + rsTRAIL tandem given group were higher than those in rsTRAIL group.	Cytarabine	37-42	TNF receptor superfamily member 10b	Homo sapiens	164-167
18538080-5	2008	The level of CD86 and NF-kappaB mRNA in Ara-c treated cells was significantly enhanced.	Cytarabine	40-45	CD86 molecule	Homo sapiens	13-17
18538080-5	2008	The level of CD86 and NF-kappaB mRNA in Ara-c treated cells was significantly enhanced.	Cytarabine	40-45	nuclear factor kappa B subunit 1	Homo sapiens	22-31
18549619-6	2008	The apoptosis rate of HL-60 cells in Ara-C + rsTRAIL tandem given group was higher than that in Ara-C + rsTRAIL simultaneously given group, the expression level of DR5 on surface of HL-60 cells and intracellular activity of caspase-8 in Ara-C + rsTRAIL tandem given group were higher than those in rsTRAIL group.	Cytarabine	37-42	caspase 8	Homo sapiens	224-233
18538080-7	2008	CONCLUSION: Ara-C can enhance CD86 and NF-kappaB expression on acute leukemia cells, which may play critical role in T cell activation and differentiation.	Cytarabine	12-17	CD86 molecule	Homo sapiens	30-34
18538080-7	2008	CONCLUSION: Ara-C can enhance CD86 and NF-kappaB expression on acute leukemia cells, which may play critical role in T cell activation and differentiation.	Cytarabine	12-17	nuclear factor kappa B subunit 1	Homo sapiens	39-48
18549619-7	2008	When HL-60 cells treated with 5 and 10 mg/L of Ara-C for 24 hours, the expression level of DR5 on surface of HL-60 cells was higher than that in control group.	Cytarabine	47-52	TNF receptor superfamily member 10b	Homo sapiens	91-94
18549619-9	2008	Ara-C can upregulate DR5 expression on the surface of HL-60 cells and enhance the effect of rsTRAIL-inducing apoptosis.	Cytarabine	0-5	TNF receptor superfamily member 10b	Homo sapiens	21-24
18549611-2	2008	Methylation specific-PCR (MS-PCR) were used to detect the status of promoter methylation of id4 gene in bone marrow samples from AML patients with CR who had accepted induction with DA or IA and 4 to 5 consolidation chemotherapy with Ara-C.	Cytarabine	234-239	inhibitor of DNA binding 4, HLH protein	Homo sapiens	92-95
18549619-12	2008	The mechanism may correlate with up-regulation of the expression level of DR5 and/or caspase-8 in HL-60 cells by Ara-C.	Cytarabine	113-118	TNF receptor superfamily member 10b	Homo sapiens	74-77
18549619-12	2008	The mechanism may correlate with up-regulation of the expression level of DR5 and/or caspase-8 in HL-60 cells by Ara-C.	Cytarabine	113-118	caspase 8	Homo sapiens	85-94
18084320-6	2008	Expression of NUP98-IQCG inhibited 32Dcl3 cell apoptosis induced by Ara-C, and partially blocked granulocyte differentiation induced by G-CSF.	Cytarabine	68-73	nucleoporin 98	Mus musculus	14-19
18084320-6	2008	Expression of NUP98-IQCG inhibited 32Dcl3 cell apoptosis induced by Ara-C, and partially blocked granulocyte differentiation induced by G-CSF.	Cytarabine	68-73	IQ motif containing G	Mus musculus	20-24
18341636-5	2008	AML samples with -17, which are more resistant to daunorubicin and cytarabine compared with samples without -17, were effectively killed by PRIMA-1.	Cytarabine	67-77	proline rich membrane anchor 1	Homo sapiens	140-147
18341639-4	2008	All three groups showed similar sensitivity to the cytotoxic effects of cytarabine but FLT3/ITD mutant level was inversely correlated with cytarabine cytotoxicity (P = 0.04) whereas FLT3/TKD mutant level had no impact.	Cytarabine	139-149	fms related receptor tyrosine kinase 3	Homo sapiens	87-91
18358726-3	2008	Then regioselective acylation of ribavirin and cytarabine with pyrimidine vinyl ester was catalyzed by CAL-B (immobilized lipase from Candida antarctica) in anhydrous acetone.	Cytarabine	47-57	PAN0_003d1715	Moesziomyces antarcticus	122-128
18279719-0	2008	Enhancement of the anti-tumor efficacy of a GM-CSF-secreting tumor cell immunotherapy in preclinical models by cytosine arabinoside.	Cytarabine	111-131	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	44-50
18273043-5	2008	Tyrosine nitration of cellular protein also increased more in MPO-expressing K562 cells than control cells after treatment with AraC.	Cytarabine	128-132	myeloperoxidase	Homo sapiens	62-65
18273043-6	2008	In clinical samples, CD34-positive AML cells from high-MPO cases showed a tendency to be sensitive to AraC in the colony-formation assay, and the generation of ROS and the nitration of protein were observed only when the percentage of MPO-expressing cells was high.	Cytarabine	102-106	myeloperoxidase	Homo sapiens	55-58
19099730-3	2008	METHODS: The drug levels of Ara-C in plasma and cerebrospinal fluid were detected with HPLC while HD-AraC was used, the expression of deoxycytidine kinase (dCK) and cytidine deaminase (CDA) mRNA in human leukemia cell lines and the bone marrow cells were investigated in 48 cases of childhood hematological malignancies with RT-PCR methods, and the relationship between the expression of these enzymes mRNA and the outcome of the patients was analyzed.	Cytarabine	28-33	deoxycytidine kinase	Homo sapiens	134-154
19099730-3	2008	METHODS: The drug levels of Ara-C in plasma and cerebrospinal fluid were detected with HPLC while HD-AraC was used, the expression of deoxycytidine kinase (dCK) and cytidine deaminase (CDA) mRNA in human leukemia cell lines and the bone marrow cells were investigated in 48 cases of childhood hematological malignancies with RT-PCR methods, and the relationship between the expression of these enzymes mRNA and the outcome of the patients was analyzed.	Cytarabine	28-33	cytidine deaminase	Homo sapiens	185-188
18401414-4	2008	Overcoming imatinib resistance in LAMA84-r with farnesyltransferase or MEK/ERK inhibitors as well as with cytosine arabinoside led to SphK1 inhibition.	Cytarabine	106-126	sphingosine kinase 1	Homo sapiens	134-139
18360721-2	2008	In this study, we developed an AML cell line (AML-2/IDAC) that is resistant to treatment with a combination of idarubicin and cytosine arabinoside (Id/AraC) by chronic exposure for more than 3 months.	Cytarabine	126-146	RUNX family transcription factor 3	Homo sapiens	46-51
18360721-6	2008	The combined treatment with indomethacin and Id/AraC caused the collapse of the mitochondrial membrane potential and was also demonstrated to enhance the activities of caspase-3 and -8 in AML-2/IDAC cells.	Cytarabine	48-52	caspase 3	Homo sapiens	168-184
18360721-6	2008	The combined treatment with indomethacin and Id/AraC caused the collapse of the mitochondrial membrane potential and was also demonstrated to enhance the activities of caspase-3 and -8 in AML-2/IDAC cells.	Cytarabine	48-52	RUNX family transcription factor 3	Homo sapiens	188-193
18279719-11	2008	CONCLUSION: GM-CSF-secreting tumor cell immunotherapy in combination with AraC prolongs survival of tumor-bearing mice, with a median survival time of 61 days observed in mice treated with AraC alone and 90% of mice treated with the combination therapy still alive by day 150.	Cytarabine	189-193	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	12-18
18076637-2	2008	Purine analogs fludarabine (FA) and cladribine (2-CdA) increase cytotoxic effect of Ara-C in leukemic blasts and inhibit DNA repair mechanisms; therefore its association with Ara-C and mitoxantrone (MIT) results in a synergistic effect.	Cytarabine	84-89	cytidine deaminase	Homo sapiens	50-53
18094719-6	2008	In the K562pTet-on/ETS2 cells, ETS2 induction conferred differences in sensitivities to ara-C and daunorubicin, depending on GATA1 levels.	Cytarabine	88-93	ETS proto-oncogene 2, transcription factor	Homo sapiens	31-35
18347158-0	2008	Preclinical modeling of cytosine arabinoside response in Mll-Enl translocator mouse leukemias.	Cytarabine	24-44	lysine (K)-specific methyltransferase 2A	Mus musculus	57-60
18347158-0	2008	Preclinical modeling of cytosine arabinoside response in Mll-Enl translocator mouse leukemias.	Cytarabine	24-44	myeloid/lymphoid or mixed-lineage leukemia; translocated to, 1	Mus musculus	61-64
18076637-2	2008	Purine analogs fludarabine (FA) and cladribine (2-CdA) increase cytotoxic effect of Ara-C in leukemic blasts and inhibit DNA repair mechanisms; therefore its association with Ara-C and mitoxantrone (MIT) results in a synergistic effect.	Cytarabine	175-180	cytidine deaminase	Homo sapiens	50-53
18974616-1	2008	Deoxycytidine kinase (dCK) is a rate-limiting enzyme in the activation of nucleoside anticancer drugs, such as gemcitabine and cytarabine (Ara-C), to their active metabolites.	Cytarabine	127-137	deoxycytidine kinase	Homo sapiens	0-20
17977830-3	2008	In this study, the relationship between p53 activation and its posttranslational modifications was investigated in the human cancer cell lines A549 and HCT116 in response to 5-aza-2"-deoxycytidine (5-aza-CdR) or cytarabine treatment.	Cytarabine	212-222	tumor protein p53	Homo sapiens	40-43
18202788-4	2008	Cells homozygous for CC at MTHFR-A1298C were significantly more sensitive to cyclocytidine, cytarabine (AraC) and floxuridine than those with AA or AC (p=0.0215, p=0.0166, and p=0.0323, respectively), and carried more methylated tumor suppressor genes (p=0.0313).	Cytarabine	92-102	methylenetetrahydrofolate reductase	Homo sapiens	27-32
18202788-4	2008	Cells homozygous for CC at MTHFR-A1298C were significantly more sensitive to cyclocytidine, cytarabine (AraC) and floxuridine than those with AA or AC (p=0.0215, p=0.0166, and p=0.0323, respectively), and carried more methylated tumor suppressor genes (p=0.0313).	Cytarabine	104-108	methylenetetrahydrofolate reductase	Homo sapiens	27-32
18202788-6	2008	In particular, cells with methylated TIMP3 had reduced mRNA levels and were significantly more sensitive to aphidicolin-glycinate, AraC and 5-FU than cells with unmethylated TIMP3.	Cytarabine	131-135	TIMP metallopeptidase inhibitor 3	Homo sapiens	37-42
18974616-1	2008	Deoxycytidine kinase (dCK) is a rate-limiting enzyme in the activation of nucleoside anticancer drugs, such as gemcitabine and cytarabine (Ara-C), to their active metabolites.	Cytarabine	127-137	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	22-25
18974616-1	2008	Deoxycytidine kinase (dCK) is a rate-limiting enzyme in the activation of nucleoside anticancer drugs, such as gemcitabine and cytarabine (Ara-C), to their active metabolites.	Cytarabine	139-144	deoxycytidine kinase	Homo sapiens	0-20
18974616-1	2008	Deoxycytidine kinase (dCK) is a rate-limiting enzyme in the activation of nucleoside anticancer drugs, such as gemcitabine and cytarabine (Ara-C), to their active metabolites.	Cytarabine	139-144	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	22-25
17574212-3	2007	In this study, K562 cells were differentiated by Ara-C treatment, and Prdx III was dramatically increased until day 5.	Cytarabine	49-54	peroxiredoxin 3	Mus musculus	70-78
17951356-3	2008	Chemosensitivity experiments with 5-fluorouracil, cytosine arabinoside (araC), and mercaptopurine (MP) demonstrated that Hmgb1(-/-) mouse embryonic fibroblasts (MEFs) were 3 to 10 times more resistant to these drugs compared with Hmgb1(+)(/)(+) MEFs.	Cytarabine	50-70	high mobility group box 1	Mus musculus	121-126
17951356-3	2008	Chemosensitivity experiments with 5-fluorouracil, cytosine arabinoside (araC), and mercaptopurine (MP) demonstrated that Hmgb1(-/-) mouse embryonic fibroblasts (MEFs) were 3 to 10 times more resistant to these drugs compared with Hmgb1(+)(/)(+) MEFs.	Cytarabine	72-76	high mobility group box 1	Mus musculus	121-126
17951356-6	2008	trans-Activation experiments demonstrated diminished activation of proapoptotic promoters Bax, Puma, and Noxa in Hmgb1-deficient cells after treatment with MP or araC, consistent with reduced transcriptional activity of p53.	Cytarabine	162-166	BCL2 associated X, apoptosis regulator	Homo sapiens	90-93
17951356-6	2008	trans-Activation experiments demonstrated diminished activation of proapoptotic promoters Bax, Puma, and Noxa in Hmgb1-deficient cells after treatment with MP or araC, consistent with reduced transcriptional activity of p53.	Cytarabine	162-166	high mobility group box 1	Mus musculus	113-118
17951356-7	2008	We have demonstrated for the first time that Hmgb1 is an essential activator of cellular response to genotoxic stress caused by chemotherapeutic agents (thiopurines, cytarabine, and 5-fluorouracil), which acts at early steps of antimetabolite-induced stress by stimulating phosphorylation of two DNA damage markers, p53 and H2AX.	Cytarabine	166-176	high mobility group box 1	Mus musculus	45-50
18067088-1	2007	OBJECTIVE: Cytidine deaminase (CDA) is a key enzyme for metabolizing chemotherapeutic agent cytosine arabinoside (Ara-C), a deoxycytidine analog used for treatment of acute leukemia and lymphomas.	Cytarabine	92-112	cytidine deaminase	Homo sapiens	11-29
18067088-1	2007	OBJECTIVE: Cytidine deaminase (CDA) is a key enzyme for metabolizing chemotherapeutic agent cytosine arabinoside (Ara-C), a deoxycytidine analog used for treatment of acute leukemia and lymphomas.	Cytarabine	92-112	cytidine deaminase	Homo sapiens	31-34
18067088-1	2007	OBJECTIVE: Cytidine deaminase (CDA) is a key enzyme for metabolizing chemotherapeutic agent cytosine arabinoside (Ara-C), a deoxycytidine analog used for treatment of acute leukemia and lymphomas.	Cytarabine	114-119	cytidine deaminase	Homo sapiens	11-29
18067088-1	2007	OBJECTIVE: Cytidine deaminase (CDA) is a key enzyme for metabolizing chemotherapeutic agent cytosine arabinoside (Ara-C), a deoxycytidine analog used for treatment of acute leukemia and lymphomas.	Cytarabine	114-119	cytidine deaminase	Homo sapiens	31-34
18067088-3	2007	Two missense mutations changing Ara-C sensitivity and toxicity had been found in the human CDA.	Cytarabine	32-37	cytidine deaminase	Homo sapiens	91-94
18067088-11	2007	CONCLUSION: This study demonstrates 3 cSNPs and their allelic frequencies of CDA in Chinese children, and provides the first step to identify genetic markers for predicting variability in Ara-C response and toxicity.	Cytarabine	188-193	cytidine deaminase	Homo sapiens	77-80
17978477-0	2007	Resistance to Ara-C up-regulates the activation of NF-kappaB, telomerase activity and Fas expression in NALM-6 cells.	Cytarabine	14-19	nuclear factor kappa B subunit 1	Homo sapiens	51-60
17978477-3	2007	The activation of nuclear factor kappaB (NF-kappaB) was accompanied by the acquisition of Ara-C resistance.	Cytarabine	90-95	nuclear factor kappa B subunit 1	Homo sapiens	41-50
17978477-5	2007	The expression of Bid, Bax, or p53 proteins have been shown to increase correlated with the acquisition of Ara-C resistance.	Cytarabine	107-112	BH3 interacting domain death agonist	Homo sapiens	18-21
17978477-5	2007	The expression of Bid, Bax, or p53 proteins have been shown to increase correlated with the acquisition of Ara-C resistance.	Cytarabine	107-112	BCL2 associated X, apoptosis regulator	Homo sapiens	23-26
17978477-5	2007	The expression of Bid, Bax, or p53 proteins have been shown to increase correlated with the acquisition of Ara-C resistance.	Cytarabine	107-112	tumor protein p53	Homo sapiens	31-34
17978477-6	2007	In contrast to the increase in these proteins, Bcl-2, Bcl-x, and Bag-1 proteins remained unchanged with the acquisition of Ara-C resistance.	Cytarabine	123-128	BAG cochaperone 1	Homo sapiens	65-70
17978477-9	2007	In conclusion, this report has shown that resistance to Ara-C up-regulates the activation of NF-kappaB, telomerase activity and Fas expression.	Cytarabine	56-61	nuclear factor kappa B subunit 1	Homo sapiens	93-102
17350683-3	2007	Patients with ara-C-containing chemotherapies whose BMMNC showed a high level of cN-II expression (greater than the median value) had shorter median overall survival (15 months versus 22 months, p&lt;0.01) and shorter median post-chemotherapy survival (10 months versus 16 months, p=0.012).	Cytarabine	14-19	5'-nucleotidase, cytosolic II	Homo sapiens	81-86
17768398-5	2007	We show that knockdown of N-CoR either transiently (siRNA) or permanently (shRNA) impairs the cytosine arabinoside (Ara-C)- but not hemin-induced erythroid differentiation of K562 cells.	Cytarabine	94-114	nuclear receptor corepressor 1	Homo sapiens	26-31
17768398-5	2007	We show that knockdown of N-CoR either transiently (siRNA) or permanently (shRNA) impairs the cytosine arabinoside (Ara-C)- but not hemin-induced erythroid differentiation of K562 cells.	Cytarabine	116-121	nuclear receptor corepressor 1	Homo sapiens	26-31
17768398-6	2007	RT-PCR analysis reveals that N-CoR is required for induction by Ara-C of 5-aminolevulinate synthase (ALA-S2), a key enzyme involved in heme biosynthesis.	Cytarabine	64-69	nuclear receptor corepressor 1	Homo sapiens	29-34
17768398-6	2007	RT-PCR analysis reveals that N-CoR is required for induction by Ara-C of 5-aminolevulinate synthase (ALA-S2), a key enzyme involved in heme biosynthesis.	Cytarabine	64-69	5'-aminolevulinate synthase 2	Homo sapiens	101-107
17855478-1	2007	Deoxycytidine kinase (DCK) is a rate-limiting enzyme in the activation of nucleoside analogs such as cytarabine (ara-C), gemcitabine, clofarabine, and others.	Cytarabine	101-111	deoxycytidine kinase	Homo sapiens	0-20
17855478-1	2007	Deoxycytidine kinase (DCK) is a rate-limiting enzyme in the activation of nucleoside analogs such as cytarabine (ara-C), gemcitabine, clofarabine, and others.	Cytarabine	101-111	deoxycytidine kinase	Homo sapiens	22-25
17855478-1	2007	Deoxycytidine kinase (DCK) is a rate-limiting enzyme in the activation of nucleoside analogs such as cytarabine (ara-C), gemcitabine, clofarabine, and others.	Cytarabine	113-118	deoxycytidine kinase	Homo sapiens	0-20
17855478-1	2007	Deoxycytidine kinase (DCK) is a rate-limiting enzyme in the activation of nucleoside analogs such as cytarabine (ara-C), gemcitabine, clofarabine, and others.	Cytarabine	113-118	deoxycytidine kinase	Homo sapiens	22-25
17855478-12	2007	These results suggest that genetic variation in DCK influences its activity and expression and may predict the variability observed in intracellular levels of the ara-C active metabolite ara-CTP.	Cytarabine	163-168	deoxycytidine kinase	Homo sapiens	48-51
17594519-4	2007	We found the accumulation and phosphorylation of p53 protein, a tumor suppressor that mediates apoptosis under various cellular stresses, in Ara-C-treated rat placentas.	Cytarabine	141-146	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	49-52
17594519-7	2007	Phosphorylation of Chk1 and H2A.X, target substrates of DNA damage transducers, was detected immediately after Ara-C treatment, suggesting activation of DNA damage cascades to phosphorylate p53.	Cytarabine	111-116	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	190-193
17594519-8	2007	Ara-C-induced trophoblastic apoptosis was almost completely abrogated in placentas of Trp53 (coding p53)-deficient mice, whereas the levels of physiological apoptosis in trophoblasts were similar among wild-type and Trp53-deficient mice.	Cytarabine	0-5	transformation related protein 53	Mus musculus	86-91
17594519-8	2007	Ara-C-induced trophoblastic apoptosis was almost completely abrogated in placentas of Trp53 (coding p53)-deficient mice, whereas the levels of physiological apoptosis in trophoblasts were similar among wild-type and Trp53-deficient mice.	Cytarabine	0-5	transformation related protein 53	Mus musculus	88-91
17594519-8	2007	Ara-C-induced trophoblastic apoptosis was almost completely abrogated in placentas of Trp53 (coding p53)-deficient mice, whereas the levels of physiological apoptosis in trophoblasts were similar among wild-type and Trp53-deficient mice.	Cytarabine	0-5	transformation related protein 53	Mus musculus	216-221
17711502-4	2007	The chemosensitivity of TMK-1 cells expressing hENT1 and hENT2 to cytarabine and 1-(3-C-ethynyl-beta-D-ribopentofuranosyl) cytosine increased markedly in comparison to that of mock cells.	Cytarabine	66-76	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	47-52
17711502-4	2007	The chemosensitivity of TMK-1 cells expressing hENT1 and hENT2 to cytarabine and 1-(3-C-ethynyl-beta-D-ribopentofuranosyl) cytosine increased markedly in comparison to that of mock cells.	Cytarabine	66-76	solute carrier family 29 member 2	Homo sapiens	57-62
17620426-6	2007	The proapoptotic IAP inhibitor, LBW242, was shown in proliferation studies done in vitro to enhance the killing of PKC412-sensitive and PKC412-resistant cell lines expressing mutant FLT3 when combined with either PKC412 or standard cytotoxic agents (doxorubicin and Ara-c).	Cytarabine	266-271	islet amyloid polypeptide	Homo sapiens	17-20
17634552-12	2007	The RIL gene, which is silenced by DNA hypermethylation, was activated by DAC, but the addition of ara-C to DAC reduced RIL gene activation.	Cytarabine	99-104	arylacetamide deacetylase	Homo sapiens	108-111
17634552-12	2007	The RIL gene, which is silenced by DNA hypermethylation, was activated by DAC, but the addition of ara-C to DAC reduced RIL gene activation.	Cytarabine	99-104	PDZ and LIM domain 4	Homo sapiens	120-123
17425403-0	2007	Signature-based small molecule screening identifies cytosine arabinoside as an EWS/FLI modulator in Ewing sarcoma.	Cytarabine	52-72	EWS RNA binding protein 1	Homo sapiens	79-82
17311927-5	2007	In the presence of cytarabine, GM-CSF-Bcl-XL was able also to promote the differentiation of the CD34+ myeloid precursor whereas Lfn-Bcl-XL, lacking the GM-CSF domain-stimulated cell proliferation and not differentiation.	Cytarabine	19-29	colony stimulating factor 2	Homo sapiens	31-37
17311927-5	2007	In the presence of cytarabine, GM-CSF-Bcl-XL was able also to promote the differentiation of the CD34+ myeloid precursor whereas Lfn-Bcl-XL, lacking the GM-CSF domain-stimulated cell proliferation and not differentiation.	Cytarabine	19-29	BCL2 like 1	Homo sapiens	38-44
17311927-5	2007	In the presence of cytarabine, GM-CSF-Bcl-XL was able also to promote the differentiation of the CD34+ myeloid precursor whereas Lfn-Bcl-XL, lacking the GM-CSF domain-stimulated cell proliferation and not differentiation.	Cytarabine	19-29	CD34 molecule	Homo sapiens	97-101
17151917-0	2007	Cytosine beta-D-arabinofuranoside used as a paradigm modifier to increase production of tau aggregates in a cellular model of tauopathy.	Cytarabine	0-33	microtubule associated protein tau	Homo sapiens	88-91
17151917-4	2007	To generate the 70-kD tau in sufficient quantity for its characterization at the molecular level, we explored and demonstrated herein that cytosine beta-D-arabinofuranoside is a useful paradigm modifier to increase production of the 70-kD tau.	Cytarabine	139-172	microtubule associated protein tau	Homo sapiens	22-25
17151917-4	2007	To generate the 70-kD tau in sufficient quantity for its characterization at the molecular level, we explored and demonstrated herein that cytosine beta-D-arabinofuranoside is a useful paradigm modifier to increase production of the 70-kD tau.	Cytarabine	139-172	microtubule associated protein tau	Homo sapiens	239-242
17425403-0	2007	Signature-based small molecule screening identifies cytosine arabinoside as an EWS/FLI modulator in Ewing sarcoma.	Cytarabine	52-72	FLII actin remodeling protein	Homo sapiens	83-86
17425403-11	2007	Screening identified cytosine arabinoside (ARA-C) as a modulator of EWS/FLI.	Cytarabine	21-41	EWS RNA binding protein 1	Homo sapiens	68-71
17425403-11	2007	Screening identified cytosine arabinoside (ARA-C) as a modulator of EWS/FLI.	Cytarabine	21-41	FLII actin remodeling protein	Homo sapiens	72-75
17414574-0	2007	"Flushing out" cytosine arabinoside from CSF to reverse neurotoxicity.	Cytarabine	15-35	colony stimulating factor 2	Homo sapiens	41-44
17425403-11	2007	Screening identified cytosine arabinoside (ARA-C) as a modulator of EWS/FLI.	Cytarabine	43-48	EWS RNA binding protein 1	Homo sapiens	68-71
17425403-11	2007	Screening identified cytosine arabinoside (ARA-C) as a modulator of EWS/FLI.	Cytarabine	43-48	FLII actin remodeling protein	Homo sapiens	72-75
17425403-12	2007	ARA-C reduced EWS/FLI protein abundance and accordingly diminished cell viability and transformation and abrogated tumor growth in a xenograft model.	Cytarabine	0-5	EWS RNA binding protein 1	Homo sapiens	14-17
17425403-12	2007	ARA-C reduced EWS/FLI protein abundance and accordingly diminished cell viability and transformation and abrogated tumor growth in a xenograft model.	Cytarabine	0-5	FLII actin remodeling protein	Homo sapiens	18-21
17342203-4	2007	Overexpression of beta1 integrins enhanced the cellular sensitivity to X-rays and Ara-C, which was counteracted by increasing concentrations of matrix proteins in association with reduced caspase-3 and -8 activation and MTP breakdown.	Cytarabine	82-87	UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase like 1	Homo sapiens	18-23
17342096-3	2007	Cripto Mab synergistically enhanced sensitivity of the MDR cells to Pgp substrates epirubicin (EPI), daunorubicin (DAU) and non-Pgp substrates nucleoside analogue cytosine arabinoside (AraC).	Cytarabine	163-183	teratocarcinoma-derived growth factor 1	Homo sapiens	0-6
17342096-3	2007	Cripto Mab synergistically enhanced sensitivity of the MDR cells to Pgp substrates epirubicin (EPI), daunorubicin (DAU) and non-Pgp substrates nucleoside analogue cytosine arabinoside (AraC).	Cytarabine	185-189	teratocarcinoma-derived growth factor 1	Homo sapiens	0-6
17327276-5	2007	The treatment of cytosine-beta-D-arabinofuranoside strikingly enhances the NER-dependent H2AX phosphorylation and induces the accumulation of replication protein A (RPA) and ATR-interacting protein (ATRIP) at locally UV-damaged subnuclear regions.	Cytarabine	17-50	H2A.X variant histone	Homo sapiens	89-93
17327276-5	2007	The treatment of cytosine-beta-D-arabinofuranoside strikingly enhances the NER-dependent H2AX phosphorylation and induces the accumulation of replication protein A (RPA) and ATR-interacting protein (ATRIP) at locally UV-damaged subnuclear regions.	Cytarabine	17-50	replication protein A1	Homo sapiens	142-163
17327276-5	2007	The treatment of cytosine-beta-D-arabinofuranoside strikingly enhances the NER-dependent H2AX phosphorylation and induces the accumulation of replication protein A (RPA) and ATR-interacting protein (ATRIP) at locally UV-damaged subnuclear regions.	Cytarabine	17-50	replication protein A1	Homo sapiens	165-168
17327276-5	2007	The treatment of cytosine-beta-D-arabinofuranoside strikingly enhances the NER-dependent H2AX phosphorylation and induces the accumulation of replication protein A (RPA) and ATR-interacting protein (ATRIP) at locally UV-damaged subnuclear regions.	Cytarabine	17-50	ATR interacting protein	Homo sapiens	174-197
17327276-5	2007	The treatment of cytosine-beta-D-arabinofuranoside strikingly enhances the NER-dependent H2AX phosphorylation and induces the accumulation of replication protein A (RPA) and ATR-interacting protein (ATRIP) at locally UV-damaged subnuclear regions.	Cytarabine	17-50	ATR interacting protein	Homo sapiens	199-204
17342203-6	2007	CONCLUSIONS/SIGNIFICANCE: The presented data suggest that the ligand status of beta1 integrins is critical for their antiapoptotic effect in leukemia cells treated with Ara-C, FasL or ionizing radiation.	Cytarabine	169-174	UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase like 1	Homo sapiens	79-84
17097625-7	2007	RESULTS: The mRNA expression of human equilibrative nucleoside transporter-1 (hENT-1), which is an uptake transporter of Ara-C, was initially decreased during the acquisition of resistance to Ara-C.	Cytarabine	121-126	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	38-76
17220902-0	2007	Total body irradiation and granulocyte colony-stimulating factor-combined high-dose cytarabine as a conditioning regimen in allogeneic hematopoietic stem cell transplantation for advanced myelodysplastic syndrome: a single-institute experience.	Cytarabine	84-94	colony stimulating factor 3	Homo sapiens	27-64
17220902-1	2007	In this study, we retrospectively evaluated the efficacy and safety of total body irradiation (TBI) and granulocyte colony-stimulating factor (G-CSF)-combined high-dose cytarabine as a conditioning regimen for allogeneic hematopoietic stem cell transplantation (HSCT) in patients with advanced myelodysplastic syndrome (MDS).	Cytarabine	169-179	colony stimulating factor 3	Homo sapiens	104-141
17220902-1	2007	In this study, we retrospectively evaluated the efficacy and safety of total body irradiation (TBI) and granulocyte colony-stimulating factor (G-CSF)-combined high-dose cytarabine as a conditioning regimen for allogeneic hematopoietic stem cell transplantation (HSCT) in patients with advanced myelodysplastic syndrome (MDS).	Cytarabine	169-179	colony stimulating factor 3	Homo sapiens	143-148
17220902-8	2007	These results suggest that G-CSF-combined high-dose cytarabine could be a promising component of the conditioning regimen of allogeneic HSCT for advanced MDS, providing a low incidence of both relapse and treatment-related mortality.	Cytarabine	52-62	colony stimulating factor 3	Homo sapiens	27-32
17241530-5	2007	Furthermore, L-valyl-ara-C appeared to be stable in the leukemia cell homogenates, and subsequently, it was far less cytotoxic than the parent, ara-C in AML2 and L1210 cells.	Cytarabine	21-26	runt related transcription factor 3	Mus musculus	153-157
17097625-7	2007	RESULTS: The mRNA expression of human equilibrative nucleoside transporter-1 (hENT-1), which is an uptake transporter of Ara-C, was initially decreased during the acquisition of resistance to Ara-C.	Cytarabine	121-126	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	78-84
17097625-7	2007	RESULTS: The mRNA expression of human equilibrative nucleoside transporter-1 (hENT-1), which is an uptake transporter of Ara-C, was initially decreased during the acquisition of resistance to Ara-C.	Cytarabine	192-197	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	38-76
17097625-7	2007	RESULTS: The mRNA expression of human equilibrative nucleoside transporter-1 (hENT-1), which is an uptake transporter of Ara-C, was initially decreased during the acquisition of resistance to Ara-C.	Cytarabine	192-197	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	78-84
17097625-9	2007	The cytotoxic effect of Ara-C on parental NALM-6 cells was ameliorated by hENT-1 inhibitors.	Cytarabine	24-29	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	74-80
17097625-11	2007	CONCLUSIONS: Decreased hENT-1 expression and function is causatively responsible for the acquisition of Ara-C resistance and alterations in dCK and CDA contribute to the higher concentration range.	Cytarabine	104-109	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	23-29
17490525-6	2007	It is concluded that NMDP and Ara-C induce apoptosis of HL-60 cells, and the mechanism of apoptosis induced by them may down-regulate the expression of bcl-2 gene and up-regulate the expression of bax gene.	Cytarabine	30-35	BCL2 apoptosis regulator	Homo sapiens	152-157
17490525-6	2007	It is concluded that NMDP and Ara-C induce apoptosis of HL-60 cells, and the mechanism of apoptosis induced by them may down-regulate the expression of bcl-2 gene and up-regulate the expression of bax gene.	Cytarabine	30-35	BCL2 associated X, apoptosis regulator	Homo sapiens	197-200
17490525-7	2007	The mechanism of HL-60 cell apoptosis induced by Ara-C and NMDP is probably associated with the down-regulation of Bcl-2 protein expression.	Cytarabine	49-54	BCL2 apoptosis regulator	Homo sapiens	115-120
16986129-0	2007	Predictable prognostic factor of CD56 expression in patients with acute myeloid leukemia with t(8:21) after high dose cytarabine or allogeneic hematopoietic stem cell transplantation.	Cytarabine	118-128	neural cell adhesion molecule 1	Homo sapiens	33-37
16989917-11	2007	Using drug inhibition analysis by a de novo protein synthesis inhibitor (cycloheximide) and a viral DNA replication inhibitor (cytosine arabinofuranoside), RGV DUT was classified as an early (E) viral gene during the in vitro infection.	Cytarabine	127-153	deoxyuridine triphosphatase	Homo sapiens	160-163
17107349-7	2006	In addition, VEGFR2 kinase inhibitor potentiated the growth inhibitory effect of cytarabine in Kasumi-1.	Cytarabine	81-91	kinase insert domain receptor	Homo sapiens	13-19
17213995-1	2007	Induction of c-jun expression in the myeloid leukemia cell line KG-1 by 1-beta-D-arabinofuranosylcytosine.	Cytarabine	72-105	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	13-18
16942854-1	2006	We studied the ability of prolyl oligopeptidase (POP) inhibitors, Z-Pro-Prolinal and JTP-4819, to prevent translocation of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and formation of reactive oxygen species (ROS), in 6-hydroxydopamine (6-OHDA) and cytosine arabinoside (Ara-C) treated monkey fibroblast (CV1-P) and human neuroblastoma (SH-SY5Y) cells.	Cytarabine	254-274	prolyl endopeptidase	Homo sapiens	26-47
16942854-1	2006	We studied the ability of prolyl oligopeptidase (POP) inhibitors, Z-Pro-Prolinal and JTP-4819, to prevent translocation of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and formation of reactive oxygen species (ROS), in 6-hydroxydopamine (6-OHDA) and cytosine arabinoside (Ara-C) treated monkey fibroblast (CV1-P) and human neuroblastoma (SH-SY5Y) cells.	Cytarabine	276-281	prolyl endopeptidase	Homo sapiens	26-47
16942854-1	2006	We studied the ability of prolyl oligopeptidase (POP) inhibitors, Z-Pro-Prolinal and JTP-4819, to prevent translocation of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and formation of reactive oxygen species (ROS), in 6-hydroxydopamine (6-OHDA) and cytosine arabinoside (Ara-C) treated monkey fibroblast (CV1-P) and human neuroblastoma (SH-SY5Y) cells.	Cytarabine	276-281	prolyl endopeptidase	Homo sapiens	49-52
17177846-0	2006	5-FdUrd-araC heterodinucleoside re-establishes sensitivity in 5-FdUrd- and AraC-resistant MCF-7 breast cancer cells overexpressing ErbB2.	Cytarabine	75-79	erb-b2 receptor tyrosine kinase 2	Homo sapiens	131-136
16942854-1	2006	We studied the ability of prolyl oligopeptidase (POP) inhibitors, Z-Pro-Prolinal and JTP-4819, to prevent translocation of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and formation of reactive oxygen species (ROS), in 6-hydroxydopamine (6-OHDA) and cytosine arabinoside (Ara-C) treated monkey fibroblast (CV1-P) and human neuroblastoma (SH-SY5Y) cells.	Cytarabine	254-274	prolyl endopeptidase	Homo sapiens	49-52
17079445-7	2006	Nutlin-3 pretreatment also conferred protection of p53-proficient cells against cytosine arabinoside but not against doxorubicin or cisplatin.	Cytarabine	80-100	tumor protein p53	Homo sapiens	51-54
16835384-1	2006	Hematopoietic stem cell gene transfer of the drug-resistance gene cytidine deaminase (CDD) protecting cells from the cytotoxic cytidine analogs cytarabine and gemcitabine was investigated in a murine transplant model.	Cytarabine	144-154	cytidine deaminase	Mus musculus	66-84
16835384-1	2006	Hematopoietic stem cell gene transfer of the drug-resistance gene cytidine deaminase (CDD) protecting cells from the cytotoxic cytidine analogs cytarabine and gemcitabine was investigated in a murine transplant model.	Cytarabine	144-154	cytidine deaminase	Mus musculus	86-89
16835384-2	2006	Following transplantation of CDD-transduced cells and cytarabine application (500 mg/kg; days 1-4; intraperitoneally) significant myeloprotection was demonstrated with nadir counts of peripheral blood granulocytes and thrombocytes of 2.9 +/- 0.6/nL versus 0.7 +/- 0.1/nL (P &lt; .001) and 509 +/- 147/nL versus 80 +/- 9/nL (P = .008), respectively (CDD versus control).	Cytarabine	54-64	cytidine deaminase	Mus musculus	349-352
16936229-5	2006	1-beta-D-Arabinofuranosylcytosine (ara-C), a chemotherapy agent often used in combination with MTX, is a nucleoside analog whose incorporation into chromosome requires prior phosphorylation by dCK.	Cytarabine	0-33	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	193-196
17080338-5	2006	There is convincing evidence that AMP is caused by spinal cord toxicity of intrathecally applied toxic agents such as cytarabin and/or methotrexate leading to spinal demyelinisation as demonstrated by elevated myelin basic protein in cerebrospinal fluid.	Cytarabine	118-127	myelin basic protein	Homo sapiens	210-230
17146554-0	2006	Cytosine arabinoside-metabolizing enzyme genes are underexpressed in children with MLL gene-rearranged acute lymphoblastic leukemia.	Cytarabine	0-20	lysine methyltransferase 2A	Homo sapiens	83-86
17146554-3	2006	We quantified mRNA expression of Ara-C key enzymes in leukemic lymphoblasts from 64 Brazilian ALL children, 15 of them presenting MLL gene rearrangement, and correlated it with clinical and biological features.	Cytarabine	33-38	lysine methyltransferase 2A	Homo sapiens	130-133
17146554-12	2006	In conclusion, the expression of the genes related to Ara-C metabolism was lower in MLL-positive children in the sample studied, suggesting the presence of population differences in the expression profile of these genes especially for HENT1.	Cytarabine	54-59	lysine methyltransferase 2A	Homo sapiens	84-87
16936229-5	2006	1-beta-D-Arabinofuranosylcytosine (ara-C), a chemotherapy agent often used in combination with MTX, is a nucleoside analog whose incorporation into chromosome requires prior phosphorylation by dCK.	Cytarabine	35-40	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	193-196
16936229-6	2006	We show that, remarkably, MTX enhances incorporation and cytotoxicity of ara-C through regulation of dCK activity in Burkitt"s lymphoma cells.	Cytarabine	73-78	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	101-104
17121229-11	2006	When the cells were treated with or without apoptosis inducer Ara-C, the apoptosis of MCF-7 cells transfected with HIF-1 alpha shRNA increased by 1.75 times (P &lt; 0.01) and 61.	Cytarabine	62-67	hypoxia inducible factor 1 subunit alpha	Homo sapiens	115-126
17094462-0	2006	Inhibition of poly (ADP-ribose) polymerase as a protective effect of nicaraven in ionizing radiation- and ara-C-induced cell death.	Cytarabine	106-111	poly(ADP-ribose) polymerase 1	Homo sapiens	14-42
16764854-7	2006	We report in this study that, when nontransformed CV1 epithelial cells and Hs578T breast cancer cells are treated with the chemotherapeutic agent cytosine arabinoside (Ara-C), Thr-821 of Rb is rapidly dephosphorylated concomitant with dissociation of the PP1 regulatory subunit PNUTS (phosphatase nuclear targeting subunit) from PP1 enzyme.	Cytarabine	146-166	inorganic pyrophosphatase 1	Homo sapiens	255-258
16764854-7	2006	We report in this study that, when nontransformed CV1 epithelial cells and Hs578T breast cancer cells are treated with the chemotherapeutic agent cytosine arabinoside (Ara-C), Thr-821 of Rb is rapidly dephosphorylated concomitant with dissociation of the PP1 regulatory subunit PNUTS (phosphatase nuclear targeting subunit) from PP1 enzyme.	Cytarabine	146-166	protein phosphatase 1 regulatory subunit 10	Homo sapiens	278-283
16764854-7	2006	We report in this study that, when nontransformed CV1 epithelial cells and Hs578T breast cancer cells are treated with the chemotherapeutic agent cytosine arabinoside (Ara-C), Thr-821 of Rb is rapidly dephosphorylated concomitant with dissociation of the PP1 regulatory subunit PNUTS (phosphatase nuclear targeting subunit) from PP1 enzyme.	Cytarabine	146-166	protein phosphatase 1 regulatory subunit 10	Homo sapiens	285-322
16764854-7	2006	We report in this study that, when nontransformed CV1 epithelial cells and Hs578T breast cancer cells are treated with the chemotherapeutic agent cytosine arabinoside (Ara-C), Thr-821 of Rb is rapidly dephosphorylated concomitant with dissociation of the PP1 regulatory subunit PNUTS (phosphatase nuclear targeting subunit) from PP1 enzyme.	Cytarabine	146-166	inorganic pyrophosphatase 1	Homo sapiens	329-332
17052966-5	2006	After 48 and 72 hours treatment with daunorubicin and Ara-C, respectively, increased cell death was observed in THP-1 cells that were pretreated with FK866, as compared to cells exposed to antineoplastic drugs alone.	Cytarabine	54-59	GLI family zinc finger 2	Homo sapiens	112-117
16627756-1	2006	In the multinational IRIS study comparing imatinib with interferon plus cytarabine (IFN/Ara-C) in patients with newly diagnosed chronic-phase chronic myelogenous leukemia (CP CML), imatinib demonstrated significantly higher rates of complete cytogenetic responses (CCyRs) and improved progression-free survival (PFS).	Cytarabine	72-82	interferon alpha 1	Homo sapiens	84-87
16573743-1	2006	The cytotoxic effect of cytarabine (Ara-C) on myeloid leukemic cells is enhanced by concomitant use of granulocyte colony-stimulating factor (G-CSF) in vitro.	Cytarabine	24-34	colony stimulating factor 3	Homo sapiens	103-140
16863913-7	2006	Also, mice injected with CXCL8, CXCL4, or the chimeric CXCL8/CXCL4 protein CXCL8M1 manifested accelerated recovery of absolute numbers of HPCs in response to the toxic effects of Ara-C administration.	Cytarabine	179-184	platelet factor 4	Mus musculus	32-37
16863913-7	2006	Also, mice injected with CXCL8, CXCL4, or the chimeric CXCL8/CXCL4 protein CXCL8M1 manifested accelerated recovery of absolute numbers of HPCs in response to the toxic effects of Ara-C administration.	Cytarabine	179-184	platelet factor 4	Mus musculus	61-66
16828706-8	2006	The [3H]uridine uptake via CNT2 was significantly decreased by the addition of cytarabin or gemcitabine, antimetabolites of cytidine analogue.	Cytarabine	79-88	solute carrier family 28 (sodium-coupled nucleoside transporter), member 2	Mus musculus	27-31
16403905-10	2006	Clofarabine plus cytarabine has activity in adult AML, achieving a good CR rate.	Cytarabine	17-27	C-reactive protein	Homo sapiens	72-74
16573743-1	2006	The cytotoxic effect of cytarabine (Ara-C) on myeloid leukemic cells is enhanced by concomitant use of granulocyte colony-stimulating factor (G-CSF) in vitro.	Cytarabine	24-34	colony stimulating factor 3	Homo sapiens	142-147
16573743-1	2006	The cytotoxic effect of cytarabine (Ara-C) on myeloid leukemic cells is enhanced by concomitant use of granulocyte colony-stimulating factor (G-CSF) in vitro.	Cytarabine	36-41	colony stimulating factor 3	Homo sapiens	103-140
16573743-1	2006	The cytotoxic effect of cytarabine (Ara-C) on myeloid leukemic cells is enhanced by concomitant use of granulocyte colony-stimulating factor (G-CSF) in vitro.	Cytarabine	36-41	colony stimulating factor 3	Homo sapiens	142-147
16573743-2	2006	The feasibility of a conditioning regimen consisting of G-CSF-combined 24 g/m2 Ara-C, 90 mg/m2 fludarabine, and 12 Gy total body irradiation was studied for five patients with acute myelogenous leukemia in cord blood transplantation (CBT).	Cytarabine	79-84	colony stimulating factor 3	Homo sapiens	56-61
16837911-1	2006	AIM: The goals of the study were to reveal the involvement of P-glycoprotein (P-gp), the product of multidrug resistance 1 gene (MDR1) in cellular resistance to vincristine (VCR) and investigate cross-resistance against cytosine arabinoside (Ara-C) in HL60 and HL60/VCR cell lines.	Cytarabine	220-240	ATP binding cassette subfamily B member 1	Homo sapiens	62-76
16818278-13	2006	INTERPRETATION AND CONCLUSIONS: In conclusion, our data indicate that Ara-C can induce apoptosis in resting G(O)-B-CLL cells using a mechanism independent of cell proliferation and DNA replication but associated with inhibition of RNA synthesis and downregulation of Mcl-1.	Cytarabine	70-75	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	267-272
16617163-6	2006	During prolonged drug exposures of CEM cells with hENT1 activity, araC was more cytotoxic than TaraC, whereas coexposures with nitrobenzylthioinosine (to pharmacologically block hENT1) yielded identical cytotoxicities for araC and TaraC.	Cytarabine	66-70	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	50-55
16805952-1	2006	This study aimed to investigate the gastrointestinal stability and the cellular uptake characteristics of L-valyl-ara-C, a peptidomimetic prodrug of ara-C (cytarabine).	Cytarabine	156-166	ATP binding cassette subfamily C member 6	Homo sapiens	114-117
16778368-1	2006	Resistance to cytosine arabinoside (Ara-C) is a major problem in the treatment of patients with acute myeloid leukemia (AML).	Cytarabine	14-34	ATP binding cassette subfamily C member 6	Homo sapiens	36-39
16395706-5	2006	Higher anti-L-Araf IgM levels in cHL patients were associated with cytosine arabinoside treatment (p &lt; 0.05).	Cytarabine	67-87	A-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	14-18
16180016-6	2006	Despite the fact that T-araC is a much poorer substrate, as compared to araC, for deoxycytidine kinase (the rate-limiting step in the formation of the triphosphates), similar intracellular concentrations of T-araC-5"-triphosphate (T-araCTP) and araCTP were formed in cells at these high, pharmacologically relevant concentrations due to similar Vmax"s.	Cytarabine	24-28	deoxycytidine kinase	Mus musculus	82-102
16837911-1	2006	AIM: The goals of the study were to reveal the involvement of P-glycoprotein (P-gp), the product of multidrug resistance 1 gene (MDR1) in cellular resistance to vincristine (VCR) and investigate cross-resistance against cytosine arabinoside (Ara-C) in HL60 and HL60/VCR cell lines.	Cytarabine	220-240	ATP binding cassette subfamily B member 1	Homo sapiens	78-82
16837911-1	2006	AIM: The goals of the study were to reveal the involvement of P-glycoprotein (P-gp), the product of multidrug resistance 1 gene (MDR1) in cellular resistance to vincristine (VCR) and investigate cross-resistance against cytosine arabinoside (Ara-C) in HL60 and HL60/VCR cell lines.	Cytarabine	220-240	ATP binding cassette subfamily B member 1	Homo sapiens	100-122
16837911-1	2006	AIM: The goals of the study were to reveal the involvement of P-glycoprotein (P-gp), the product of multidrug resistance 1 gene (MDR1) in cellular resistance to vincristine (VCR) and investigate cross-resistance against cytosine arabinoside (Ara-C) in HL60 and HL60/VCR cell lines.	Cytarabine	220-240	ATP binding cassette subfamily B member 1	Homo sapiens	129-133
16837911-1	2006	AIM: The goals of the study were to reveal the involvement of P-glycoprotein (P-gp), the product of multidrug resistance 1 gene (MDR1) in cellular resistance to vincristine (VCR) and investigate cross-resistance against cytosine arabinoside (Ara-C) in HL60 and HL60/VCR cell lines.	Cytarabine	242-247	ATP binding cassette subfamily B member 1	Homo sapiens	62-76
16837911-1	2006	AIM: The goals of the study were to reveal the involvement of P-glycoprotein (P-gp), the product of multidrug resistance 1 gene (MDR1) in cellular resistance to vincristine (VCR) and investigate cross-resistance against cytosine arabinoside (Ara-C) in HL60 and HL60/VCR cell lines.	Cytarabine	242-247	ATP binding cassette subfamily B member 1	Homo sapiens	78-82
16837911-1	2006	AIM: The goals of the study were to reveal the involvement of P-glycoprotein (P-gp), the product of multidrug resistance 1 gene (MDR1) in cellular resistance to vincristine (VCR) and investigate cross-resistance against cytosine arabinoside (Ara-C) in HL60 and HL60/VCR cell lines.	Cytarabine	242-247	ATP binding cassette subfamily B member 1	Homo sapiens	100-122
16837911-1	2006	AIM: The goals of the study were to reveal the involvement of P-glycoprotein (P-gp), the product of multidrug resistance 1 gene (MDR1) in cellular resistance to vincristine (VCR) and investigate cross-resistance against cytosine arabinoside (Ara-C) in HL60 and HL60/VCR cell lines.	Cytarabine	242-247	ATP binding cassette subfamily B member 1	Homo sapiens	129-133
16837911-6	2006	CONCLUSION: Aquired resistance to VCR and cross-resistance to Ara-C correlates with MDR1 gene expression in vitro.	Cytarabine	62-67	ATP binding cassette subfamily B member 1	Homo sapiens	84-88
16706835-7	2006	Intracerebroventricular infusion of cytosine-beta-d-arabiofuranoside (Ara-C) eliminated trophinin-positive cells in the SVZ.	Cytarabine	70-75	trophinin	Rattus norvegicus	88-97
16647569-0	2006	Trp53 loss during in vitro selection contributes to acquired Ara-C resistance in acute myeloid leukemia.	Cytarabine	61-66	transformation related protein 53	Mus musculus	0-5
16419075-0	2006	Competition of cytarabine and aspirin in binding to serum albumin in multidrug therapy.	Cytarabine	15-25	albumin	Homo sapiens	52-65
16647569-6	2006	p21Cip1 was dramatically downregulated and p53 protein accumulation induced by Ara-C treatment was impaired in one resistant line.	Cytarabine	79-84	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	0-7
16647569-6	2006	p21Cip1 was dramatically downregulated and p53 protein accumulation induced by Ara-C treatment was impaired in one resistant line.	Cytarabine	79-84	transformation related protein 53	Mus musculus	43-46
16647569-7	2006	In this line, repeated Ara-C exposure had selected for cells that harbor a genomic deletion affecting the splicing of Trp53 mRNA.	Cytarabine	23-28	transformation related protein 53	Mus musculus	118-123
16609362-1	2006	The human equilibrative nucleoside transporter 1 gene (hENT1) is the primary nucleoside transporter for cytosine arabinoside (AraC), a deoxycytidine analog used for treatment of acute leukemias and lymphomas.	Cytarabine	104-124	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	10-48
16609362-1	2006	The human equilibrative nucleoside transporter 1 gene (hENT1) is the primary nucleoside transporter for cytosine arabinoside (AraC), a deoxycytidine analog used for treatment of acute leukemias and lymphomas.	Cytarabine	104-124	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	55-60
16609362-1	2006	The human equilibrative nucleoside transporter 1 gene (hENT1) is the primary nucleoside transporter for cytosine arabinoside (AraC), a deoxycytidine analog used for treatment of acute leukemias and lymphomas.	Cytarabine	126-130	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	10-48
16609362-1	2006	The human equilibrative nucleoside transporter 1 gene (hENT1) is the primary nucleoside transporter for cytosine arabinoside (AraC), a deoxycytidine analog used for treatment of acute leukemias and lymphomas.	Cytarabine	126-130	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	55-60
16609362-10	2006	hENT1 promoter region haplotypes may influence gene expression and alter AraC chemosensitivity.	Cytarabine	73-77	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	0-5
16419075-1	2006	The aim of this study was to describe a competition between cytarabine (araC) and aspirin (ASA) in binding with bovine serum albumin (BSA).	Cytarabine	60-70	albumin	Homo sapiens	119-132
16419075-1	2006	The aim of this study was to describe a competition between cytarabine (araC) and aspirin (ASA) in binding with bovine serum albumin (BSA).	Cytarabine	72-76	albumin	Homo sapiens	119-132
16581899-0	2006	Cytosine arabinoside induces programmed endothelial cell death through the caspase-3 pathway.	Cytarabine	0-20	caspase 3	Homo sapiens	75-84
16581899-14	2006	Caspase-3 activity increased after ARA-C addition; hydrocortisone blunted this increase.	Cytarabine	35-40	caspase 3	Homo sapiens	0-9
16581899-16	2006	Hydrocortisone may protect against ARA-C-induced apoptosis by reducing caspase-3 activity.	Cytarabine	35-40	caspase 3	Homo sapiens	71-80
16249385-6	2006	CMK sublines, transfected with the BST2 cDNA and incubated with HS-5 bone marrow stromal cells, exhibited up to 1.7-fold reduced cytosine arabinoside (ara-C)-induced apoptosis, compared with mock-transfected cells.	Cytarabine	129-149	C-X-C motif chemokine ligand 9	Homo sapiens	0-3
16482209-0	2006	Targeting Hsp90 by 17-AAG in leukemia cells: mechanisms for synergistic and antagonistic drug combinations with arsenic trioxide and Ara-C.	Cytarabine	133-138	heat shock protein 90 alpha family class A member 1	Homo sapiens	10-15
16482209-0	2006	Targeting Hsp90 by 17-AAG in leukemia cells: mechanisms for synergistic and antagonistic drug combinations with arsenic trioxide and Ara-C.	Cytarabine	133-138	N-methylpurine DNA glycosylase	Homo sapiens	22-25
16482209-3	2006	Here we report that 17-AAG has striking opposite effects on the activity of arsenic trioxide (ATO) and ara-C.	Cytarabine	103-108	N-methylpurine DNA glycosylase	Homo sapiens	23-26
16482209-7	2006	In contrast, treatment of leukemia cells with 17-AAG caused a G1 arrest, a decrease in DNA synthesis and reduced ara-C incorporation into DNA, leading to antagonism.	Cytarabine	113-118	N-methylpurine DNA glycosylase	Homo sapiens	49-52
16478523-3	2006	Using rat sympathetic neurons as an in vitro model of neuronal apoptosis, we show that cytosine arabinoside is a DNA damaging drug that induces the expression of the BH3-only pro-apoptotic genes Noxa, Puma and Bim.	Cytarabine	87-107	phorbol-12-myristate-13-acetate-induced protein 1	Rattus norvegicus	195-199
16364248-5	2006	Transduced HURP was capable of specifically enhancing the chemosensitivity of deoxycytosine analogs, such as gemcitabine, ARA-C, and 5-AZA-CdR, but neither had an effect on the response of DNA intercalating agents, such as cisplatin, carboplatin, and doxorubicin, nor on the response of microtubule stabilizers, such as paclitaxel, docetaxel, and vinblastine.	Cytarabine	122-127	DLG associated protein 5	Mus musculus	11-15
16609039-15	2006	Cytarabine and daunorubicin interfered with EPO signaling in F-MEL cells.	Cytarabine	0-10	erythropoietin	Homo sapiens	44-47
16293603-2	2006	Activation of Chk1 in response to cytarabine (ara-C) induced an S-phase checkpoint characterized by the inhibition of Cdk2, cell cycle arrest, no change in constitutively active Akt, or low-stress kinase signaling in ML-1 cells.	Cytarabine	34-44	checkpoint kinase 1	Homo sapiens	14-18
16293603-2	2006	Activation of Chk1 in response to cytarabine (ara-C) induced an S-phase checkpoint characterized by the inhibition of Cdk2, cell cycle arrest, no change in constitutively active Akt, or low-stress kinase signaling in ML-1 cells.	Cytarabine	34-44	cyclin dependent kinase 2	Homo sapiens	118-122
16293603-2	2006	Activation of Chk1 in response to cytarabine (ara-C) induced an S-phase checkpoint characterized by the inhibition of Cdk2, cell cycle arrest, no change in constitutively active Akt, or low-stress kinase signaling in ML-1 cells.	Cytarabine	46-51	checkpoint kinase 1	Homo sapiens	14-18
16293603-2	2006	Activation of Chk1 in response to cytarabine (ara-C) induced an S-phase checkpoint characterized by the inhibition of Cdk2, cell cycle arrest, no change in constitutively active Akt, or low-stress kinase signaling in ML-1 cells.	Cytarabine	46-51	cyclin dependent kinase 2	Homo sapiens	118-122
16293603-7	2006	Constitutively phosphorylated Akt kinase declined on addition of UCN-01 to the ara-C infusion, an action accompanied by an activation of JNK and reduction in absolute AML blast counts.	Cytarabine	79-84	AKT serine/threonine kinase 1	Homo sapiens	30-33
16293603-7	2006	Constitutively phosphorylated Akt kinase declined on addition of UCN-01 to the ara-C infusion, an action accompanied by an activation of JNK and reduction in absolute AML blast counts.	Cytarabine	79-84	mitogen-activated protein kinase 8	Homo sapiens	137-140
16293603-8	2006	Thus, use of UCN-01 in combination with ara-C decreases Chk1 phosphorylation, inhibits the Akt survival pathway, and activates JNK during the course of therapy, offering a rationale for the cytotoxic action of this combination during AML treatment.	Cytarabine	40-45	checkpoint kinase 1	Homo sapiens	56-60
16293603-8	2006	Thus, use of UCN-01 in combination with ara-C decreases Chk1 phosphorylation, inhibits the Akt survival pathway, and activates JNK during the course of therapy, offering a rationale for the cytotoxic action of this combination during AML treatment.	Cytarabine	40-45	AKT serine/threonine kinase 1	Homo sapiens	91-94
16293603-8	2006	Thus, use of UCN-01 in combination with ara-C decreases Chk1 phosphorylation, inhibits the Akt survival pathway, and activates JNK during the course of therapy, offering a rationale for the cytotoxic action of this combination during AML treatment.	Cytarabine	40-45	mitogen-activated protein kinase 8	Homo sapiens	127-130
16430862-5	2006	Our results showed that JWA was not only regulated by ATRA but also by several other differentiation inducers such as phorbol-12-myristate-13-acetate (TPA), arabinoside (Ara-C), and hemin, involved in the mechanisms of differentiation along different lineages of myeloid leukemia cells arrested at different stages of development.	Cytarabine	170-175	ADP ribosylation factor like GTPase 6 interacting protein 5	Homo sapiens	24-27
16538382-9	2006	The phosphate conjugated 5-FdUrd-araC heterodimer (5-Fluoro-2"-desoxyuridylyl-(3"--&gt;5")-Arabinocytidine), which is a prodrug of AraC-monophosphate, reactivated AIF and down-regulated cyclin D1 in AraC-resistant cells and circumvented resistance to apoptosis and to cell cycle inhibition.	Cytarabine	131-135	cyclin D1	Homo sapiens	186-195
16112192-4	2006	Therefore, the present study was performed to evaluate whether stem cell factor-antibody (anti-SCF) can enhance the efficacy of the two main chemotherapeutic drugs used in AML therapy: cytarabine and daunorubicin at low doses in human-resistant CD34+ AML cells, in an attempt to identify a novel effective regimen with tolerable side-effects for elderly AML patients.	Cytarabine	185-195	KIT ligand	Homo sapiens	95-98
16112192-6	2006	Anti-SCF has significantly enhanced the low dose cytarabine- and daunorubicin-induced apoptosis+necrosis in KG1a CD34+ AML cells from 12.0+/-1.7 to 40.9+/-5.9% and from 16.3+/-0.9 to 48.9+/-1.0%, respectively, p&lt;0.01.	Cytarabine	49-59	KIT ligand	Homo sapiens	5-8
16112192-6	2006	Anti-SCF has significantly enhanced the low dose cytarabine- and daunorubicin-induced apoptosis+necrosis in KG1a CD34+ AML cells from 12.0+/-1.7 to 40.9+/-5.9% and from 16.3+/-0.9 to 48.9+/-1.0%, respectively, p&lt;0.01.	Cytarabine	49-59	CD34 molecule	Homo sapiens	113-117
16112192-7	2006	It has also exerted its significant enhancement activity on the low dose cytarabine- and daunorubicin-induced apoptosis+necrosis in KG1a CD34+ AML cells in the presence of SCF, p&lt;0.05.	Cytarabine	73-83	CD34 molecule	Homo sapiens	137-141
16112192-8	2006	Anti-SCF has significantly enhanced the low dose cytarabine- and daunorubicin-induced bcl-2 reduction in KG1a CD34+ AML cells from 26.7+/-0.6 to 64.6+/-1.0% and from 59.8+/-3.1 to 80.1+/-7.9%, respectively, p&lt;0.01.	Cytarabine	49-59	KIT ligand	Homo sapiens	5-8
16112192-8	2006	Anti-SCF has significantly enhanced the low dose cytarabine- and daunorubicin-induced bcl-2 reduction in KG1a CD34+ AML cells from 26.7+/-0.6 to 64.6+/-1.0% and from 59.8+/-3.1 to 80.1+/-7.9%, respectively, p&lt;0.01.	Cytarabine	49-59	BCL2 apoptosis regulator	Homo sapiens	86-91
16112192-8	2006	Anti-SCF has significantly enhanced the low dose cytarabine- and daunorubicin-induced bcl-2 reduction in KG1a CD34+ AML cells from 26.7+/-0.6 to 64.6+/-1.0% and from 59.8+/-3.1 to 80.1+/-7.9%, respectively, p&lt;0.01.	Cytarabine	49-59	CD34 molecule	Homo sapiens	110-114
16112192-10	2006	Anti-SCF has also significantly enhanced the low dose cytarabine- and daunorubicin-induced bcl-2 reduction in KG1a CD34+ AML cells in the presence of SCF, p&lt;0.05.	Cytarabine	54-64	KIT ligand	Homo sapiens	5-8
16112192-10	2006	Anti-SCF has also significantly enhanced the low dose cytarabine- and daunorubicin-induced bcl-2 reduction in KG1a CD34+ AML cells in the presence of SCF, p&lt;0.05.	Cytarabine	54-64	BCL2 apoptosis regulator	Homo sapiens	91-96
16112192-10	2006	Anti-SCF has also significantly enhanced the low dose cytarabine- and daunorubicin-induced bcl-2 reduction in KG1a CD34+ AML cells in the presence of SCF, p&lt;0.05.	Cytarabine	54-64	CD34 molecule	Homo sapiens	115-119
16112192-10	2006	Anti-SCF has also significantly enhanced the low dose cytarabine- and daunorubicin-induced bcl-2 reduction in KG1a CD34+ AML cells in the presence of SCF, p&lt;0.05.	Cytarabine	54-64	KIT ligand	Homo sapiens	150-153
16200630-2	2006	APE (cytosine arabinoside, cisplatin, etoposide) is a non-cross-resistant regimen with limited toxicities.	Cytarabine	5-25	apurinic/apyrimidinic endodeoxyribonuclease 1	Homo sapiens	0-3
16200630-4	2006	METHODS: Patients with recurrent Hodgkin disease who were &lt;or=21 years of age and had previously received standard alkylating agent and doxorubicin-based therapy, were treated with APE chemotherapy (cytosine arabinoside 750 mg/m(2), cisplatin 15 mg/m(2), etoposide 20 mg/m(2)) every 12 hr, administered three or four times per cycle.	Cytarabine	202-222	apurinic/apyrimidinic endodeoxyribonuclease 1	Homo sapiens	184-187
16249385-6	2006	CMK sublines, transfected with the BST2 cDNA and incubated with HS-5 bone marrow stromal cells, exhibited up to 1.7-fold reduced cytosine arabinoside (ara-C)-induced apoptosis, compared with mock-transfected cells.	Cytarabine	129-149	bone marrow stromal cell antigen 2	Homo sapiens	35-39
16249385-6	2006	CMK sublines, transfected with the BST2 cDNA and incubated with HS-5 bone marrow stromal cells, exhibited up to 1.7-fold reduced cytosine arabinoside (ara-C)-induced apoptosis, compared with mock-transfected cells.	Cytarabine	151-156	C-X-C motif chemokine ligand 9	Homo sapiens	0-3
16249385-6	2006	CMK sublines, transfected with the BST2 cDNA and incubated with HS-5 bone marrow stromal cells, exhibited up to 1.7-fold reduced cytosine arabinoside (ara-C)-induced apoptosis, compared with mock-transfected cells.	Cytarabine	151-156	bone marrow stromal cell antigen 2	Homo sapiens	35-39
16611405-3	2006	GrB/scFvMEL showed synergistic cytotoxicity when coadministered with doxorubicin, vincristine or cisplatin, and additive effects, in combination with etoposide or cytarabine.	Cytarabine	163-173	granzyme B	Homo sapiens	0-3
16467107-7	2006	The combination of pralatrexate and gemcitabine was superior to any methotrexate and ara-C combination in inducing apoptosis and in activating caspase-3.	Cytarabine	85-90	caspase 3	Homo sapiens	143-152
16307021-0	2006	Nfl gene inactivation in acute myeloid leukemia cells confers cytarabine resistance through MAPK and mTOR pathways.	Cytarabine	62-72	neurofilament light chain	Homo sapiens	0-3
16307021-0	2006	Nfl gene inactivation in acute myeloid leukemia cells confers cytarabine resistance through MAPK and mTOR pathways.	Cytarabine	62-72	mechanistic target of rapamycin kinase	Homo sapiens	101-105
16219908-3	2006	In contrast, Bcl-2 and Bcl-x(L) largely blocked these events in cells exposed to the cytotoxic agent 1-beta-d-arabinofuranosylcytosine (ara-C).	Cytarabine	101-134	BCL2 apoptosis regulator	Homo sapiens	13-18
16219908-3	2006	In contrast, Bcl-2 and Bcl-x(L) largely blocked these events in cells exposed to the cytotoxic agent 1-beta-d-arabinofuranosylcytosine (ara-C).	Cytarabine	101-134	BCL2 like 1	Homo sapiens	23-28
16219908-3	2006	In contrast, Bcl-2 and Bcl-x(L) largely blocked these events in cells exposed to the cytotoxic agent 1-beta-d-arabinofuranosylcytosine (ara-C).	Cytarabine	136-141	BCL2 apoptosis regulator	Homo sapiens	13-18
16219908-3	2006	In contrast, Bcl-2 and Bcl-x(L) largely blocked these events in cells exposed to the cytotoxic agent 1-beta-d-arabinofuranosylcytosine (ara-C).	Cytarabine	136-141	BCL2 like 1	Homo sapiens	23-28
16219908-5	2006	Ectopic expression of a phosphorylation loop-deleted Bcl-2 or Bcl-2 lacking the serine(70) phosphorylation site, which dramatically protected cells from ara-C lethality, delayed but did not prevent flavopiridol/HDAC inhibitor-induced mitochondrial injury, cell death, or loss of clonogenicity.	Cytarabine	153-158	BCL2 apoptosis regulator	Homo sapiens	53-58
16219908-5	2006	Ectopic expression of a phosphorylation loop-deleted Bcl-2 or Bcl-2 lacking the serine(70) phosphorylation site, which dramatically protected cells from ara-C lethality, delayed but did not prevent flavopiridol/HDAC inhibitor-induced mitochondrial injury, cell death, or loss of clonogenicity.	Cytarabine	153-158	BCL2 apoptosis regulator	Homo sapiens	62-67
16333246-10	2005	In conclusion, decreased expression of hENT1, which transports ara-C across the cell membrane, appears to be a major factor in ara-C resistance in childhood AML.	Cytarabine	63-68	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	39-44
16944754-4	2006	RESULTS: Cytarabine effects manifested with EC-induced expression of cell surface P- and E-selectines and VCAM-1; ICAM-1 expression rapidly enhanced, leukocyte adhesion to endothelium also activates.	Cytarabine	9-19	vascular cell adhesion molecule 1	Homo sapiens	106-112
16944754-4	2006	RESULTS: Cytarabine effects manifested with EC-induced expression of cell surface P- and E-selectines and VCAM-1; ICAM-1 expression rapidly enhanced, leukocyte adhesion to endothelium also activates.	Cytarabine	9-19	intercellular adhesion molecule 1	Homo sapiens	114-120
16333246-6	2005	Human equilibrative nucleoside transporter-1 (hENT1) mRNA expression and ara-C sensitivity were significantly correlated (rp=-0.46; P=0.001), with three-fold lower hENT1 mRNA levels in resistant patients (P=0.003).	Cytarabine	73-78	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	46-51
16333246-6	2005	Human equilibrative nucleoside transporter-1 (hENT1) mRNA expression and ara-C sensitivity were significantly correlated (rp=-0.46; P=0.001), with three-fold lower hENT1 mRNA levels in resistant patients (P=0.003).	Cytarabine	73-78	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	164-169
16333246-10	2005	In conclusion, decreased expression of hENT1, which transports ara-C across the cell membrane, appears to be a major factor in ara-C resistance in childhood AML.	Cytarabine	127-132	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	39-44
16126823-6	2005	Cells lacking Rad9, Chk1, or ATR were more sensitive to gemcitabine and cytarabine, consistent with the fact that these agents stall replication forks, and this sensitization was independent of p53 status.	Cytarabine	72-82	RAD9 checkpoint clamp component A	Homo sapiens	14-18
16304576-1	2005	Overexpression of the detoxifying enzyme cytidine deaminase (CDD) renders normal and leukemic hematopoietic cells resistant to cytarabine (1-beta-D-arabinofuranosylcytosine), and studies on murine cells have suggested transgenic CDD overexpression as a way to reduce the substantial myelotoxicity induced by the deoxycytidine analogs cytarabine and gemcitabine (2",2"-difluorodeoxycytidine).	Cytarabine	334-344	cytidine deaminase	Mus musculus	41-59
16304576-1	2005	Overexpression of the detoxifying enzyme cytidine deaminase (CDD) renders normal and leukemic hematopoietic cells resistant to cytarabine (1-beta-D-arabinofuranosylcytosine), and studies on murine cells have suggested transgenic CDD overexpression as a way to reduce the substantial myelotoxicity induced by the deoxycytidine analogs cytarabine and gemcitabine (2",2"-difluorodeoxycytidine).	Cytarabine	334-344	cytidine deaminase	Mus musculus	61-64
16304576-3	2005	Retroviral gene transfer significantly increased the resistance of CDD-transduced cord blood and peripheral blood-derived progenitor cells for doses ranging from 20-100 nM cytarabine and 8-10 nM gemcitabine.	Cytarabine	172-182	cytidine deaminase	Homo sapiens	67-70
16304576-5	2005	In addition, significant selection of CDD-transduced cells was obtained after a 4-day culture in 30-100 nM cytarabine.	Cytarabine	107-117	cytidine deaminase	Homo sapiens	38-41
16304576-6	2005	Thus, our data demonstrate that overexpression of CDD cDNA results in significant protection of human progenitors from cytarabine- as well as gemcitabine-induced toxicity, and allows in vitro selection of transduced cells.	Cytarabine	119-129	cytidine deaminase	Homo sapiens	50-53
16304576-1	2005	Overexpression of the detoxifying enzyme cytidine deaminase (CDD) renders normal and leukemic hematopoietic cells resistant to cytarabine (1-beta-D-arabinofuranosylcytosine), and studies on murine cells have suggested transgenic CDD overexpression as a way to reduce the substantial myelotoxicity induced by the deoxycytidine analogs cytarabine and gemcitabine (2",2"-difluorodeoxycytidine).	Cytarabine	127-137	cytidine deaminase	Mus musculus	41-59
16304576-1	2005	Overexpression of the detoxifying enzyme cytidine deaminase (CDD) renders normal and leukemic hematopoietic cells resistant to cytarabine (1-beta-D-arabinofuranosylcytosine), and studies on murine cells have suggested transgenic CDD overexpression as a way to reduce the substantial myelotoxicity induced by the deoxycytidine analogs cytarabine and gemcitabine (2",2"-difluorodeoxycytidine).	Cytarabine	127-137	cytidine deaminase	Mus musculus	61-64
16304576-1	2005	Overexpression of the detoxifying enzyme cytidine deaminase (CDD) renders normal and leukemic hematopoietic cells resistant to cytarabine (1-beta-D-arabinofuranosylcytosine), and studies on murine cells have suggested transgenic CDD overexpression as a way to reduce the substantial myelotoxicity induced by the deoxycytidine analogs cytarabine and gemcitabine (2",2"-difluorodeoxycytidine).	Cytarabine	139-172	cytidine deaminase	Mus musculus	41-59
16304576-1	2005	Overexpression of the detoxifying enzyme cytidine deaminase (CDD) renders normal and leukemic hematopoietic cells resistant to cytarabine (1-beta-D-arabinofuranosylcytosine), and studies on murine cells have suggested transgenic CDD overexpression as a way to reduce the substantial myelotoxicity induced by the deoxycytidine analogs cytarabine and gemcitabine (2",2"-difluorodeoxycytidine).	Cytarabine	139-172	cytidine deaminase	Mus musculus	61-64
16126823-6	2005	Cells lacking Rad9, Chk1, or ATR were more sensitive to gemcitabine and cytarabine, consistent with the fact that these agents stall replication forks, and this sensitization was independent of p53 status.	Cytarabine	72-82	checkpoint kinase 1	Homo sapiens	20-24
16126823-6	2005	Cells lacking Rad9, Chk1, or ATR were more sensitive to gemcitabine and cytarabine, consistent with the fact that these agents stall replication forks, and this sensitization was independent of p53 status.	Cytarabine	72-82	ATR serine/threonine kinase	Homo sapiens	29-32
16126823-8	2005	Together, these results demonstrate that 1) gemcitabine triggers both checkpoint signaling pathways, 2) both pathways contribute to cell survival after gemcitabine-induced replication stress, and 3) although gemcitabine and cytarabine both stall replication forks, ATM plays differential roles in cell survival after treatment with these agents.	Cytarabine	224-234	ATM serine/threonine kinase	Homo sapiens	265-268
15936818-0	2005	Increase in Ara-C cytotoxicity in the presence of valproate, a histone deacetylase inhibitor, is associated with the concurrent expression of cyclin D1 and p27(Kip 1) in acute myeloblastic leukemia cells.	Cytarabine	12-17	cyclin D1	Homo sapiens	142-151
16288046-6	2005	Pretreatment with 17-AAG, which induced hsp70, inhibited 1-beta-D-arabinofuranosylcytosine or etoposide-induced apoptosis in HL-60 cells.	Cytarabine	57-90	N-methylpurine DNA glycosylase	Homo sapiens	21-24
16288046-6	2005	Pretreatment with 17-AAG, which induced hsp70, inhibited 1-beta-D-arabinofuranosylcytosine or etoposide-induced apoptosis in HL-60 cells.	Cytarabine	57-90	heat shock protein family A (Hsp70) member 4	Homo sapiens	40-45
16014563-9	2005	MDM2 inhibition synergistically enhanced cytotoxicity of cytosine arabinoside and doxorubicin in AML blasts but not in normal hematopoietic progenitor cells.	Cytarabine	57-77	transformed mouse 3T3 cell double minute 2	Mus musculus	0-4
16094422-8	2005	The LYL1-transfected U937 cells were also more resistant to the cytotoxic drug cytarabine.	Cytarabine	79-89	LYL1 basic helix-loop-helix family member	Homo sapiens	4-8
15936818-0	2005	Increase in Ara-C cytotoxicity in the presence of valproate, a histone deacetylase inhibitor, is associated with the concurrent expression of cyclin D1 and p27(Kip 1) in acute myeloblastic leukemia cells.	Cytarabine	12-17	interferon alpha inducible protein 27	Homo sapiens	156-159
15936818-0	2005	Increase in Ara-C cytotoxicity in the presence of valproate, a histone deacetylase inhibitor, is associated with the concurrent expression of cyclin D1 and p27(Kip 1) in acute myeloblastic leukemia cells.	Cytarabine	12-17	cyclin dependent kinase inhibitor 1B	Homo sapiens	160-165
15936818-4	2005	Valproate induced a clear G1 phase arrest and up-regulated cyclin D1 expression in the presence of Ara-C and etoposide.	Cytarabine	99-104	cyclin D1	Homo sapiens	59-68
15936818-5	2005	In addition, valporate was able to block the Ara-C-induced down-regulation of p27(Kip1) expression but not that induced by etoposide.	Cytarabine	45-50	interferon alpha inducible protein 27	Homo sapiens	78-81
15936818-5	2005	In addition, valporate was able to block the Ara-C-induced down-regulation of p27(Kip1) expression but not that induced by etoposide.	Cytarabine	45-50	cyclin dependent kinase inhibitor 1B	Homo sapiens	82-86
16254185-4	2005	Coadministration of the mitotic blocker cytosine-beta-d-arabinofuranoside (Ara-C) eliminates the proliferation of neural cells and abrogates the long-term, but not the short-term, effect of CNTF on body weight.	Cytarabine	40-73	ciliary neurotrophic factor	Mus musculus	190-194
16254185-4	2005	Coadministration of the mitotic blocker cytosine-beta-d-arabinofuranoside (Ara-C) eliminates the proliferation of neural cells and abrogates the long-term, but not the short-term, effect of CNTF on body weight.	Cytarabine	75-80	ciliary neurotrophic factor	Mus musculus	190-194
16277846-0	2005	[JWA gene in regulating committed differentiation of HL-60 cells induced by ATRA, Ara-C and TPA].	Cytarabine	82-87	ADP ribosylation factor like GTPase 6 interacting protein 5	Homo sapiens	1-4
16277846-9	2005	In this study, we also exposed HL-60 cells in higher dose of Ara-C (20 ng/ml), and JWA expression underwent opposite trend comparing with in lower dose of Ara-C (10 ng/ml).	Cytarabine	155-160	ADP ribosylation factor like GTPase 6 interacting protein 5	Homo sapiens	83-86
16197446-1	2005	Fludarabine plus cytarabine (Ara-C) and idarubicin (FLAI) is an effective and well-tolerated induction regimen for the treatment of acute myeloid leukaemia (AML).	Cytarabine	17-27	ATP binding cassette subfamily C member 6	Homo sapiens	29-32
16277846-2	2005	By using FCM, the changes of CD13, CD14, CD15, CD11b and cell cycles were detected in HL-60 cells treated with ATRA (10(-6) mol/L), Ara-C (10 ng/ml) and TPA (10(-8) mol/L) respectively.	Cytarabine	132-137	fucosyltransferase 4	Homo sapiens	41-45
16277846-2	2005	By using FCM, the changes of CD13, CD14, CD15, CD11b and cell cycles were detected in HL-60 cells treated with ATRA (10(-6) mol/L), Ara-C (10 ng/ml) and TPA (10(-8) mol/L) respectively.	Cytarabine	132-137	integrin subunit alpha M	Homo sapiens	47-52
16277846-2	2005	By using FCM, the changes of CD13, CD14, CD15, CD11b and cell cycles were detected in HL-60 cells treated with ATRA (10(-6) mol/L), Ara-C (10 ng/ml) and TPA (10(-8) mol/L) respectively.	Cytarabine	132-137	alanyl aminopeptidase, membrane	Homo sapiens	29-33
16277846-2	2005	By using FCM, the changes of CD13, CD14, CD15, CD11b and cell cycles were detected in HL-60 cells treated with ATRA (10(-6) mol/L), Ara-C (10 ng/ml) and TPA (10(-8) mol/L) respectively.	Cytarabine	132-137	CD14 molecule	Homo sapiens	35-39
16044347-2	2005	H9-araC cells obtained by cultivation of H9 cells in the presence of 0.5 microM arabinosylcytosine (araC) had lower deoxycytidine kinase (dCK) than the parental cell line.	Cytarabine	80-98	deoxycytidine kinase	Homo sapiens	116-136
15856358-2	2005	Synergistic interaction between FAMP or 2-CdA with cytarabine (cytosine arabinoside, Ara-C) has been demonstrated in preclinical and clinical studies.	Cytarabine	51-61	cytidine deaminase	Homo sapiens	42-45
15856358-2	2005	Synergistic interaction between FAMP or 2-CdA with cytarabine (cytosine arabinoside, Ara-C) has been demonstrated in preclinical and clinical studies.	Cytarabine	63-83	cytidine deaminase	Homo sapiens	42-45
15856358-2	2005	Synergistic interaction between FAMP or 2-CdA with cytarabine (cytosine arabinoside, Ara-C) has been demonstrated in preclinical and clinical studies.	Cytarabine	85-90	cytidine deaminase	Homo sapiens	42-45
16144928-20	2005	This branched 40-kDa PEG-IFN was well tolerated both as a monotherapy as well as in combination with ara-C.	Cytarabine	101-106	interferon alpha 1	Homo sapiens	25-28
16190908-3	2005	We demonstrate that telencephalic cells from embryonic Gli3Xt/Xt embryos survive better and are more resistant to death induced by cytosine arabinoside, a nucleoside analogue that induces death in neuronal progenitors and neurons, than are control counterparts in vitro.	Cytarabine	131-151	GLI-Kruppel family member GLI3	Mus musculus	55-64
16044347-2	2005	H9-araC cells obtained by cultivation of H9 cells in the presence of 0.5 microM arabinosylcytosine (araC) had lower deoxycytidine kinase (dCK) than the parental cell line.	Cytarabine	80-98	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	138-141
16044347-2	2005	H9-araC cells obtained by cultivation of H9 cells in the presence of 0.5 microM arabinosylcytosine (araC) had lower deoxycytidine kinase (dCK) than the parental cell line.	Cytarabine	3-7	deoxycytidine kinase	Homo sapiens	116-136
16044347-2	2005	H9-araC cells obtained by cultivation of H9 cells in the presence of 0.5 microM arabinosylcytosine (araC) had lower deoxycytidine kinase (dCK) than the parental cell line.	Cytarabine	3-7	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	138-141
16044347-7	2005	CdA metabolic studies (influx and activation) in the presence of deoxyadenosine, deoxycytidine, or araC suggested that CdA enters cells by a deoxyadenosine-inhibitable transport system, which is different than that of araC and deoxycytidine transport system.	Cytarabine	99-103	cytidine deaminase	Homo sapiens	0-3
16044347-7	2005	CdA metabolic studies (influx and activation) in the presence of deoxyadenosine, deoxycytidine, or araC suggested that CdA enters cells by a deoxyadenosine-inhibitable transport system, which is different than that of araC and deoxycytidine transport system.	Cytarabine	99-103	cytidine deaminase	Homo sapiens	119-122
16044347-7	2005	CdA metabolic studies (influx and activation) in the presence of deoxyadenosine, deoxycytidine, or araC suggested that CdA enters cells by a deoxyadenosine-inhibitable transport system, which is different than that of araC and deoxycytidine transport system.	Cytarabine	218-222	cytidine deaminase	Homo sapiens	0-3
16044347-7	2005	CdA metabolic studies (influx and activation) in the presence of deoxyadenosine, deoxycytidine, or araC suggested that CdA enters cells by a deoxyadenosine-inhibitable transport system, which is different than that of araC and deoxycytidine transport system.	Cytarabine	218-222	cytidine deaminase	Homo sapiens	119-122
15950950-3	2005	The expression of the dCK gene in araC resistant cells was reduced to 60% of H9 cells, which correlated with lower dCK protein and activity.	Cytarabine	34-38	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	22-25
16077982-6	2005	To investigate the possible molecular mechanism of the protective effect, the influence of Jagged1 on Ara-C-induced activation of caspase-3 and PARP, and dephosphorylation of NF-kappaB was examined in NB4 cells.	Cytarabine	102-107	jagged canonical Notch ligand 1	Homo sapiens	91-98
16077982-6	2005	To investigate the possible molecular mechanism of the protective effect, the influence of Jagged1 on Ara-C-induced activation of caspase-3 and PARP, and dephosphorylation of NF-kappaB was examined in NB4 cells.	Cytarabine	102-107	caspase 3	Homo sapiens	130-139
16077982-6	2005	To investigate the possible molecular mechanism of the protective effect, the influence of Jagged1 on Ara-C-induced activation of caspase-3 and PARP, and dephosphorylation of NF-kappaB was examined in NB4 cells.	Cytarabine	102-107	poly(ADP-ribose) polymerase 1	Homo sapiens	144-148
15950950-3	2005	The expression of the dCK gene in araC resistant cells was reduced to 60% of H9 cells, which correlated with lower dCK protein and activity.	Cytarabine	34-38	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	115-118
16194358-1	2005	OBJECTIVE: To explore the feasibility of transferring fusion gene of dihydrofolate reductase (DHFR) gene and cytidine deaminase (CD) gene into mouse bone marrow cells in order to observe the drug resistance of high dose methotrexate (MTX) and cytosine arabinoside (Ara-C) in the bone marrow cells and to improve the tolerance of myelosuppression following combination chemotherapy.	Cytarabine	243-263	dihydrofolate reductase	Mus musculus	69-92
16129037-7	2005	It is concluded that Ara-c can effectively induce apoptosis of HL-60 cells and simultaneously decrease the level of expression of Bcl-2 protein and elevate the level of expression of Bax protein.	Cytarabine	21-26	BCL2 apoptosis regulator	Homo sapiens	130-135
16129037-7	2005	It is concluded that Ara-c can effectively induce apoptosis of HL-60 cells and simultaneously decrease the level of expression of Bcl-2 protein and elevate the level of expression of Bax protein.	Cytarabine	21-26	BCL2 associated X, apoptosis regulator	Homo sapiens	183-186
16129037-8	2005	Decrease of expression ratio of Bcl-2/Bax proteins may be one of the main mechanisms in HL-60 apoptosis induced by Ara-C.	Cytarabine	115-120	BCL2 apoptosis regulator	Homo sapiens	32-37
16129037-8	2005	Decrease of expression ratio of Bcl-2/Bax proteins may be one of the main mechanisms in HL-60 apoptosis induced by Ara-C.	Cytarabine	115-120	BCL2 associated X, apoptosis regulator	Homo sapiens	38-41
16194358-1	2005	OBJECTIVE: To explore the feasibility of transferring fusion gene of dihydrofolate reductase (DHFR) gene and cytidine deaminase (CD) gene into mouse bone marrow cells in order to observe the drug resistance of high dose methotrexate (MTX) and cytosine arabinoside (Ara-C) in the bone marrow cells and to improve the tolerance of myelosuppression following combination chemotherapy.	Cytarabine	243-263	dihydrofolate reductase	Mus musculus	94-98
16194358-1	2005	OBJECTIVE: To explore the feasibility of transferring fusion gene of dihydrofolate reductase (DHFR) gene and cytidine deaminase (CD) gene into mouse bone marrow cells in order to observe the drug resistance of high dose methotrexate (MTX) and cytosine arabinoside (Ara-C) in the bone marrow cells and to improve the tolerance of myelosuppression following combination chemotherapy.	Cytarabine	243-263	cytidine deaminase	Mus musculus	129-131
16194358-1	2005	OBJECTIVE: To explore the feasibility of transferring fusion gene of dihydrofolate reductase (DHFR) gene and cytidine deaminase (CD) gene into mouse bone marrow cells in order to observe the drug resistance of high dose methotrexate (MTX) and cytosine arabinoside (Ara-C) in the bone marrow cells and to improve the tolerance of myelosuppression following combination chemotherapy.	Cytarabine	265-270	dihydrofolate reductase	Mus musculus	69-92
16194358-1	2005	OBJECTIVE: To explore the feasibility of transferring fusion gene of dihydrofolate reductase (DHFR) gene and cytidine deaminase (CD) gene into mouse bone marrow cells in order to observe the drug resistance of high dose methotrexate (MTX) and cytosine arabinoside (Ara-C) in the bone marrow cells and to improve the tolerance of myelosuppression following combination chemotherapy.	Cytarabine	265-270	dihydrofolate reductase	Mus musculus	94-98
16194358-1	2005	OBJECTIVE: To explore the feasibility of transferring fusion gene of dihydrofolate reductase (DHFR) gene and cytidine deaminase (CD) gene into mouse bone marrow cells in order to observe the drug resistance of high dose methotrexate (MTX) and cytosine arabinoside (Ara-C) in the bone marrow cells and to improve the tolerance of myelosuppression following combination chemotherapy.	Cytarabine	265-270	cytidine deaminase	Mus musculus	129-131
16194358-6	2005	RESULTS: Bone marrow cells after coculture with the retroviral producer cells transduced with the genes (SFG-F/S-CD) showed the drug resistance colonies yield (Colony formation after exposure to Ara-C, MTX and Ara-C + MTX were 56%, 22% and 14%, respectively) and the increase in drug resistant to both MTX and Ara-C (P &lt; 0.005).	Cytarabine	195-200	cytidine deaminase	Mus musculus	113-115
16194358-6	2005	RESULTS: Bone marrow cells after coculture with the retroviral producer cells transduced with the genes (SFG-F/S-CD) showed the drug resistance colonies yield (Colony formation after exposure to Ara-C, MTX and Ara-C + MTX were 56%, 22% and 14%, respectively) and the increase in drug resistant to both MTX and Ara-C (P &lt; 0.005).	Cytarabine	210-215	cytidine deaminase	Mus musculus	113-115
16194358-6	2005	RESULTS: Bone marrow cells after coculture with the retroviral producer cells transduced with the genes (SFG-F/S-CD) showed the drug resistance colonies yield (Colony formation after exposure to Ara-C, MTX and Ara-C + MTX were 56%, 22% and 14%, respectively) and the increase in drug resistant to both MTX and Ara-C (P &lt; 0.005).	Cytarabine	210-215	cytidine deaminase	Mus musculus	113-115
15784732-0	2005	Heat shock protein 90 inhibition sensitizes acute myelogenous leukemia cells to cytarabine.	Cytarabine	80-90	heat shock protein 90 alpha family class A member 1	Homo sapiens	0-21
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.	Cytarabine	74-84	cytochrome c oxidase subunit 8A	Homo sapiens	19-22
15876539-1	2005	5"-Phosphorylation, catalyzed by human deoxycytidine kinase (dCK), is a crucial step in the metabolic activation of anticancer and antiviral nucleoside antimetabolites, such as cytarabine (AraC), gemcitabine, cladribine (CdA), and lamivudine.	Cytarabine	177-187	deoxycytidine kinase	Homo sapiens	39-59
15876539-1	2005	5"-Phosphorylation, catalyzed by human deoxycytidine kinase (dCK), is a crucial step in the metabolic activation of anticancer and antiviral nucleoside antimetabolites, such as cytarabine (AraC), gemcitabine, cladribine (CdA), and lamivudine.	Cytarabine	177-187	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	61-64
15876539-1	2005	5"-Phosphorylation, catalyzed by human deoxycytidine kinase (dCK), is a crucial step in the metabolic activation of anticancer and antiviral nucleoside antimetabolites, such as cytarabine (AraC), gemcitabine, cladribine (CdA), and lamivudine.	Cytarabine	177-187	cytidine deaminase	Homo sapiens	221-224
15876539-1	2005	5"-Phosphorylation, catalyzed by human deoxycytidine kinase (dCK), is a crucial step in the metabolic activation of anticancer and antiviral nucleoside antimetabolites, such as cytarabine (AraC), gemcitabine, cladribine (CdA), and lamivudine.	Cytarabine	189-193	deoxycytidine kinase	Homo sapiens	39-59
15876539-1	2005	5"-Phosphorylation, catalyzed by human deoxycytidine kinase (dCK), is a crucial step in the metabolic activation of anticancer and antiviral nucleoside antimetabolites, such as cytarabine (AraC), gemcitabine, cladribine (CdA), and lamivudine.	Cytarabine	189-193	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	61-64
15876539-1	2005	5"-Phosphorylation, catalyzed by human deoxycytidine kinase (dCK), is a crucial step in the metabolic activation of anticancer and antiviral nucleoside antimetabolites, such as cytarabine (AraC), gemcitabine, cladribine (CdA), and lamivudine.	Cytarabine	189-193	cytidine deaminase	Homo sapiens	221-224
15784732-4	2005	Cytarabine, at concentrations as low as 30 nM, caused activating phosphorylation of Chk1, loss of the phosphatase Cdc25A, and S-phase slowing.	Cytarabine	0-10	checkpoint kinase 1	Homo sapiens	84-88
15784732-4	2005	Cytarabine, at concentrations as low as 30 nM, caused activating phosphorylation of Chk1, loss of the phosphatase Cdc25A, and S-phase slowing.	Cytarabine	0-10	cell division cycle 25A	Homo sapiens	114-120
15935150-1	2005	Cytarabine (ara-C), a major antileukemic agent, is phosphorylated in the cell to cytarabine triphosphate (ara-CTP), which is then partly incorporated into DNA.	Cytarabine	0-10	solute carrier family 25 member 1	Homo sapiens	110-113
15784732-5	2005	Conversely, treatment with 100 to 300 nM 17-AAG for 24 hours caused Chk1 depletion that was accompanied by diminished cytarabine-induced S-phase accumulation, decreased Cdc25A degradation, and enhanced cytotoxicity as measured by inhibition of colony formation and induction of apoptosis.	Cytarabine	118-128	N-methylpurine DNA glycosylase	Homo sapiens	44-47
15784732-6	2005	Additional studies demonstrated that small inhibitory RNA (siRNA) depletion of Chk1 also sensitized cells to cytarabine, whereas disruption of the phosphatidylinositol 3-kinase (PI3k) signaling pathway, which is also blocked by Hsp90 inhibition, did not.	Cytarabine	109-119	checkpoint kinase 1	Homo sapiens	79-83
15784732-7	2005	Collectively, these results suggest that treatment with 17-AAG might represent a means of reversing checkpoint-mediated cytarabine resistance in AML.	Cytarabine	120-130	N-methylpurine DNA glycosylase	Homo sapiens	59-62
15935150-1	2005	Cytarabine (ara-C), a major antileukemic agent, is phosphorylated in the cell to cytarabine triphosphate (ara-CTP), which is then partly incorporated into DNA.	Cytarabine	12-17	solute carrier family 25 member 1	Homo sapiens	110-113
15935150-11	2005	ara-C incorporation into DNA appeared to be associated with intracellular retention of ara-CTP or persistence of plasma ara-C.	Cytarabine	0-5	solute carrier family 25 member 1	Homo sapiens	91-94
16158821-4	2005	Interestingly, L1210/F showed a modest level of cross-resistance to deoxycytidine analogues phosphorylated by dCK, for instance, 1-beta-D-arabinofuranosylcytosine (ara-C).	Cytarabine	129-162	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	110-113
16158821-4	2005	Interestingly, L1210/F showed a modest level of cross-resistance to deoxycytidine analogues phosphorylated by dCK, for instance, 1-beta-D-arabinofuranosylcytosine (ara-C).	Cytarabine	164-169	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	110-113
16158825-3	2005	Granulocyte colony-stimulating factor was infused continuously, starting 12 hours before Ara-C therapy and continuing until the end of Ara-C therapy.	Cytarabine	89-94	colony stimulating factor 3	Homo sapiens	0-37
16158825-3	2005	Granulocyte colony-stimulating factor was infused continuously, starting 12 hours before Ara-C therapy and continuing until the end of Ara-C therapy.	Cytarabine	135-140	colony stimulating factor 3	Homo sapiens	0-37
15815728-4	2005	Here we show that CML CD34(+) progenitors are sensitive to several apoptosis-inducing stimuli including the chemotherapeutic agents Ara-C and VP-16, radiation, arsenic trioxide, ceramide, growth factor withdrawal, and the death receptor activators TNFalpha and TRAIL.	Cytarabine	132-137	CD34 molecule	Homo sapiens	22-26
15815728-6	2005	We further demonstrate that apoptosis was restricted to dividing cells, whereas nonproliferating BCR/ABL(+) CD34(+) cells were resistant to apoptosis induced by imatinib, Ara-C or arsenic, either alone or in combination.	Cytarabine	171-176	CD34 molecule	Homo sapiens	108-112
15529184-1	2005	The human equilibrative nucleoside transporter 1 (hENT1) is a member of the equilibrative nucleoside transporter family that mediates cellular entry of gemcitabine, cytarabine, and fludarabine.	Cytarabine	165-175	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	10-48
15540985-0	2005	Modulation of the p38 MAPK (mitogen-activated protein kinase) pathway through Bcr/Abl: implications in the cellular response to Ara-C.	Cytarabine	128-133	mitogen-activated protein kinase 14	Mus musculus	18-26
15540985-0	2005	Modulation of the p38 MAPK (mitogen-activated protein kinase) pathway through Bcr/Abl: implications in the cellular response to Ara-C.	Cytarabine	128-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-85
15540985-8	2005	While Bcr/Abl-negative cells activated p38 MAPK in response to Ara-C (1-beta-D-arabinofuranosylcytosine), Bcr/Abl-positive cells were unable to activate p38 MAPK, suggesting that the p38 MAPK pathway is not sensitive to Abl-dependent stimuli in Bcr/Abl-positive cells.	Cytarabine	63-68	BCR activator of RhoGEF and GTPase	Homo sapiens	6-9
15540985-8	2005	While Bcr/Abl-negative cells activated p38 MAPK in response to Ara-C (1-beta-D-arabinofuranosylcytosine), Bcr/Abl-positive cells were unable to activate p38 MAPK, suggesting that the p38 MAPK pathway is not sensitive to Abl-dependent stimuli in Bcr/Abl-positive cells.	Cytarabine	63-68	mitogen-activated protein kinase 14	Mus musculus	39-47
15540985-8	2005	While Bcr/Abl-negative cells activated p38 MAPK in response to Ara-C (1-beta-D-arabinofuranosylcytosine), Bcr/Abl-positive cells were unable to activate p38 MAPK, suggesting that the p38 MAPK pathway is not sensitive to Abl-dependent stimuli in Bcr/Abl-positive cells.	Cytarabine	70-103	mitogen-activated protein kinase 14	Mus musculus	39-47
15540985-9	2005	Our results demonstrate that the involvement of Bcr/Abl in the p38 MAPK pathway is a key mechanism for explaining resistance to Ara-C, and could provide a clue for new therapeutic approaches based on the use of specific Abl inhibitors.	Cytarabine	128-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-55
15540985-9	2005	Our results demonstrate that the involvement of Bcr/Abl in the p38 MAPK pathway is a key mechanism for explaining resistance to Ara-C, and could provide a clue for new therapeutic approaches based on the use of specific Abl inhibitors.	Cytarabine	128-133	mitogen-activated protein kinase 14	Mus musculus	63-71
15540985-9	2005	Our results demonstrate that the involvement of Bcr/Abl in the p38 MAPK pathway is a key mechanism for explaining resistance to Ara-C, and could provide a clue for new therapeutic approaches based on the use of specific Abl inhibitors.	Cytarabine	128-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-55
15723262-9	2005	With 10 microM ara-C alone, 86 microM ara-CTP had accumulated after 3 h. The optimal sequence for the drug combination, i.e., clofarabine followed 4 h later by ara-C, resulted in 248 microM ara-CTP at 3 h. Clofarabine accumulated maximally in the monophosphate form.	Cytarabine	15-20	solute carrier family 25 member 1	Homo sapiens	42-45
15723262-13	2005	CONCLUSIONS: These findings demonstrate that combination of clofarabine followed by ara-C results in a biochemical modulation of ara-CTP and synergistic cell kill.	Cytarabine	84-89	solute carrier family 25 member 1	Homo sapiens	133-136
15925997-6	2005	A complete although short lasting clinical and radiological response was achieved by means of systemic high dose methotrexate treatment combined with rituximab and intra-CSF injections of cytarabine.	Cytarabine	188-198	colony stimulating factor 2	Homo sapiens	170-173
15703783-8	2005	An inducible activated form of Akt protects normal myeloid cells from Ara-C and etoposide-mediated apoptosis.	Cytarabine	70-75	AKT serine/threonine kinase 1	Homo sapiens	31-34
15529184-1	2005	The human equilibrative nucleoside transporter 1 (hENT1) is a member of the equilibrative nucleoside transporter family that mediates cellular entry of gemcitabine, cytarabine, and fludarabine.	Cytarabine	165-175	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	50-55
15854290-0	2005	[Influence of anti-CXCR4 monoclonal antibody 12G5 on killing effect of cytosine arabinoside to HL-60 cell].	Cytarabine	71-91	C-X-C motif chemokine receptor 4	Homo sapiens	19-24
15934494-11	2005	Overall, our study showed that low-dose cytosine arabinoside given by continuous infusion together with continuous infusion GM-CSF and hydroxyurea was well-tolerated and effective in treating elderly AML and MDS patients who were not eligible for standard induction therapy.	Cytarabine	40-60	colony stimulating factor 2	Homo sapiens	124-130
15854290-1	2005	This study was aimed to explore the influence of anti-CXCR4 monoclonal antibody 12G5 on killing effect of cytosine arabinoside (Ara C) to HL-60 cell, and to assess its therapeutic value in marrow residual disease.	Cytarabine	106-126	C-X-C motif chemokine receptor 4	Homo sapiens	54-59
15854290-1	2005	This study was aimed to explore the influence of anti-CXCR4 monoclonal antibody 12G5 on killing effect of cytosine arabinoside (Ara C) to HL-60 cell, and to assess its therapeutic value in marrow residual disease.	Cytarabine	128-133	C-X-C motif chemokine receptor 4	Homo sapiens	54-59
15388581-1	2005	Bcr-Abl-expressing primary or cultured leukemia cells display high levels of the antiapoptotic heat shock protein (hsp) 70 and are resistant to cytarabine (Ara-C), etoposide, or Apo-2L/TRAIL (TNF-related apoptosis-inducing ligand)-induced apoptosis.	Cytarabine	144-154	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
15687366-4	2005	Stable transfection of wild-type GATA1 cDNA into the Down syndrome AMkL cell line CMK resulted in decreased (8- to 17-fold) ara-C sensitivity and a threefold-lower generation of the active ara-C metabolite ara-CTP compared with that for mock-transfected CMK cells.	Cytarabine	124-129	GATA binding protein 1	Homo sapiens	33-38
15687366-4	2005	Stable transfection of wild-type GATA1 cDNA into the Down syndrome AMkL cell line CMK resulted in decreased (8- to 17-fold) ara-C sensitivity and a threefold-lower generation of the active ara-C metabolite ara-CTP compared with that for mock-transfected CMK cells.	Cytarabine	124-129	cytidine/uridine monophosphate kinase 1	Homo sapiens	82-85
15687366-4	2005	Stable transfection of wild-type GATA1 cDNA into the Down syndrome AMkL cell line CMK resulted in decreased (8- to 17-fold) ara-C sensitivity and a threefold-lower generation of the active ara-C metabolite ara-CTP compared with that for mock-transfected CMK cells.	Cytarabine	189-194	GATA binding protein 1	Homo sapiens	33-38
15687366-4	2005	Stable transfection of wild-type GATA1 cDNA into the Down syndrome AMkL cell line CMK resulted in decreased (8- to 17-fold) ara-C sensitivity and a threefold-lower generation of the active ara-C metabolite ara-CTP compared with that for mock-transfected CMK cells.	Cytarabine	189-194	cytidine/uridine monophosphate kinase 1	Homo sapiens	82-85
15687366-7	2005	These results suggest that GATA1 transcriptionally upregulates cytidine deaminase and that the presence or absence of GATA1 mutations in AML blasts likely confers differences in ara-C sensitivities due to effects on cytidine deaminase gene expression, which, in turn, contributes to the high cure rate of Down syndrome AMkL patients.	Cytarabine	178-183	GATA binding protein 1	Homo sapiens	118-123
15687366-7	2005	These results suggest that GATA1 transcriptionally upregulates cytidine deaminase and that the presence or absence of GATA1 mutations in AML blasts likely confers differences in ara-C sensitivities due to effects on cytidine deaminase gene expression, which, in turn, contributes to the high cure rate of Down syndrome AMkL patients.	Cytarabine	178-183	cytidine deaminase	Homo sapiens	216-234
15388581-7	2005	Expression of the dominant negative (DN) STAT5 resensitized HL-60/hsp70 cells to cytarabine, etoposide, and Apo-2L/TRAIL-induced apoptosis.	Cytarabine	81-91	signal transducer and activator of transcription 5A	Homo sapiens	41-46
15388581-7	2005	Expression of the dominant negative (DN) STAT5 resensitized HL-60/hsp70 cells to cytarabine, etoposide, and Apo-2L/TRAIL-induced apoptosis.	Cytarabine	81-91	heat shock protein family A (Hsp70) member 4	Homo sapiens	66-71
15668113-9	2005	Pre-treatment with Ara C and hydroxyurea made the Min-mice slightly more sensitive to MN induction by glycidamide compared to wt-mice.	Cytarabine	19-24	APC, WNT signaling pathway regulator	Mus musculus	50-53
15388581-1	2005	Bcr-Abl-expressing primary or cultured leukemia cells display high levels of the antiapoptotic heat shock protein (hsp) 70 and are resistant to cytarabine (Ara-C), etoposide, or Apo-2L/TRAIL (TNF-related apoptosis-inducing ligand)-induced apoptosis.	Cytarabine	156-161	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
15388581-4	2005	Ectopic expression of hsp70 in HL-60 cells (HL-60/hsp70) inhibited Ara-C and etoposide-induced Bax conformation change and translocation to the mitochondria; attenuated the accumulation of cytochrome c, Smac, and Omi/HtrA2 in the cytosol; and inhibited the processing and activity of caspase-9 and caspase-3.	Cytarabine	67-72	heat shock protein family A (Hsp70) member 4	Homo sapiens	22-27
15388581-4	2005	Ectopic expression of hsp70 in HL-60 cells (HL-60/hsp70) inhibited Ara-C and etoposide-induced Bax conformation change and translocation to the mitochondria; attenuated the accumulation of cytochrome c, Smac, and Omi/HtrA2 in the cytosol; and inhibited the processing and activity of caspase-9 and caspase-3.	Cytarabine	67-72	heat shock protein family A (Hsp70) member 4	Homo sapiens	50-55
15539958-3	2005	In this manuscript we investigated the potential of chemo-sensitization via ablation of Chk1 in cells treated with anti-metabolite cancer drugs, hydroxyurea (HU) and cytosine arabinoside (ara-C).	Cytarabine	166-186	checkpoint kinase 1	Homo sapiens	88-92
15676214-0	2005	Anti-CD33 monoclonal antibodies enhance the cytotoxic effects of cytosine arabinoside and idarubicin on acute myeloid leukemia cells through similarities in their signaling pathways.	Cytarabine	65-85	CD33 molecule	Homo sapiens	5-9
15676214-5	2005	RESULTS: CD33 ligation induced a significant increase in ara-C- or IDA- but not VP-16-or Bryostatin-mediated inhibition of proliferation and colony formation.	Cytarabine	57-62	CD33 molecule	Homo sapiens	9-13
15676214-6	2005	Ara-C and IDA induced SHP-1 and SHP-2 protein tyrosine phosphatase (PTPs) phosphorylation and Lyn/SHP-1 complex formation, while VP-16 and Bryostatin did not.	Cytarabine	0-5	protein tyrosine phosphatase non-receptor type 6	Homo sapiens	22-27
15676214-6	2005	Ara-C and IDA induced SHP-1 and SHP-2 protein tyrosine phosphatase (PTPs) phosphorylation and Lyn/SHP-1 complex formation, while VP-16 and Bryostatin did not.	Cytarabine	0-5	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	94-97
15676214-6	2005	Ara-C and IDA induced SHP-1 and SHP-2 protein tyrosine phosphatase (PTPs) phosphorylation and Lyn/SHP-1 complex formation, while VP-16 and Bryostatin did not.	Cytarabine	0-5	protein tyrosine phosphatase non-receptor type 6	Homo sapiens	98-103
15676214-8	2005	Combined treatment of AML cells by ara-C or IDA with anti-CD33 mAb resulted in higher levels of SHP-1 phosphorylation.	Cytarabine	35-40	CD33 molecule	Homo sapiens	58-62
15676214-8	2005	Combined treatment of AML cells by ara-C or IDA with anti-CD33 mAb resulted in higher levels of SHP-1 phosphorylation.	Cytarabine	35-40	protein tyrosine phosphatase non-receptor type 6	Homo sapiens	96-101
15676214-10	2005	CONCLUSION: These data suggest that combined incubation of leukemia cells with anti-CD33 mAb and ara-C or IDA, but not VP-16 or Bryostatin, independently triggers similar events in the downstream signaling cascade, and therefore leads to additive antiproliferative effects and enhanced cytotoxicity.	Cytarabine	97-102	CD33 molecule	Homo sapiens	84-88
15676021-1	2005	Human chronic myelogenous leukemia K562 cells are relatively resistant to the anti-metabolite cytosine arabinoside (Ara-C) and, when treated with Ara-C, they differentiate into erythrocytes without undergoing apoptosis.	Cytarabine	94-114	ATP binding cassette subfamily C member 6	Homo sapiens	116-119
15853657-3	2005	The novel ara-C molecules reveal different pharmacological profiles from the parent compound such as decreased catabolism by cytidine deaminase, increased plasma half-life, and release of nucleoside monophosphate, a reaction that bypasses the rate limiting initial nucleoside phosphorylation.	Cytarabine	10-15	cytidine deaminase	Homo sapiens	125-143
15567516-5	2005	K252a, an inhibitor of the tropomyosin-related kinase (Trk) tyrosine kinase receptor family which showed no toxicity by itself, blocked BDNF protection of AraC-induced apoptosis in a concentration-dependent manner.	Cytarabine	155-159	neurotrophic receptor tyrosine kinase 1	Rattus norvegicus	27-53
16041392-8	2005	Cytidine deaminase (CDD) and 5"-nucleotidase (5NT) gene polymorphisms and CDD, 5NT, deoxycytidine kinase and MRP5 gene expression levels and their potential relation to dFdC and ara-C cytotoxicity are reviewed.	Cytarabine	178-183	cytidine deaminase	Homo sapiens	0-18
15567516-5	2005	K252a, an inhibitor of the tropomyosin-related kinase (Trk) tyrosine kinase receptor family which showed no toxicity by itself, blocked BDNF protection of AraC-induced apoptosis in a concentration-dependent manner.	Cytarabine	155-159	neurotrophic receptor tyrosine kinase 1	Rattus norvegicus	55-58
15567516-5	2005	K252a, an inhibitor of the tropomyosin-related kinase (Trk) tyrosine kinase receptor family which showed no toxicity by itself, blocked BDNF protection of AraC-induced apoptosis in a concentration-dependent manner.	Cytarabine	155-159	brain-derived neurotrophic factor	Rattus norvegicus	136-140
15567516-11	2005	These results show that neurotrophins protect against AraC-induced apoptosis, at least in part, through TrkB-mediated activation of the PI 3-kinase/Akt and MEK signaling pathways.	Cytarabine	54-58	neurotrophic receptor tyrosine kinase 2	Rattus norvegicus	104-108
15567516-11	2005	These results show that neurotrophins protect against AraC-induced apoptosis, at least in part, through TrkB-mediated activation of the PI 3-kinase/Akt and MEK signaling pathways.	Cytarabine	54-58	AKT serine/threonine kinase 1	Rattus norvegicus	148-151
15390307-3	2005	The high event-free survival (EFS) rates of DS AML patients and in particular, patients with megakaryocytic leukemia (AMkL), at least in part reflects an increased sensitivity to cytosine arabinoside (ara-C) secondary to increased expression of the chromosome 21-localized gene, cystathionine-beta-synthase, and potentially global mechanisms which increase the susceptibility of cells to undergo apoptosis.	Cytarabine	201-206	cystathionine beta-synthase	Homo sapiens	279-306
15390307-4	2005	Somatic mutations of the X-linked transcription factor gene, GATA1, have been detected uniformly and exclusively in DS AMkL cases, which may lead to altered expression of GATA1 target genes and alter the metabolism of drugs including ara-C.	Cytarabine	234-239	GATA binding protein 1	Homo sapiens	61-66
15390307-4	2005	Somatic mutations of the X-linked transcription factor gene, GATA1, have been detected uniformly and exclusively in DS AMkL cases, which may lead to altered expression of GATA1 target genes and alter the metabolism of drugs including ara-C.	Cytarabine	234-239	GATA binding protein 1	Homo sapiens	171-176
15548380-0	2004	Polymerization of the triphosphates of AraC, 2",2"-difluorodeoxycytidine (dFdC) and OSI-7836 (T-araC) by human DNA polymerase alpha and DNA primase.	Cytarabine	39-43	DNA polymerase alpha 1, catalytic subunit	Homo sapiens	111-131
15304385-7	2004	Combining SU11248 and cytarabine synergistically inhibited the proliferation of primary AML myeloblasts expressing FLT3 ITD but not WT FLT3 protein.	Cytarabine	22-32	fms related receptor tyrosine kinase 3	Homo sapiens	115-119
15548380-2	2004	We examined how the triphosphates of OSI-7836 (T-araCTP), cytarabine (araCTP), and gemcitabine (dFdCTP) affected the initiation of new DNA strands by the pol alpha primase complex.	Cytarabine	58-68	DNA polymerase alpha 1, catalytic subunit	Homo sapiens	154-163
15631654-0	2004	[A novel bcl-2 antisense oligodeoxynucleotide F951 increases sensitivity of HL-60 cells to Ara-C].	Cytarabine	91-96	BCL2 apoptosis regulator	Homo sapiens	9-14
15547723-0	2004	The effect of G-CSF on the in vitro cytotoxicity of cytarabine and fludarabine in the FLAG combination in pediatric acute myeloid leukemia.	Cytarabine	52-62	colony stimulating factor 3	Homo sapiens	14-19
15547723-4	2004	The LCS decreased significantly from 69.7 to 54.0% when blasts were exposed to G-CSF 21 h prior to incubation with ara-C (p=0.01).	Cytarabine	115-120	colony stimulating factor 3	Homo sapiens	79-84
15217836-4	2004	The ETV6/RUNX1(+) samples were significantly more sensitive than ETV6/RUNX1(-) samples to doxorubicin, etoposide, amsacrine, and dexamethasone, whereas the opposite was true for cytarabine.	Cytarabine	178-188	ETS variant transcription factor 6	Homo sapiens	4-8
15736462-3	2004	CSF involvement could be managed by intrathecal Ara-C.	Cytarabine	48-53	colony stimulating factor 2	Homo sapiens	0-3
15632314-0	2004	Gene-expression profiling reveals down-regulation of equilibrative nucleoside transporter 1 (ENT1) in Ara-C-resistant CCRF-CEM-derived cells.	Cytarabine	102-107	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	53-91
15632314-0	2004	Gene-expression profiling reveals down-regulation of equilibrative nucleoside transporter 1 (ENT1) in Ara-C-resistant CCRF-CEM-derived cells.	Cytarabine	102-107	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	93-97
15632314-3	2004	The adenosine deaminase (ADA) gene was highly up-regulated in Ara-C-resistant cells, while equilibrative nucleoside transporter 1 (ENT1) and several cell-cycle-related genes were down-regulated.	Cytarabine	62-67	adenosine deaminase	Homo sapiens	4-23
15632314-3	2004	The adenosine deaminase (ADA) gene was highly up-regulated in Ara-C-resistant cells, while equilibrative nucleoside transporter 1 (ENT1) and several cell-cycle-related genes were down-regulated.	Cytarabine	62-67	adenosine deaminase	Homo sapiens	25-28
15632314-3	2004	The adenosine deaminase (ADA) gene was highly up-regulated in Ara-C-resistant cells, while equilibrative nucleoside transporter 1 (ENT1) and several cell-cycle-related genes were down-regulated.	Cytarabine	62-67	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	131-135
15632314-4	2004	Of all these genes, ENT1 seemed the most likely to be relevant to Ara-C resistance.	Cytarabine	66-71	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	20-24
15632314-5	2004	To investigate the role of ENT1 in Ara-C-resistant cells, we transfected the cells with the gene.	Cytarabine	35-40	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	27-31
15632314-6	2004	ENT1-transfected Ara-C-resistant cells resembled wild-type CCRF-CEM cells more closely than untransfected Ara-C-resistant cells in terms of growth rate, Ara-C-uptake characteristics, and ADA expression levels.	Cytarabine	17-22	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	0-4
15632314-6	2004	ENT1-transfected Ara-C-resistant cells resembled wild-type CCRF-CEM cells more closely than untransfected Ara-C-resistant cells in terms of growth rate, Ara-C-uptake characteristics, and ADA expression levels.	Cytarabine	17-22	adenosine deaminase	Homo sapiens	187-190
15632314-6	2004	ENT1-transfected Ara-C-resistant cells resembled wild-type CCRF-CEM cells more closely than untransfected Ara-C-resistant cells in terms of growth rate, Ara-C-uptake characteristics, and ADA expression levels.	Cytarabine	106-111	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	0-4
15632314-6	2004	ENT1-transfected Ara-C-resistant cells resembled wild-type CCRF-CEM cells more closely than untransfected Ara-C-resistant cells in terms of growth rate, Ara-C-uptake characteristics, and ADA expression levels.	Cytarabine	106-111	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	0-4
15632314-7	2004	The down-regulation of the ENT1 gene is expected to result in nucleotide deficiency in addition to blockage of Ara-C influx.	Cytarabine	111-116	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	27-31
15632314-8	2004	Accordingly, Ara-C-resistant cells showed low growth rates, which were restored by transfection with ENT1.	Cytarabine	13-18	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	101-105
15380349-1	2004	Addition of cytosine arabinoside (Ara-C) to truncated diphtheria toxin (DT388) fused to granulocyte macrophage-colony stimulating factor (GMCSF) or interleukin-3 (IL3) was studied in a NOD/SCID mouse model of human AML.	Cytarabine	12-32	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	138-143
15380349-1	2004	Addition of cytosine arabinoside (Ara-C) to truncated diphtheria toxin (DT388) fused to granulocyte macrophage-colony stimulating factor (GMCSF) or interleukin-3 (IL3) was studied in a NOD/SCID mouse model of human AML.	Cytarabine	34-39	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	88-136
15543344-6	2004	Treatment with increasing concentrations of daunorubicin or cytosine-beta-D-arabinofuranoside, two cytotoxic drugs commonly used in AML therapy, induced apoptosis and secondary necrosis of HL60 cells and resulted in marked decryption of TF PCA independent of de novo protein synthesis.	Cytarabine	60-93	coagulation factor III, tissue factor	Homo sapiens	237-239
15492802-0	2004	Impact of cytidine deaminase activity on intrinsic resistance to cytarabine in carcinoma cells.	Cytarabine	65-75	cytidine deaminase	Homo sapiens	10-28
15492802-10	2004	In conclusion, carcinomas are intrinsically resistant to cytarabine through high CDA activity and low cellular transport, but not low DCK activity.	Cytarabine	57-67	cytidine deaminase	Homo sapiens	81-84
15571257-0	2004	Immunocytochemical detection of deoxycytidine kinase in pediatric malignancies in relation to in vitro cytarabine sensitivity.	Cytarabine	103-113	deoxycytidine kinase	Homo sapiens	32-52
15571257-1	2004	Deoxycytidine kinase (dCK) is essential for the phosphorylation of cytarabine (ara-C), a deoxycytidine analog active against acute leukemias.	Cytarabine	67-77	deoxycytidine kinase	Homo sapiens	0-20
15571257-1	2004	Deoxycytidine kinase (dCK) is essential for the phosphorylation of cytarabine (ara-C), a deoxycytidine analog active against acute leukemias.	Cytarabine	67-77	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	22-25
15571257-1	2004	Deoxycytidine kinase (dCK) is essential for the phosphorylation of cytarabine (ara-C), a deoxycytidine analog active against acute leukemias.	Cytarabine	79-84	deoxycytidine kinase	Homo sapiens	0-20
15571257-1	2004	Deoxycytidine kinase (dCK) is essential for the phosphorylation of cytarabine (ara-C), a deoxycytidine analog active against acute leukemias.	Cytarabine	79-84	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	22-25
15571257-2	2004	Resistance to ara-C has been linked to dCK deficiency.	Cytarabine	14-19	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	39-42
15571257-3	2004	In this study we determined the expression of the dCK protein in pediatric malignancies, using immunocytochemistry and related the expression levels to in vitro ara-C sensitivity (measured with the MTT-assay).	Cytarabine	161-166	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	50-53
15571257-9	2004	Samples with low dCK expression were significantly more resistant to ara-C compared to samples with high dCK expression.	Cytarabine	69-74	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	17-20
15571257-10	2004	In conclusion, dCK expression varies between individual samples and between different types of malignancies and may play a role in resistance to ara-C in particular tumor types.	Cytarabine	145-150	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	15-18
15161671-4	2004	We now report that the levels of mRNAs encoding the cholesterol synthesis-regulating enzyme, 3-hydroxy-3-methylglutaryl coenzyme A reductase, and the cholesterol-importing low-density lipoprotein (LDL) receptor were both increased by daunorubicin (DNR) or cytarabine (ARA-C) treatments in almost three fourths of cultured AML samples.	Cytarabine	256-266	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	93-140
15161671-4	2004	We now report that the levels of mRNAs encoding the cholesterol synthesis-regulating enzyme, 3-hydroxy-3-methylglutaryl coenzyme A reductase, and the cholesterol-importing low-density lipoprotein (LDL) receptor were both increased by daunorubicin (DNR) or cytarabine (ARA-C) treatments in almost three fourths of cultured AML samples.	Cytarabine	256-266	low density lipoprotein receptor	Homo sapiens	172-210
15161671-4	2004	We now report that the levels of mRNAs encoding the cholesterol synthesis-regulating enzyme, 3-hydroxy-3-methylglutaryl coenzyme A reductase, and the cholesterol-importing low-density lipoprotein (LDL) receptor were both increased by daunorubicin (DNR) or cytarabine (ARA-C) treatments in almost three fourths of cultured AML samples.	Cytarabine	268-273	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	93-140
15161671-4	2004	We now report that the levels of mRNAs encoding the cholesterol synthesis-regulating enzyme, 3-hydroxy-3-methylglutaryl coenzyme A reductase, and the cholesterol-importing low-density lipoprotein (LDL) receptor were both increased by daunorubicin (DNR) or cytarabine (ARA-C) treatments in almost three fourths of cultured AML samples.	Cytarabine	268-273	low density lipoprotein receptor	Homo sapiens	172-210
15347263-5	2004	However, a significant number of patients may relapse in spite of low expression of MDR1 or MRP1, suggesting the involvement of other intracellular mechanisms, possibly related to cytarabine resistance.	Cytarabine	180-190	ATP binding cassette subfamily B member 1	Homo sapiens	84-88
15302096-3	2004	NALM-6, which had a high expression level of p53, a tumor suppressor gene, was most susceptible to Ara-C.	Cytarabine	99-104	tumor protein p53	Homo sapiens	45-48
15302096-7	2004	Pifithrin-alpha, a chemical inhibitor of wild-type p53, ameliorated the cytotoxicity of Ara-C in NALM-6 and MOLT-4, but not Jurkat, U937 or HL-60.	Cytarabine	88-93	tumor protein p53	Homo sapiens	51-54
15302096-8	2004	Our data suggest that the mechanism of Ara-C-induced cell death is a common one, involving an increase in the production of ROS and p53-dependent cell death.	Cytarabine	39-44	tumor protein p53	Homo sapiens	132-135
15287952-7	2004	When employed at 5 micromol/l, the Akt inhibitors markedly reduced the resistance of the leukaemic cell lines to etoposide or cytarabine.	Cytarabine	126-136	AKT serine/threonine kinase 1	Homo sapiens	35-38
15336657-1	2004	An SFG-based retroviral bicistronic vector containing a double-mutant dihydrofolate reductase-cytidine deaminase fusion cDNA (F/S DHFR-CD) with IRES-eGFP confers resistance to both methotrexate (MTX) and cytarabine (ara-C).	Cytarabine	204-214	dihydrofolate reductase	Homo sapiens	130-134
15336657-1	2004	An SFG-based retroviral bicistronic vector containing a double-mutant dihydrofolate reductase-cytidine deaminase fusion cDNA (F/S DHFR-CD) with IRES-eGFP confers resistance to both methotrexate (MTX) and cytarabine (ara-C).	Cytarabine	216-221	dihydrofolate reductase	Homo sapiens	130-134
15122323-9	2004	Two leukemic cell lines, ALL-1 and HL-60 lacking ARTS, were resistant to apoptotic induction by ara-C.	Cytarabine	96-101	ALL1	Homo sapiens	25-30
15122323-9	2004	Two leukemic cell lines, ALL-1 and HL-60 lacking ARTS, were resistant to apoptotic induction by ara-C.	Cytarabine	96-101	septin 4	Homo sapiens	49-53
15138809-3	2004	Here, we present five consecutive neonates with trisomy 21 and TAM, four of whom were critically ill and were therefore treated with cytosine-arabinoside.	Cytarabine	133-153	Myeloproliferative syndrome, transient (transient abnormal myelopoiesis)	Homo sapiens	63-66
15152266-4	2004	In vivo experiments in the mouse DA1-3b/C3H whole-animal acute myeloid leukemia (AML) model showed that injection of Ara-C induced expression of CD80 and CD86, and decreased expression of B7-H1, indicating that chemotherapy can modify costimulatory molecule expression in vivo, in a way not necessarily observed in vitro.	Cytarabine	117-122	RT1 class II, locus Da	Rattus norvegicus	33-36
15257929-0	2004	Clinical effects and P-glycoprotein inhibition in patients with acute myeloid leukemia treated with zosuquidar trihydrochloride, daunorubicin and cytarabine.	Cytarabine	146-156	ATP binding cassette subfamily B member 1	Homo sapiens	21-35
15832507-6	2004	Similarly, the deoxycytidine kinase-deficient cell line (CEM/dCK-) was highly resistant to cytarabine (13900-fold) but more sensitive (106-fold resistant vs CCRF-CEM cells) to prodrug 1.	Cytarabine	91-101	sticky	Drosophila melanogaster	61-64
15149862-0	2004	Distinct functions for WRN and TP53 in a shared pathway of cellular response to 1-beta-D-arabinofuranosylcytosine and bleomycin.	Cytarabine	80-113	WRN RecQ like helicase	Homo sapiens	23-26
15149862-0	2004	Distinct functions for WRN and TP53 in a shared pathway of cellular response to 1-beta-D-arabinofuranosylcytosine and bleomycin.	Cytarabine	80-113	tumor protein p53	Homo sapiens	31-35
15149862-2	2004	We investigated the hypothesis that WRN and TP53 are involved in cellular responses to DNA replication-blocking lesions by exposing WRN deficient and TP53 mutant lymphoblastoid cell lines (LCLs) to 1-beta-d-arabinofuranosylcytosine (AraC) and bleomycin.	Cytarabine	198-231	WRN RecQ like helicase	Homo sapiens	36-39
15158140-11	2004	Ghrelin did not modify the viability of HL-1 cells subjected to 12-h starvation, but did protect against the apoptosis inducer cytosine arabinoside (AraC).	Cytarabine	127-147	ghrelin	Mus musculus	0-7
15158140-11	2004	Ghrelin did not modify the viability of HL-1 cells subjected to 12-h starvation, but did protect against the apoptosis inducer cytosine arabinoside (AraC).	Cytarabine	149-153	ghrelin	Mus musculus	0-7
15158140-12	2004	Finally, production of ghrelin mRNA in HL-1 cardiomyocytes was reduced by AraC but increased if exposure to AraC was preceded by GH treatment.	Cytarabine	74-78	ghrelin and obestatin prepropeptide	Homo sapiens	23-30
15217378-10	2004	With continuous Ara-C infusion, the likelihood of developing SRS was decreased and, during the latent period, the development of ectopic granule cells in the hilus and new glia in the CA1 area was reduced when compared with the vehicle-infused group, while MFS was not altered.	Cytarabine	16-21	carbonic anhydrase 1	Rattus norvegicus	184-187
15204103-0	2004	In vitro evaluation of cytochrome P450-mediated drug interactions between cytarabine, idarubicin, itraconazole and caspofungin.	Cytarabine	74-84	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	23-38
15204103-3	2004	In vitro assays were performed to assess whether cytochrome P450 (CYP450) enzymes were affected by combinations of cytarabine or idarubicin with itraconazole or caspofungin.	Cytarabine	115-125	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	49-64
15204103-3	2004	In vitro assays were performed to assess whether cytochrome P450 (CYP450) enzymes were affected by combinations of cytarabine or idarubicin with itraconazole or caspofungin.	Cytarabine	115-125	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	66-72
15204103-4	2004	METHODS: The high throughput microtiter assay was used to determine whether cytarabine, idarubicin and itraconazole or caspofungin were CYP450 isoenzyme substrates, inhibitors of CYP450 isoenzymes, and to determine potential CYP450 metabolism interactions between these agents.	Cytarabine	76-86	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	136-142
15204103-4	2004	METHODS: The high throughput microtiter assay was used to determine whether cytarabine, idarubicin and itraconazole or caspofungin were CYP450 isoenzyme substrates, inhibitors of CYP450 isoenzymes, and to determine potential CYP450 metabolism interactions between these agents.	Cytarabine	76-86	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	179-185
15204103-4	2004	METHODS: The high throughput microtiter assay was used to determine whether cytarabine, idarubicin and itraconazole or caspofungin were CYP450 isoenzyme substrates, inhibitors of CYP450 isoenzymes, and to determine potential CYP450 metabolism interactions between these agents.	Cytarabine	76-86	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	179-185
15204103-6	2004	Cytarabine is a substrate of CYP450 3A4.	Cytarabine	0-10	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	29-35
15204103-7	2004	Idarubicin inhibits CYP450 2D6, and cytarabine, itraconazole, and caspofungin inhibit CYP450 3A4.	Cytarabine	36-46	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	86-92
14999001-6	2004	In concert with these results, MUC1 attenuated (i) the loss of mitochondrial transmembrane potential, (ii) mitochondrial cytochrome c release, (iii) activation of caspase-9, and (iv) induction of apoptosis by the antimetabolite, 1-beta-d-arabinofuranosylcytosine.	Cytarabine	229-262	mucin 1, cell surface associated	Rattus norvegicus	31-35
15136231-1	2004	We analyzed cytosolic 5"-(3")-nucleotidase (dNT-1) mRNA expression by quantitative polymerase chain reaction at diagnosis in leukemic blasts from 114 patients with acute myeloid leukemia (AML) treated with ara-C.	Cytarabine	206-211	Neurotrophin 1	Drosophila melanogaster	44-49
15136231-2	2004	Our results show that low dNT-1 mRNA expression in leukemic blasts at diagnosis is correlated with a worse clinical outcome and suggest that this enzyme may have a role in sensitivity to ara-C in AML patients.	Cytarabine	187-192	Neurotrophin 1	Drosophila melanogaster	26-31
15087713-4	2004	Infusion of an antimitotic agent (cytosine-beta-D-arabiofuranoside, Ara-C) onto the ipsilateral cortex eliminated more than 98% of actively proliferating cells in the SVZ and doublecortin-positive cells in the ipsilateral striatum.	Cytarabine	68-73	doublecortin	Rattus norvegicus	175-187
15152266-0	2004	Cytosine arabinoside induces costimulatory molecule expression in acute myeloid leukemia cells.	Cytarabine	0-20	CD276 antigen	Mus musculus	29-51
15152266-3	2004	In this study, we show that cytosine arabinoside (Ara-C), even at low doses, induced CD80 expression in vitro in mouse DA1-3b leukemic cells, by a mechanism that involved reactive oxygen species.	Cytarabine	28-48	CD80 antigen	Mus musculus	85-89
15152266-3	2004	In this study, we show that cytosine arabinoside (Ara-C), even at low doses, induced CD80 expression in vitro in mouse DA1-3b leukemic cells, by a mechanism that involved reactive oxygen species.	Cytarabine	28-48	RT1 class II, locus Da	Rattus norvegicus	119-122
15152266-3	2004	In this study, we show that cytosine arabinoside (Ara-C), even at low doses, induced CD80 expression in vitro in mouse DA1-3b leukemic cells, by a mechanism that involved reactive oxygen species.	Cytarabine	50-55	CD80 antigen	Mus musculus	85-89
15152266-3	2004	In this study, we show that cytosine arabinoside (Ara-C), even at low doses, induced CD80 expression in vitro in mouse DA1-3b leukemic cells, by a mechanism that involved reactive oxygen species.	Cytarabine	50-55	RT1 class II, locus Da	Rattus norvegicus	119-122
15152266-4	2004	In vivo experiments in the mouse DA1-3b/C3H whole-animal acute myeloid leukemia (AML) model showed that injection of Ara-C induced expression of CD80 and CD86, and decreased expression of B7-H1, indicating that chemotherapy can modify costimulatory molecule expression in vivo, in a way not necessarily observed in vitro.	Cytarabine	117-122	CD80 antigen	Mus musculus	145-149
15152266-4	2004	In vivo experiments in the mouse DA1-3b/C3H whole-animal acute myeloid leukemia (AML) model showed that injection of Ara-C induced expression of CD80 and CD86, and decreased expression of B7-H1, indicating that chemotherapy can modify costimulatory molecule expression in vivo, in a way not necessarily observed in vitro.	Cytarabine	117-122	CD86 antigen	Mus musculus	154-158
15152266-4	2004	In vivo experiments in the mouse DA1-3b/C3H whole-animal acute myeloid leukemia (AML) model showed that injection of Ara-C induced expression of CD80 and CD86, and decreased expression of B7-H1, indicating that chemotherapy can modify costimulatory molecule expression in vivo, in a way not necessarily observed in vitro.	Cytarabine	117-122	CD276 antigen	Mus musculus	235-257
15152266-6	2004	Ara-C also induced CD80 or CD86 expression in 14 of 21 primary cultured human AML samples.	Cytarabine	0-5	CD80 molecule	Homo sapiens	19-23
15152266-6	2004	Ara-C also induced CD80 or CD86 expression in 14 of 21 primary cultured human AML samples.	Cytarabine	0-5	CD86 molecule	Homo sapiens	27-31
15158086-8	2004	More significantly, ajoene profoundly enhanced the apoptotic effect of the two chemotherapeutic drugs: cytarabine and fludarabine in human CD34-positive resistant myeloid leukaemia cells through enhancing their bcl-2 inhibitory and caspase-3 activation activities.	Cytarabine	103-113	CD34 molecule	Homo sapiens	139-143
15203180-0	2004	Involvement of p53 in 1-beta-D-arabinofuranosylcytosine-induced rat fetal brain lesions.	Cytarabine	22-55	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	15-18
15203180-3	2004	Histopathological examinations revealed marked induction of apoptotic cell death and decrease of mitosis in neuroepithelial cells in the brain of Ara-C-treated fetus, and these changes were most prominent from 9 to 12 h. Expression of p53 protein, which mediates apoptosis and cell cycle arrest after DNA damage, was elevated remarkably and peaked at 3 h. p21, a cyclin-dependent kinase inhibitor responsible for p53-mediated cell cycle arrest, showed intense overexpression in protein and mRNA levels following the increase of p53 protein.	Cytarabine	146-151	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	235-238
15203180-3	2004	Histopathological examinations revealed marked induction of apoptotic cell death and decrease of mitosis in neuroepithelial cells in the brain of Ara-C-treated fetus, and these changes were most prominent from 9 to 12 h. Expression of p53 protein, which mediates apoptosis and cell cycle arrest after DNA damage, was elevated remarkably and peaked at 3 h. p21, a cyclin-dependent kinase inhibitor responsible for p53-mediated cell cycle arrest, showed intense overexpression in protein and mRNA levels following the increase of p53 protein.	Cytarabine	146-151	KRAS proto-oncogene, GTPase	Rattus norvegicus	356-359
15203180-3	2004	Histopathological examinations revealed marked induction of apoptotic cell death and decrease of mitosis in neuroepithelial cells in the brain of Ara-C-treated fetus, and these changes were most prominent from 9 to 12 h. Expression of p53 protein, which mediates apoptosis and cell cycle arrest after DNA damage, was elevated remarkably and peaked at 3 h. p21, a cyclin-dependent kinase inhibitor responsible for p53-mediated cell cycle arrest, showed intense overexpression in protein and mRNA levels following the increase of p53 protein.	Cytarabine	146-151	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	413-416
15203180-3	2004	Histopathological examinations revealed marked induction of apoptotic cell death and decrease of mitosis in neuroepithelial cells in the brain of Ara-C-treated fetus, and these changes were most prominent from 9 to 12 h. Expression of p53 protein, which mediates apoptosis and cell cycle arrest after DNA damage, was elevated remarkably and peaked at 3 h. p21, a cyclin-dependent kinase inhibitor responsible for p53-mediated cell cycle arrest, showed intense overexpression in protein and mRNA levels following the increase of p53 protein.	Cytarabine	146-151	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	413-416
15203180-4	2004	The mRNA expressions of other p53 transcriptional target genes, bax, cyclinG1, and fas, also significantly increased and peaked at around 9 h. In conclusion, prenatal treatment of Ara-C is thought to induce apoptosis and inhibition of cell proliferation mediated by p53 and its target genes in the fetal brain.	Cytarabine	180-185	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	30-33
15203180-4	2004	The mRNA expressions of other p53 transcriptional target genes, bax, cyclinG1, and fas, also significantly increased and peaked at around 9 h. In conclusion, prenatal treatment of Ara-C is thought to induce apoptosis and inhibition of cell proliferation mediated by p53 and its target genes in the fetal brain.	Cytarabine	180-185	BCL2 associated X, apoptosis regulator	Rattus norvegicus	64-67
15203180-4	2004	The mRNA expressions of other p53 transcriptional target genes, bax, cyclinG1, and fas, also significantly increased and peaked at around 9 h. In conclusion, prenatal treatment of Ara-C is thought to induce apoptosis and inhibition of cell proliferation mediated by p53 and its target genes in the fetal brain.	Cytarabine	180-185	cyclin G1	Rattus norvegicus	69-77
15203180-4	2004	The mRNA expressions of other p53 transcriptional target genes, bax, cyclinG1, and fas, also significantly increased and peaked at around 9 h. In conclusion, prenatal treatment of Ara-C is thought to induce apoptosis and inhibition of cell proliferation mediated by p53 and its target genes in the fetal brain.	Cytarabine	180-185	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	266-269
15150801-1	2004	The mechanism of cooperative binding of both cytarabine and fluorouracil, used in combination therapy, to the transporting protein [bovine serum albumin (BSA)] has been investigated.	Cytarabine	45-55	albumin	Homo sapiens	139-152
15150801-7	2004	The competition of these two drugs and the removal of 5-fluorouracil by cytarabine from the common binding site in serum albumin tertiary structure are observed.	Cytarabine	72-82	albumin	Homo sapiens	115-128
15149862-2	2004	We investigated the hypothesis that WRN and TP53 are involved in cellular responses to DNA replication-blocking lesions by exposing WRN deficient and TP53 mutant lymphoblastoid cell lines (LCLs) to 1-beta-d-arabinofuranosylcytosine (AraC) and bleomycin.	Cytarabine	233-237	WRN RecQ like helicase	Homo sapiens	36-39
15149862-3	2004	Loss of WRN or TP53 function resulted in induction of apoptosis and lesser proliferative survival in response to AraC and bleomycin.	Cytarabine	113-117	WRN RecQ like helicase	Homo sapiens	8-11
15149862-3	2004	Loss of WRN or TP53 function resulted in induction of apoptosis and lesser proliferative survival in response to AraC and bleomycin.	Cytarabine	113-117	tumor protein p53	Homo sapiens	15-19
15169628-0	2004	Abrogation of Chk1-mediated S/G2 checkpoint by UCN-01 enhances ara-C-induced cytotoxicity in human colon cancer cells.	Cytarabine	63-68	checkpoint kinase 1	Homo sapiens	14-18
14766721-0	2004	Involvement of p53 in 1-beta-D-arabinofuranosylcytosine-induced trophoblastic cell apoptosis and impaired proliferation in rat placenta.	Cytarabine	22-55	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	15-18
14766721-8	2004	These results indicate that Ara-C would induce apoptosis and impair cell proliferation in the placental labyrinth zone, and p53 and its transcriptional target genes may play an important role in the pathogenesis of the Ara-C-induced placental toxicity.	Cytarabine	219-224	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	124-127
15173063-0	2004	Targeting vascular endothelial growth factor for relapsed and refractory adult acute myelogenous leukemias: therapy with sequential 1-beta-d-arabinofuranosylcytosine, mitoxantrone, and bevacizumab.	Cytarabine	132-165	vascular endothelial growth factor A	Homo sapiens	10-44
14988409-7	2004	Interestingly, the ability of cytarabine to activate the S-phase checkpoint was severely compromised in Rad9(-/-) cells, whereas activation of this checkpoint by camptothecin and etoposide was unaltered, suggesting that the action of cytarabine is readily distinguished from that of classical topoisomerase poisons.	Cytarabine	30-40	RAD9 checkpoint clamp component A	Homo sapiens	104-108
14871251-3	2004	Strikingly, high-dose cytarabine and etoposide plus granulocyte colony stimulating factor (G-CSF) mobilized PBSC harvests from acute myeloid leukaemia (AML) patients containing the highest number of myeloid lin(neg)CD11c(pos) DC (mean: 7.04 x 106/kg, range: 1.46-19.67) which was 18.1-fold higher than in non-AML patients mobilized using chemotherapy (CT) regimens plus G-CSF.	Cytarabine	22-32	integrin subunit alpha X	Homo sapiens	215-220
14871251-3	2004	Strikingly, high-dose cytarabine and etoposide plus granulocyte colony stimulating factor (G-CSF) mobilized PBSC harvests from acute myeloid leukaemia (AML) patients containing the highest number of myeloid lin(neg)CD11c(pos) DC (mean: 7.04 x 106/kg, range: 1.46-19.67) which was 18.1-fold higher than in non-AML patients mobilized using chemotherapy (CT) regimens plus G-CSF.	Cytarabine	22-32	colony stimulating factor 3	Homo sapiens	370-375
14973255-5	2004	In this report we show that the G1 phase-specific expression of the replication factor Mcm2 is a useful marker for detecting slowly cycling putative NSCs in situ and confirm the identity of these cells using both cytosine beta-D-arabinofuranoside (Ara-C) treatment and a double nucleoside analog-labeling technique.	Cytarabine	213-246	minichromosome maintenance complex component 2	Mus musculus	87-91
14973255-5	2004	In this report we show that the G1 phase-specific expression of the replication factor Mcm2 is a useful marker for detecting slowly cycling putative NSCs in situ and confirm the identity of these cells using both cytosine beta-D-arabinofuranoside (Ara-C) treatment and a double nucleoside analog-labeling technique.	Cytarabine	248-253	minichromosome maintenance complex component 2	Mus musculus	87-91
14765985-9	2004	GH also reduced AraC-induced phosphorylation of mitogen-activated protein kinase p38 (MAPK p38) in HL-1 cells.	Cytarabine	16-20	mitogen activated protein kinase 14	Rattus norvegicus	81-84
14984497-0	2004	Granulocyte-macrophage colony-stimulating factor to increase efficacy of mitoxantrone, etoposide and cytarabine in previously untreated elderly patients with acute myeloid leukaemia: a Swedish multicentre randomized trial.	Cytarabine	101-111	colony stimulating factor 2	Homo sapiens	0-48
14973057-7	2004	A decrease in copy numbers of genes encoding deoxycytidine kinase, DNA topoisomerase I, and DNA topoisomerase II alpha reduced their expression levels in one cytosine arabinoside-resistant line, two of three camptothecin-resistant lines, and two of five VP-16-resistant cell lines, respectively.	Cytarabine	158-178	deoxycytidine kinase	Homo sapiens	45-65
15037202-1	2004	1-beta-D-arabinofuranosylcytosine (ara-C) is a deoxycytidine analog with activity in leukemia, which requires phosphorylation by deoxycytidine kinase (dCK) to allow formation of its active phosphate 1-beta-D-arabinofuranosylcytosine triphosphate, but can be deaminated by deoxycytidine deaminase.	Cytarabine	0-33	deoxycytidine kinase	Mus musculus	129-149
15037202-1	2004	1-beta-D-arabinofuranosylcytosine (ara-C) is a deoxycytidine analog with activity in leukemia, which requires phosphorylation by deoxycytidine kinase (dCK) to allow formation of its active phosphate 1-beta-D-arabinofuranosylcytosine triphosphate, but can be deaminated by deoxycytidine deaminase.	Cytarabine	0-33	sticky	Drosophila melanogaster	151-154
15037202-1	2004	1-beta-D-arabinofuranosylcytosine (ara-C) is a deoxycytidine analog with activity in leukemia, which requires phosphorylation by deoxycytidine kinase (dCK) to allow formation of its active phosphate 1-beta-D-arabinofuranosylcytosine triphosphate, but can be deaminated by deoxycytidine deaminase.	Cytarabine	35-40	deoxycytidine kinase	Mus musculus	129-149
15037202-1	2004	1-beta-D-arabinofuranosylcytosine (ara-C) is a deoxycytidine analog with activity in leukemia, which requires phosphorylation by deoxycytidine kinase (dCK) to allow formation of its active phosphate 1-beta-D-arabinofuranosylcytosine triphosphate, but can be deaminated by deoxycytidine deaminase.	Cytarabine	35-40	sticky	Drosophila melanogaster	151-154
14765985-9	2004	GH also reduced AraC-induced phosphorylation of mitogen-activated protein kinase p38 (MAPK p38) in HL-1 cells.	Cytarabine	16-20	mitogen activated protein kinase 14	Rattus norvegicus	91-94
14744791-0	2004	The role of cytidine deaminase and GATA1 mutations in the increased cytosine arabinoside sensitivity of Down syndrome myeloblasts and leukemia cell lines.	Cytarabine	68-88	cytidine deaminase	Homo sapiens	12-30
14671640-5	2004	In response to cytostatic drug treatment (arabinoside cytosine (Ara-C) and methotrexate (MTX)), NF-kappaB was activated in intestinal epithelial cells (IEC-6) resulting in an NF-kappaB-related induction of tumour necrosis factor alpha and monocyte chemoattractant protein-1.	Cytarabine	42-62	C-C motif chemokine ligand 2	Rattus norvegicus	239-273
14671640-5	2004	In response to cytostatic drug treatment (arabinoside cytosine (Ara-C) and methotrexate (MTX)), NF-kappaB was activated in intestinal epithelial cells (IEC-6) resulting in an NF-kappaB-related induction of tumour necrosis factor alpha and monocyte chemoattractant protein-1.	Cytarabine	64-69	C-C motif chemokine ligand 2	Rattus norvegicus	239-273
14744791-0	2004	The role of cytidine deaminase and GATA1 mutations in the increased cytosine arabinoside sensitivity of Down syndrome myeloblasts and leukemia cell lines.	Cytarabine	68-88	GATA binding protein 1	Homo sapiens	35-40
14744791-4	2004	The ratio of deoxycytidine kinase/CDA transcripts significantly correlated with ara-C sensitivities and ara-CTP generation.	Cytarabine	80-85	cytidine deaminase	Homo sapiens	34-37
14744791-5	2004	In clinically relevant AML cell line models, high cystathionine-beta-synthase transcripts in DS CMK cells were accompanied by 10-fold greater ara-C sensitivity and 2.4-fold higher levels of ara-CTP compared with non-DS CMS cells.	Cytarabine	142-147	cystathionine beta-synthase	Homo sapiens	50-77
14744791-6	2004	Overexpression of CDA in non-DS THP-1 cells was associated with a 100-fold decreased ara-C sensitivity and 40-fold decreased ara-CTP generation.	Cytarabine	85-90	cytidine deaminase	Homo sapiens	18-21
14744791-7	2004	THP-1 cells secreted CDA into the incubation media and converted extracellular ara-C completely to 1-beta-D-arabinofuranosyluracil within 30 min.	Cytarabine	79-84	cytidine deaminase	Homo sapiens	21-24
15069761-4	2004	In this study we have investigated the effects of increased intracellular levels of CD on the antineoplastic action of troxacitabine and the related antileukemic drug, cytosine arabinoside (ARA-C).	Cytarabine	168-188	cytidine deaminase	Homo sapiens	84-86
15124675-0	2004	Imatinib mesylate selectively influences the cellular metabolism of cytarabine in BCR/ABL negative leukemia cell lines and normal CD34+ progenitor cells.	Cytarabine	68-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
15124675-1	2004	STI-571 (Imatinib/Glivec) has been shown to have synergism with various chemotherapeutic agents including cytosine arabinoside (Ara-C) in BCR/ABL positive leukemia cells.	Cytarabine	106-126	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-145
15124675-1	2004	STI-571 (Imatinib/Glivec) has been shown to have synergism with various chemotherapeutic agents including cytosine arabinoside (Ara-C) in BCR/ABL positive leukemia cells.	Cytarabine	128-133	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	138-145
15124675-8	2004	The synergism between Ara-C and STI-571 was even more pronounced in Raji and HL-60 cells when 300 ng/ml G-CSF were added at the beginning of the culture period.	Cytarabine	22-27	colony stimulating factor 3	Homo sapiens	104-109
15069761-4	2004	In this study we have investigated the effects of increased intracellular levels of CD on the antineoplastic action of troxacitabine and the related antileukemic drug, cytosine arabinoside (ARA-C).	Cytarabine	190-195	cytidine deaminase	Homo sapiens	84-86
15069761-6	2004	The A549-CD cells were more resistant to the cytotoxic action of ARA-C than the wild type A549 cells as determined by clonogenic assays.	Cytarabine	65-70	cytidine deaminase	Homo sapiens	9-11
14654957-4	2004	Among the conjugates, 1-beta-D-arabino-furanosylcytosine 5"-diphosphate-rac-1-O-octadecyl-2-O-palmitoylglycerol [(ara-CDP-DL-PBA); ara-C conjugate of ether phospholipid], was employed to investigate its mode of activation, since ether phospholipid has been reported to be a regulator of the PKC.	Cytarabine	114-119	Rac family small GTPase 1	Homo sapiens	72-77
15193284-3	2004	We have investigated the involvement of ERK activation/inhibition in hemin-, butyrate-, cisplatin- and ara-C-induced erythroid differentiation using the K562 cell line.	Cytarabine	103-108	mitogen-activated protein kinase 1	Homo sapiens	40-43
15193284-5	2004	ERK was then activated by hemin and cisplatin, while ERK phosphorylation remained decreased during incubation with butyrate and ara-C.	Cytarabine	128-133	mitogen-activated protein kinase 1	Homo sapiens	53-56
14654957-8	2004	These results suggest that the ara-C conjugate of phospholipid activates PKC in a co-operative manner with diacylglycerol and/or phosphatidylserine, however, the exact mechanism of the antineoplastic effect of ara-CDP-DL-PBA through PKC activation still remains speculative.	Cytarabine	31-36	cut like homeobox 1	Homo sapiens	214-217
14586480-0	2004	Successful CD34+ cell mobilization by intermediate-dose Ara-C in chronic lymphocytic leukemia patients treated with sequential fludarabine and Campath-1H.	Cytarabine	56-61	CD34 molecule	Homo sapiens	11-15
14669283-1	2003	BACKGROUND: The International Randomized study of Interferon-alpha plus cytarabine (IFN-alpha plus ara-C) versus STI571 (imatinib mesylate) [IRIS trial] in patients with newly diagnosed Philadelphia chromosome (Ph)-positive, chronic-phase chronic myelogenous leukemia (CML) has not shown (to date) a survival advantage for imatinib.	Cytarabine	72-82	interferon alpha 1	Homo sapiens	84-93
14574327-7	2004	MDR gene expression levels did not correlate to prednisolone, vincristine, daunorubicin or Ara-C cytotoxicity, except for BCRP expression, which correlated with resistance to Ara-C (Rs=0.53, P=0.012), suggesting that Ara-C might be a BCRP substrate.	Cytarabine	175-180	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	122-126
14574327-7	2004	MDR gene expression levels did not correlate to prednisolone, vincristine, daunorubicin or Ara-C cytotoxicity, except for BCRP expression, which correlated with resistance to Ara-C (Rs=0.53, P=0.012), suggesting that Ara-C might be a BCRP substrate.	Cytarabine	175-180	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	122-126
14713572-9	2003	Moreover, in the G2/M-phase, an increase in p53 and a decrease in survivin occurred that were X-ray and Ara-C dose dependent.	Cytarabine	104-109	tumor protein p53	Homo sapiens	44-47
14514691-1	2003	Deoxycytidine kinase (EC 2.7.1.74, dCK) is central to drug activity of anticancer and antiviral agents such as cytosine arabinoside (araC) and gemcitabine.	Cytarabine	111-131	deoxycytidine kinase	Homo sapiens	0-20
14514691-1	2003	Deoxycytidine kinase (EC 2.7.1.74, dCK) is central to drug activity of anticancer and antiviral agents such as cytosine arabinoside (araC) and gemcitabine.	Cytarabine	111-131	dreadlocks	Drosophila melanogaster	35-38
14514691-1	2003	Deoxycytidine kinase (EC 2.7.1.74, dCK) is central to drug activity of anticancer and antiviral agents such as cytosine arabinoside (araC) and gemcitabine.	Cytarabine	133-137	deoxycytidine kinase	Homo sapiens	0-20
14514691-1	2003	Deoxycytidine kinase (EC 2.7.1.74, dCK) is central to drug activity of anticancer and antiviral agents such as cytosine arabinoside (araC) and gemcitabine.	Cytarabine	133-137	dreadlocks	Drosophila melanogaster	35-38
14514691-12	2003	Identifying the physical and functional interactions between Sp and USF proteins may lead to a better understanding of the basis for differential expression of the dCK gene in tumor cells and may foster strategies for up-regulating dCK gene expression and improving chemotherapy with araC and gemcitabine.	Cytarabine	284-288	upstream transcription factor 1	Homo sapiens	68-71
14514691-12	2003	Identifying the physical and functional interactions between Sp and USF proteins may lead to a better understanding of the basis for differential expression of the dCK gene in tumor cells and may foster strategies for up-regulating dCK gene expression and improving chemotherapy with araC and gemcitabine.	Cytarabine	284-288	dreadlocks	Drosophila melanogaster	164-167
14523462-0	2003	Dynamics of BCR-ABL mRNA expression in first-line therapy of chronic myelogenous leukemia patients with imatinib or interferon alpha/ara-C.	Cytarabine	133-138	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
12859994-0	2003	Effects of TNFalpha on the growth and sensitivity to cytosine arabinoside of blast progenitors in acute myelogenous leukemia with special reference to the role of NF-kappaB.	Cytarabine	53-73	tumor necrosis factor	Homo sapiens	11-19
12829606-7	2003	Clones overexpressing BACH2 were more sensitive to etoposide, doxorubicin, and cytarabine than control RAJI cells, whereas there were no significant differences in the sensitivity of either cells to methotrexate or vincristine.	Cytarabine	79-89	BTB domain and CNC homolog 2	Homo sapiens	22-27
14598320-3	2003	In this study, we found that NPCs deficient in Apaf-1, or both the pro-apoptotic multidomain Bcl-2 family members Bax and Bak, were resistant to cytosine arabinoside and gamma-irradiation-induced apoptosis.	Cytarabine	145-165	apoptotic peptidase activating factor 1	Homo sapiens	47-53
12859994-5	2003	However, the combination of TNFalpha with IL-3 uniformly rendered blast progenitors more resistant to Ara-C irrespective of whether TNFalpha suppressed or augmented IL-3-supported growth, indicating that TNFalpha regulates the Ara-C sensitivity of leukemic progenitors independently of their cell cycle status.	Cytarabine	102-107	tumor necrosis factor	Homo sapiens	28-36
12931228-8	2003	Importantly, low-concentration HA14-1 (5 muM) was nontoxic to normal colony-forming cells, whereas it enhanced the cytotoxicity of the antileukemia drug cytarabine in Bcl-2-positive lymphoblastic leukemia cells.	Cytarabine	153-163	BCL2 apoptosis regulator	Homo sapiens	167-172
12859994-5	2003	However, the combination of TNFalpha with IL-3 uniformly rendered blast progenitors more resistant to Ara-C irrespective of whether TNFalpha suppressed or augmented IL-3-supported growth, indicating that TNFalpha regulates the Ara-C sensitivity of leukemic progenitors independently of their cell cycle status.	Cytarabine	102-107	interleukin 3	Homo sapiens	42-46
12859994-5	2003	However, the combination of TNFalpha with IL-3 uniformly rendered blast progenitors more resistant to Ara-C irrespective of whether TNFalpha suppressed or augmented IL-3-supported growth, indicating that TNFalpha regulates the Ara-C sensitivity of leukemic progenitors independently of their cell cycle status.	Cytarabine	227-232	interleukin 3	Homo sapiens	42-46
14502542-1	2003	Tetrahydrouridine (THU) is an inhibitor of cytidine deaminase (CDA), the enzyme responsible for the deactivation of ara-C and other cytidine analogues in vivo, and therefore is capable of improving the therapeutic efficacy of these antitumor agents.	Cytarabine	116-121	cytidine deaminase	Mus musculus	43-61
12970762-8	2003	Targeting XIAP by XIAP antisense oligonucleotide resulted in downregulation of XIAP, activation of caspases and cell death, and sensitized HL-60 cells to Ara-C.	Cytarabine	154-159	X-linked inhibitor of apoptosis	Homo sapiens	10-14
12970762-8	2003	Targeting XIAP by XIAP antisense oligonucleotide resulted in downregulation of XIAP, activation of caspases and cell death, and sensitized HL-60 cells to Ara-C.	Cytarabine	154-159	X-linked inhibitor of apoptosis	Homo sapiens	18-22
12970762-8	2003	Targeting XIAP by XIAP antisense oligonucleotide resulted in downregulation of XIAP, activation of caspases and cell death, and sensitized HL-60 cells to Ara-C.	Cytarabine	154-159	X-linked inhibitor of apoptosis	Homo sapiens	18-22
14534335-5	2003	RESULTS: In patients who had a complete cytogenetic remission, levels of BCR-ABL transcripts after 12 months of treatment had fallen by at least 3 log in 57 percent of those in the imatinib group and 24 percent of those in the group given interferon plus cytarabine (P=0.003).	Cytarabine	255-265	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	73-80
14534335-8	2003	CONCLUSIONS: The proportion of patients with CML who had a reduction in BCR-ABL transcript levels of at least 3 log by 12 months of therapy was far greater with imatinib treatment than with treatment with interferon plus cytarabine.	Cytarabine	221-231	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
14720446-8	2003	Vp16 or Ara-C upregulated DR5 gene expression and augmented Apo2L-induced apoptosis in HL-60 cells.	Cytarabine	8-13	TNF receptor superfamily member 10b	Homo sapiens	26-29
14720446-8	2003	Vp16 or Ara-C upregulated DR5 gene expression and augmented Apo2L-induced apoptosis in HL-60 cells.	Cytarabine	8-13	TNF superfamily member 10	Homo sapiens	60-65
14720446-10	2003	Ara-C or Vp16 upregulated DR5 gene expression and increased the sensitivity of HL-60 to Apo2L-induced cytotoxicity.	Cytarabine	0-5	TNF receptor superfamily member 10b	Homo sapiens	26-29
14720446-10	2003	Ara-C or Vp16 upregulated DR5 gene expression and increased the sensitivity of HL-60 to Apo2L-induced cytotoxicity.	Cytarabine	0-5	TNF superfamily member 10	Homo sapiens	88-93
12925971-2	2003	The critical step for ara-CMP formation is intracellular phosphorylation of ara-C by deoxycytidine kinase (dCK).	Cytarabine	22-27	deoxycytidine kinase	Homo sapiens	85-105
12925971-2	2003	The critical step for ara-CMP formation is intracellular phosphorylation of ara-C by deoxycytidine kinase (dCK).	Cytarabine	22-27	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	107-110
12925971-4	2003	We describe the ability of a tert-butyl S-acyl-thioethyl (SATE) derivative of ara-CMP (UA911) to circumvent ara-C resistance in a dCK-deficient human follicular lymphoma cell line (RL-G).	Cytarabine	78-83	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	130-133
12925971-5	2003	The RL-G cell line was produced by continuous exposure to gemcitabine and displayed low dCK mRNA and protein expression that conferred resistance both to ara-C (2,250-fold) and to gemcitabine (2,092-fold).	Cytarabine	154-159	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	88-91
14502542-1	2003	Tetrahydrouridine (THU) is an inhibitor of cytidine deaminase (CDA), the enzyme responsible for the deactivation of ara-C and other cytidine analogues in vivo, and therefore is capable of improving the therapeutic efficacy of these antitumor agents.	Cytarabine	116-121	cytidine deaminase	Mus musculus	63-66
12934079-0	2003	Cytosine arabinoside rapidly activates Bax-dependent apoptosis and a delayed Bax-independent death pathway in sympathetic neurons.	Cytarabine	0-20	BCL2 associated X, apoptosis regulator	Homo sapiens	39-42
12951057-5	2003	In K562 cells, Ara-C treatment induced significant down-regulation of the asparagine synthetase gene, which is involved in resistance to L-asparaginase.	Cytarabine	15-20	asparaginase and isoaspartyl peptidase 1	Homo sapiens	137-151
12934079-0	2003	Cytosine arabinoside rapidly activates Bax-dependent apoptosis and a delayed Bax-independent death pathway in sympathetic neurons.	Cytarabine	0-20	BCL2 associated X, apoptosis regulator	Homo sapiens	77-80
12934079-4	2003	Similar to neurons undergoing trophic factor deprivation-induced apoptosis, ara-C-exposed neurons became hypometabolic before death and upregulated c-myb, c-fos, and Bim.	Cytarabine	76-81	MYB proto-oncogene, transcription factor	Homo sapiens	148-153
12934079-4	2003	Similar to neurons undergoing trophic factor deprivation-induced apoptosis, ara-C-exposed neurons became hypometabolic before death and upregulated c-myb, c-fos, and Bim.	Cytarabine	76-81	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	155-160
12934079-4	2003	Similar to neurons undergoing trophic factor deprivation-induced apoptosis, ara-C-exposed neurons became hypometabolic before death and upregulated c-myb, c-fos, and Bim.	Cytarabine	76-81	BCL2 like 11	Homo sapiens	166-169
12934079-7	2003	p53-deficient neurons demonstrated decreased sensitivity to ara-C, but neither p53 nor multiple p53-regulated genes were induced.	Cytarabine	60-65	tumor protein p53	Homo sapiens	0-3
12970779-9	2003	Our findings demonstrate that, at a concentration which does not affect PI3K activity, the Akt inhibitor markedly reduced resistance of HL60AR cells to etoposide, cytarabine, TRAIL, ATRA, and ionizing radiation.	Cytarabine	163-173	AKT serine/threonine kinase 1	Homo sapiens	91-94
13677932-2	2003	Recently, low doses of cytosine arabinoside (ara-C) were reported to enhance Fas antigen expression in the human myeloid leukemia cell line HL60.	Cytarabine	23-43	Fas cell surface death receptor	Homo sapiens	77-88
12886238-2	2003	The rationales for the study design were based (i) on previous favorable results with high-dose cytarabine in AML with t(8;21), inv/t(16q22) and in AML with normal karyotype, and ii) on encouraging results obtained in several phase II trials using autologous stem cell transplantation (SCT).	Cytarabine	96-106	inversin	Homo sapiens	128-131
13677932-2	2003	Recently, low doses of cytosine arabinoside (ara-C) were reported to enhance Fas antigen expression in the human myeloid leukemia cell line HL60.	Cytarabine	45-50	Fas cell surface death receptor	Homo sapiens	77-88
13677932-5	2003	The ratios for Fas antigen expression induced in non-treated U937 by 24 h incubations with ara-C, VP-16 or VCR were 1.90, 1.36 and 1.00, respectively.	Cytarabine	91-96	Fas cell surface death receptor	Homo sapiens	15-26
12853972-0	2003	Mechanism of cytosine arabinoside-mediated apoptosis: role of Rel A (p65) dephosphorylation.	Cytarabine	13-33	RELA proto-oncogene, NF-kB subunit	Homo sapiens	62-67
12853972-0	2003	Mechanism of cytosine arabinoside-mediated apoptosis: role of Rel A (p65) dephosphorylation.	Cytarabine	13-33	RELA proto-oncogene, NF-kB subunit	Homo sapiens	69-72
12853972-5	2003	AraC, but not TNF or ceramide was able to induce apoptosis in these cells as detected by assays for lipid peroxidation, reactive oxygen intermediates generation, caspase activation, cytotoxicity, Bcl-2 degradation, and DNA fragmentation.	Cytarabine	0-4	BCL2 apoptosis regulator	Homo sapiens	196-201
12853972-7	2003	AraC was able to induce protein phosphatases (PP) 2A and 2B-A, and phosphorylation of p65 subunit of NF-kappaB in the HuT-78 and SA-LPS/Jkt cells was downregulated by araC treatment.	Cytarabine	0-4	protein phosphatase 2 phosphatase activator	Homo sapiens	46-61
12853972-7	2003	AraC was able to induce protein phosphatases (PP) 2A and 2B-A, and phosphorylation of p65 subunit of NF-kappaB in the HuT-78 and SA-LPS/Jkt cells was downregulated by araC treatment.	Cytarabine	0-4	RELA proto-oncogene, NF-kB subunit	Homo sapiens	86-110
12853972-7	2003	AraC was able to induce protein phosphatases (PP) 2A and 2B-A, and phosphorylation of p65 subunit of NF-kappaB in the HuT-78 and SA-LPS/Jkt cells was downregulated by araC treatment.	Cytarabine	167-171	RELA proto-oncogene, NF-kB subunit	Homo sapiens	86-110
12853972-9	2003	These observations collectively suggest that araC induces apoptosis in NF-kappaB-expressing cells by dephosphorylating the p65 subunit of NF-kappaB.	Cytarabine	45-49	nuclear factor kappa B subunit 1	Homo sapiens	71-80
12853972-9	2003	These observations collectively suggest that araC induces apoptosis in NF-kappaB-expressing cells by dephosphorylating the p65 subunit of NF-kappaB.	Cytarabine	45-49	RELA proto-oncogene, NF-kB subunit	Homo sapiens	123-147
12787880-0	2003	Enforced expression of the tumor suppressor p53 renders human leukemia cells (U937) more sensitive to 1-[beta-D-arabinofuranosyl]cytosine (ara-C)-induced apoptosis.	Cytarabine	102-137	tumor protein p53	Homo sapiens	44-47
12823345-0	2003	Deoxycytidine kinase and cN-II nucleotidase expression in blast cells predict survival in acute myeloid leukaemia patients treated with cytarabine.	Cytarabine	136-146	deoxycytidine kinase	Homo sapiens	0-20
12823345-0	2003	Deoxycytidine kinase and cN-II nucleotidase expression in blast cells predict survival in acute myeloid leukaemia patients treated with cytarabine.	Cytarabine	136-146	5'-nucleotidase, cytosolic II	Homo sapiens	25-30
12823345-1	2003	The cytotoxic activity of cytarabine (ara-C) in leukaemic blasts depends on activating enzymes such as deoxycytidine kinase (dCK) and inactivating enzymes such as the 5"-nucleotidases.	Cytarabine	26-36	deoxycytidine kinase	Homo sapiens	103-123
12823345-1	2003	The cytotoxic activity of cytarabine (ara-C) in leukaemic blasts depends on activating enzymes such as deoxycytidine kinase (dCK) and inactivating enzymes such as the 5"-nucleotidases.	Cytarabine	26-36	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	125-128
12823345-1	2003	The cytotoxic activity of cytarabine (ara-C) in leukaemic blasts depends on activating enzymes such as deoxycytidine kinase (dCK) and inactivating enzymes such as the 5"-nucleotidases.	Cytarabine	38-43	deoxycytidine kinase	Homo sapiens	103-123
12823345-1	2003	The cytotoxic activity of cytarabine (ara-C) in leukaemic blasts depends on activating enzymes such as deoxycytidine kinase (dCK) and inactivating enzymes such as the 5"-nucleotidases.	Cytarabine	38-43	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	125-128
12823345-7	2003	Our results suggest that dCK and cN-II mRNA expression in leukaemic blasts at diagnosis is correlated with clinical outcome and may play a functional role in the resistance to ara-C in patients with AML.	Cytarabine	176-181	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	25-28
12823345-7	2003	Our results suggest that dCK and cN-II mRNA expression in leukaemic blasts at diagnosis is correlated with clinical outcome and may play a functional role in the resistance to ara-C in patients with AML.	Cytarabine	176-181	5'-nucleotidase, cytosolic II	Homo sapiens	33-38
12808445-3	2003	To determine the factors that limit the phosphorylation efficiency of the prodrug, we solved the crystal structure of dCK to a resolution of 1.6 A in complex with its physiological substrate deoxycytidine and with the prodrugs AraC and gemcitabine.	Cytarabine	227-231	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	118-121
12787880-7	2003	Significantly, ptsp53 cells synchronized in S phase were markedly more sensitive to ara-C-mediated mitochondrial injury and apoptosis at 32 degrees, indicating that wild-type p53 specifically enhances the susceptibility of this subpopulation to ara-C lethality.	Cytarabine	84-89	tumor protein p53	Homo sapiens	18-21
12787880-8	2003	Consistent with these results, transient transfection of human wild-type p53 cDNA rendered parental U937 cells more sensitive to ara-C-mediated cell death.	Cytarabine	129-134	tumor protein p53	Homo sapiens	73-76
12787880-9	2003	Collectively, these findings indicate that p53 expression renders S-phase U937 cells more susceptible to ara-C-mediated mitochondrial dysfunction, cytochrome c release, apoptosis, and loss of clonogenic survival without enhancing ara-C metabolism.	Cytarabine	105-110	tumor protein p53	Homo sapiens	43-46
12787880-0	2003	Enforced expression of the tumor suppressor p53 renders human leukemia cells (U937) more sensitive to 1-[beta-D-arabinofuranosyl]cytosine (ara-C)-induced apoptosis.	Cytarabine	139-144	tumor protein p53	Homo sapiens	44-47
12730959-10	2003	Cytosine arabinoside (10 micro M), a DNA synthesis blocker, inhibited the ET-1-induced BrdU uptake without affecting the ET-1-induced increase in astrocytic protein content.	Cytarabine	0-20	endothelin 1	Rattus norvegicus	74-78
12684520-2	2003	Ara-C-induced DNA damage caused rapid sympathetic neuronal death that was associated with an increase of c-jun expression.	Cytarabine	0-5	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	105-110
12780785-4	2003	However, incubation with TRAIL combined with fludarabine, cytosine arabinoside or daunorubicin resulted in additive or super-additive apoptosis induction in approximately half of the isolates.	Cytarabine	58-78	TNF superfamily member 10	Homo sapiens	25-30
12781215-7	2003	Ara-C increased the level of p53 in both CV1-P and SH-SY5Y cells compared to control.	Cytarabine	0-5	tumor protein p53	Homo sapiens	29-32
12764361-0	2003	In BCR-ABL-positive cells, STAT-5 tyrosine-phosphorylation integrates signals induced by imatinib mesylate and Ara-C.	Cytarabine	111-116	signal transducer and activator of transcription 5A	Homo sapiens	27-33
12764361-3	2003	Here, we investigated the effects of imatinib mesylate and cytosine arabinoside (Ara-C) on STAT-5 tyrosine-phosphorylation, cellular proliferation and induction of apoptosis in cell lines and primary hematopoietic cells.	Cytarabine	59-79	signal transducer and activator of transcription 5A	Homo sapiens	91-97
12764361-3	2003	Here, we investigated the effects of imatinib mesylate and cytosine arabinoside (Ara-C) on STAT-5 tyrosine-phosphorylation, cellular proliferation and induction of apoptosis in cell lines and primary hematopoietic cells.	Cytarabine	81-86	signal transducer and activator of transcription 5A	Homo sapiens	91-97
12764361-7	2003	In addition, we investigated the effects of Ara-C on STAT-5 tyrosine-phosphorylation.	Cytarabine	44-49	signal transducer and activator of transcription 5A	Homo sapiens	53-59
12764361-8	2003	Exposure to Ara-C resulted in significant downregulation of STAT-5 tyrosine-phosphorylation and inhibition of DNA binding.	Cytarabine	12-17	signal transducer and activator of transcription 5A	Homo sapiens	60-66
12764361-9	2003	Treatment of K562 cells with Ara-C in combination with imatinib mesylate revealed synergistic effects at the level of STAT-5 tyrosine-phosphorylation and DNA binding, Hck tyrosine-phosphorylation, cell growth and induction of apoptosis.	Cytarabine	29-34	signal transducer and activator of transcription 5A	Homo sapiens	118-124
12764361-9	2003	Treatment of K562 cells with Ara-C in combination with imatinib mesylate revealed synergistic effects at the level of STAT-5 tyrosine-phosphorylation and DNA binding, Hck tyrosine-phosphorylation, cell growth and induction of apoptosis.	Cytarabine	29-34	HCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	167-170
12764361-10	2003	Overall, in this report we demonstrate that STAT-5 tyrosine-phosphorylation is a specific target of imatinib mesylate and Ara-C.	Cytarabine	122-127	signal transducer and activator of transcription 5A	Homo sapiens	44-50
12590940-2	2003	When hippocampal cultures of neurons and astrocytes were treated from day 2-4 in vitro (DIV 2-4) with 1 microM cytosine arabinofuranoside (AraC), we observed a stellation of astrocytes, an increase in glial fibrillary acidic protein (GFAP) level as well as a higher susceptibility of the neurons to glutamate compared with cultures treated from DIV 2-4 with vehicle.	Cytarabine	111-137	glial fibrillary acidic protein	Homo sapiens	201-232
12590940-2	2003	When hippocampal cultures of neurons and astrocytes were treated from day 2-4 in vitro (DIV 2-4) with 1 microM cytosine arabinofuranoside (AraC), we observed a stellation of astrocytes, an increase in glial fibrillary acidic protein (GFAP) level as well as a higher susceptibility of the neurons to glutamate compared with cultures treated from DIV 2-4 with vehicle.	Cytarabine	111-137	glial fibrillary acidic protein	Homo sapiens	234-238
12884821-0	2003	[High dose ara-C therapy induced bradycardia in an acute myeloid leukemia patient with inv (16)(p13q22)].	Cytarabine	11-16	inversin	Homo sapiens	87-90
12781215-10	2003	Our results prove that Ara-C- induced apoptosis in CV1-P cells is associated with an increase of p53 and activation of caspase-3.	Cytarabine	23-28	tumor protein p53	Homo sapiens	97-100
12781215-10	2003	Our results prove that Ara-C- induced apoptosis in CV1-P cells is associated with an increase of p53 and activation of caspase-3.	Cytarabine	23-28	caspase 3	Homo sapiens	119-128
12699351-1	2003	Most antitumor 2"-deoxycytidine (dCyd) analogues, such as Ara-C (1-beta-arabinofuranosylcytosine) and gemcitabine (2"-deoxy-2",2"-difluolo-cytidine), have common antitumor mechanisms and metabolic pathways.	Cytarabine	58-63	Cyd	Drosophila melanogaster	33-37
12699351-1	2003	Most antitumor 2"-deoxycytidine (dCyd) analogues, such as Ara-C (1-beta-arabinofuranosylcytosine) and gemcitabine (2"-deoxy-2",2"-difluolo-cytidine), have common antitumor mechanisms and metabolic pathways.	Cytarabine	65-96	Cyd	Drosophila melanogaster	33-37
12699351-6	2003	Such high resistance is generally attributed to deficiency of dCyd kinase activity, but the clinical resistance index of Ara-C-resistant patients is estimated to be increased a maximum of 20 times compared with non-treated patients.	Cytarabine	121-126	Cyd	Drosophila melanogaster	62-66
12531222-4	2003	We designed a trial of ATRA plus ara-C-based TST in an attempt to enhance drug-induced apoptosis and clinical outcome.	Cytarabine	33-38	thiosulfate sulfurtransferase	Homo sapiens	45-48
12839679-3	2003	RESULTS: The activation of NF-kappa B induced by Ara-C and Vp-16 was obviously correlated to apoptosis in P388 cells.	Cytarabine	49-54	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	27-37
12760263-1	2003	BACKGROUND: The t (8;21) (q22;q22), which produces the fusion gene AML1/ETO, is associated with relatively good prognosis and, in particular, with a good response to cytosine arabinoside.	Cytarabine	166-186	RUNX family transcription factor 1	Homo sapiens	67-71
12579303-0	2003	Atypical nuclear apoptosis downstream to caspase-3 activation in ara-C treated CCRF-CEM cells.	Cytarabine	65-70	caspase 3	Homo sapiens	41-50
12627512-4	2003	Patients with CD19 negative ALL received high-dose cytarabine.	Cytarabine	51-61	CD19 molecule	Homo sapiens	14-18
12688309-3	2003	Synergistic interaction between FA or 2-CdA with cytarabine (Ara-C) have been demonstrated in both preclinical and clinical studies.	Cytarabine	49-59	cytidine deaminase	Homo sapiens	40-43
12688309-3	2003	Synergistic interaction between FA or 2-CdA with cytarabine (Ara-C) have been demonstrated in both preclinical and clinical studies.	Cytarabine	61-66	cytidine deaminase	Homo sapiens	40-43
12760263-1	2003	BACKGROUND: The t (8;21) (q22;q22), which produces the fusion gene AML1/ETO, is associated with relatively good prognosis and, in particular, with a good response to cytosine arabinoside.	Cytarabine	166-186	RUNX1 partner transcriptional co-repressor 1	Homo sapiens	72-75
12662441-2	2003	Present studies evaluated the myeloprotective capabilities of Lkn-1 in vivo against Ara-C and 5-fluorouracil (5-FU).	Cytarabine	84-89	C-C motif chemokine ligand 15	Homo sapiens	62-67
12406912-2	2003	One exception is cytosine arabinoside (Ara-C), to which infant ALL cells are highly sensitive.	Cytarabine	17-37	ATP binding cassette subfamily C member 6	Homo sapiens	39-42
12586797-8	2003	CONCLUSION: These results suggest that a moderate dose of IL-2 after high-dose cytarabine-idarubicin-mobilized ASCT is associated with a low regimen-related toxicity and may improve DFS.	Cytarabine	79-89	interleukin 2	Homo sapiens	58-62
12667288-0	2003	[Design of antisense oligodeoxynucleotide targeting at bcl-2 mRNA and observation on its effect on the sensitivity of leukemia cells to arabinosyl cytosine].	Cytarabine	136-155	BCL2 apoptosis regulator	Homo sapiens	55-60
12667288-1	2003	The effective target sites for antisense oligodeoxynucleotides (AS-ODN) on bcl-2 mRNA, except its start region, were looked for and their effects on the sensitivity of HL-60 and K562 leukemia cells to arabinosyl cytosine (Ara-C) were observed.	Cytarabine	201-220	BCL2 apoptosis regulator	Homo sapiens	75-80
12667288-1	2003	The effective target sites for antisense oligodeoxynucleotides (AS-ODN) on bcl-2 mRNA, except its start region, were looked for and their effects on the sensitivity of HL-60 and K562 leukemia cells to arabinosyl cytosine (Ara-C) were observed.	Cytarabine	222-227	BCL2 apoptosis regulator	Homo sapiens	75-80
12667288-4	2003	The results showed that 10 micro mol/L bcl-2 AS-ODN combined with Ara-C inhibited the expression of bcl-2 protein, increased apoptosis in HL-60 and K562 cells and decresed IC(50) of Ara-C significantly.	Cytarabine	66-71	BCL2 apoptosis regulator	Homo sapiens	39-44
12667288-4	2003	The results showed that 10 micro mol/L bcl-2 AS-ODN combined with Ara-C inhibited the expression of bcl-2 protein, increased apoptosis in HL-60 and K562 cells and decresed IC(50) of Ara-C significantly.	Cytarabine	66-71	BCL2 apoptosis regulator	Homo sapiens	100-105
12667288-4	2003	The results showed that 10 micro mol/L bcl-2 AS-ODN combined with Ara-C inhibited the expression of bcl-2 protein, increased apoptosis in HL-60 and K562 cells and decresed IC(50) of Ara-C significantly.	Cytarabine	182-187	BCL2 apoptosis regulator	Homo sapiens	39-44
12757405-1	2003	Decitabine [NSC 127716, DAC, dezocitidine, Aza dC, 2"-deoxy-5-azacytidine] is a deoxycytidine and cytarabine derivative with potent antileukaemic activity, which was originated by Pharmachemie.	Cytarabine	98-108	arylacetamide deacetylase	Homo sapiens	24-27
12417182-7	2003	Expression of PCNA was suppressed in the presence of Cytochalasin B, Cytochalasin D, Aphidicolin, and AraC.	Cytarabine	102-106	proliferating cell nuclear antigen	Ovis aries	14-18
12488556-2	2003	Whereas bryostatin 1 and UCN-01 both markedly enhanced ara-C-induced mitochondrial injury (e.g., cytochrome c and Smac/DIABLO release, loss of mitochondrial membrane potential), caspase activation, and apoptosis, ectopic expression of an N-terminal loop-deleted Bcl-2 mutant protein protected cells from ara-C/UCN-01- but not ara-C/bryostatin 1-mediated lethality.	Cytarabine	55-60	cytochrome c, somatic	Homo sapiens	97-109
12488556-2	2003	Whereas bryostatin 1 and UCN-01 both markedly enhanced ara-C-induced mitochondrial injury (e.g., cytochrome c and Smac/DIABLO release, loss of mitochondrial membrane potential), caspase activation, and apoptosis, ectopic expression of an N-terminal loop-deleted Bcl-2 mutant protein protected cells from ara-C/UCN-01- but not ara-C/bryostatin 1-mediated lethality.	Cytarabine	55-60	diablo IAP-binding mitochondrial protein	Homo sapiens	114-118
12488556-2	2003	Whereas bryostatin 1 and UCN-01 both markedly enhanced ara-C-induced mitochondrial injury (e.g., cytochrome c and Smac/DIABLO release, loss of mitochondrial membrane potential), caspase activation, and apoptosis, ectopic expression of an N-terminal loop-deleted Bcl-2 mutant protein protected cells from ara-C/UCN-01- but not ara-C/bryostatin 1-mediated lethality.	Cytarabine	55-60	BCL2 apoptosis regulator	Homo sapiens	262-267
12488556-3	2003	Conversely, ectopic expression of CrmA or dominant-negative caspase-8 abrogated potentiation of ara-C-mediated apoptosis by bryostatin 1 but not by UCN-01.	Cytarabine	96-101	caspase 8	Homo sapiens	60-69
12488556-4	2003	Exposure of cells to ara-C and bryostatin 1 (but not UCN-01) resulted in sustained release of tumor necrosis factor (TNF) alpha; moreover, potentiation of ara-C lethality by bryostatin 1 (but not by UCN-01) was reversed by coadministration of TNF soluble receptors or the selective PKC inhibitor bisindolylmaleimide (1 microM).	Cytarabine	21-26	tumor necrosis factor	Homo sapiens	94-127
12459171-0	2002	p53 codon 72 genotype affects apoptosis by cytosine arabinoside in blood leukocytes.	Cytarabine	43-63	tumor protein p53	Homo sapiens	0-3
12544510-0	2003	A functional single-nucleotide polymorphism in the human cytidine deaminase gene contributing to ara-C sensitivity.	Cytarabine	97-102	cytidine deaminase	Homo sapiens	57-75
12563609-5	2003	Combining IFNalpha with other drugs, like arabinosyl cytosine (AC), and with other treatments, like autologous stem cell transplantation (autoSCT), may provide additional benefit, although this has not been proven.	Cytarabine	42-61	interferon alpha 1	Homo sapiens	10-18
12563609-5	2003	Combining IFNalpha with other drugs, like arabinosyl cytosine (AC), and with other treatments, like autologous stem cell transplantation (autoSCT), may provide additional benefit, although this has not been proven.	Cytarabine	63-65	interferon alpha 1	Homo sapiens	10-18
12377781-3	2002	The present studies demonstrate that PKCdelta is required in part for induction of the stress-activated protein kinase (SAPK/JNK) in cells treated with 1-beta-d-arabinofuranosylcytosine (araC) and other genotoxic agents.	Cytarabine	152-185	protein kinase C delta	Homo sapiens	37-45
12377781-3	2002	The present studies demonstrate that PKCdelta is required in part for induction of the stress-activated protein kinase (SAPK/JNK) in cells treated with 1-beta-d-arabinofuranosylcytosine (araC) and other genotoxic agents.	Cytarabine	152-185	mitogen-activated protein kinase 9	Homo sapiens	120-124
12377781-3	2002	The present studies demonstrate that PKCdelta is required in part for induction of the stress-activated protein kinase (SAPK/JNK) in cells treated with 1-beta-d-arabinofuranosylcytosine (araC) and other genotoxic agents.	Cytarabine	152-185	mitogen-activated protein kinase 9	Homo sapiens	125-128
13678233-2	2003	The treatment of the cells with arabinosylcytosine and green tea extract results in a strong enhancement of cellular NEP activity whereas cellular ACE activity was not changed significantly, indicating a green tea extract-specific regulation of NEP expression.	Cytarabine	32-50	membrane metalloendopeptidase	Homo sapiens	117-120
13678233-2	2003	The treatment of the cells with arabinosylcytosine and green tea extract results in a strong enhancement of cellular NEP activity whereas cellular ACE activity was not changed significantly, indicating a green tea extract-specific regulation of NEP expression.	Cytarabine	32-50	membrane metalloendopeptidase	Homo sapiens	245-248
12393388-9	2002	FLT3 mutations identify a subset of young AML patients with normal cytogenetics who do not benefit from intensive chemotherapy, including double-induction and postremission therapy with high-dose cytarabine.	Cytarabine	196-206	fms related receptor tyrosine kinase 3	Homo sapiens	0-4
12377781-3	2002	The present studies demonstrate that PKCdelta is required in part for induction of the stress-activated protein kinase (SAPK/JNK) in cells treated with 1-beta-d-arabinofuranosylcytosine (araC) and other genotoxic agents.	Cytarabine	187-191	protein kinase C delta	Homo sapiens	37-45
12377781-3	2002	The present studies demonstrate that PKCdelta is required in part for induction of the stress-activated protein kinase (SAPK/JNK) in cells treated with 1-beta-d-arabinofuranosylcytosine (araC) and other genotoxic agents.	Cytarabine	187-191	mitogen-activated protein kinase 9	Homo sapiens	120-124
12377781-3	2002	The present studies demonstrate that PKCdelta is required in part for induction of the stress-activated protein kinase (SAPK/JNK) in cells treated with 1-beta-d-arabinofuranosylcytosine (araC) and other genotoxic agents.	Cytarabine	187-191	mitogen-activated protein kinase 9	Homo sapiens	125-128
12459171-2	2002	In this report, we addressed the question whether the natural variability at p53 locus (the proline-arginine substitution at codon 72) affects the capacity of peripheral-blood mononuclear cells from healthy subjects to undergo in vitro apoptosis in response to the cytotoxic drug cytosine arabinoside.	Cytarabine	280-300	tumor protein p53	Homo sapiens	77-80
12435813-4	2002	We show that PKCzeta overexpression resulted in delayed apoptosis and significant resistance to both 1-beta-D-arabinofuranosylcytosine (ara-C) and daunorubicin (DNR), but there was no significant protection against cell-permeant C(6)-CER.	Cytarabine	101-134	protein kinase C zeta	Homo sapiens	13-20
12520735-1	2002	BACKGROUND &amp; OBJECTIVE: The previous study has identified two novel antisense oligonucleotides (AS-ODN) of new target point in the translation initiation and the coding region of bcl-2 mRNA that could increase the sensitivity of HL-60 and K562 cells lines to etoposide, daunorubicin, and araninosyl cytosine (Ara-C).	Cytarabine	313-318	BCL2 apoptosis regulator	Homo sapiens	183-188
12520735-2	2002	This study was designed to investigate whether the two novel bcl-2 AS-ODNs could increase Ara-C-induced apoptosis of cultured primary acute leukemia (AL) and chronic lymphocytic leukemia (CLL) Cells.	Cytarabine	90-95	BCL2 apoptosis regulator	Homo sapiens	61-66
12520735-8	2002	It was found that the two AS-ODNs respectively combined with Ara-C could significantly downregulate bcl-2 protein expression (P &lt; 0.05).	Cytarabine	61-66	BCL2 apoptosis regulator	Homo sapiens	100-105
12520735-11	2002	CONCLUSIONS: The two novel AS-ODNs of new target point in the translation initiation and the coding region of bcl-2 mRNA could enhance Ara-C induced apoptosis of AL and CLL cells.	Cytarabine	135-140	BCL2 apoptosis regulator	Homo sapiens	110-115
12435813-4	2002	We show that PKCzeta overexpression resulted in delayed apoptosis and significant resistance to both 1-beta-D-arabinofuranosylcytosine (ara-C) and daunorubicin (DNR), but there was no significant protection against cell-permeant C(6)-CER.	Cytarabine	136-141	protein kinase C zeta	Homo sapiens	13-20
12435813-6	2002	We further investigated p53/p56 Lyn activation in PKCzeta-overexpressing U937 cells treated with ara-C or DNR.	Cytarabine	97-102	tumor protein p53	Homo sapiens	24-27
12435813-6	2002	We further investigated p53/p56 Lyn activation in PKCzeta-overexpressing U937 cells treated with ara-C or DNR.	Cytarabine	97-102	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	28-35
12435813-6	2002	We further investigated p53/p56 Lyn activation in PKCzeta-overexpressing U937 cells treated with ara-C or DNR.	Cytarabine	97-102	protein kinase C zeta	Homo sapiens	50-57
12642689-2	2002	We have observed that exogenous expression of MRITalpha1/cFLIP(L) isoform also protects against cell death induced by a diverse group of chemotherapeutic drugs with different mechanisms of action, including doxorubicin, etoposide, cytosine arabinoside, daunorubicin, chlorambucil and cisplatin.	Cytarabine	231-251	CASP8 and FADD like apoptosis regulator	Homo sapiens	57-62
12439044-2	2002	The authors describe the clinical course and the pharmacokinetics of 2-CdA in a child with acute monoblastic leukemia who experienced acute renal failure during treatment with cytarabine and 2-CdA.	Cytarabine	176-186	cytidine deaminase	Homo sapiens	71-74
12481403-13	2002	This is the case in chronic myeloid leukemia where IFN alpha could be associated with aracytine or the inhibitors of tyrosine kinase.	Cytarabine	86-95	interferon alpha 1	Homo sapiens	51-60
12533044-4	2002	JM-1, SUP-B 15 and RS4 leukemic cell lines cleaved Bcl-2 to its 23 kDa form when exposed to the chemotherapeutic agents 1-beta-D-arabinofuranosyl-cytosine (Ara-C) or etoposide (VP-16).	Cytarabine	120-154	BCL2 apoptosis regulator	Homo sapiens	51-56
12533044-4	2002	JM-1, SUP-B 15 and RS4 leukemic cell lines cleaved Bcl-2 to its 23 kDa form when exposed to the chemotherapeutic agents 1-beta-D-arabinofuranosyl-cytosine (Ara-C) or etoposide (VP-16).	Cytarabine	156-161	BCL2 apoptosis regulator	Homo sapiens	51-56
12866723-1	2002	Effects of theophylline, lidocaine, cyclophosphamide, hyoscine N-butyl bromide, tranexamic acid and cytarabine on hexokinase (HK) from human erythrocytes have been investigated in vitro.	Cytarabine	100-110	hexokinase 1	Homo sapiens	114-124
12866723-1	2002	Effects of theophylline, lidocaine, cyclophosphamide, hyoscine N-butyl bromide, tranexamic acid and cytarabine on hexokinase (HK) from human erythrocytes have been investigated in vitro.	Cytarabine	100-110	hexokinase 1	Homo sapiens	126-128
12384536-5	2002	The decline in Bcr-Abl expression and TK activity in K562 R (-Bcr-Abl) cells was associated with reduced AKT kinase and signal transducers and activators of transcription-5 DNA binding activities and increased sensitivity to the death ligand Apo-2 ligand/tumor necrosis factor-related apoptosis-inducing ligand and 1-beta-D-arabinofuranosylcytosine-induced apoptosis.	Cytarabine	324-348	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	15-22
12377965-10	2002	CONCLUSION: Intracellular accumulation of ara-CTP is increased when 2-CdA is given with ara-C, but no schedule-dependent differences in this effect were seen.	Cytarabine	42-47	cytidine deaminase	Homo sapiens	70-73
12384536-5	2002	The decline in Bcr-Abl expression and TK activity in K562 R (-Bcr-Abl) cells was associated with reduced AKT kinase and signal transducers and activators of transcription-5 DNA binding activities and increased sensitivity to the death ligand Apo-2 ligand/tumor necrosis factor-related apoptosis-inducing ligand and 1-beta-D-arabinofuranosylcytosine-induced apoptosis.	Cytarabine	324-348	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
12716468-10	2002	Resistance to ara-C excluded MDR-1 gene involvement and highlighted other key genes such as MXR gene.	Cytarabine	14-19	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	92-95
12232794-3	2002	Bcl-X(L)-deficient primary telencephalic neuron cultures were highly susceptible to the apoptotic effects of cytosine arabinoside (AraC), a known genotoxic agent.	Cytarabine	109-129	BCL2-like 1	Mus musculus	0-8
12232794-3	2002	Bcl-X(L)-deficient primary telencephalic neuron cultures were highly susceptible to the apoptotic effects of cytosine arabinoside (AraC), a known genotoxic agent.	Cytarabine	131-135	BCL2-like 1	Mus musculus	0-8
12232794-4	2002	In contrast, neurons lacking p53, or both Bcl-X(L) and p53, were markedly, and equivalently, resistant to AraC-induced caspase-3 activation and death in vitro indicating that Bcl-X(L) lies downstream of p53 in DNA damage-induced neuronal death.	Cytarabine	106-110	transformation related protein 53, pseudogene	Mus musculus	29-32
12232794-4	2002	In contrast, neurons lacking p53, or both Bcl-X(L) and p53, were markedly, and equivalently, resistant to AraC-induced caspase-3 activation and death in vitro indicating that Bcl-X(L) lies downstream of p53 in DNA damage-induced neuronal death.	Cytarabine	106-110	BCL2-like 1	Mus musculus	42-50
12232794-4	2002	In contrast, neurons lacking p53, or both Bcl-X(L) and p53, were markedly, and equivalently, resistant to AraC-induced caspase-3 activation and death in vitro indicating that Bcl-X(L) lies downstream of p53 in DNA damage-induced neuronal death.	Cytarabine	106-110	transformation related protein 53, pseudogene	Mus musculus	55-58
12232794-4	2002	In contrast, neurons lacking p53, or both Bcl-X(L) and p53, were markedly, and equivalently, resistant to AraC-induced caspase-3 activation and death in vitro indicating that Bcl-X(L) lies downstream of p53 in DNA damage-induced neuronal death.	Cytarabine	106-110	caspase 3	Mus musculus	119-128
12232794-4	2002	In contrast, neurons lacking p53, or both Bcl-X(L) and p53, were markedly, and equivalently, resistant to AraC-induced caspase-3 activation and death in vitro indicating that Bcl-X(L) lies downstream of p53 in DNA damage-induced neuronal death.	Cytarabine	106-110	BCL2-like 1	Mus musculus	175-183
12232794-4	2002	In contrast, neurons lacking p53, or both Bcl-X(L) and p53, were markedly, and equivalently, resistant to AraC-induced caspase-3 activation and death in vitro indicating that Bcl-X(L) lies downstream of p53 in DNA damage-induced neuronal death.	Cytarabine	106-110	transformation related protein 53, pseudogene	Mus musculus	55-58
12182997-12	2002	CONCLUSIONS: In the dFdC-resistant lung tumor cell line SWg, the deficiency in dCK is related to the resistance to dFdC and ara-C.	Cytarabine	124-129	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	79-82
12077112-1	2002	While investigating the ability of p38 MAPK to regulate cytarabine (Ara C)-dependent differentiation of erythroleukemia K562 cells, we observed effects that indicated that the imidazoline class of p38 MAPK inhibitors prevented nucleoside transport.	Cytarabine	56-66	mitogen-activated protein kinase 14	Homo sapiens	35-38
12077112-1	2002	While investigating the ability of p38 MAPK to regulate cytarabine (Ara C)-dependent differentiation of erythroleukemia K562 cells, we observed effects that indicated that the imidazoline class of p38 MAPK inhibitors prevented nucleoside transport.	Cytarabine	56-66	mitogen-activated protein kinase 14	Homo sapiens	197-200
12077112-1	2002	While investigating the ability of p38 MAPK to regulate cytarabine (Ara C)-dependent differentiation of erythroleukemia K562 cells, we observed effects that indicated that the imidazoline class of p38 MAPK inhibitors prevented nucleoside transport.	Cytarabine	68-73	mitogen-activated protein kinase 14	Homo sapiens	35-38
12077112-1	2002	While investigating the ability of p38 MAPK to regulate cytarabine (Ara C)-dependent differentiation of erythroleukemia K562 cells, we observed effects that indicated that the imidazoline class of p38 MAPK inhibitors prevented nucleoside transport.	Cytarabine	68-73	mitogen-activated protein kinase 14	Homo sapiens	197-200
12210815-5	2002	We suggest that the muscle damage might be related to the known ability of cytarabine to trigger the release of cytochrome c from the mitochondria, which could lead to uncoupling of the oxidative phosphorylation with subsequent depletion of ATP reserves at the skeletal muscle and rhabdomyolysis.	Cytarabine	75-85	cytochrome c, somatic	Homo sapiens	112-124
12206990-0	2002	Ara-C- and daunorubicin-induced recruitment of Lyn in sphingomyelinase-enriched membrane rafts.	Cytarabine	0-5	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	47-50
12206990-1	2002	Induction of apoptosis by DNA-damaging agents such as 1-beta-D-arabinofuranosylcytosine (Ara-C) includes the activation of Lyn protein tyrosine kinase.	Cytarabine	54-87	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	123-126
12206990-1	2002	Induction of apoptosis by DNA-damaging agents such as 1-beta-D-arabinofuranosylcytosine (Ara-C) includes the activation of Lyn protein tyrosine kinase.	Cytarabine	89-94	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	123-126
12206990-2	2002	We have previously established that Ara-C-induced activation of Lyn results in its binding to a neutral sphingomyelinase (SMase) and is requisite for its stimulation and the induction of apoptosis in U937 cells.	Cytarabine	36-41	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	64-67
12206990-5	2002	Under Ara-C and daunorubicin (DNR) treatment, Lyn is rapidly activated and translocated into rafts.	Cytarabine	6-11	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	46-49
12481430-13	2002	UCN-01 potently enhanced the activity of 1-beta-D-arabinofuranosylcytosine in both p53 wild-type and mutant cells, whereas ICP-1 was inactive in this combination.	Cytarabine	41-74	tumor protein p53	Homo sapiens	83-86
12153475-1	2002	Treatment of mixed hippocampal cultures of neurones and astrocytes from day 2-4 in vitro (DIV 2-4) with 1 micro m cytosine arabinofuranoside (AraC) caused an activation of astrocytes as detected by a stellate morphology and a 10-fold increase in glial fibrillary acidic protein (GFAP) level compared with vehicle-treated cultures.	Cytarabine	114-140	glial fibrillary acidic protein	Homo sapiens	246-277
12153475-1	2002	Treatment of mixed hippocampal cultures of neurones and astrocytes from day 2-4 in vitro (DIV 2-4) with 1 micro m cytosine arabinofuranoside (AraC) caused an activation of astrocytes as detected by a stellate morphology and a 10-fold increase in glial fibrillary acidic protein (GFAP) level compared with vehicle-treated cultures.	Cytarabine	114-140	glial fibrillary acidic protein	Homo sapiens	279-283
12153475-5	2002	In cultures treated with vehicle and AraC, glutamate-induced neurotoxicity was mediated through stimulation of the NR1-NR2B subtype of NMDA receptors, because it was blocked by the NMDA receptor antagonist MK-801 and the NR1-NR2B selective receptor antagonist ifenprodil.	Cytarabine	37-41	glutamate ionotropic receptor NMDA type subunit 1	Homo sapiens	115-118
12153475-5	2002	In cultures treated with vehicle and AraC, glutamate-induced neurotoxicity was mediated through stimulation of the NR1-NR2B subtype of NMDA receptors, because it was blocked by the NMDA receptor antagonist MK-801 and the NR1-NR2B selective receptor antagonist ifenprodil.	Cytarabine	37-41	glutamate ionotropic receptor NMDA type subunit 2B	Homo sapiens	119-123
12153475-5	2002	In cultures treated with vehicle and AraC, glutamate-induced neurotoxicity was mediated through stimulation of the NR1-NR2B subtype of NMDA receptors, because it was blocked by the NMDA receptor antagonist MK-801 and the NR1-NR2B selective receptor antagonist ifenprodil.	Cytarabine	37-41	glutamate ionotropic receptor NMDA type subunit 1	Homo sapiens	221-224
12153475-5	2002	In cultures treated with vehicle and AraC, glutamate-induced neurotoxicity was mediated through stimulation of the NR1-NR2B subtype of NMDA receptors, because it was blocked by the NMDA receptor antagonist MK-801 and the NR1-NR2B selective receptor antagonist ifenprodil.	Cytarabine	37-41	glutamate ionotropic receptor NMDA type subunit 2B	Homo sapiens	225-229
12049569-0	2002	Enhancement of cytarabine sensitivity in squamous cell carcinoma cell line transfected with deoxycytidine kinase.	Cytarabine	15-25	deoxycytidine kinase	Homo sapiens	92-112
12008078-3	2002	These results suggest that expression of 5NT and reduced hENT1 in leukemic blasts at diagnosis are correlated with clinical outcome and may play a role in resistance mechanisms to ara-C in patients with AML.	Cytarabine	180-185	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	57-62
12136643-6	2002	Deoxycytidine kinase (dCK) is a rate-limiting enzyme for the activation of ara-C.	Cytarabine	75-80	deoxycytidine kinase	Mus musculus	0-20
12136643-6	2002	Deoxycytidine kinase (dCK) is a rate-limiting enzyme for the activation of ara-C.	Cytarabine	75-80	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	22-25
12049569-4	2002	The reason for this is thought to be that in cell lines of solid tumors the expression of cytidine deaminase, an enzyme that degrades cytarabine, is high, whereas the expression of deoxycytidine kinase (dCK), which phosphorylates cytarabine (a prodrug), is weak.	Cytarabine	134-144	cytidine deaminase	Homo sapiens	90-108
12049569-4	2002	The reason for this is thought to be that in cell lines of solid tumors the expression of cytidine deaminase, an enzyme that degrades cytarabine, is high, whereas the expression of deoxycytidine kinase (dCK), which phosphorylates cytarabine (a prodrug), is weak.	Cytarabine	134-144	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	203-206
12049569-4	2002	The reason for this is thought to be that in cell lines of solid tumors the expression of cytidine deaminase, an enzyme that degrades cytarabine, is high, whereas the expression of deoxycytidine kinase (dCK), which phosphorylates cytarabine (a prodrug), is weak.	Cytarabine	230-240	cytidine deaminase	Homo sapiens	90-108
12049569-4	2002	The reason for this is thought to be that in cell lines of solid tumors the expression of cytidine deaminase, an enzyme that degrades cytarabine, is high, whereas the expression of deoxycytidine kinase (dCK), which phosphorylates cytarabine (a prodrug), is weak.	Cytarabine	230-240	deoxycytidine kinase	Homo sapiens	181-201
12049569-4	2002	The reason for this is thought to be that in cell lines of solid tumors the expression of cytidine deaminase, an enzyme that degrades cytarabine, is high, whereas the expression of deoxycytidine kinase (dCK), which phosphorylates cytarabine (a prodrug), is weak.	Cytarabine	230-240	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	203-206
12049569-8	2002	RESULTS: Both retroviral and adenoviral vector-mediated transduction of the dCK complementary DNA resulted in marked sensitization of tongue squamous carcinoma cell lines to the cytotoxic effects of cytarabine in vitro.	Cytarabine	199-209	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	76-79
12049569-9	2002	CONCLUSION: The dCK-cytarabine system may be a useful approach for gene therapy of squamous cell carcinomas of the head and neck.	Cytarabine	20-30	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	16-19
12036920-5	2002	Only the dCK+ cell line phosphorylated 1-beta-D-arabinofuranosylcytosine (used as a substrate for dCK) in a cell-free system; phosphorylation of this compound by dGK+ was below the limit of detection.	Cytarabine	39-72	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	9-12
12060121-1	2002	Factors that reduce the intracellular concentration of triphosphorylated cytarabine (ara-CTP), the active form of cytarabine (ara-C), may induce chemoresistance in acute myeloid leukaemia (AML) patients.	Cytarabine	73-83	solute carrier family 25 member 1	Homo sapiens	89-92
12060121-1	2002	Factors that reduce the intracellular concentration of triphosphorylated cytarabine (ara-CTP), the active form of cytarabine (ara-C), may induce chemoresistance in acute myeloid leukaemia (AML) patients.	Cytarabine	114-124	solute carrier family 25 member 1	Homo sapiens	89-92
12060121-2	2002	These factors include reduced influx of ara-C by the hENT1 transporter, reduced phosphorylation by deoxycytidine kinase (dCK), and increased degradation by high Km cytoplasmic 5"-nucleotidase (5NT) and/or cytidine deaminase (CDD).	Cytarabine	40-45	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	53-58
12060121-3	2002	Increased levels of DNA polymerase alpha (DNA POL) and reduced levels of topoisomerase I (TOPO I) and topoisomerase II (TOPO II) have also been detected in ara-C-resistant cell lines.	Cytarabine	156-161	DNA polymerase alpha 1, catalytic subunit	Homo sapiens	20-40
12060121-10	2002	These results suggest that expression of DNA POL, 5NT and hENT1 at diagnosis may be resistance mechanisms to ara-C in AML patients.	Cytarabine	109-114	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	58-63
12036920-5	2002	Only the dCK+ cell line phosphorylated 1-beta-D-arabinofuranosylcytosine (used as a substrate for dCK) in a cell-free system; phosphorylation of this compound by dGK+ was below the limit of detection.	Cytarabine	39-72	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	98-101
11961058-4	2002	In contrast, ectopic expression of Bcl-x(L) blocked cytochrome c redistribution as well as all other events involved in ara-C/bryostatin 1-mediated apoptosis.	Cytarabine	120-125	BCL2 like 1	Homo sapiens	35-43
11961058-0	2002	Bryostatin 1 increases 1-beta-D-arabinofuranosylcytosine-induced cytochrome c release and apoptosis in human leukemia cells ectopically expressing Bcl-x(L).	Cytarabine	23-56	cytochrome c, somatic	Homo sapiens	65-77
11961058-0	2002	Bryostatin 1 increases 1-beta-D-arabinofuranosylcytosine-induced cytochrome c release and apoptosis in human leukemia cells ectopically expressing Bcl-x(L).	Cytarabine	23-56	BCL2 like 1	Homo sapiens	147-155
12021410-0	2002	Inhibition of c-Abl with STI571 attenuates stress-activated protein kinase activation and apoptosis in the cellular response to 1-beta-D-arabinofuranosylcytosine.	Cytarabine	128-161	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	14-19
12021410-1	2002	The response of myeloid leukemia cells to treatment with 1-beta-D-arabinofuranosylcytosine (ara-C) includes activation of the c-Abl protein tyrosine kinase and the stress-activated protein kinase (SAPK).	Cytarabine	57-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-131
12021410-1	2002	The response of myeloid leukemia cells to treatment with 1-beta-D-arabinofuranosylcytosine (ara-C) includes activation of the c-Abl protein tyrosine kinase and the stress-activated protein kinase (SAPK).	Cytarabine	57-90	mitogen-activated protein kinase 9	Homo sapiens	197-201
12021410-1	2002	The response of myeloid leukemia cells to treatment with 1-beta-D-arabinofuranosylcytosine (ara-C) includes activation of the c-Abl protein tyrosine kinase and the stress-activated protein kinase (SAPK).	Cytarabine	92-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-131
12021410-1	2002	The response of myeloid leukemia cells to treatment with 1-beta-D-arabinofuranosylcytosine (ara-C) includes activation of the c-Abl protein tyrosine kinase and the stress-activated protein kinase (SAPK).	Cytarabine	92-97	mitogen-activated protein kinase 9	Homo sapiens	197-201
12021410-2	2002	The present studies demonstrate that treatment of human U-937 leukemia cells with ara-C is associated with translocation of SAPK to mitochondria.	Cytarabine	82-87	mitogen-activated protein kinase 9	Homo sapiens	124-128
12021410-3	2002	STI571 (imatinib mesylate), an inhibitor of c-Abl, blocked both activation and mitochondrial targeting of SAPK in the ara-C response.	Cytarabine	118-123	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-49
12021410-3	2002	STI571 (imatinib mesylate), an inhibitor of c-Abl, blocked both activation and mitochondrial targeting of SAPK in the ara-C response.	Cytarabine	118-123	mitogen-activated protein kinase 9	Homo sapiens	106-110
12021410-5	2002	The results further show that STI571 inhibits ara-C-induced loss of mitochondrial transmembrane potential, caspase-3 activation, and apoptosis.	Cytarabine	46-51	caspase 3	Homo sapiens	107-116
12021410-6	2002	These findings demonstrate that STI571 down-regulates c-Abl-mediated signals that target the mitochondria in the apoptotic response to ara-C.	Cytarabine	135-140	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-59
12054682-0	2002	Cytotoxic activity of 2",2"-difluorodeoxycytidine, 5-aza-2"-deoxycytidine and cytosine arabinoside in cells transduced with deoxycytidine kinase gene.	Cytarabine	78-98	deoxycytidine kinase	Mus musculus	124-144
12054682-5	2002	The dCK-transduced cells showed an increase in cytotoxicity to the analogs, cytosine arabinoside (ARA-C), and 5-aza-2"-deoxycytidine (5-AZA-CdR).	Cytarabine	76-96	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	4-7
12054682-5	2002	The dCK-transduced cells showed an increase in cytotoxicity to the analogs, cytosine arabinoside (ARA-C), and 5-aza-2"-deoxycytidine (5-AZA-CdR).	Cytarabine	98-103	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	4-7
12168812-11	2002	Conversely, the caspase-3 activity increased in a dose-dependent manner and inversely-correlated with loss of cell viability (r= 0.91) after exposure to IDA + TXR combination in the double drug-resistant line to both ara-C and ASNase.	Cytarabine	217-222	caspase 3	Homo sapiens	16-25
12125986-2	2002	DepoCyt is a slow-release formulation of cytarabine that maintains cytotoxic concentrations of free cytarabine in the CSF for &gt;14 days following a single injection.	Cytarabine	41-51	colony stimulating factor 2	Homo sapiens	118-121
12125986-2	2002	DepoCyt is a slow-release formulation of cytarabine that maintains cytotoxic concentrations of free cytarabine in the CSF for &gt;14 days following a single injection.	Cytarabine	100-110	colony stimulating factor 2	Homo sapiens	118-121
11961058-2	2002	Coadministration of bryostatin 1 with ara-C resulted in enhanced cytosolic release of cytochrome c and Smac/DIABLO, procaspase-3 and -9 activation, loss of mitochondrial membrane potential (Deltapsi(m)), poly(ADP-ribosyl)phosphorylase degradation, apoptosis, and loss of clonogenic survival in U937/Bcl-x(L) cells, although effects were not as marked as in empty-vector control cells.	Cytarabine	38-43	cytochrome c, somatic	Homo sapiens	86-98
11961058-2	2002	Coadministration of bryostatin 1 with ara-C resulted in enhanced cytosolic release of cytochrome c and Smac/DIABLO, procaspase-3 and -9 activation, loss of mitochondrial membrane potential (Deltapsi(m)), poly(ADP-ribosyl)phosphorylase degradation, apoptosis, and loss of clonogenic survival in U937/Bcl-x(L) cells, although effects were not as marked as in empty-vector control cells.	Cytarabine	38-43	diablo IAP-binding mitochondrial protein	Homo sapiens	103-107
11961058-2	2002	Coadministration of bryostatin 1 with ara-C resulted in enhanced cytosolic release of cytochrome c and Smac/DIABLO, procaspase-3 and -9 activation, loss of mitochondrial membrane potential (Deltapsi(m)), poly(ADP-ribosyl)phosphorylase degradation, apoptosis, and loss of clonogenic survival in U937/Bcl-x(L) cells, although effects were not as marked as in empty-vector control cells.	Cytarabine	38-43	diablo IAP-binding mitochondrial protein	Homo sapiens	108-114
11961058-2	2002	Coadministration of bryostatin 1 with ara-C resulted in enhanced cytosolic release of cytochrome c and Smac/DIABLO, procaspase-3 and -9 activation, loss of mitochondrial membrane potential (Deltapsi(m)), poly(ADP-ribosyl)phosphorylase degradation, apoptosis, and loss of clonogenic survival in U937/Bcl-x(L) cells, although effects were not as marked as in empty-vector control cells.	Cytarabine	38-43	caspase 3	Homo sapiens	116-135
11961058-2	2002	Coadministration of bryostatin 1 with ara-C resulted in enhanced cytosolic release of cytochrome c and Smac/DIABLO, procaspase-3 and -9 activation, loss of mitochondrial membrane potential (Deltapsi(m)), poly(ADP-ribosyl)phosphorylase degradation, apoptosis, and loss of clonogenic survival in U937/Bcl-x(L) cells, although effects were not as marked as in empty-vector control cells.	Cytarabine	38-43	BCL2 like 1	Homo sapiens	299-304
11956089-5	2002	The experimental data indicate that the disruption of UPase activity in murine ES cells leads to a 10-fold increase in 5-FU IC(50) and a 2-3-fold reduction in its incorporation into nucleic acids, whereas no differences in toxicity is seen with other pyrimidine nucleoside analogues such as 5-fluorouridine, 2"-deoxy-5-fluorouridine, and 1-beta-D-arabinofuranosylcytosine compared with WT (wild-type) ES cells.	Cytarabine	338-371	uridine phosphorylase 1	Mus musculus	54-59
11867204-7	2002	Importantly, we found that hTERT-transfected K562 cells are protected against apoptosis induced by serum deprivation and double-stranded DNA break inducing agents (ionizing irradiation, and etoposide (VP-16)), but not against DNA synthesis inhibitors (1-beta-D-arabinofuranosylcytosine and hydroxyurea).	Cytarabine	252-285	telomerase reverse transcriptase	Homo sapiens	27-32
11849208-1	2002	2-chlorodeoxyadenosine (2-CdA) and arabinosylcytosine (araC) are nucleoside drugs that are used to treat various leukaemias, although 2-CdA has not been tested extensively in children with acute lymphoblastic leukaemia (ALL).	Cytarabine	35-53	cytidine deaminase	Homo sapiens	136-139
12034328-7	2002	Addition of 10(-5) M cytosine arabinoside (CAr) at the 4th day in vitro (DIV) improved TRH cell content per dish compared to addition at 5 DIV; 2.5-5x10(-5) M bromodeoxyuridine added at seeding reduced cell survival and did not enhance TRH levels, in comparison to CAr-treated cultures.	Cytarabine	21-41	thyrotropin releasing hormone	Rattus norvegicus	87-90
12034328-7	2002	Addition of 10(-5) M cytosine arabinoside (CAr) at the 4th day in vitro (DIV) improved TRH cell content per dish compared to addition at 5 DIV; 2.5-5x10(-5) M bromodeoxyuridine added at seeding reduced cell survival and did not enhance TRH levels, in comparison to CAr-treated cultures.	Cytarabine	21-41	thyrotropin releasing hormone	Rattus norvegicus	236-239
12034328-7	2002	Addition of 10(-5) M cytosine arabinoside (CAr) at the 4th day in vitro (DIV) improved TRH cell content per dish compared to addition at 5 DIV; 2.5-5x10(-5) M bromodeoxyuridine added at seeding reduced cell survival and did not enhance TRH levels, in comparison to CAr-treated cultures.	Cytarabine	43-46	thyrotropin releasing hormone	Rattus norvegicus	87-90
12034328-7	2002	Addition of 10(-5) M cytosine arabinoside (CAr) at the 4th day in vitro (DIV) improved TRH cell content per dish compared to addition at 5 DIV; 2.5-5x10(-5) M bromodeoxyuridine added at seeding reduced cell survival and did not enhance TRH levels, in comparison to CAr-treated cultures.	Cytarabine	43-46	thyrotropin releasing hormone	Rattus norvegicus	236-239
11938460-3	2002	Human cytidine deaminase (hCD) is a chemoresistance gene that inactivates cytotoxic cytosine nucleoside analogs, such as cytosine arabinoside (Ara-C).	Cytarabine	121-141	cytidine deaminase	Homo sapiens	6-24
11938460-3	2002	Human cytidine deaminase (hCD) is a chemoresistance gene that inactivates cytotoxic cytosine nucleoside analogs, such as cytosine arabinoside (Ara-C).	Cytarabine	121-141	DIH1	Homo sapiens	26-29
11938460-3	2002	Human cytidine deaminase (hCD) is a chemoresistance gene that inactivates cytotoxic cytosine nucleoside analogs, such as cytosine arabinoside (Ara-C).	Cytarabine	143-148	cytidine deaminase	Homo sapiens	6-24
11938460-3	2002	Human cytidine deaminase (hCD) is a chemoresistance gene that inactivates cytotoxic cytosine nucleoside analogs, such as cytosine arabinoside (Ara-C).	Cytarabine	143-148	DIH1	Homo sapiens	26-29
11938460-8	2002	Increased selective pressure with 2.5 microM Ara-C allowed for enrichment of a mixed population of MSCs expressing approximately six-fold higher levels of GFP and of CD activity when compared with unmanipulated engineered MSCs.	Cytarabine	45-50	DIH1	Homo sapiens	166-168
12165291-0	2002	Arsenic trioxide, retinoic acid and Ara-c regulated the expression of annexin II on the surface of APL cells, a novel co-receptor for plasminogen/tissue plasminogen activator.	Cytarabine	36-41	annexin A2	Homo sapiens	70-80
12165291-5	2002	Consistent with in vivo findings, annexin II on NB(4) cell surface and its mRNA content were downregulated with 1 microM As(2)O(3) or 1 microM ATRA, while 2 microg Ara-c enhanced the expression of annexin II and the generation of cell-surface plasmin before its induction of apoptosis.	Cytarabine	164-169	annexin A2	Homo sapiens	34-44
12165291-5	2002	Consistent with in vivo findings, annexin II on NB(4) cell surface and its mRNA content were downregulated with 1 microM As(2)O(3) or 1 microM ATRA, while 2 microg Ara-c enhanced the expression of annexin II and the generation of cell-surface plasmin before its induction of apoptosis.	Cytarabine	164-169	annexin A2	Homo sapiens	197-207
12165291-5	2002	Consistent with in vivo findings, annexin II on NB(4) cell surface and its mRNA content were downregulated with 1 microM As(2)O(3) or 1 microM ATRA, while 2 microg Ara-c enhanced the expression of annexin II and the generation of cell-surface plasmin before its induction of apoptosis.	Cytarabine	164-169	plasminogen	Homo sapiens	243-250
12170773-2	2002	A 3-fold increase in full-length Bcl-2 protein conferred substantial resistance to ara-C-associated lethality, but not to FP-mediated cytochrome c release, caspase-3 and-9 activation and apoptosis.	Cytarabine	83-88	BCL2 apoptosis regulator	Homo sapiens	33-38
12575210-5	2002	The combination of IFN with Ara-c enhanced the cytotoxic effect of IFN or Ara-c alone on CML cells.	Cytarabine	28-33	interferon alpha 1	Homo sapiens	67-70
12575210-5	2002	The combination of IFN with Ara-c enhanced the cytotoxic effect of IFN or Ara-c alone on CML cells.	Cytarabine	74-79	interferon alpha 1	Homo sapiens	19-22
11849208-1	2002	2-chlorodeoxyadenosine (2-CdA) and arabinosylcytosine (araC) are nucleoside drugs that are used to treat various leukaemias, although 2-CdA has not been tested extensively in children with acute lymphoblastic leukaemia (ALL).	Cytarabine	55-59	cytidine deaminase	Homo sapiens	136-139
11853918-6	2002	The greater loading of the PEG backbone appears to have achieved a minimum threshold concentration for the therapeutic delivery of ara-C.	Cytarabine	131-136	progestagen associated endometrial protein	Homo sapiens	27-30
11830489-0	2002	Functional role of alternatively spliced deoxycytidine kinase in sensitivity to cytarabine of acute myeloid leukemic cells.	Cytarabine	80-90	deoxycytidine kinase	Homo sapiens	41-61
11830489-10	2002	However, a cell expressing alternatively spliced dCK forms that has lost wt dCK expression is resistant to the cytotoxic effects of AraC.	Cytarabine	132-136	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	76-79
11830489-5	2002	In the current study, the biologic role of the alternatively spliced dCK forms in AraC resistance was further investigated by retroviral transductions in rat leukemic cells.	Cytarabine	82-86	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	69-72
11830489-6	2002	Introduction of inactive, alternatively spliced dCK forms into AraC-resistant K7 cells, with no endogenous wild-type (wt) dCK activity, could not restore AraC sensitivity, whereas wt dCK fully restored the AraC-sensitive phenotype.	Cytarabine	63-67	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	48-51
11830489-10	2002	However, a cell expressing alternatively spliced dCK forms that has lost wt dCK expression is resistant to the cytotoxic effects of AraC.	Cytarabine	132-136	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	49-52
11860280-7	2002	Ara C toxicity is known to utilize the p53-dependent signaling pathway to initiate apoptosis.	Cytarabine	0-5	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	39-42
11830549-0	2002	An MCL1-overexpressing Burkitt lymphoma subline exhibits enhanced survival on exposure to serum deprivation, topoisomerase inhibitors, or staurosporine but remains sensitive to 1-beta-D-arabinofuranosylcytosine.	Cytarabine	177-210	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	3-7
12127861-5	2002	Similar to the structurally and functionally related deoxycytidine analog ara-C, the first, crucial step in phosphorylation is catalyzed by deoxycytidine kinase (dCK).	Cytarabine	74-79	deoxycytidine kinase	Homo sapiens	140-160
12127861-5	2002	Similar to the structurally and functionally related deoxycytidine analog ara-C, the first, crucial step in phosphorylation is catalyzed by deoxycytidine kinase (dCK).	Cytarabine	74-79	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	162-165
11821962-5	2002	Mutant p53 stimulates recombination induced by the replication elongation inhibitors (aphidicolin, hydroxyurea and Ara-C) but is without effect on recombination induced by the initiation inhibitors (mimosine and ciclopirox olamine).	Cytarabine	115-120	tumor protein p53	Homo sapiens	7-10
12803126-1	2002	BACKGROUND: Big ICE chemotherapy (consisting of Idarubicin, high dose Cytosine arabinoside and Etoposide), has proven its efficacy in the treatment of patients with relapse/refractory acute myeloblastic leukemia.	Cytarabine	70-90	carboxylesterase 2	Homo sapiens	16-19
12145468-0	2002	CD7+ and CD56+ myeloid/natural killer cell precursor acute leukemia treated with idarubicin and cytosine arabinoside.	Cytarabine	96-116	CD7 molecule	Homo sapiens	0-3
12145468-0	2002	CD7+ and CD56+ myeloid/natural killer cell precursor acute leukemia treated with idarubicin and cytosine arabinoside.	Cytarabine	96-116	neural cell adhesion molecule 1	Homo sapiens	9-13
12658802-4	2002	Induced by FasL+ CD34+ + DNR, FasL+ CD34+ + Ara-C, the ratio was (13.4 +/- 1.0)% (P &lt; 0.05), (17.9 +/- 1.3)% (P &lt; 0.01), respectively.	Cytarabine	44-49	Fas ligand	Homo sapiens	30-34
12658802-4	2002	Induced by FasL+ CD34+ + DNR, FasL+ CD34+ + Ara-C, the ratio was (13.4 +/- 1.0)% (P &lt; 0.05), (17.9 +/- 1.3)% (P &lt; 0.01), respectively.	Cytarabine	44-49	CD34 molecule	Homo sapiens	36-40
12111518-10	2002	Furthermore, c-myc amplification may play an important role in altering phenotype and growth characteristics in vitro and in vivo, and for increasing sensitivity to Ara C and the potential of cancer cells to metastasize to lymph nodes.	Cytarabine	165-170	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	13-18
11698292-9	2001	In contrast, in vitro treatment with cytarabine and etoposide induced p53 protein, CD95 receptor expression, CD95 sensitivity, and CD95 receptor-ligand interaction in stimulated cycling lymphocytes, but no such induction was seen in resting cells.	Cytarabine	37-47	tumor protein p53	Homo sapiens	70-73
11726320-7	2001	In the following 4 patients the Ara-C was reduced to 300 mg: 2 had severe hematologic and 2 moderate gastrointestinal toxicity; IFN and Ara-C were reduced in 2 patients and treatment discontinued in 2 due to progression or toxicity; the other 2 achieved a minor cytogenetic response, progressing in one to a major response after 6 more cycles.	Cytarabine	32-37	interferon alpha 1	Homo sapiens	128-131
11726320-8	2001	In 8 patients the starting Ara-C dose was 200 mg: 5 had moderate-severe hematologic and 5 mild gastrointestinal toxicity; IFN was reduced in 5, Ara-C in 1, and treatment discontinued in 1; Ara-C was increased in 7 cases; hematologic response was obtained in 4 patients, 2 of whom attained a minor and 1 a major cytogenetic response.	Cytarabine	27-32	interferon alpha 1	Homo sapiens	122-125
11723252-7	2001	In addition, treatment of U-937 human myeloid leukemia cells with 1-beta-D-arabinofuranosylcytosine (ara-C) was associated with induction of the PKCdelta kinase function and inhibition of SHPTP1 activity.	Cytarabine	66-99	protein kinase C delta	Homo sapiens	145-153
11723252-7	2001	In addition, treatment of U-937 human myeloid leukemia cells with 1-beta-D-arabinofuranosylcytosine (ara-C) was associated with induction of the PKCdelta kinase function and inhibition of SHPTP1 activity.	Cytarabine	66-99	protein tyrosine phosphatase non-receptor type 6	Homo sapiens	188-194
11723252-7	2001	In addition, treatment of U-937 human myeloid leukemia cells with 1-beta-D-arabinofuranosylcytosine (ara-C) was associated with induction of the PKCdelta kinase function and inhibition of SHPTP1 activity.	Cytarabine	101-106	protein kinase C delta	Homo sapiens	145-153
11723252-7	2001	In addition, treatment of U-937 human myeloid leukemia cells with 1-beta-D-arabinofuranosylcytosine (ara-C) was associated with induction of the PKCdelta kinase function and inhibition of SHPTP1 activity.	Cytarabine	101-106	protein tyrosine phosphatase non-receptor type 6	Homo sapiens	188-194
11723252-8	2001	Down-regulation of SHPTP1 by ara-C was blocked by the PKCdelta inhibitor rottlerin but not by the PKCalpha and -beta inhibitor Go6976.	Cytarabine	29-34	protein tyrosine phosphatase non-receptor type 6	Homo sapiens	19-25
11723252-8	2001	Down-regulation of SHPTP1 by ara-C was blocked by the PKCdelta inhibitor rottlerin but not by the PKCalpha and -beta inhibitor Go6976.	Cytarabine	29-34	protein kinase C delta	Homo sapiens	54-62
11698292-9	2001	In contrast, in vitro treatment with cytarabine and etoposide induced p53 protein, CD95 receptor expression, CD95 sensitivity, and CD95 receptor-ligand interaction in stimulated cycling lymphocytes, but no such induction was seen in resting cells.	Cytarabine	37-47	Fas cell surface death receptor	Homo sapiens	83-87
11698292-9	2001	In contrast, in vitro treatment with cytarabine and etoposide induced p53 protein, CD95 receptor expression, CD95 sensitivity, and CD95 receptor-ligand interaction in stimulated cycling lymphocytes, but no such induction was seen in resting cells.	Cytarabine	37-47	Fas cell surface death receptor	Homo sapiens	109-113
11698292-9	2001	In contrast, in vitro treatment with cytarabine and etoposide induced p53 protein, CD95 receptor expression, CD95 sensitivity, and CD95 receptor-ligand interaction in stimulated cycling lymphocytes, but no such induction was seen in resting cells.	Cytarabine	37-47	Fas cell surface death receptor	Homo sapiens	109-113
11745875-9	2001	CONCLUSIONS: We conclude that high-dose cytarabine treatment often induces release of TNF-alpha followed by the sequential release of other proinflammatory cytokines.	Cytarabine	40-50	tumor necrosis factor	Homo sapiens	86-95
11593419-4	2001	When HL-60 cells synchronized at the G1/S boundary were treated with pro-apoptotic cytosine arabinoside (araC), PP1alpha protein increased twofold and PP1 activity about 30% within 1 h. This was followed by pRB dephosphorylation, pRB cleavage by caspases, DNA fragmentation, the appearance of cells with &lt;2n DNA content and finally, dying and dead cells.	Cytarabine	83-103	protein phosphatase 1 catalytic subunit alpha	Homo sapiens	112-120
11860442-0	2001	FAB M4 and high CD14 surface expression is associated with high cellular resistance to Ara-C and daunorubicin: implications for clinical outcome in acute myeloid leukaemia.	Cytarabine	87-92	FA complementation group B	Homo sapiens	0-3
11860442-0	2001	FAB M4 and high CD14 surface expression is associated with high cellular resistance to Ara-C and daunorubicin: implications for clinical outcome in acute myeloid leukaemia.	Cytarabine	87-92	CD14 molecule	Homo sapiens	16-20
11860442-2	2001	We demonstrate that high CD14 expression is highly significantly associated with high cellular Ara-C and Dau resistance in univariate as well as multivariate analyses.	Cytarabine	95-100	CD14 molecule	Homo sapiens	25-29
11860442-3	2001	FAB subtypes with highest and lowest cellular Ara-C resistance were M4 and M5, respectively (P &lt; 0.01, one-way anova), whereas FAB subtypes with highest and lowest cellular Dau resistance were M4 and M1, respectively (P &lt; 0.01, one-way anova).	Cytarabine	46-51	FA complementation group B	Homo sapiens	0-3
11860442-8	2001	We conclude that although cases with high blast cell CD14 expression (and FAB-M4 cases) were more resistant to Ara-C as well as Dau in vitro, the clinical and biological significance of this may be debatable because of interactions with major prognostic factors in AML.	Cytarabine	111-116	CD14 molecule	Homo sapiens	53-57
11860442-8	2001	We conclude that although cases with high blast cell CD14 expression (and FAB-M4 cases) were more resistant to Ara-C as well as Dau in vitro, the clinical and biological significance of this may be debatable because of interactions with major prognostic factors in AML.	Cytarabine	111-116	FA complementation group B	Homo sapiens	74-77
11585758-3	2001	The CCRF-CEM leukemia cell line was highly sensitive to the antiproliferative effects of troxacitabine, gemcitabine, and cytarabine with inhibition of proliferation by 50% observed at 160, 20, and 10 nM, respectively, whereas a deoxycytidine kinase (dCK)-deficient variant (CEM/dCK(-)) was resistant to all three drugs.	Cytarabine	121-131	deoxycytidine kinase	Homo sapiens	228-248
11585758-3	2001	The CCRF-CEM leukemia cell line was highly sensitive to the antiproliferative effects of troxacitabine, gemcitabine, and cytarabine with inhibition of proliferation by 50% observed at 160, 20, and 10 nM, respectively, whereas a deoxycytidine kinase (dCK)-deficient variant (CEM/dCK(-)) was resistant to all three drugs.	Cytarabine	121-131	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	250-253
11585758-3	2001	The CCRF-CEM leukemia cell line was highly sensitive to the antiproliferative effects of troxacitabine, gemcitabine, and cytarabine with inhibition of proliferation by 50% observed at 160, 20, and 10 nM, respectively, whereas a deoxycytidine kinase (dCK)-deficient variant (CEM/dCK(-)) was resistant to all three drugs.	Cytarabine	121-131	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	278-281
11532524-3	2001	Following treatment with Ara-C or VP-16 in vitro, caspase 3 activity in leukemic cells was consistently reduced by co-culture of leukemic cells with human bone marrow stromal cell layers.	Cytarabine	25-30	caspase 3	Homo sapiens	50-59
11593419-4	2001	When HL-60 cells synchronized at the G1/S boundary were treated with pro-apoptotic cytosine arabinoside (araC), PP1alpha protein increased twofold and PP1 activity about 30% within 1 h. This was followed by pRB dephosphorylation, pRB cleavage by caspases, DNA fragmentation, the appearance of cells with &lt;2n DNA content and finally, dying and dead cells.	Cytarabine	83-103	inorganic pyrophosphatase 1	Homo sapiens	112-115
11593419-4	2001	When HL-60 cells synchronized at the G1/S boundary were treated with pro-apoptotic cytosine arabinoside (araC), PP1alpha protein increased twofold and PP1 activity about 30% within 1 h. This was followed by pRB dephosphorylation, pRB cleavage by caspases, DNA fragmentation, the appearance of cells with &lt;2n DNA content and finally, dying and dead cells.	Cytarabine	83-103	RB transcriptional corepressor 1	Homo sapiens	207-210
11593419-4	2001	When HL-60 cells synchronized at the G1/S boundary were treated with pro-apoptotic cytosine arabinoside (araC), PP1alpha protein increased twofold and PP1 activity about 30% within 1 h. This was followed by pRB dephosphorylation, pRB cleavage by caspases, DNA fragmentation, the appearance of cells with &lt;2n DNA content and finally, dying and dead cells.	Cytarabine	83-103	RB transcriptional corepressor 1	Homo sapiens	230-233
11593419-7	2001	Similarly, araC-resistant cells, normally unable to die in response to araC, initiated apoptosis when electroporated with active PP1alpha.	Cytarabine	11-15	protein phosphatase 1 catalytic subunit alpha	Homo sapiens	129-137
11535530-2	2001	Cytoplasmic 5"-nucleotidase (5NT) dephosphorylates ara-CMP, a key intermediate, preventing accumulation of ara-CTP and may reduce cellular sensitivity to the cytotoxic activity of ara-C.	Cytarabine	51-56	5'-nucleotidase ecto	Homo sapiens	12-27
11535530-2	2001	Cytoplasmic 5"-nucleotidase (5NT) dephosphorylates ara-CMP, a key intermediate, preventing accumulation of ara-CTP and may reduce cellular sensitivity to the cytotoxic activity of ara-C.	Cytarabine	51-56	5'-nucleotidase ecto	Homo sapiens	29-32
11527401-0	2001	MEK1/2 inhibitors promote Ara-C-induced apoptosis but not loss of Deltapsi(m) in HL-60 cells.	Cytarabine	26-31	mitogen-activated protein kinase kinase 1	Homo sapiens	0-6
11527401-2	2001	Coadministration of subtoxic concentrations of the MEK1/2 inhibitors U0126 (20 microM), PD98059 (40 microM), or PD184352 (10 microM) with 10-100 microM ara-C (6 h) potentiated apoptosis (i.e., by approx twofold), and pro-caspase 3, pro-caspase 8, Bid, and PARP cleavage.	Cytarabine	152-157	mitogen-activated protein kinase kinase 1	Homo sapiens	51-57
11527401-5	2001	Together, these findings indicate that potentiation of ara-C-mediated lethality in HL-60 cells by MEK1/2 inhibitors involves enhanced cytosolic release of cytochrome c and Smac/DIABLO but not discharge of DeltaPsi(m), implicating activation of an apoptotic pathway that differs, at least with respect to the nature of the accompanying mitochondrial injury, from that triggered by ara-C alone.	Cytarabine	55-60	mitogen-activated protein kinase kinase 1	Homo sapiens	98-104
11527401-4	2001	U0126/ara-C-mediated apoptosis and pro-caspase 3 activation, but not cytochrome c or Smac/DIABLO release, were blocked by the pan-caspase inhibitor ZVAD-fmk.	Cytarabine	6-11	caspase 3	Homo sapiens	35-48
11527401-5	2001	Together, these findings indicate that potentiation of ara-C-mediated lethality in HL-60 cells by MEK1/2 inhibitors involves enhanced cytosolic release of cytochrome c and Smac/DIABLO but not discharge of DeltaPsi(m), implicating activation of an apoptotic pathway that differs, at least with respect to the nature of the accompanying mitochondrial injury, from that triggered by ara-C alone.	Cytarabine	55-60	cytochrome c, somatic	Homo sapiens	155-167
11527401-5	2001	Together, these findings indicate that potentiation of ara-C-mediated lethality in HL-60 cells by MEK1/2 inhibitors involves enhanced cytosolic release of cytochrome c and Smac/DIABLO but not discharge of DeltaPsi(m), implicating activation of an apoptotic pathway that differs, at least with respect to the nature of the accompanying mitochondrial injury, from that triggered by ara-C alone.	Cytarabine	55-60	diablo IAP-binding mitochondrial protein	Homo sapiens	172-176
11417479-7	2001	Exposure of WT cells to either dexamethasone or the cytotoxic agents cytarabine and methotrexate caused translocation of the glucocorticoid receptor from the cytoplasm into the nucleus.	Cytarabine	69-79	nuclear receptor subfamily 3 group C member 1	Homo sapiens	125-148
11527401-5	2001	Together, these findings indicate that potentiation of ara-C-mediated lethality in HL-60 cells by MEK1/2 inhibitors involves enhanced cytosolic release of cytochrome c and Smac/DIABLO but not discharge of DeltaPsi(m), implicating activation of an apoptotic pathway that differs, at least with respect to the nature of the accompanying mitochondrial injury, from that triggered by ara-C alone.	Cytarabine	55-60	diablo IAP-binding mitochondrial protein	Homo sapiens	177-183
11527401-5	2001	Together, these findings indicate that potentiation of ara-C-mediated lethality in HL-60 cells by MEK1/2 inhibitors involves enhanced cytosolic release of cytochrome c and Smac/DIABLO but not discharge of DeltaPsi(m), implicating activation of an apoptotic pathway that differs, at least with respect to the nature of the accompanying mitochondrial injury, from that triggered by ara-C alone.	Cytarabine	380-385	mitogen-activated protein kinase kinase 1	Homo sapiens	98-104
11564071-2	2001	Granulocyte colony-stimulating factor (G-CSF) was infused continuously from 12 h before until the end of Ara-C therapy to enhance the antileukaemia effect of Ara-C.	Cytarabine	105-110	colony stimulating factor 3	Homo sapiens	0-37
11564071-2	2001	Granulocyte colony-stimulating factor (G-CSF) was infused continuously from 12 h before until the end of Ara-C therapy to enhance the antileukaemia effect of Ara-C.	Cytarabine	105-110	colony stimulating factor 3	Homo sapiens	39-44
11564071-2	2001	Granulocyte colony-stimulating factor (G-CSF) was infused continuously from 12 h before until the end of Ara-C therapy to enhance the antileukaemia effect of Ara-C.	Cytarabine	158-163	colony stimulating factor 3	Homo sapiens	0-37
11564071-2	2001	Granulocyte colony-stimulating factor (G-CSF) was infused continuously from 12 h before until the end of Ara-C therapy to enhance the antileukaemia effect of Ara-C.	Cytarabine	158-163	colony stimulating factor 3	Homo sapiens	39-44
11561778-0	2001	Reversal of cytosine arabinoside (ara-C) resistance by the synergistic combination of 6-thioguanine plus ara-C plus PEG-asparaginase (TGAP) in human leukemia lines lacking or expressing p53 protein.	Cytarabine	34-39	tumor protein p53	Homo sapiens	186-189
11461962-7	2001	These data support a model in which AraC induces neuronal apoptosis by provoking the generation of reactive oxygen species, causing oxidative DNA damage and initiating the p53-dependent apoptotic program.	Cytarabine	36-40	tumor protein p53	Homo sapiens	172-175
11526598-5	2001	Combination regimens of IFN-alpha with other drugs such as cytarabine (Ara-C) appear to enhance efficacy and are currently under investigation.	Cytarabine	59-69	interferon alpha 1	Homo sapiens	24-33
11526598-5	2001	Combination regimens of IFN-alpha with other drugs such as cytarabine (Ara-C) appear to enhance efficacy and are currently under investigation.	Cytarabine	71-76	interferon alpha 1	Homo sapiens	24-33
11412905-2	2001	Bax-deficient embryos show decreased neuronal programmed cell death in vivo and resistance to cytosine arabinoside (AraC)-induced neuronal apoptosis in vitro.	Cytarabine	94-114	BCL2 associated X, apoptosis regulator	Homo sapiens	0-3
11412905-2	2001	Bax-deficient embryos show decreased neuronal programmed cell death in vivo and resistance to cytosine arabinoside (AraC)-induced neuronal apoptosis in vitro.	Cytarabine	116-120	BCL2 associated X, apoptosis regulator	Homo sapiens	0-3
11848518-11	2001	Ajoene significantly enhanced the inhibitory effect of the two chemotherapeutic drugs, cytarabine and fludarabine, on bcl-2-expression in KGI cells.	Cytarabine	87-97	BCL2 apoptosis regulator	Homo sapiens	118-123
11848518-14	2001	Quantitative measurement of activated caspase-3 (pg per million cells) showed the two drugs, cytarabine and fludarabine, significantly increased the activated caspase-3 level in KGI myeloid leukaemia cells.	Cytarabine	93-103	caspase 3	Homo sapiens	38-47
11848518-14	2001	Quantitative measurement of activated caspase-3 (pg per million cells) showed the two drugs, cytarabine and fludarabine, significantly increased the activated caspase-3 level in KGI myeloid leukaemia cells.	Cytarabine	93-103	caspase 3	Homo sapiens	159-168
11848518-15	2001	CONCLUSION: The addition of ajoene enhanced the activation of caspase-3 in both cytarabine- and fludarabine-treated KGI cells.	Cytarabine	80-90	caspase 3	Homo sapiens	62-71
11593336-2	2001	We have shown previously that the human cytidine deaminase (CD) gene can confer drug resistance in murine bone marrow cells (BMCs) to the nucleoside analog, cytosine arabinoside (ARA-C).	Cytarabine	157-177	cytidine deaminase	Homo sapiens	40-58
11593336-2	2001	We have shown previously that the human cytidine deaminase (CD) gene can confer drug resistance in murine bone marrow cells (BMCs) to the nucleoside analog, cytosine arabinoside (ARA-C).	Cytarabine	157-177	cytidine deaminase	Homo sapiens	60-62
11593336-2	2001	We have shown previously that the human cytidine deaminase (CD) gene can confer drug resistance in murine bone marrow cells (BMCs) to the nucleoside analog, cytosine arabinoside (ARA-C).	Cytarabine	179-184	cytidine deaminase	Homo sapiens	40-58
11593336-2	2001	We have shown previously that the human cytidine deaminase (CD) gene can confer drug resistance in murine bone marrow cells (BMCs) to the nucleoside analog, cytosine arabinoside (ARA-C).	Cytarabine	179-184	cytidine deaminase	Homo sapiens	60-62
11516093-1	2001	The Australian Leukaemia Study Group (ALSG) investigated whether G-CSF would accelerate haemopoietic recovery after induction treatment for acute myeloid leukaemia (AML) intensified with high-dose cytarabine, and therefore improve response rates and survival.	Cytarabine	197-207	colony stimulating factor 3	Homo sapiens	65-70
11516093-9	2001	We conclude that the granulopoietic stimulating effect of G-CSF is observed after induction therapy for AML intensified by high-dose cytarabine, resulting in an improvement in a number of clinically important parameters with no major adverse effects.	Cytarabine	133-143	colony stimulating factor 3	Homo sapiens	58-63
11517422-2	2001	Nineteen patients with PML proven by brain biopsy or spinal fluid polymerase chain reaction were treated with intravenous cytosine arabinoside 2 mg/kg per day for 5 days and followed for neurologic outcome by neurologic examination and MRI scanning.	Cytarabine	122-142	PML nuclear body scaffold	Homo sapiens	23-26
11517422-3	2001	Seven of 19 PML patients treated with cytosine arabinoside intravenously improved neurologically.	Cytarabine	38-58	PML nuclear body scaffold	Homo sapiens	12-15
11517422-8	2001	Cytosine arabinoside given intravenously to non-AIDS PML patients in this small study was associated with a 36% chance of developing stabilization at 1 year.	Cytarabine	0-20	PML nuclear body scaffold	Homo sapiens	53-56
11427493-0	2001	Oxidative stress-induced activation of Lyn recruits sphingomyelinase and is requisite for its stimulation by Ara-C.	Cytarabine	109-114	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	39-42
11473731-1	2001	We studied mutational events in deoxycytidine (dCyd) kinase mRNA expression, focusing on aberrant dCyd kinase mRNA, which has been frequently observed in established cell lines resistant to antitumor dCyd nucleoside analogues such as 1-beta-D-arabinofuranosyl cytosine (Ara-C), gemcitabine (dFdC) and 2"-C-cyano-2"-deoxy-1-beta-D-arabinofuranosylcytosine (CNDAC).	Cytarabine	234-268	Cyd	Drosophila melanogaster	98-102
11473731-1	2001	We studied mutational events in deoxycytidine (dCyd) kinase mRNA expression, focusing on aberrant dCyd kinase mRNA, which has been frequently observed in established cell lines resistant to antitumor dCyd nucleoside analogues such as 1-beta-D-arabinofuranosyl cytosine (Ara-C), gemcitabine (dFdC) and 2"-C-cyano-2"-deoxy-1-beta-D-arabinofuranosylcytosine (CNDAC).	Cytarabine	234-268	Cyd	Drosophila melanogaster	98-102
11473731-1	2001	We studied mutational events in deoxycytidine (dCyd) kinase mRNA expression, focusing on aberrant dCyd kinase mRNA, which has been frequently observed in established cell lines resistant to antitumor dCyd nucleoside analogues such as 1-beta-D-arabinofuranosyl cytosine (Ara-C), gemcitabine (dFdC) and 2"-C-cyano-2"-deoxy-1-beta-D-arabinofuranosylcytosine (CNDAC).	Cytarabine	270-275	Cyd	Drosophila melanogaster	98-102
11473731-1	2001	We studied mutational events in deoxycytidine (dCyd) kinase mRNA expression, focusing on aberrant dCyd kinase mRNA, which has been frequently observed in established cell lines resistant to antitumor dCyd nucleoside analogues such as 1-beta-D-arabinofuranosyl cytosine (Ara-C), gemcitabine (dFdC) and 2"-C-cyano-2"-deoxy-1-beta-D-arabinofuranosylcytosine (CNDAC).	Cytarabine	270-275	Cyd	Drosophila melanogaster	98-102
11331076-5	2001	dCK catalyzes the first rate-limiting activation step of both gemcitabine and ara-C.	Cytarabine	78-83	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	0-3
11331076-6	2001	In addition, deoxycytidine deaminase, responsible for inactivation of dFdC and ara-C, was 9.0-fold lower in H69/DAU cells.	Cytarabine	79-84	apolipoprotein B mRNA editing enzyme catalytic subunit 3G	Homo sapiens	13-36
11351258-8	2001	The model we developed here will allow further studies on the role of post-translational events involving bcl-2 (such as translocation and/or phosphorylation) in the cellular response to ara-C treatment.	Cytarabine	187-192	BCL2 apoptosis regulator	Homo sapiens	106-111
11368357-5	2001	We also assessed the expressions of pRb, cyclin E, p21 and p27 and the activity of cdk2, the major regulator of S-phase entry, after exposure to cytosine-arabinoside (AraC) and daunorubicin (DNR), and found these proteins could characterize time- and dose-dependent cellular response to each drug.	Cytarabine	167-171	cyclin dependent kinase 2	Homo sapiens	83-87
11380397-7	2001	The activity of deoxycytidine kinase (dCK), responsible for activation of CdA and ara-C, was the same for resistant and wild-type cells.	Cytarabine	82-87	deoxycytidine kinase	Homo sapiens	16-36
11380397-7	2001	The activity of deoxycytidine kinase (dCK), responsible for activation of CdA and ara-C, was the same for resistant and wild-type cells.	Cytarabine	82-87	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	38-41
11376564-2	2001	Ara-C therapy may be optimal if it is directed by the clinical pharmacokinetics of the intracellular active metabolite of ara-C, 1-beta-D-arabinofuranosylcytosine 5"-triphosphate (ara-CTP).	Cytarabine	0-5	solute carrier family 25 member 1	Homo sapiens	184-187
11376564-2	2001	Ara-C therapy may be optimal if it is directed by the clinical pharmacokinetics of the intracellular active metabolite of ara-C, 1-beta-D-arabinofuranosylcytosine 5"-triphosphate (ara-CTP).	Cytarabine	122-127	solute carrier family 25 member 1	Homo sapiens	184-187
11376564-6	2001	There was a close correlation between the elimination half-life values of the plasma ara-C and the intracellular ara-CTP.	Cytarabine	85-90	solute carrier family 25 member 1	Homo sapiens	117-120
11376564-7	2001	The presence of ara-C in the plasma was important to maintain ara-CTP.	Cytarabine	16-21	solute carrier family 25 member 1	Homo sapiens	66-69
11376564-8	2001	The continuous ara-C and the 2-h N(4)-behenoyl-1-beta-D-arabinofuranosylcytosine infusions maintained ara-CTP and the plasma ara-C longer than the subcutaneous ara-C or the 2-h ara-C infusion.	Cytarabine	15-20	solute carrier family 25 member 1	Homo sapiens	106-109
11335788-0	2001	Increased sensitivity to cytosine arabinoside in human leukemia by c-raf-1 antisense oligonucleotides.	Cytarabine	25-45	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	67-72
11335788-5	2001	Expression of c-raf-1 was increased in U937 and in Ara-C-resistant K562AC cells compared with the parental cells.	Cytarabine	51-56	TNF receptor associated factor 3	Homo sapiens	14-21
11335788-8	2001	These results suggest that c-raf-1 is one of the factors involved in Ara-C resistance in leukemia and lend weight to the case for development of anti-cancer therapeutics involving oncogene-targeted antisense oligonucleotides.	Cytarabine	69-74	TNF receptor associated factor 3	Homo sapiens	27-34
11380602-9	2001	IL-6 decreases after a low dose of Ara-C and increases after a high dose.	Cytarabine	35-40	interleukin 6	Mus musculus	0-4
11376869-0	2001	Transfection of caspase-3 in the caspase-3-deficient Hodgkin"s disease cell line, KMH2, results in enhanced sensitivity to CD95-, TRAIL-, and ARA-C-induced apoptosis.	Cytarabine	142-147	caspase 3	Homo sapiens	16-25
11376869-0	2001	Transfection of caspase-3 in the caspase-3-deficient Hodgkin"s disease cell line, KMH2, results in enhanced sensitivity to CD95-, TRAIL-, and ARA-C-induced apoptosis.	Cytarabine	142-147	caspase 3	Homo sapiens	33-42
11376869-8	2001	In addition, pro-caspase-3-transfected KM-H2 cells showed significantly increased sensitivity to other caspase-3-dependent apoptotic stimuli, including the death-inducing ligand, TRAIL, and the chemotherapeutic agent, Ara-C.	Cytarabine	218-223	caspase 3	Homo sapiens	13-26
11376869-8	2001	In addition, pro-caspase-3-transfected KM-H2 cells showed significantly increased sensitivity to other caspase-3-dependent apoptotic stimuli, including the death-inducing ligand, TRAIL, and the chemotherapeutic agent, Ara-C.	Cytarabine	218-223	caspase 3	Homo sapiens	17-26
11368436-2	2001	Forty-nine consecutive patients (median age 49, range 21-70) with acute myelogenous leukemia in first remission were enrolled on a study of high-dose cytarabine/mitoxantrone consolidation chemotherapy with post-recovery IL-2 used as a method of in vivo purging for the purpose of autologous peripheral blood progenitor cell transplantation.	Cytarabine	150-160	interleukin 2	Homo sapiens	220-224
11286995-8	2001	Ara-C induced ROS release from PMNs in the presence of subthreshold concentrations of f-MLP (priming effect).	Cytarabine	0-5	cysteine and glycine rich protein 3	Homo sapiens	88-91
11368357-6	2001	We observed hyperphosphorylated pRb, increased levels of cyclin E and a high cdk2 activity, but no p21 induction, in AML cells exposed to 10(-6) M AraC.	Cytarabine	147-151	RB transcriptional corepressor 1	Homo sapiens	32-35
11368357-6	2001	We observed hyperphosphorylated pRb, increased levels of cyclin E and a high cdk2 activity, but no p21 induction, in AML cells exposed to 10(-6) M AraC.	Cytarabine	147-151	cyclin dependent kinase 2	Homo sapiens	77-81
11368357-7	2001	After exposure to 10(-5) M AraC, corresponding to the serum concentration reached in high-dose AraC regimens (HDAraC), a strong p21 induction was observed, associated with similarly overexpressed cyclin E and even higher cdk2 activity than after 10(-6) M AraC, while apoptosis was significantly increased.	Cytarabine	27-31	cyclin dependent kinase inhibitor 1A	Homo sapiens	128-131
11368357-7	2001	After exposure to 10(-5) M AraC, corresponding to the serum concentration reached in high-dose AraC regimens (HDAraC), a strong p21 induction was observed, associated with similarly overexpressed cyclin E and even higher cdk2 activity than after 10(-6) M AraC, while apoptosis was significantly increased.	Cytarabine	27-31	cyclin dependent kinase 2	Homo sapiens	221-225
11368357-7	2001	After exposure to 10(-5) M AraC, corresponding to the serum concentration reached in high-dose AraC regimens (HDAraC), a strong p21 induction was observed, associated with similarly overexpressed cyclin E and even higher cdk2 activity than after 10(-6) M AraC, while apoptosis was significantly increased.	Cytarabine	95-99	cyclin dependent kinase inhibitor 1A	Homo sapiens	128-131
11368357-7	2001	After exposure to 10(-5) M AraC, corresponding to the serum concentration reached in high-dose AraC regimens (HDAraC), a strong p21 induction was observed, associated with similarly overexpressed cyclin E and even higher cdk2 activity than after 10(-6) M AraC, while apoptosis was significantly increased.	Cytarabine	95-99	cyclin dependent kinase 2	Homo sapiens	221-225
11342363-10	2001	Cost-effectiveness estimates for cytarabine added to IFN-alpha range from $7,000 per quality-adjusted life year (QALY) to $35,000 per QALY, under all plausible assumptions superior to IFN-alpha alone.	Cytarabine	33-43	interferon alpha 1	Homo sapiens	53-62
11563038-1	2001	Continuous cultivation of T-lymphoid C8166 cells in the presence of pharmacological relevant concentration of cytarabine (Ara-C) results in significantly decreased expression of CD4 and CXCR4 molecules, the major cellular receptor and co-receptor of T-lymphotropic HIV-1 isolates.	Cytarabine	110-120	CD4 molecule	Homo sapiens	178-181
11563038-1	2001	Continuous cultivation of T-lymphoid C8166 cells in the presence of pharmacological relevant concentration of cytarabine (Ara-C) results in significantly decreased expression of CD4 and CXCR4 molecules, the major cellular receptor and co-receptor of T-lymphotropic HIV-1 isolates.	Cytarabine	110-120	C-X-C motif chemokine receptor 4	Homo sapiens	186-191
11563038-1	2001	Continuous cultivation of T-lymphoid C8166 cells in the presence of pharmacological relevant concentration of cytarabine (Ara-C) results in significantly decreased expression of CD4 and CXCR4 molecules, the major cellular receptor and co-receptor of T-lymphotropic HIV-1 isolates.	Cytarabine	122-127	CD4 molecule	Homo sapiens	178-181
11563038-1	2001	Continuous cultivation of T-lymphoid C8166 cells in the presence of pharmacological relevant concentration of cytarabine (Ara-C) results in significantly decreased expression of CD4 and CXCR4 molecules, the major cellular receptor and co-receptor of T-lymphotropic HIV-1 isolates.	Cytarabine	122-127	C-X-C motif chemokine receptor 4	Homo sapiens	186-191
11237055-3	2001	We tested whether combinations of STI571 and cytarabine or other chemotherapeutic agents such as hydroxyurea, mafosfamide or etoposide would display synergistic activity in BCR-ABL-positive chronic myelogenous leukemia (CML) cell lines derived from patients in blast crisis.	Cytarabine	45-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	177-180
11342363-10	2001	Cost-effectiveness estimates for cytarabine added to IFN-alpha range from $7,000 per quality-adjusted life year (QALY) to $35,000 per QALY, under all plausible assumptions superior to IFN-alpha alone.	Cytarabine	33-43	interferon alpha 1	Homo sapiens	184-193
11372732-0	2001	Effect of granulocyte colony-stimulating factor on chemotherapeutic activity of cytosine arabinoside in acute leukemic cell lines.	Cytarabine	80-100	colony stimulating factor 3	Homo sapiens	10-47
11372740-5	2001	The mean number of CD34+ cells harvested per apheresis was larger in the group receiving high-dose cytosine arabinoside or high-dose etoposide plus granulocyte colony-stimulating factor (G-CSF) than in the group receiving conventional chemotherapy plus G-CSF.	Cytarabine	99-119	CD34 molecule	Homo sapiens	19-23
11280917-6	2001	This case suggests that Ph/-7 ALL with major BCR/ABL gene rearrangement showing coexpression of myeloid antigens may be sensitive to intermediate- and high-dose ara-C.	Cytarabine	161-166	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
11299723-6	2001	Moreover, the data imply that upregulation of bcl-2 is critical in the development of resistance to ara-C and ASNase in these leukemic lines.	Cytarabine	100-105	BCL2 apoptosis regulator	Homo sapiens	46-51
11440177-2	2001	The level of dCK activity is especially important in chemotherapy with the use of deoxynucleoside analogues like arabinosyl cytosine (Citarabid, ara-C), or 2-chloro-deoxyadenosine (Cladribine, CdA).	Cytarabine	113-132	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	13-16
11440177-2	2001	The level of dCK activity is especially important in chemotherapy with the use of deoxynucleoside analogues like arabinosyl cytosine (Citarabid, ara-C), or 2-chloro-deoxyadenosine (Cladribine, CdA).	Cytarabine	145-150	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	13-16
11163333-1	2001	Deoxycytidine kinase (dCK, EC.2.7.1.74) is a key enzyme in the intracellular metabolism of 2-chlorodeoxyadenosine, 1-beta-D-arabinofuranosylcytosine, difluorodeoxycytidine, and other drugs used in chemotherapy of different leukaemias and solid tumours.	Cytarabine	115-148	deoxycytidine kinase	Homo sapiens	0-20
11163333-1	2001	Deoxycytidine kinase (dCK, EC.2.7.1.74) is a key enzyme in the intracellular metabolism of 2-chlorodeoxyadenosine, 1-beta-D-arabinofuranosylcytosine, difluorodeoxycytidine, and other drugs used in chemotherapy of different leukaemias and solid tumours.	Cytarabine	115-148	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	22-25
11150333-8	2001	AraC caused extensive apoptosis of wild-type and Bcl-X(L)-deficient neurons.	Cytarabine	0-4	BCL2-like 1	Mus musculus	49-57
11196157-0	2001	Induction of differentiation of acute promyelocytic leukemia cells by a cytidine deaminase-resistant analogue of 1-beta-D-arabinofuranosylcytosine, 1-(2-deoxy-2-methylene-beta-D-erythro-pentofuranosyl)cytidine.	Cytarabine	113-146	cytidine deaminase	Homo sapiens	72-90
11196157-6	2001	A cytidine deaminase-resistant analogue of araC, 1-(2-deoxy-2-methylene-beta-D-erythro-pentofuranosyl)cytidine (DMDC), inhibited the growth of NB4 and HT-93 cells and was also effective on HL-60 and U937 cells.	Cytarabine	43-47	cytidine deaminase	Homo sapiens	2-20
11150333-10	2001	These findings contrast with our previous investigation of AraC-induced apoptosis of telencephalic neural precursor cells in which death was completely blocked by p53 or Caspase-9 deficiency but not Bax deficiency.	Cytarabine	59-63	transformation related protein 53, pseudogene	Mus musculus	163-166
11090076-6	2000	Treatment of human leukemic cells with etoposide, Ara-C, or doxorubicin increased DR5 but not DR4, Fas, DcR1, DcR2, Fas ligand, or Apo-2L levels.	Cytarabine	50-55	TNF superfamily member 10	Homo sapiens	131-137
11123359-1	2001	Expression of the transforming oncogene bcr-abl in chronic myelogenous leukemia (CML) cells is reported to confer resistance against apoptosis induced by many chemotherapeutic agents such as etoposide, ara-C, and staurosporine.	Cytarabine	202-207	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
11243402-1	2001	The rate of ara-cytosine triphosphate (ara-CTP) accumulation and its retention has been correlated with 1-beta-D-arabinofuranosylcytosine (ara-C)-mediated toxicity and clinical outcome in childhood and adult leukemia.	Cytarabine	104-137	solute carrier family 25 member 1	Homo sapiens	43-46
11243402-7	2001	In conclusion, our data suggest that combinations of ara-C and ribonucleotide reductase inhibitors are apt to increase ara-CTP levels depending on the individual cell type and its sensitivity towards ara-C modulators.	Cytarabine	53-58	solute carrier family 25 member 1	Homo sapiens	123-126
10993893-7	2000	The cells expressing Dm-dNK exhibited increased sensitivity to several cytotoxic nucleoside analogs, such as 1-beta-d-arabinofuranosylcytosine, 1-beta-d-arabinofuranosylthymine, (E)-5-(2-bromovinyl)-2"-deoxyuridine, 2-chloro-2"-deoxyadenosine, and 2",2"-difluorodeoxycytidine.	Cytarabine	109-142	deoxyribonucleoside kinase	Drosophila melanogaster	21-27
11090076-6	2000	Treatment of human leukemic cells with etoposide, Ara-C, or doxorubicin increased DR5 but not DR4, Fas, DcR1, DcR2, Fas ligand, or Apo-2L levels.	Cytarabine	50-55	TNF receptor superfamily member 10b	Homo sapiens	82-85
11090076-7	2000	Importantly, sequential treatment of HL-60 cells with etoposide, Ara-C, or doxorubicin followed by Apo-2L induced significantly more apoptosis than treatment with Apo-2L, etoposide, doxorubicin, or Ara-C alone, or cotreatment with Apo-2L and the antileukemic drugs, or treatment with the reverse sequence of Apo-2L followed by one of the antileukemic drugs.	Cytarabine	198-203	TNF superfamily member 10	Homo sapiens	99-105
11090076-6	2000	Treatment of human leukemic cells with etoposide, Ara-C, or doxorubicin increased DR5 but not DR4, Fas, DcR1, DcR2, Fas ligand, or Apo-2L levels.	Cytarabine	50-55	TNF receptor superfamily member 10a	Homo sapiens	94-97
11090076-8	2000	These findings indicate that treatment with etoposide, Ara-C, or doxorubicin up-regulates DR5 levels in a p53-independent manner and sensitizes human acute leukemia cells to Apo-2L-induced apoptosis.	Cytarabine	55-60	TNF receptor superfamily member 10b	Homo sapiens	90-93
11090076-8	2000	These findings indicate that treatment with etoposide, Ara-C, or doxorubicin up-regulates DR5 levels in a p53-independent manner and sensitizes human acute leukemia cells to Apo-2L-induced apoptosis.	Cytarabine	55-60	tumor protein p53	Homo sapiens	106-109
11090076-6	2000	Treatment of human leukemic cells with etoposide, Ara-C, or doxorubicin increased DR5 but not DR4, Fas, DcR1, DcR2, Fas ligand, or Apo-2L levels.	Cytarabine	50-55	TNF receptor superfamily member 10c	Homo sapiens	104-108
11090076-8	2000	These findings indicate that treatment with etoposide, Ara-C, or doxorubicin up-regulates DR5 levels in a p53-independent manner and sensitizes human acute leukemia cells to Apo-2L-induced apoptosis.	Cytarabine	55-60	TNF superfamily member 10	Homo sapiens	174-180
11090076-6	2000	Treatment of human leukemic cells with etoposide, Ara-C, or doxorubicin increased DR5 but not DR4, Fas, DcR1, DcR2, Fas ligand, or Apo-2L levels.	Cytarabine	50-55	TNF receptor superfamily member 10d	Homo sapiens	110-114
11135355-3	2000	Interaction between fludarabine or cladribine with deoxycytidine kinase results in a significant enhancement of the activity of cytarabine.	Cytarabine	128-138	deoxycytidine kinase	Homo sapiens	51-71
11090076-6	2000	Treatment of human leukemic cells with etoposide, Ara-C, or doxorubicin increased DR5 but not DR4, Fas, DcR1, DcR2, Fas ligand, or Apo-2L levels.	Cytarabine	50-55	Fas ligand	Homo sapiens	116-126
11103808-2	2000	The cystathionine-beta-synthase (CBS) gene (localized to chromosome 21q22.3) may have downstream effects on reduced folate and S-adenosylmethionine pathways; ara-C metabolism and folate pools are linked by the known synergistic effect of sequential methotrexate and ara-C therapy.	Cytarabine	158-163	cystathionine beta-synthase	Homo sapiens	4-31
11426620-4	2000	However, we show here that cytosine beta-D-arabinofuranoside (Ara C) and 12-O-tetradecanoylphorbol 13-acetate (TPA), agents that activated the MDR1 gene in the H9 T-cell leukemia line, caused different effects on PKC.	Cytarabine	62-67	ATP binding cassette subfamily B member 1	Homo sapiens	143-147
11426620-4	2000	However, we show here that cytosine beta-D-arabinofuranoside (Ara C) and 12-O-tetradecanoylphorbol 13-acetate (TPA), agents that activated the MDR1 gene in the H9 T-cell leukemia line, caused different effects on PKC.	Cytarabine	27-60	ATP binding cassette subfamily B member 1	Homo sapiens	143-147
11103808-0	2000	Cystathionine-beta-synthase cDNA transfection alters the sensitivity and metabolism of 1-beta-D-arabinofuranosylcytosine in CCRF-CEM leukemia cells in vitro and in vivo: a model of leukemia in Down syndrome.	Cytarabine	87-120	cystathionine beta-synthase	Homo sapiens	0-27
11103808-2	2000	The cystathionine-beta-synthase (CBS) gene (localized to chromosome 21q22.3) may have downstream effects on reduced folate and S-adenosylmethionine pathways; ara-C metabolism and folate pools are linked by the known synergistic effect of sequential methotrexate and ara-C therapy.	Cytarabine	158-163	cystathionine beta-synthase	Homo sapiens	33-36
11103808-3	2000	We have shown that relative CBS transcripts were significantly higher in DS compared with non-DS myeloblasts, and CBS transcript levels correlated with in vitro ara-C sensitivity (J. W. Taub et al., Blood, 94: 1393-1400, 1999).	Cytarabine	161-166	cystathionine beta-synthase	Homo sapiens	28-31
11103808-3	2000	We have shown that relative CBS transcripts were significantly higher in DS compared with non-DS myeloblasts, and CBS transcript levels correlated with in vitro ara-C sensitivity (J. W. Taub et al., Blood, 94: 1393-1400, 1999).	Cytarabine	161-166	cystathionine beta-synthase	Homo sapiens	114-117
11103808-5	2000	CBS-transfected cells were a median 15-fold more sensitive in vitro to ara-C compared with wild-type cells and generated 8.5-fold higher [3H]ara-C triphosphate levels after in vitro incubation with [3H]ara-C.	Cytarabine	71-76	cystathionine beta-synthase	Homo sapiens	0-3
11103808-5	2000	CBS-transfected cells were a median 15-fold more sensitive in vitro to ara-C compared with wild-type cells and generated 8.5-fold higher [3H]ara-C triphosphate levels after in vitro incubation with [3H]ara-C.	Cytarabine	141-146	cystathionine beta-synthase	Homo sapiens	0-3
11103808-6	2000	Severe combined immunodeficient mice implanted with CBS-transfected CEM cells demonstrated greater responsiveness to therapy, reflected in significantly prolonged survivals after ara-C administration compared with mice implanted with wild-type cells and treated with the same dosage schedule.	Cytarabine	179-184	cystathionine beta-synthase	Mus musculus	52-55
11103808-10	2000	Collectively, these results suggest a posttranscriptional regulation of dCK in CBS-overexpressing cells that contributes to increased ara-C phosphorylation and drug activity.	Cytarabine	134-139	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	72-75
11103808-10	2000	Collectively, these results suggest a posttranscriptional regulation of dCK in CBS-overexpressing cells that contributes to increased ara-C phosphorylation and drug activity.	Cytarabine	134-139	cystathionine beta-synthase	Homo sapiens	79-82
11103808-11	2000	Further elucidating the mechanisms of increased sensitivity of DS cells to ara-C related to the CBS gene may lead to the application of these novel approaches to acute myeloid leukemia therapy for non-DS patients.	Cytarabine	75-80	cystathionine beta-synthase	Homo sapiens	96-99
11045730-9	2000	In addition, exposure of XPA and XPG fibroblasts to UV (5, 10 or 20 J/m2) followed by incubation without araC resulted in a strong upregulation of p53.	Cytarabine	105-109	tumor protein p53	Homo sapiens	147-150
11122104-0	2000	Contrasting in vitro effects for the combination of fludarabine, cytosine arabinoside (Ara-C) and granulocyte colony-stimulating factor (FLAG) compared with daunorubicin and Ara-C in P-glycoprotein-positive and P-glycoprotein-negative acute myeloblastic leukaemia.	Cytarabine	65-85	ATP binding cassette subfamily B member 1	Homo sapiens	183-197
11122104-0	2000	Contrasting in vitro effects for the combination of fludarabine, cytosine arabinoside (Ara-C) and granulocyte colony-stimulating factor (FLAG) compared with daunorubicin and Ara-C in P-glycoprotein-positive and P-glycoprotein-negative acute myeloblastic leukaemia.	Cytarabine	174-179	ATP binding cassette subfamily B member 1	Homo sapiens	183-197
11122104-0	2000	Contrasting in vitro effects for the combination of fludarabine, cytosine arabinoside (Ara-C) and granulocyte colony-stimulating factor (FLAG) compared with daunorubicin and Ara-C in P-glycoprotein-positive and P-glycoprotein-negative acute myeloblastic leukaemia.	Cytarabine	174-179	ATP binding cassette subfamily B member 1	Homo sapiens	211-225
11122104-1	2000	It has been suggested that the FLAG remission induction regimen comprising fludarabine (F-ara), cytosine arabinoside (Ara-C) and granulocyte colony-stimulating factor (G-CSF) may be capable of overcoming P-glycoprotein (P-gp)-related multidrug resistance (MDR) in patients with acute myeloblastic leukaemia (AML).	Cytarabine	96-116	ATP binding cassette subfamily B member 1	Homo sapiens	204-218
11122104-1	2000	It has been suggested that the FLAG remission induction regimen comprising fludarabine (F-ara), cytosine arabinoside (Ara-C) and granulocyte colony-stimulating factor (G-CSF) may be capable of overcoming P-glycoprotein (P-gp)-related multidrug resistance (MDR) in patients with acute myeloblastic leukaemia (AML).	Cytarabine	96-116	ATP binding cassette subfamily B member 1	Homo sapiens	220-224
11032593-10	2000	CONCLUSION: The combination regimen of HHT and ara-C is effective and safe in patients with CML who have experienced treatment failure with IFNalpha and needs to be investigated together with IFNalpha as part of front-line CML therapy.	Cytarabine	47-52	interferon alpha 1	Homo sapiens	140-148
11089918-9	2000	Co-treatment of HL-60 cells with VD3 plus TNF-alpha or ara-C produced an additive effect on CD157 upregulation.	Cytarabine	55-60	bone marrow stromal cell antigen 1	Homo sapiens	92-97
11006103-3	2000	Hydroxyurea showed synergistic cytotoxicity with the nucleoside analogs 1-beta-d-arabinofuranosylcytosine and 2-chloro-2"-deoxyadenosine when dCK was expressed in the cytosol or in the nucleus, but not when dCK was expressed in the mitochondria.	Cytarabine	72-105	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	142-145
11020446-0	2000	Potentiation of 1-beta-D-arabinofuranosylcytosine-mediated mitochondrial damage and apoptosis in human leukemia cells (U937) overexpressing bcl-2 by the kinase inhibitor 7-hydroxystaurosporine (UCN-01).	Cytarabine	16-49	BCL2 apoptosis regulator	Homo sapiens	140-145
11020446-0	2000	Potentiation of 1-beta-D-arabinofuranosylcytosine-mediated mitochondrial damage and apoptosis in human leukemia cells (U937) overexpressing bcl-2 by the kinase inhibitor 7-hydroxystaurosporine (UCN-01).	Cytarabine	16-49	urocortin	Homo sapiens	194-197
11020446-1	2000	Antileukemic interactions between the nucleoside analog 1-beta-D-arabinofuranosylcytosine (ara-C) and the kinase inhibitor 7-hydroxystaurosporine (UCN-01) have been examined in relation to Bcl-2 expression/phosphorylation, mitochondrial damage, caspase activation, and loss of clonogenic potential.	Cytarabine	91-96	urocortin	Homo sapiens	147-150
11020446-2	2000	Subsequent exposure of ara-C-pretreated U937 cells (1 microM; 6 hr) to UCN-01 (300 nM; 24 hr) resulted in marked potentiation of pro-caspase-3 and -9 cleavage/activation, poly(ADP-ribose)polymerase degradation, diminished mitochondrial membrane potential (Deltapsi(m)), enhanced cytochrome c release, reduction in the S-phase fraction, and induction of classic apoptotic morphologic features.	Cytarabine	23-28	urocortin	Homo sapiens	71-74
11020446-2	2000	Subsequent exposure of ara-C-pretreated U937 cells (1 microM; 6 hr) to UCN-01 (300 nM; 24 hr) resulted in marked potentiation of pro-caspase-3 and -9 cleavage/activation, poly(ADP-ribose)polymerase degradation, diminished mitochondrial membrane potential (Deltapsi(m)), enhanced cytochrome c release, reduction in the S-phase fraction, and induction of classic apoptotic morphologic features.	Cytarabine	23-28	caspase 3	Homo sapiens	129-149
11020446-2	2000	Subsequent exposure of ara-C-pretreated U937 cells (1 microM; 6 hr) to UCN-01 (300 nM; 24 hr) resulted in marked potentiation of pro-caspase-3 and -9 cleavage/activation, poly(ADP-ribose)polymerase degradation, diminished mitochondrial membrane potential (Deltapsi(m)), enhanced cytochrome c release, reduction in the S-phase fraction, and induction of classic apoptotic morphologic features.	Cytarabine	23-28	cytochrome c, somatic	Homo sapiens	279-291
11020446-5	2000	Examination of cells at later intervals revealed that ectopic expression of Bcl-2 or Bcl-2Delta(32-80) could only delay, but not prevent, mitochondrial damage, caspase activation, and cell death induced by ara-C/UCN-01 treatment.	Cytarabine	206-211	BCL2 apoptosis regulator	Homo sapiens	76-81
11020446-5	2000	Examination of cells at later intervals revealed that ectopic expression of Bcl-2 or Bcl-2Delta(32-80) could only delay, but not prevent, mitochondrial damage, caspase activation, and cell death induced by ara-C/UCN-01 treatment.	Cytarabine	206-211	BCL2 apoptosis regulator	Homo sapiens	85-90
11020446-7	2000	These findings indicate that subsequent exposure of ara-C-pretreated human leukemia cells to UCN-01 potently triggers mitochondrial damage and apoptosis, and that these events are postponed but not prevented by ectopic expression of Bcl-2 or its phosphorylation loop-deleted counterpart.	Cytarabine	52-57	urocortin	Homo sapiens	93-96
10930419-4	2000	The results demonstrate that XIAP inhibits apoptosis induced by 1-[beta-d-arabinofuranosyl]cytosine (ara-C) and other genotoxic agents.	Cytarabine	64-99	X-linked inhibitor of apoptosis	Homo sapiens	29-33
10930419-4	2000	The results demonstrate that XIAP inhibits apoptosis induced by 1-[beta-d-arabinofuranosyl]cytosine (ara-C) and other genotoxic agents.	Cytarabine	101-106	X-linked inhibitor of apoptosis	Homo sapiens	29-33
10930419-6	2000	In addition, we show that ara-C induces the association of XIAP with the cleaved fragments of caspase-9 and thereby inhibition of caspase-9 activity.	Cytarabine	26-31	X-linked inhibitor of apoptosis	Homo sapiens	59-63
10930419-6	2000	In addition, we show that ara-C induces the association of XIAP with the cleaved fragments of caspase-9 and thereby inhibition of caspase-9 activity.	Cytarabine	26-31	caspase 9	Homo sapiens	94-103
10930419-6	2000	In addition, we show that ara-C induces the association of XIAP with the cleaved fragments of caspase-9 and thereby inhibition of caspase-9 activity.	Cytarabine	26-31	caspase 9	Homo sapiens	130-139
10930419-7	2000	The results also demonstrate that ara-C induces cleavage of procaspase-3 by a caspase-8-dependent mechanism and that XIAP inhibits caspase-3 activity.	Cytarabine	34-39	caspase 3	Homo sapiens	60-72
10930419-7	2000	The results also demonstrate that ara-C induces cleavage of procaspase-3 by a caspase-8-dependent mechanism and that XIAP inhibits caspase-3 activity.	Cytarabine	34-39	caspase 8	Homo sapiens	78-87
10930419-7	2000	The results also demonstrate that ara-C induces cleavage of procaspase-3 by a caspase-8-dependent mechanism and that XIAP inhibits caspase-3 activity.	Cytarabine	34-39	caspase 3	Homo sapiens	63-72
10979973-3	2000	Exposure to low-dose cytosine arabinoside (Ara-C; 10 nmol/L) increased hemoglobin levels in HL-60/Bcr-Abl and in the chronic myeloid leukemia (CML) blast crisis K562 cells, which express the p210 Bcr-Abl protein.	Cytarabine	21-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
10979973-3	2000	Exposure to low-dose cytosine arabinoside (Ara-C; 10 nmol/L) increased hemoglobin levels in HL-60/Bcr-Abl and in the chronic myeloid leukemia (CML) blast crisis K562 cells, which express the p210 Bcr-Abl protein.	Cytarabine	21-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	196-203
10979973-3	2000	Exposure to low-dose cytosine arabinoside (Ara-C; 10 nmol/L) increased hemoglobin levels in HL-60/Bcr-Abl and in the chronic myeloid leukemia (CML) blast crisis K562 cells, which express the p210 Bcr-Abl protein.	Cytarabine	43-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
10979973-3	2000	Exposure to low-dose cytosine arabinoside (Ara-C; 10 nmol/L) increased hemoglobin levels in HL-60/Bcr-Abl and in the chronic myeloid leukemia (CML) blast crisis K562 cells, which express the p210 Bcr-Abl protein.	Cytarabine	43-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	196-203
10979973-4	2000	As compared with HL-60/neo, HL-60/Bcr-Abl and K562 cells were resistant to apoptosis induced by Ara-C, doxorubicin, or tumor necrosis factor-alpha (TNF-alpha), which was associated with reduced processing of caspase-8 and Bid protein and decreased cytosolic accumulation of cytochrome c (cyt c).	Cytarabine	96-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	34-41
10979973-8	2000	Attenuation of NFkappaB activity by ectopic expression of transdominant repressor of IkappaB sensitized HL-60/Bcr-Abl and K562 cells to TNF-alpha but not to apoptosis induced by Ara-C or doxorubicin.	Cytarabine	178-183	nuclear factor kappa B subunit 1	Homo sapiens	15-23
10979973-9	2000	Importantly, cotreatment with CGP57148B significantly increased Ara-C- or doxorubicin-induced apoptosis of HL-60/Bcr-Abl and K562 cells.	Cytarabine	64-69	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
10979973-11	2000	These in vitro data indicate that combinations of CGP57148B and antileukemic drugs such as Ara-C may have improved in vivo efficacy against Bcr-Abl-positive acute leukemia.	Cytarabine	91-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	140-147
10995016-1	2000	In vitro studies have demonstrated that deoxycytidine kinase (dCK) plays a crucial role in the mechanism of resistance to cytarabine (AraC).	Cytarabine	122-132	deoxycytidine kinase	Homo sapiens	40-60
10978779-3	2000	We found that the expression of trkA was dramatically induced by the two megakaryocyte lineage inducers sodium butyrate (NaBut) and phorbol 12-myristate 13-acetate (PMA), but not by the two erythrocyte lineage inducers hemin or 1-beta-D-arabinofuranosyl cytosine (Ara-C).	Cytarabine	228-262	neurotrophic receptor tyrosine kinase 1	Homo sapiens	32-36
10978779-3	2000	We found that the expression of trkA was dramatically induced by the two megakaryocyte lineage inducers sodium butyrate (NaBut) and phorbol 12-myristate 13-acetate (PMA), but not by the two erythrocyte lineage inducers hemin or 1-beta-D-arabinofuranosyl cytosine (Ara-C).	Cytarabine	264-269	neurotrophic receptor tyrosine kinase 1	Homo sapiens	32-36
10961894-6	2000	Moreover, ionizing radiation, aracytine, and etoposide not only increase GrB and PFN expression but also conferred potent cellular cytotoxicity to these cells toward various cellular targets.	Cytarabine	30-39	granzyme B	Homo sapiens	73-76
10961896-6	2000	Specifically, signaling mediated through interaction with the stromal cell adhesion molecule VCAM-1 was required to maintain the maximum viability of leukemic cells during Ara-C and VP-16 exposure.	Cytarabine	172-177	vascular cell adhesion molecule 1	Homo sapiens	93-99
10995016-1	2000	In vitro studies have demonstrated that deoxycytidine kinase (dCK) plays a crucial role in the mechanism of resistance to cytarabine (AraC).	Cytarabine	122-132	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	62-65
10995016-1	2000	In vitro studies have demonstrated that deoxycytidine kinase (dCK) plays a crucial role in the mechanism of resistance to cytarabine (AraC).	Cytarabine	134-138	deoxycytidine kinase	Homo sapiens	40-60
10995016-1	2000	In vitro studies have demonstrated that deoxycytidine kinase (dCK) plays a crucial role in the mechanism of resistance to cytarabine (AraC).	Cytarabine	134-138	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	62-65
10997587-0	2000	Evidence of a functional role for the cyclin-dependent kinase inhibitor p21CIP1 in leukemic cell (U937) differentiation induced by low concentrations of 1-beta-D-arabinofuranosylcytosine.	Cytarabine	153-186	cyclin dependent kinase inhibitor 3	Homo sapiens	38-71
10942400-1	2000	Deficiency of functional deoxycytidine kinase (dCK) is a common characteristic for in vitro resistance to cytarabine (AraC).	Cytarabine	106-116	deoxycytidine kinase	Homo sapiens	25-45
10942400-1	2000	Deficiency of functional deoxycytidine kinase (dCK) is a common characteristic for in vitro resistance to cytarabine (AraC).	Cytarabine	106-116	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	47-50
10942400-1	2000	Deficiency of functional deoxycytidine kinase (dCK) is a common characteristic for in vitro resistance to cytarabine (AraC).	Cytarabine	118-122	deoxycytidine kinase	Homo sapiens	25-45
10942400-1	2000	Deficiency of functional deoxycytidine kinase (dCK) is a common characteristic for in vitro resistance to cytarabine (AraC).	Cytarabine	118-122	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	47-50
10942400-2	2000	To investigate whether dCK is also a target for induction of AraC resistance in patients with acute myeloid leukemia (AML), we determined dCK messenger RNA (mRNA) expression in (purified) leukemic blasts and phytohemagglutinin-stimulated T cells (PHA T cells) from patients with chemotherapy-sensitive and chemotherapy-resistant AML.	Cytarabine	61-65	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	23-26
10910927-6	2000	However, the TEL/AML1-positive patients were relatively more sensitive to L-asparaginase (ASP; 5.9-fold; P =.029) and slightly but significantly more resistant to vincristine (1.5-fold; P =.011) and cytarabine (1.5-fold; P =.014).	Cytarabine	199-209	ETS variant transcription factor 6	Homo sapiens	13-16
10910927-6	2000	However, the TEL/AML1-positive patients were relatively more sensitive to L-asparaginase (ASP; 5.9-fold; P =.029) and slightly but significantly more resistant to vincristine (1.5-fold; P =.011) and cytarabine (1.5-fold; P =.014).	Cytarabine	199-209	RUNX family transcription factor 1	Homo sapiens	17-21
10997587-0	2000	Evidence of a functional role for the cyclin-dependent kinase inhibitor p21CIP1 in leukemic cell (U937) differentiation induced by low concentrations of 1-beta-D-arabinofuranosylcytosine.	Cytarabine	153-186	cyclin dependent kinase inhibitor 1A	Homo sapiens	72-79
10997587-1	2000	The functional role of the cyclin-dependent kinase inhibitor (CDKI) p21CIP1 in differentiation of human myelomonocytic leukemia cells (U937) exposed to low concentrations of the antimetabolite 1-beta-D-arabino-furanosylcytosine (ara-C) was examined utilizing a cell line stably expressing a p21CIP1 antisense construct.	Cytarabine	193-227	cyclin dependent kinase inhibitor 3	Homo sapiens	27-60
10997587-1	2000	The functional role of the cyclin-dependent kinase inhibitor (CDKI) p21CIP1 in differentiation of human myelomonocytic leukemia cells (U937) exposed to low concentrations of the antimetabolite 1-beta-D-arabino-furanosylcytosine (ara-C) was examined utilizing a cell line stably expressing a p21CIP1 antisense construct.	Cytarabine	193-227	cyclin dependent kinase inhibitor 3	Homo sapiens	62-66
10997587-1	2000	The functional role of the cyclin-dependent kinase inhibitor (CDKI) p21CIP1 in differentiation of human myelomonocytic leukemia cells (U937) exposed to low concentrations of the antimetabolite 1-beta-D-arabino-furanosylcytosine (ara-C) was examined utilizing a cell line stably expressing a p21CIP1 antisense construct.	Cytarabine	193-227	cyclin dependent kinase inhibitor 1A	Homo sapiens	68-75
10997587-1	2000	The functional role of the cyclin-dependent kinase inhibitor (CDKI) p21CIP1 in differentiation of human myelomonocytic leukemia cells (U937) exposed to low concentrations of the antimetabolite 1-beta-D-arabino-furanosylcytosine (ara-C) was examined utilizing a cell line stably expressing a p21CIP1 antisense construct.	Cytarabine	229-234	cyclin dependent kinase inhibitor 3	Homo sapiens	62-66
10997587-2	2000	Continuous exposure to 50 nM ara-C led to marked induction of p21CIP1 at 48-72 h in empty-vector control cells but not in their antisense-expressing counterparts (p21AS/F4 and B8).	Cytarabine	29-34	cyclin dependent kinase inhibitor 1A	Homo sapiens	62-69
10997587-4	2000	However, antisense-expressing cells exposed to low concentrations of ara-C exhibited a reciprocal increase in apoptosis, manifested by the appearance of cells with classic morphologic features and hypodiploid quantities of DNA, reduced mitochondrial membrane potential (deltapsim), an increase in cytochrome c release into the cytosol, cleavage/activation of procaspases-9 and -3, and degradation of PARP and p27Kip1.	Cytarabine	69-74	cytochrome c, somatic	Homo sapiens	297-309
10997587-4	2000	However, antisense-expressing cells exposed to low concentrations of ara-C exhibited a reciprocal increase in apoptosis, manifested by the appearance of cells with classic morphologic features and hypodiploid quantities of DNA, reduced mitochondrial membrane potential (deltapsim), an increase in cytochrome c release into the cytosol, cleavage/activation of procaspases-9 and -3, and degradation of PARP and p27Kip1.	Cytarabine	69-74	caspase 3	Homo sapiens	359-379
10997587-4	2000	However, antisense-expressing cells exposed to low concentrations of ara-C exhibited a reciprocal increase in apoptosis, manifested by the appearance of cells with classic morphologic features and hypodiploid quantities of DNA, reduced mitochondrial membrane potential (deltapsim), an increase in cytochrome c release into the cytosol, cleavage/activation of procaspases-9 and -3, and degradation of PARP and p27Kip1.	Cytarabine	69-74	collagen type XI alpha 2 chain	Homo sapiens	400-404
10997587-4	2000	However, antisense-expressing cells exposed to low concentrations of ara-C exhibited a reciprocal increase in apoptosis, manifested by the appearance of cells with classic morphologic features and hypodiploid quantities of DNA, reduced mitochondrial membrane potential (deltapsim), an increase in cytochrome c release into the cytosol, cleavage/activation of procaspases-9 and -3, and degradation of PARP and p27Kip1.	Cytarabine	69-74	cyclin dependent kinase inhibitor 1B	Homo sapiens	409-416
10997587-5	2000	Whereas empty-vector control cells exposed to 50 nM ara-C exhibited a decline in Bcl-2 expression, dephosphorylation of pRb, and an initial accumulation in S-phase, antisense-expressing cells did not.	Cytarabine	52-57	BCL2 apoptosis regulator	Homo sapiens	81-86
10997587-5	2000	Whereas empty-vector control cells exposed to 50 nM ara-C exhibited a decline in Bcl-2 expression, dephosphorylation of pRb, and an initial accumulation in S-phase, antisense-expressing cells did not.	Cytarabine	52-57	RB transcriptional corepressor 1	Homo sapiens	120-123
10997587-6	2000	However, c-Myc down-regulation induced by low concentrations of ara-C was, if anything, more complete in antisense-expressing cells.	Cytarabine	64-69	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	9-14
10997587-8	2000	Lastly, exposure to 50 nM ara-C for 72 h resulted in detectable levels of cytoplasmic p21CIP1, a phenomenon associated with resistance to apoptosis, only in empty vector controls.	Cytarabine	26-31	cyclin dependent kinase inhibitor 1A	Homo sapiens	86-93
10997587-9	2000	Collectively, these findings demonstrate a functional role for p21CIP1 in leukemic cell maturation induced by low concentrations of ara-C.	Cytarabine	132-137	cyclin dependent kinase inhibitor 1A	Homo sapiens	63-70
10997587-10	2000	They also indicate that, as in the case of more conventional differentiation-inducers such as phorbol esters, disruption of the p21CIP1 response after exposure to low concentrations of the cytotoxic drug ara-C prevents leukemic cells from engaging a maturation program, but instead directs them along an apoptotic pathway.	Cytarabine	204-209	cyclin dependent kinase inhibitor 1A	Homo sapiens	128-135
10930995-2	2000	The activity of key enzymes of AraC metabolism-deoxycytidine kinase (DCK), cytidine deaminase (DCD) and polymerase alpha (PolyA) were determined in blast cells from 33 patients.	Cytarabine	31-35	deoxycytidine kinase	Homo sapiens	69-72
10942234-5	2000	When Ara-C was added to cultures containing IFN-alpha, the inhibition of replating by CML progenitors was abrogated.	Cytarabine	5-10	interferon alpha 1	Homo sapiens	44-53
10942234-12	2000	Thus we conclude that combining IFN-alpha with Ara-C or ATRA neutralises the effect of IFN-alpha on CML CFU-GM.	Cytarabine	47-52	interferon alpha 1	Homo sapiens	87-96
10825466-4	2000	Experiments reported herein demonstrated that the cloned rat kidney rOCT1 transports dTub, cytosine arabinoside, 2-chlorodeoxyadenosine, and azidothymidine when expressed in the Xenopus laevis oocyte translation system.	Cytarabine	91-111	solute carrier family 22 member 1	Rattus norvegicus	68-73
10930995-4	2000	Similarly, priming with GM-CSF or G-CSF increased both the proliferative activity of AML blasts by a median of 1.84- and 1.64-fold, respectively, and the incorporation of AraC into the DNA (1.29- and 1.40-fold respectively).	Cytarabine	171-175	colony stimulating factor 2	Homo sapiens	24-30
10930995-4	2000	Similarly, priming with GM-CSF or G-CSF increased both the proliferative activity of AML blasts by a median of 1.84- and 1.64-fold, respectively, and the incorporation of AraC into the DNA (1.29- and 1.40-fold respectively).	Cytarabine	171-175	colony stimulating factor 3	Homo sapiens	34-39
10891478-2	2000	Using cells deficient in Lyn expression, the present studies demonstrate that Lyn is required in part for induction of the stress-activated protein kinase (SAPK) in the response to 1-beta-D-arabinofuranosylcytosine (ara-C) and other genotoxic agents.	Cytarabine	181-214	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	25-28
10891478-2	2000	Using cells deficient in Lyn expression, the present studies demonstrate that Lyn is required in part for induction of the stress-activated protein kinase (SAPK) in the response to 1-beta-D-arabinofuranosylcytosine (ara-C) and other genotoxic agents.	Cytarabine	181-214	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	78-81
10891478-2	2000	Using cells deficient in Lyn expression, the present studies demonstrate that Lyn is required in part for induction of the stress-activated protein kinase (SAPK) in the response to 1-beta-D-arabinofuranosylcytosine (ara-C) and other genotoxic agents.	Cytarabine	181-214	mitogen-activated protein kinase 9	Homo sapiens	123-154
10891478-2	2000	Using cells deficient in Lyn expression, the present studies demonstrate that Lyn is required in part for induction of the stress-activated protein kinase (SAPK) in the response to 1-beta-D-arabinofuranosylcytosine (ara-C) and other genotoxic agents.	Cytarabine	181-214	mitogen-activated protein kinase 9	Homo sapiens	156-160
10891478-2	2000	Using cells deficient in Lyn expression, the present studies demonstrate that Lyn is required in part for induction of the stress-activated protein kinase (SAPK) in the response to 1-beta-D-arabinofuranosylcytosine (ara-C) and other genotoxic agents.	Cytarabine	216-221	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	78-81
10891478-2	2000	Using cells deficient in Lyn expression, the present studies demonstrate that Lyn is required in part for induction of the stress-activated protein kinase (SAPK) in the response to 1-beta-D-arabinofuranosylcytosine (ara-C) and other genotoxic agents.	Cytarabine	216-221	mitogen-activated protein kinase 9	Homo sapiens	123-154
10891478-2	2000	Using cells deficient in Lyn expression, the present studies demonstrate that Lyn is required in part for induction of the stress-activated protein kinase (SAPK) in the response to 1-beta-D-arabinofuranosylcytosine (ara-C) and other genotoxic agents.	Cytarabine	216-221	mitogen-activated protein kinase 9	Homo sapiens	156-160
10891478-3	2000	By contrast, exposure of Lyn-deficient cells to ara-C, ionizing radiation, or cisplatin had no effect on activation of extracellular signal-regulated protein kinase or p38 mitogen-activated protein kinase.	Cytarabine	48-53	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	25-28
10926348-3	2000	Cytarabine is principally active in the S phase of the cell cycle and is most toxic to replicating cells, whereas pentostatin, fludarabine and cladribine are incorporated into DNA during the process in which strand breaks are repaired and are therefore cytotoxic to slowly replicating cells (although the action of pentostatin results from its inhibition of adenosine deaminase).	Cytarabine	0-10	adenosine deaminase	Homo sapiens	358-377
10929040-0	2000	Respiratory failure during induction chemotherapy for acute myelomonocytic leukaemia (FAB M4Eo) with ara-C and all-trans retinoic acid.	Cytarabine	101-106	FA complementation group B	Homo sapiens	86-89
11005568-7	2000	Results also suggest that the decrease of telomeric-repeat binding factor 2 (TRF2) may be the earliest event in the ara-C-induced telomere shortening, induction of endoreduplication and chromosomal fragmentation leading to cell death.	Cytarabine	116-121	telomeric repeat binding factor 2	Homo sapiens	42-75
11005568-7	2000	Results also suggest that the decrease of telomeric-repeat binding factor 2 (TRF2) may be the earliest event in the ara-C-induced telomere shortening, induction of endoreduplication and chromosomal fragmentation leading to cell death.	Cytarabine	116-121	telomeric repeat binding factor 2	Homo sapiens	77-81
10764790-0	2000	Proteolytic cleavage and activation of protein kinase C [micro] by caspase-3 in the apoptotic response of cells to 1-beta -D-arabinofuranosylcytosine and other genotoxic agents.	Cytarabine	115-149	caspase 3	Homo sapiens	67-76
10764790-3	2000	The present studies demonstrate that PKCmu is cleaved during apoptosis induced by 1-beta-d-arabinofuranosylcytosine (ara-C) and other genotoxic agents.	Cytarabine	82-115	protein kinase D1	Homo sapiens	37-42
10764790-3	2000	The present studies demonstrate that PKCmu is cleaved during apoptosis induced by 1-beta-d-arabinofuranosylcytosine (ara-C) and other genotoxic agents.	Cytarabine	117-122	protein kinase D1	Homo sapiens	37-42
10764790-10	2000	These findings demonstrate that PKCmu is cleaved by caspase-3 and that expression of the catalytic domain sensitizes cells to the cytotoxic effects of ara-C and other anticancer agents.	Cytarabine	151-156	protein kinase D1	Homo sapiens	32-37
10764790-10	2000	These findings demonstrate that PKCmu is cleaved by caspase-3 and that expression of the catalytic domain sensitizes cells to the cytotoxic effects of ara-C and other anticancer agents.	Cytarabine	151-156	caspase 3	Homo sapiens	52-61
10918492-0	2000	Enhancement of cytosine arabinoside-induced apoptosis in human myeloblastic leukemia cells by NF-kappa B/Rel- specific decoy oligodeoxynucleotides.	Cytarabine	15-35	nuclear factor kappa B subunit 1	Homo sapiens	94-104
10845930-0	2000	Liposomal Bcl-2 antisense oligonucleotides enhance proliferation, sensitize acute myeloid leukemia to cytosine-arabinoside, and induce apoptosis independent of other antiapoptotic proteins.	Cytarabine	102-122	BCL2 apoptosis regulator	Homo sapiens	10-15
10845930-4	2000	Down-regulation of Bcl-2 by Bcl-2-AS reduced the viability of HL-60 cells and, less effectively, HL-60-DOX cells and increased ara-C cytotoxicity in both cell lines.	Cytarabine	127-132	BCL2 apoptosis regulator	Homo sapiens	19-24
10845930-4	2000	Down-regulation of Bcl-2 by Bcl-2-AS reduced the viability of HL-60 cells and, less effectively, HL-60-DOX cells and increased ara-C cytotoxicity in both cell lines.	Cytarabine	127-132	BCL2 apoptosis regulator	Homo sapiens	28-33
10845930-5	2000	Incubation of primary AML blasts with Bcl-2-AS decreased Bcl-2 expression in CD34(+) blast cells after induction of apoptosis and enhancement of ara-C cytotoxicity in 11 of 19 primary AML samples.	Cytarabine	145-150	BCL2 apoptosis regulator	Homo sapiens	38-43
10865967-0	2000	P-glycoprotein in primary acute myeloid leukemia and treatment outcome of idarubicin/cytosine arabinoside-based induction therapy.	Cytarabine	85-105	ATP binding cassette subfamily B member 1	Homo sapiens	0-14
10781689-4	2000	Gene analysis revealed that this cell line lacked expression of the deoxycytidine kinase (dCK) gene, which was evident in Ara-C-sensitive cells.	Cytarabine	122-127	deoxycytidine kinase	Homo sapiens	68-88
10781689-4	2000	Gene analysis revealed that this cell line lacked expression of the deoxycytidine kinase (dCK) gene, which was evident in Ara-C-sensitive cells.	Cytarabine	122-127	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	90-93
10781689-6	2000	We also established an in vitro model of Ara-C resistance using phosphorothioate antisense oligonucleotides to dCK (dCK-AS).	Cytarabine	41-46	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	111-114
10781689-6	2000	We also established an in vitro model of Ara-C resistance using phosphorothioate antisense oligonucleotides to dCK (dCK-AS).	Cytarabine	41-46	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	116-119
10781689-7	2000	Treatment of K562 with dCK-AS caused decreased dCK expression and 6- to 10-fold increases in resistance to Ara-C, compared with that in cells treated with sense oligonucleotides to dCK (dCK-S) or in non-transfected cells.	Cytarabine	107-112	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	23-26
10781689-8	2000	The cells described here may contribute to the study of a novel mechanism associated with Ara-C resistance, in which reduced dCK activity may play an important role.	Cytarabine	90-95	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	125-128
10784625-6	2000	AHS rates increased with age less than 10 years (odds ratio [OR], 2.0; P = .007), intensively timed induction (OR, 1.8 to 1.9; P = .02), and high-dose cytarabine intensification (OR, 3.7; P&lt;.0001).	Cytarabine	151-161	alpha 2-HS glycoprotein	Homo sapiens	0-3
10830723-0	2000	Coexpression of rat glutathione S-transferase A3 and human cytidine deaminase by a bicistronic retroviral vector confers in vitro resistance to nitrogen mustards and cytosine arabinoside in murine fibroblasts.	Cytarabine	166-186	cytidine deaminase	Homo sapiens	59-77
10830723-6	2000	After selection with Ara-C, the peroxidase and CD activities of GIC cells were augmented 2.6- and 2.9-fold, respectively, in comparison with unselected cells, and the resistance to melphalan, chlorambucil, and Ara-C was further increased to 3.7-, 5.9-, and 53-fold, respectively.	Cytarabine	21-26	cytidine deaminase	Homo sapiens	47-49
10830723-6	2000	After selection with Ara-C, the peroxidase and CD activities of GIC cells were augmented 2.6- and 2.9-fold, respectively, in comparison with unselected cells, and the resistance to melphalan, chlorambucil, and Ara-C was further increased to 3.7-, 5.9-, and 53-fold, respectively.	Cytarabine	210-215	cytidine deaminase	Homo sapiens	47-49
10815900-5	2000	High levels of XIAP protein in tumor cell lines were unexpectedly correlated with sensitivity to some anticancer drugs, particularly cytarabine and other nucleosides, whereas higher levels of cIAP1 protein levels were associated with resistance to several anticancer drugs.	Cytarabine	133-143	X-linked inhibitor of apoptosis	Homo sapiens	15-19
10815900-6	2000	The relevance of XIAP to in vivo responses to cytarabine was explored in AML, making correlations with patient outcome (n = 78).	Cytarabine	46-56	X-linked inhibitor of apoptosis	Homo sapiens	17-21
10845427-3	2000	Similar to 1-beta-D-arabinofuranosylcytosine (ara-C), another agent that inhibits growth and induces apoptosis of these cells, CDDO induced the release of mitochondrial cytochrome c and activation of caspase-3.	Cytarabine	46-51	caspase 3	Homo sapiens	200-209
10845427-4	2000	Overexpression of Bcl-X(L) blocked cytochrome c release, caspase-3 activation, and apoptosis in ara-C-treated cells.	Cytarabine	96-101	BCL2 like 1	Homo sapiens	18-26
10845427-4	2000	Overexpression of Bcl-X(L) blocked cytochrome c release, caspase-3 activation, and apoptosis in ara-C-treated cells.	Cytarabine	96-101	cytochrome c, somatic	Homo sapiens	35-47
10845427-4	2000	Overexpression of Bcl-X(L) blocked cytochrome c release, caspase-3 activation, and apoptosis in ara-C-treated cells.	Cytarabine	96-101	caspase 3	Homo sapiens	57-66
10785262-5	2000	Among 40 patients who completed standard-/high-dose cytarabine-containing induction/consolidation treatment and were evaluable for treatment response, a higher complete remission (CR) rate was achieved in c-mpl- than in c-mpl(+) patients (95 vs. 68%; P = 0.026).	Cytarabine	52-62	MPL proto-oncogene, thrombopoietin receptor	Homo sapiens	205-210
10785262-5	2000	Among 40 patients who completed standard-/high-dose cytarabine-containing induction/consolidation treatment and were evaluable for treatment response, a higher complete remission (CR) rate was achieved in c-mpl- than in c-mpl(+) patients (95 vs. 68%; P = 0.026).	Cytarabine	52-62	MPL proto-oncogene, thrombopoietin receptor	Homo sapiens	220-225
11603759-9	2000	Treatment of EGF stimulated P0 explants with an antimitotic drug, cytosine arabinoside (ARAc), demonstrated that the production of supernumerary hair cells occurred independently of cell division.	Cytarabine	66-86	epidermal growth factor like 1	Rattus norvegicus	13-16
10797445-12	2000	On the other hand, PCNA-gated cell-cycle distributions in untreated cells and G1 versus S phase cell-cycle arrests after cytosine arabinoside treatments were completely concordant in 4C and 3C assays.	Cytarabine	121-141	proliferating cell nuclear antigen	Homo sapiens	19-23
10722727-5	2000	In contrast, the ERK pathway-selective protein Ras(Val-12)T35S had no protective effects on NGF-deprived neurons but was almost as strongly protective as Ras(Val-12) against cytosine arabinoside-induced apoptosis.	Cytarabine	174-194	mitogen-activated protein kinase 1	Homo sapiens	17-20
10722727-6	2000	The protective effects of Ras(Val-12)T35S against cytosine arabinoside were completely abolished by the ERK pathway inhibitor PD98059.	Cytarabine	50-70	mitogen-activated protein kinase 1	Homo sapiens	104-107
11603759-9	2000	Treatment of EGF stimulated P0 explants with an antimitotic drug, cytosine arabinoside (ARAc), demonstrated that the production of supernumerary hair cells occurred independently of cell division.	Cytarabine	88-92	epidermal growth factor like 1	Rattus norvegicus	13-16
10644049-0	2000	Role of c-Jun N-terminal kinase/p38 stress signaling in 1-beta-D-arabinofuranosylcytosine-induced apoptosis.	Cytarabine	56-89	mitogen-activated protein kinase 14	Homo sapiens	32-35
10737723-1	2000	A clonogenic assay was tested in order to determine the effects of low intensity ultrasound on HL-60 cells in the presence of cytosine arabinoside (Ara-C).	Cytarabine	126-146	p21 (RAC1) activated kinase 3	Homo sapiens	148-151
10644049-1	2000	1-beta-D-Arabinofuranosylcytosine (ara-C) induced apoptosis in HL-60 cells, which was preceded by the activation of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK), and p38 mitogen-activated protein kinase (MAPK).	Cytarabine	0-33	mitogen-activated protein kinase 1	Homo sapiens	116-153
10644049-7	2000	These results suggest that ara-C-induced apoptotic DNA fragmentation and loss of clonogenicity occur through a p38-dependent pathway.	Cytarabine	27-32	mitogen-activated protein kinase 14	Homo sapiens	111-114
10644049-1	2000	1-beta-D-Arabinofuranosylcytosine (ara-C) induced apoptosis in HL-60 cells, which was preceded by the activation of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK), and p38 mitogen-activated protein kinase (MAPK).	Cytarabine	0-33	mitogen-activated protein kinase 1	Homo sapiens	155-158
10644049-1	2000	1-beta-D-Arabinofuranosylcytosine (ara-C) induced apoptosis in HL-60 cells, which was preceded by the activation of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK), and p38 mitogen-activated protein kinase (MAPK).	Cytarabine	0-33	mitogen-activated protein kinase 8	Homo sapiens	218-226
10679746-4	2000	We compared the two different techniques, DiOC(6)(3) uptake and Annexin V-propidium iodide co-labeling in the quantification of cytarabine, vincristine and daunorubicin induced apoptosis on three leukemia cell lines (HL-60, CEM, U937), and bone marrow blasts from 26 children with acute myeloid leukemia, 14 with T cell acute lymphoblastic leukemia.	Cytarabine	128-138	annexin A5	Homo sapiens	64-73
10644049-1	2000	1-beta-D-Arabinofuranosylcytosine (ara-C) induced apoptosis in HL-60 cells, which was preceded by the activation of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK), and p38 mitogen-activated protein kinase (MAPK).	Cytarabine	0-33	mitogen-activated protein kinase 14	Homo sapiens	233-269
10644049-1	2000	1-beta-D-Arabinofuranosylcytosine (ara-C) induced apoptosis in HL-60 cells, which was preceded by the activation of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK), and p38 mitogen-activated protein kinase (MAPK).	Cytarabine	0-33	mitogen-activated protein kinase 1	Homo sapiens	271-275
10644049-1	2000	1-beta-D-Arabinofuranosylcytosine (ara-C) induced apoptosis in HL-60 cells, which was preceded by the activation of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK), and p38 mitogen-activated protein kinase (MAPK).	Cytarabine	35-40	mitogen-activated protein kinase 1	Homo sapiens	116-153
10644049-1	2000	1-beta-D-Arabinofuranosylcytosine (ara-C) induced apoptosis in HL-60 cells, which was preceded by the activation of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK), and p38 mitogen-activated protein kinase (MAPK).	Cytarabine	35-40	mitogen-activated protein kinase 1	Homo sapiens	155-158
10644049-1	2000	1-beta-D-Arabinofuranosylcytosine (ara-C) induced apoptosis in HL-60 cells, which was preceded by the activation of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK), and p38 mitogen-activated protein kinase (MAPK).	Cytarabine	35-40	mitogen-activated protein kinase 8	Homo sapiens	218-226
10644049-1	2000	1-beta-D-Arabinofuranosylcytosine (ara-C) induced apoptosis in HL-60 cells, which was preceded by the activation of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK), and p38 mitogen-activated protein kinase (MAPK).	Cytarabine	35-40	mitogen-activated protein kinase 14	Homo sapiens	233-269
10644049-1	2000	1-beta-D-Arabinofuranosylcytosine (ara-C) induced apoptosis in HL-60 cells, which was preceded by the activation of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK), and p38 mitogen-activated protein kinase (MAPK).	Cytarabine	35-40	mitogen-activated protein kinase 1	Homo sapiens	271-275
10751606-2	2000	To further characterize p53-mediated DNA repair, we studied the effect of p53 status on the ability of the DNA repair inhibitor 1-ss-D-arabinofuranosylcytosine (AraC) to sensitize MEF to bleomycin-induced chromatid aberrations.	Cytarabine	161-165	tumor protein p53	Homo sapiens	24-27
10751606-2	2000	To further characterize p53-mediated DNA repair, we studied the effect of p53 status on the ability of the DNA repair inhibitor 1-ss-D-arabinofuranosylcytosine (AraC) to sensitize MEF to bleomycin-induced chromatid aberrations.	Cytarabine	161-165	tumor protein p53	Homo sapiens	74-77
10639579-5	2000	The addition of AraC rapidly initiated differentiation in these cell lines, which continued to differentiate to erythrocyte cells possessing a high level of hemoglobin even after the decrease in AMY-1 expression.	Cytarabine	16-20	MYC binding protein	Homo sapiens	195-200
10784401-6	2000	The combination of 2-CdA with doxorubicin or mitoxantrone had a synergistic effect on the induction of apoptosis (p&lt;0.001) in both normal and neoplastic lymphocytes, whereas 2-CdA plus etoposide or cytosine arabinoside were only additive.	Cytarabine	201-221	cytidine deaminase	Homo sapiens	21-24
10784405-2	2000	In the present study, we report that the expression of trkA was also induced by several other differentiation inducers, including 1alpha, 25-dihydroxyvitamin D3 (Vit D3), 1-beta-D-arabinofuranosyl cytosine (Ara-C), sodium butyrate (NaBut), and phorbol 12-myristate 13-acetate (PMA).	Cytarabine	171-205	neurotrophic receptor tyrosine kinase 1	Homo sapiens	55-59
10784405-2	2000	In the present study, we report that the expression of trkA was also induced by several other differentiation inducers, including 1alpha, 25-dihydroxyvitamin D3 (Vit D3), 1-beta-D-arabinofuranosyl cytosine (Ara-C), sodium butyrate (NaBut), and phorbol 12-myristate 13-acetate (PMA).	Cytarabine	207-212	neurotrophic receptor tyrosine kinase 1	Homo sapiens	55-59
10786621-1	2000	The luciferase reporter gene system was used to assay the basal and Ara-C induced promoter activity of the human CR1 gene in K-562 erythroleukemia cells.	Cytarabine	68-73	complement C3b/C4b receptor 1 (Knops blood group)	Homo sapiens	113-116
10574931-6	1999	We also demonstrate that treatment of cells with 1-beta-D-arabinofuranosylcytosine and other genotoxic agents induces Lyn-dependent phosphorylation and activation of SHPTP1.	Cytarabine	49-82	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	118-121
10769646-10	2000	All of the cell lines studied, CEM/0 (wt) and the ara-C resistant clones, showed functional p53 protein.	Cytarabine	50-55	tumor protein p53	Homo sapiens	92-95
10769646-11	2000	The cell treatment with 0.1, 1 and 10 microM ara-C for 48 hours showed increased p53 protein expression in most of these lines.	Cytarabine	45-50	tumor protein p53	Homo sapiens	81-84
10769646-13	2000	Three cell lines resistant to ara-C (CEM/ara-C/B, CEM/ara-C/D and CEM/ara-C/I) showed an important increased expression of bcl-2 protein after treatment with 1 microM ara-C, but not after 10 microM.	Cytarabine	30-35	BCL2 apoptosis regulator	Homo sapiens	123-128
10769646-13	2000	Three cell lines resistant to ara-C (CEM/ara-C/B, CEM/ara-C/D and CEM/ara-C/I) showed an important increased expression of bcl-2 protein after treatment with 1 microM ara-C, but not after 10 microM.	Cytarabine	41-46	BCL2 apoptosis regulator	Homo sapiens	123-128
10769646-13	2000	Three cell lines resistant to ara-C (CEM/ara-C/B, CEM/ara-C/D and CEM/ara-C/I) showed an important increased expression of bcl-2 protein after treatment with 1 microM ara-C, but not after 10 microM.	Cytarabine	41-46	BCL2 apoptosis regulator	Homo sapiens	123-128
10769646-13	2000	Three cell lines resistant to ara-C (CEM/ara-C/B, CEM/ara-C/D and CEM/ara-C/I) showed an important increased expression of bcl-2 protein after treatment with 1 microM ara-C, but not after 10 microM.	Cytarabine	41-46	BCL2 apoptosis regulator	Homo sapiens	123-128
10769646-13	2000	Three cell lines resistant to ara-C (CEM/ara-C/B, CEM/ara-C/D and CEM/ara-C/I) showed an important increased expression of bcl-2 protein after treatment with 1 microM ara-C, but not after 10 microM.	Cytarabine	41-46	BCL2 apoptosis regulator	Homo sapiens	123-128
10769646-17	2000	However, three ara-C resistant cell clones, CEM/ara-C/7A, CEM/ara-C/B and CEM/ara-C/G, were positive for P-gp expression and functional activity.	Cytarabine	15-20	ATP binding cassette subfamily B member 1	Homo sapiens	105-109
10769646-17	2000	However, three ara-C resistant cell clones, CEM/ara-C/7A, CEM/ara-C/B and CEM/ara-C/G, were positive for P-gp expression and functional activity.	Cytarabine	48-53	ATP binding cassette subfamily B member 1	Homo sapiens	105-109
10769646-17	2000	However, three ara-C resistant cell clones, CEM/ara-C/7A, CEM/ara-C/B and CEM/ara-C/G, were positive for P-gp expression and functional activity.	Cytarabine	48-53	ATP binding cassette subfamily B member 1	Homo sapiens	105-109
10769646-17	2000	However, three ara-C resistant cell clones, CEM/ara-C/7A, CEM/ara-C/B and CEM/ara-C/G, were positive for P-gp expression and functional activity.	Cytarabine	48-53	ATP binding cassette subfamily B member 1	Homo sapiens	105-109
10769646-18	2000	It is apparent that selection for ara-C resistance confers cross-resistance to many other classes of drugs and gamma radiation, probably due to bcl-2 protein overexpression or P-gp and MRP expression, as independent mechanisms.	Cytarabine	34-39	BCL2 apoptosis regulator	Homo sapiens	144-149
10769646-18	2000	It is apparent that selection for ara-C resistance confers cross-resistance to many other classes of drugs and gamma radiation, probably due to bcl-2 protein overexpression or P-gp and MRP expression, as independent mechanisms.	Cytarabine	34-39	ATP binding cassette subfamily B member 1	Homo sapiens	176-180
10769646-18	2000	It is apparent that selection for ara-C resistance confers cross-resistance to many other classes of drugs and gamma radiation, probably due to bcl-2 protein overexpression or P-gp and MRP expression, as independent mechanisms.	Cytarabine	34-39	chromosome 19 open reading frame 48	Homo sapiens	185-188
11399618-7	2000	Addition of low-dose cytosine arabinoside (Ara-C)(1 to 10 ng/ml) enhanced TPO- or EPO- induced megakaryocytic differentiation in MO7ER cells while mildly suppressing cell growth.	Cytarabine	21-41	thrombopoietin	Homo sapiens	74-77
11399618-7	2000	Addition of low-dose cytosine arabinoside (Ara-C)(1 to 10 ng/ml) enhanced TPO- or EPO- induced megakaryocytic differentiation in MO7ER cells while mildly suppressing cell growth.	Cytarabine	21-41	erythropoietin	Homo sapiens	82-85
11399618-7	2000	Addition of low-dose cytosine arabinoside (Ara-C)(1 to 10 ng/ml) enhanced TPO- or EPO- induced megakaryocytic differentiation in MO7ER cells while mildly suppressing cell growth.	Cytarabine	43-48	thrombopoietin	Homo sapiens	74-77
11399618-7	2000	Addition of low-dose cytosine arabinoside (Ara-C)(1 to 10 ng/ml) enhanced TPO- or EPO- induced megakaryocytic differentiation in MO7ER cells while mildly suppressing cell growth.	Cytarabine	43-48	erythropoietin	Homo sapiens	82-85
11399618-8	2000	Treatment the cells with low-dose Ara-C plus TPO plus SLF overrode the proliferative enhancing effects of SLF and induced GPIIb/IIIa and GPIb expression as efficient as TPO alone.	Cytarabine	34-39	kit ligand	Mus musculus	106-109
11399618-8	2000	Treatment the cells with low-dose Ara-C plus TPO plus SLF overrode the proliferative enhancing effects of SLF and induced GPIIb/IIIa and GPIb expression as efficient as TPO alone.	Cytarabine	34-39	integrin subunit alpha 2b	Homo sapiens	122-127
11399618-8	2000	Treatment the cells with low-dose Ara-C plus TPO plus SLF overrode the proliferative enhancing effects of SLF and induced GPIIb/IIIa and GPIb expression as efficient as TPO alone.	Cytarabine	34-39	thrombopoietin	Homo sapiens	169-172
10574931-6	1999	We also demonstrate that treatment of cells with 1-beta-D-arabinofuranosylcytosine and other genotoxic agents induces Lyn-dependent phosphorylation and activation of SHPTP1.	Cytarabine	49-82	protein tyrosine phosphatase non-receptor type 6	Homo sapiens	166-172
10574931-7	1999	The significance of the Lyn-SHPTP1 interaction is supported by the demonstration that activation of Lyn contributes in part to the apoptotic response to ara-C treatment and that SHPTP1 attenuates this response.	Cytarabine	153-158	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	24-27
10574931-7	1999	The significance of the Lyn-SHPTP1 interaction is supported by the demonstration that activation of Lyn contributes in part to the apoptotic response to ara-C treatment and that SHPTP1 attenuates this response.	Cytarabine	153-158	protein tyrosine phosphatase non-receptor type 6	Homo sapiens	28-34
10574931-7	1999	The significance of the Lyn-SHPTP1 interaction is supported by the demonstration that activation of Lyn contributes in part to the apoptotic response to ara-C treatment and that SHPTP1 attenuates this response.	Cytarabine	153-158	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	100-103
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).	Cytarabine	68-78	solute carrier family 1 member 4	Homo sapiens	0-5
10606241-10	1999	The HL60/CdA cells showed cross-resistance to 2-chloro-2"-arabino-fluoro-2"-deoxyadenosine, Fara-A, arabinofuranosyl cytosine, difluorodeoxyguanosine, and difluorodeoxycytidine toxicity, most likely because of the decreased phosphorylation of these analogues by dCK.	Cytarabine	100-125	cytidine deaminase	Homo sapiens	9-12
10556184-16	1999	These results also suggest a minor role for cytarabine and etoposide in the treatment of newly diagnosed PML/RARalpha-positive APL patients.	Cytarabine	44-54	PML nuclear body scaffold	Homo sapiens	105-108
10547616-3	1999	A six-tube flow cytometric assay for measuring the sensitivity to ara-C of CD45/side-scatter-gated or of CD34-positive leukemic blasts with 7AAD was established, using fixed stained normal mononuclear cells as an internal standard for quantitation of viable cells following culture.	Cytarabine	66-71	protein tyrosine phosphatase receptor type C	Homo sapiens	75-79
10602423-2	1999	Here, we tested the hypothesis that MIP-1alpha protects normal, but not CML, CFC from the cytotoxic effects of the cell-cycle active drug cytosine arabinoside (Ara-C).	Cytarabine	138-158	C-C motif chemokine ligand 3	Homo sapiens	36-46
10602423-2	1999	Here, we tested the hypothesis that MIP-1alpha protects normal, but not CML, CFC from the cytotoxic effects of the cell-cycle active drug cytosine arabinoside (Ara-C).	Cytarabine	160-165	C-C motif chemokine ligand 3	Homo sapiens	36-46
10602423-3	1999	Using a 24-h Ara-C protection assay we showed that MIP-1alpha confers protection to normal CFC but also sensitizes CML CFC to Ara-C.	Cytarabine	13-18	C-C motif chemokine ligand 3	Homo sapiens	51-61
10602423-3	1999	Using a 24-h Ara-C protection assay we showed that MIP-1alpha confers protection to normal CFC but also sensitizes CML CFC to Ara-C.	Cytarabine	126-131	C-C motif chemokine ligand 3	Homo sapiens	51-61
10613356-4	1999	In contrast, the mRNA expression of LIF was induced by the two erythroid inducers 1-beta-D-arabinofuranosyl cytosine (Ara-C) and hemin.	Cytarabine	82-116	LIF interleukin 6 family cytokine	Homo sapiens	36-39
10613356-4	1999	In contrast, the mRNA expression of LIF was induced by the two erythroid inducers 1-beta-D-arabinofuranosyl cytosine (Ara-C) and hemin.	Cytarabine	118-123	LIF interleukin 6 family cytokine	Homo sapiens	36-39
10602895-4	1999	However, cytidine deaminase activity in particular has a major impact on AraC pharmacokinetics by degrading AraC to its inactive metabolite AraU, and it has been shown to be of prognostic relevance in the treatment of acute myeloid leukemia.	Cytarabine	73-77	cytidine deaminase	Homo sapiens	9-27
10602895-4	1999	However, cytidine deaminase activity in particular has a major impact on AraC pharmacokinetics by degrading AraC to its inactive metabolite AraU, and it has been shown to be of prognostic relevance in the treatment of acute myeloid leukemia.	Cytarabine	108-112	cytidine deaminase	Homo sapiens	9-27
10556184-16	1999	These results also suggest a minor role for cytarabine and etoposide in the treatment of newly diagnosed PML/RARalpha-positive APL patients.	Cytarabine	44-54	retinoic acid receptor alpha	Homo sapiens	109-117
11721472-5	1999	CONCLUSION: It suggests that L-4-oxalysine and arabinosyl cytosine may even exhibit antimetastatic effect through thrombin-fibrinogen pathway, and thrombin might operate in tumor metastasis for only limited step but crucial to fibrin formation in tumor nodules.	Cytarabine	47-66	coagulation factor II, thrombin	Homo sapiens	114-122
10583228-3	1999	We describe a patient who presented with CD56-negative t(8;21) AML who achieved a complete remission and was subsequently treated with three consolidative courses of high-dose cytarabine therapy.	Cytarabine	176-186	neural cell adhesion molecule 1	Homo sapiens	41-45
11721472-5	1999	CONCLUSION: It suggests that L-4-oxalysine and arabinosyl cytosine may even exhibit antimetastatic effect through thrombin-fibrinogen pathway, and thrombin might operate in tumor metastasis for only limited step but crucial to fibrin formation in tumor nodules.	Cytarabine	47-66	fibrinogen beta chain	Homo sapiens	123-133
10557062-3	1999	Treatment with anticancer drugs such as doxorubicin, methotrexate, cytarabine, etoposide and cisplatin at therapeutic concentrations leads to induction of CD95-ligand (CD95-L).	Cytarabine	67-77	Fas ligand	Homo sapiens	155-166
10531467-1	1999	We recently reported that cytosine arabinoside (AraC)-induced apoptosis of cerebellar neurons involves the overexpression of glyceraldehyde-3-phosphate dehydrogenase (GAPDH).	Cytarabine	26-46	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	125-165
10531467-1	1999	We recently reported that cytosine arabinoside (AraC)-induced apoptosis of cerebellar neurons involves the overexpression of glyceraldehyde-3-phosphate dehydrogenase (GAPDH).	Cytarabine	26-46	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	167-172
10531467-1	1999	We recently reported that cytosine arabinoside (AraC)-induced apoptosis of cerebellar neurons involves the overexpression of glyceraldehyde-3-phosphate dehydrogenase (GAPDH).	Cytarabine	48-52	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	125-165
10531467-1	1999	We recently reported that cytosine arabinoside (AraC)-induced apoptosis of cerebellar neurons involves the overexpression of glyceraldehyde-3-phosphate dehydrogenase (GAPDH).	Cytarabine	48-52	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	167-172
10531467-3	1999	AraC-induced apoptosis of cerebellar granule cells was preceded by an increase in levels of p53 mRNA and protein detected between 1 and 8 hr after treatment.	Cytarabine	0-4	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	92-95
10531467-11	1999	These results suggest that AraC-induced apoptosis of cerebellar granule cells involves the expression of both GAPDH and p53 and that, similar to Bax, GAPDH is upregulated by p53 after exposure to the apoptotic insult.	Cytarabine	27-31	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	110-115
10531467-11	1999	These results suggest that AraC-induced apoptosis of cerebellar granule cells involves the expression of both GAPDH and p53 and that, similar to Bax, GAPDH is upregulated by p53 after exposure to the apoptotic insult.	Cytarabine	27-31	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	120-123
10531467-11	1999	These results suggest that AraC-induced apoptosis of cerebellar granule cells involves the expression of both GAPDH and p53 and that, similar to Bax, GAPDH is upregulated by p53 after exposure to the apoptotic insult.	Cytarabine	27-31	BCL2 associated X, apoptosis regulator	Rattus norvegicus	145-148
10531467-11	1999	These results suggest that AraC-induced apoptosis of cerebellar granule cells involves the expression of both GAPDH and p53 and that, similar to Bax, GAPDH is upregulated by p53 after exposure to the apoptotic insult.	Cytarabine	27-31	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	150-155
10531467-11	1999	These results suggest that AraC-induced apoptosis of cerebellar granule cells involves the expression of both GAPDH and p53 and that, similar to Bax, GAPDH is upregulated by p53 after exposure to the apoptotic insult.	Cytarabine	27-31	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	174-177
10557046-11	1999	Within the limitations of this retrospective study, this analysis suggests that, similar to de novo AML with inv(16), secondary cases may also potentially benefit from treatment with escalated-dose ara-C.	Cytarabine	198-203	inversin	Homo sapiens	109-112
10576510-1	1999	In order to investigate whether transfer of the cytidine deaminase (CDD) cDNA would increase chemotherapy resistance to cytosine arabinoside (ara-C) we used a retroviral vector expressing both, neomycin phosphotransferase and the CDD cDNA, to transduce hematopoietic cells from cell lines and from murine bone marrow (BM).	Cytarabine	120-140	cytidine deaminase	Mus musculus	48-66
10576510-1	1999	In order to investigate whether transfer of the cytidine deaminase (CDD) cDNA would increase chemotherapy resistance to cytosine arabinoside (ara-C) we used a retroviral vector expressing both, neomycin phosphotransferase and the CDD cDNA, to transduce hematopoietic cells from cell lines and from murine bone marrow (BM).	Cytarabine	120-140	cytidine deaminase	Mus musculus	68-71
10576510-1	1999	In order to investigate whether transfer of the cytidine deaminase (CDD) cDNA would increase chemotherapy resistance to cytosine arabinoside (ara-C) we used a retroviral vector expressing both, neomycin phosphotransferase and the CDD cDNA, to transduce hematopoietic cells from cell lines and from murine bone marrow (BM).	Cytarabine	142-147	cytidine deaminase	Mus musculus	48-66
10576510-1	1999	In order to investigate whether transfer of the cytidine deaminase (CDD) cDNA would increase chemotherapy resistance to cytosine arabinoside (ara-C) we used a retroviral vector expressing both, neomycin phosphotransferase and the CDD cDNA, to transduce hematopoietic cells from cell lines and from murine bone marrow (BM).	Cytarabine	142-147	cytidine deaminase	Mus musculus	68-71
10557062-3	1999	Treatment with anticancer drugs such as doxorubicin, methotrexate, cytarabine, etoposide and cisplatin at therapeutic concentrations leads to induction of CD95-ligand (CD95-L).	Cytarabine	67-77	Fas ligand	Homo sapiens	168-174
10557064-2	1999	At first, the sensitive and P-glycoprotein (P-gp)-related resistant cell lines were tested to induce apoptosis by a non-P-gp transported drug, such as cytosine arabinoside (ara-C).	Cytarabine	151-171	ATP binding cassette subfamily B member 1	Homo sapiens	28-42
10557064-2	1999	At first, the sensitive and P-glycoprotein (P-gp)-related resistant cell lines were tested to induce apoptosis by a non-P-gp transported drug, such as cytosine arabinoside (ara-C).	Cytarabine	151-171	ATP binding cassette subfamily B member 1	Homo sapiens	44-48
10557064-2	1999	At first, the sensitive and P-glycoprotein (P-gp)-related resistant cell lines were tested to induce apoptosis by a non-P-gp transported drug, such as cytosine arabinoside (ara-C).	Cytarabine	173-178	ATP binding cassette subfamily B member 1	Homo sapiens	28-42
10609785-2	1999	The aim of this study combining IFN-alpha, low-dose cytosine arabinoside (ara-C) and ATRA was to increase the proportion of patients achieving a major cytogenetic response, in comparison with a group of 140 patients previously treated with IFN-alpha plus low-dose ara-C.	Cytarabine	264-269	interferon alpha 1	Homo sapiens	32-41
10557064-2	1999	At first, the sensitive and P-glycoprotein (P-gp)-related resistant cell lines were tested to induce apoptosis by a non-P-gp transported drug, such as cytosine arabinoside (ara-C).	Cytarabine	173-178	ATP binding cassette subfamily B member 1	Homo sapiens	44-48
10557064-3	1999	It was demonstrated that ara-C induces apoptosis in sensitive as well as in P-gp-related resistant cell lines, as expected.	Cytarabine	25-30	ATP binding cassette subfamily B member 1	Homo sapiens	76-80
10557066-10	1999	Downregulation of Bcl-2 mRNA and protein was observed by ATRA and the combination of Ara-C, followed by ATRA, resulted in markedly increased cytotoxicity in HL-60 cells, as compared to Ara-C alone or ATRA followed by Ara-C.	Cytarabine	85-90	BCL2 apoptosis regulator	Homo sapiens	18-23
10557066-10	1999	Downregulation of Bcl-2 mRNA and protein was observed by ATRA and the combination of Ara-C, followed by ATRA, resulted in markedly increased cytotoxicity in HL-60 cells, as compared to Ara-C alone or ATRA followed by Ara-C.	Cytarabine	185-190	BCL2 apoptosis regulator	Homo sapiens	18-23
10557066-10	1999	Downregulation of Bcl-2 mRNA and protein was observed by ATRA and the combination of Ara-C, followed by ATRA, resulted in markedly increased cytotoxicity in HL-60 cells, as compared to Ara-C alone or ATRA followed by Ara-C.	Cytarabine	185-190	BCL2 apoptosis regulator	Homo sapiens	18-23
10531298-5	1999	UV (80 J/m(2)) and the DNA-damaging drugs cytosine beta-D-arabinofuranoside (AraC) and cis-platinum(II)diammine dichloride (cisplatin) also induce gamma-PAK activation.	Cytarabine	42-75	p21 (RAC1) activated kinase 2	Mus musculus	147-156
10502284-2	1999	By using cultured cerebellar granule cells, two types of apoptosis can be induced, one by adding cytosine arabinoside (Ara-c; p53-dependent apoptosis) and one by lowering the K(+) concentrations of the medium (p53-independent apoptosis).	Cytarabine	97-117	tumor protein p53	Homo sapiens	126-129
10543614-0	1999	Expression of a novel double-mutant dihydrofolate reductase-cytidine deaminase fusion gene confers resistance to both methotrexate and cytosine arabinoside.	Cytarabine	135-155	cytidine deaminase	Mus musculus	60-78
10543614-1	1999	A novel fusion gene consisting of the open reading frame of a double-mutant (Phe22-Ser31) dihydrofolate reductase (dmDHFR) cDNA fused to the open reading frame of cytidine deaminase (CD) was constructed and characterized for the purpose of conferring simultaneous resistance to methotrexate (MTX) and cytosine arabinoside (ara-C).	Cytarabine	301-321	cytidine deaminase	Mus musculus	163-181
10543614-1	1999	A novel fusion gene consisting of the open reading frame of a double-mutant (Phe22-Ser31) dihydrofolate reductase (dmDHFR) cDNA fused to the open reading frame of cytidine deaminase (CD) was constructed and characterized for the purpose of conferring simultaneous resistance to methotrexate (MTX) and cytosine arabinoside (ara-C).	Cytarabine	301-321	cytidine deaminase	Mus musculus	183-185
10543614-1	1999	A novel fusion gene consisting of the open reading frame of a double-mutant (Phe22-Ser31) dihydrofolate reductase (dmDHFR) cDNA fused to the open reading frame of cytidine deaminase (CD) was constructed and characterized for the purpose of conferring simultaneous resistance to methotrexate (MTX) and cytosine arabinoside (ara-C).	Cytarabine	323-328	cytidine deaminase	Mus musculus	163-181
10543614-1	1999	A novel fusion gene consisting of the open reading frame of a double-mutant (Phe22-Ser31) dihydrofolate reductase (dmDHFR) cDNA fused to the open reading frame of cytidine deaminase (CD) was constructed and characterized for the purpose of conferring simultaneous resistance to methotrexate (MTX) and cytosine arabinoside (ara-C).	Cytarabine	323-328	cytidine deaminase	Mus musculus	183-185
10543614-4	1999	Retrovirus-mediated expression of dmDHFR-CD in NIH 3T3 cells conferred significant resistance (10- to 12-fold) against MTX and ara-C, compared with mock- and single gene-infected cells and the level of resistance obtained was similar to that of cells expressing both CD and dmDHFR from a retroviral bicistronic vector.	Cytarabine	127-132	cytidine deaminase	Mus musculus	41-43
10456672-13	1999	The addition of RA to cytarabine enhanced its induced reduction of Bcl-2 in KG1 CD34+CD7- but not in KGla CD34+CD7+ human myeloid leukaemia cells.	Cytarabine	22-32	BCL2 apoptosis regulator	Homo sapiens	67-72
10573139-1	1999	In some studies the GM-CSF (granulocyte-macrophage colony-stimulating factor) increased the in vitro sensitivity of acute myeloid leukemia (AML) cells to cytosine arabinoside (Ara-C), however, in clinical trials no favorable effects were shown.	Cytarabine	154-174	colony stimulating factor 2	Homo sapiens	20-26
10573139-1	1999	In some studies the GM-CSF (granulocyte-macrophage colony-stimulating factor) increased the in vitro sensitivity of acute myeloid leukemia (AML) cells to cytosine arabinoside (Ara-C), however, in clinical trials no favorable effects were shown.	Cytarabine	154-174	colony stimulating factor 2	Homo sapiens	28-76
10573139-1	1999	In some studies the GM-CSF (granulocyte-macrophage colony-stimulating factor) increased the in vitro sensitivity of acute myeloid leukemia (AML) cells to cytosine arabinoside (Ara-C), however, in clinical trials no favorable effects were shown.	Cytarabine	176-181	colony stimulating factor 2	Homo sapiens	20-26
10573139-1	1999	In some studies the GM-CSF (granulocyte-macrophage colony-stimulating factor) increased the in vitro sensitivity of acute myeloid leukemia (AML) cells to cytosine arabinoside (Ara-C), however, in clinical trials no favorable effects were shown.	Cytarabine	176-181	colony stimulating factor 2	Homo sapiens	28-76
10573139-3	1999	In 6 days continuous exposure, dose dependent Ara-C cytotoxicity was counteracted by GM-CSF.	Cytarabine	46-51	colony stimulating factor 2	Homo sapiens	85-91
10573139-5	1999	However, in a short term treatment (24 h, high doses) the GM-CSF increased both MTX and Ara-C cytotoxicity.	Cytarabine	88-93	colony stimulating factor 2	Homo sapiens	58-64
10520005-13	1999	We conclude that a clinical benefit for the addition of cytarabine to the treatment of CML with IFN might only be achieved by the administration of a higher cumulative dose of cytarabine, suggesting that lower leucocyte counts of 2-4 x 109/l have to be tolerated.	Cytarabine	56-66	interferon alpha 1	Homo sapiens	96-99
10520005-13	1999	We conclude that a clinical benefit for the addition of cytarabine to the treatment of CML with IFN might only be achieved by the administration of a higher cumulative dose of cytarabine, suggesting that lower leucocyte counts of 2-4 x 109/l have to be tolerated.	Cytarabine	176-186	interferon alpha 1	Homo sapiens	96-99
10561359-1	1999	PURPOSE: The Cancer and Leukemia Group B conducted parallel phase I trials of cytarabine, daunorubicin, and etoposide (ADE) with or without PSC-833 (P), a modulator of p-glycoprotein-mediated multidrug resistance.	Cytarabine	78-88	ATP binding cassette subfamily B member 1	Homo sapiens	168-182
10470825-4	1999	Constitutive overexpression of murine bax was achieved in U138 and U373 only, which resulted in an increased sensitivity of these lines to the apoptosis-inducing effect of cytosine arabinoside (ara-C).	Cytarabine	172-192	BCL2-associated X protein	Mus musculus	38-41
10470825-4	1999	Constitutive overexpression of murine bax was achieved in U138 and U373 only, which resulted in an increased sensitivity of these lines to the apoptosis-inducing effect of cytosine arabinoside (ara-C).	Cytarabine	194-199	BCL2-associated X protein	Mus musculus	38-41
10470825-11	1999	In contrast, the lines that had mutant, nonfunctional P53 did not undergo spontaneous apoptosis, but they were rendered more sensitive to the apoptosis-inducing effect of ara-C.	Cytarabine	171-176	tumor protein p53	Homo sapiens	54-57
10462544-6	1999	We further showed, in a combined enzymatic assay, that human deoxycytidine kinase and UMP-CMP kinase together phosphorylated araC, dFdC, and 2",3"-dideoxycytidine to their diphosphate forms.	Cytarabine	125-129	cytidine/uridine monophosphate kinase 1	Homo sapiens	86-100
10450749-0	1999	Granulocyte-macrophage colony-stimulating factor (GM-CSF) to increase efficacy of intensive sequential chemotherapy with etoposide, mitoxantrone and cytarabine (EMA) in previously treated acute myeloid leukemia: a multicenter randomized placebo-controlled trial (EMA91 Trial).	Cytarabine	149-159	colony stimulating factor 2	Homo sapiens	0-48
10450749-0	1999	Granulocyte-macrophage colony-stimulating factor (GM-CSF) to increase efficacy of intensive sequential chemotherapy with etoposide, mitoxantrone and cytarabine (EMA) in previously treated acute myeloid leukemia: a multicenter randomized placebo-controlled trial (EMA91 Trial).	Cytarabine	149-159	colony stimulating factor 2	Homo sapiens	50-56
10564345-4	1999	The antimitotic cytosine-beta,D-arabinofuranoside (AraC) blocked glial cell proliferation induced by bFGF, but not neuroprotection.	Cytarabine	16-49	fibroblast growth factor 2	Homo sapiens	101-105
10564345-4	1999	The antimitotic cytosine-beta,D-arabinofuranoside (AraC) blocked glial cell proliferation induced by bFGF, but not neuroprotection.	Cytarabine	51-55	fibroblast growth factor 2	Homo sapiens	101-105
10456672-7	1999	Both cytarabine and fludarabine induced a dose dependent increase in the number of apoptotic cells in both CD34 positive cell types.	Cytarabine	5-15	CD34 molecule	Homo sapiens	107-111
10456672-11	1999	As single agents, RA, cytarabine and fludarabine reduced Bcl-2 expression in a dose dependent manner in both cell types.	Cytarabine	22-32	BCL2 apoptosis regulator	Homo sapiens	57-62
10456672-12	1999	Using a quantitative ELISA assay, the Bcl-2 protein concentration was reduced by 86 or 100%, after 72 h of treatment with 10 microM cytarabine or fludarabine, respectively, in both CD34 positive leukaemia cell types.	Cytarabine	132-142	BCL2 apoptosis regulator	Homo sapiens	38-43
10456672-12	1999	Using a quantitative ELISA assay, the Bcl-2 protein concentration was reduced by 86 or 100%, after 72 h of treatment with 10 microM cytarabine or fludarabine, respectively, in both CD34 positive leukaemia cell types.	Cytarabine	132-142	CD34 molecule	Homo sapiens	181-185
10456672-13	1999	The addition of RA to cytarabine enhanced its induced reduction of Bcl-2 in KG1 CD34+CD7- but not in KGla CD34+CD7+ human myeloid leukaemia cells.	Cytarabine	22-32	CD34 molecule	Homo sapiens	80-84
10456672-15	1999	In conclusion, the present results suggest a potential role for the combination of RA and cytarabine in the treatment of refractory and/or relapsed AML patients with CD34+CD7- but not CD34+CD7+ blast cells.	Cytarabine	90-100	CD34 molecule	Homo sapiens	166-170
10403525-4	1999	Unexpectedly, pretreatment of cells with ara-C or dFdC opposed BRY- and PMA-related induction of the cyclin-dependent kinase inhibitors (CDKIs) p21CIP1 and/or p27KIP1.	Cytarabine	41-46	cyclin dependent kinase inhibitor 1A	Homo sapiens	144-151
10511810-2	1999	In the present study, using leukemic cell lines, time course of cytarabine-induced apoptosis was examined morphologically, using annexin V method, TUNEL method and fluorometric assay for caspase-3 activity.	Cytarabine	64-74	annexin A5	Homo sapiens	129-138
10511810-2	1999	In the present study, using leukemic cell lines, time course of cytarabine-induced apoptosis was examined morphologically, using annexin V method, TUNEL method and fluorometric assay for caspase-3 activity.	Cytarabine	64-74	caspase 3	Homo sapiens	187-196
10511810-4	1999	In annexin V method and assay for caspase-3 activity, changes accompanied by apoptosis could also be detected at 4-hour incubation with cytarabine, but in TUNEL method, they were not found until 24-hour incubation.	Cytarabine	136-146	annexin A5	Homo sapiens	3-12
10511810-4	1999	In annexin V method and assay for caspase-3 activity, changes accompanied by apoptosis could also be detected at 4-hour incubation with cytarabine, but in TUNEL method, they were not found until 24-hour incubation.	Cytarabine	136-146	caspase 3	Homo sapiens	34-43
10511810-5	1999	The advantage of annexin V method which detects phosphatidylserine emerging on cell surface during the early course of apoptosis included simplicity and rapidity of the procedure and short time requirement for apoptosis to appear after incubation with cytarabine.	Cytarabine	252-262	annexin A5	Homo sapiens	17-26
10403525-4	1999	Unexpectedly, pretreatment of cells with ara-C or dFdC opposed BRY- and PMA-related induction of the cyclin-dependent kinase inhibitors (CDKIs) p21CIP1 and/or p27KIP1.	Cytarabine	41-46	cyclin dependent kinase inhibitor 1B	Homo sapiens	159-166
10400371-4	1999	Among acute myeloid leukemia patients, AML1-ETO and CBFbeta-MYH11 fusions are associated with a favorable response, especially when the chemotherapy regimen includes high-dose cytarabine.	Cytarabine	176-186	RUNX family transcription factor 1	Homo sapiens	39-43
10400371-4	1999	Among acute myeloid leukemia patients, AML1-ETO and CBFbeta-MYH11 fusions are associated with a favorable response, especially when the chemotherapy regimen includes high-dose cytarabine.	Cytarabine	176-186	RUNX1 partner transcriptional co-repressor 1	Homo sapiens	44-47
10400371-4	1999	Among acute myeloid leukemia patients, AML1-ETO and CBFbeta-MYH11 fusions are associated with a favorable response, especially when the chemotherapy regimen includes high-dose cytarabine.	Cytarabine	176-186	core-binding factor subunit beta	Homo sapiens	52-59
10400371-4	1999	Among acute myeloid leukemia patients, AML1-ETO and CBFbeta-MYH11 fusions are associated with a favorable response, especially when the chemotherapy regimen includes high-dose cytarabine.	Cytarabine	176-186	myosin heavy chain 11	Homo sapiens	60-65
10448422-2	1999	In cell lines derived from the rat neostriatum immortalized with tsA58, the toxic agents Adriamycin, cytosine arabinoside, and glutamate induced apoptosis and increased p53 activity and differentiation.	Cytarabine	101-121	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	169-172
10386996-4	1999	Expression of SM-20 also increases during neuronal death caused by cytosine arabinoside or the phosphatidylinositol 3-kinase inhibitor LY294002.	Cytarabine	67-87	egl-9 family hypoxia inducible factor 1	Homo sapiens	14-19
10361105-11	1999	In 1 patient with AML, an increase in Pgp levels was observed in vivo at 4 and 16 hours after the administration of standard chemotherapy with DAU/AraC.	Cytarabine	147-151	ATP binding cassette subfamily B member 1	Homo sapiens	38-41
10374846-7	1999	These finding suggest that co-treatment with DT388-GM-CSF may lead to a lowered apoptotic threshold and clonogenic survival of human AML blasts due to Ara-C.	Cytarabine	151-156	colony stimulating factor 2	Homo sapiens	51-57
10374846-1	1999	Human granulocyte-macrophage colony-stimulating factor fused to truncated diphtheria toxin (DT388-GM-CSF) sensitized wild-type and Bcl2-overexpressing HL60 human leukemia cells to intoxication by Ara-C based on proliferation and clonogenic assays.	Cytarabine	196-201	colony stimulating factor 2	Homo sapiens	6-54
10374846-1	1999	Human granulocyte-macrophage colony-stimulating factor fused to truncated diphtheria toxin (DT388-GM-CSF) sensitized wild-type and Bcl2-overexpressing HL60 human leukemia cells to intoxication by Ara-C based on proliferation and clonogenic assays.	Cytarabine	196-201	colony stimulating factor 2	Homo sapiens	98-104
10096557-0	1999	Dysregulation of the cyclin-dependent kinase inhibitor p21WAF1/CIP1/MDA6 increases the susceptibility of human leukemia cells (U937) to 1-beta-D-arabinofuranosylcytosine-mediated mitochondrial dysfunction and apoptosis.	Cytarabine	136-169	cyclin dependent kinase inhibitor 1A	Homo sapiens	63-67
10374846-5	1999	As compared to exposure to DT388-GM-CSF or Ara-C alone, co-treatment produced significant increases in cytosolic accumulation of cytochrome c, a higher percentage of cells with loss of mitochondrial membrane potential and an increase in reactive oxygen species and morphologic changes of apoptosis, and a greater induction of poly(ADP-ribose) polymerase (PARP) and DNA fragmentation factor 45 (DFF45) cleavage activities of caspase 3.	Cytarabine	43-48	cytochrome c, somatic	Homo sapiens	129-141
10374846-5	1999	As compared to exposure to DT388-GM-CSF or Ara-C alone, co-treatment produced significant increases in cytosolic accumulation of cytochrome c, a higher percentage of cells with loss of mitochondrial membrane potential and an increase in reactive oxygen species and morphologic changes of apoptosis, and a greater induction of poly(ADP-ribose) polymerase (PARP) and DNA fragmentation factor 45 (DFF45) cleavage activities of caspase 3.	Cytarabine	43-48	poly(ADP-ribose) polymerase 1	Homo sapiens	326-353
10374846-5	1999	As compared to exposure to DT388-GM-CSF or Ara-C alone, co-treatment produced significant increases in cytosolic accumulation of cytochrome c, a higher percentage of cells with loss of mitochondrial membrane potential and an increase in reactive oxygen species and morphologic changes of apoptosis, and a greater induction of poly(ADP-ribose) polymerase (PARP) and DNA fragmentation factor 45 (DFF45) cleavage activities of caspase 3.	Cytarabine	43-48	poly(ADP-ribose) polymerase 1	Homo sapiens	355-359
10374846-5	1999	As compared to exposure to DT388-GM-CSF or Ara-C alone, co-treatment produced significant increases in cytosolic accumulation of cytochrome c, a higher percentage of cells with loss of mitochondrial membrane potential and an increase in reactive oxygen species and morphologic changes of apoptosis, and a greater induction of poly(ADP-ribose) polymerase (PARP) and DNA fragmentation factor 45 (DFF45) cleavage activities of caspase 3.	Cytarabine	43-48	DNA fragmentation factor subunit alpha	Homo sapiens	365-392
10374846-5	1999	As compared to exposure to DT388-GM-CSF or Ara-C alone, co-treatment produced significant increases in cytosolic accumulation of cytochrome c, a higher percentage of cells with loss of mitochondrial membrane potential and an increase in reactive oxygen species and morphologic changes of apoptosis, and a greater induction of poly(ADP-ribose) polymerase (PARP) and DNA fragmentation factor 45 (DFF45) cleavage activities of caspase 3.	Cytarabine	43-48	DNA fragmentation factor subunit alpha	Homo sapiens	394-399
10374846-5	1999	As compared to exposure to DT388-GM-CSF or Ara-C alone, co-treatment produced significant increases in cytosolic accumulation of cytochrome c, a higher percentage of cells with loss of mitochondrial membrane potential and an increase in reactive oxygen species and morphologic changes of apoptosis, and a greater induction of poly(ADP-ribose) polymerase (PARP) and DNA fragmentation factor 45 (DFF45) cleavage activities of caspase 3.	Cytarabine	43-48	caspase 3	Homo sapiens	424-433
10196170-2	1999	In cells exposed to genotoxic agents including etoposide and cytosine arabinoside, MEKK1 is cleaved at Asp874 by caspases.	Cytarabine	61-81	mitogen-activated protein kinase kinase kinase 1	Homo sapiens	83-88
10233409-0	1999	Leukaemic blasts differ from normal bone marrow mononuclear cells and CD34+ haemopoietic stem cells in their metabolism of cytosine arabinoside.	Cytarabine	123-143	CD34 molecule	Homo sapiens	70-74
10218969-7	1999	Cytosine arabinoside lowered cultured islet IP3R-II and -III mRNA levels, but glucose effects remained evident.	Cytarabine	0-20	inositol 1,4,5-trisphosphate receptor, type 1	Rattus norvegicus	44-48
11601208-1	1999	OBJECTIVE: To study the in vitro effect of cord blood plasma(CBP) on the sensitivity of acute myeloid leukemia(AML) cells to cytosine arabinoside (Ara-C).	Cytarabine	125-145	CREB binding protein	Homo sapiens	61-64
11601208-1	1999	OBJECTIVE: To study the in vitro effect of cord blood plasma(CBP) on the sensitivity of acute myeloid leukemia(AML) cells to cytosine arabinoside (Ara-C).	Cytarabine	147-152	CREB binding protein	Homo sapiens	61-64
11601208-3	1999	RESULTS AND CONCLUSION: The sensitivity of AML cells to Ara-C was heterogeneous, but CBP could significantly enhanced the cytotoxic activity of Ara-C to drug resistant AML cells.	Cytarabine	144-149	CREB binding protein	Homo sapiens	85-88
10348147-8	1999	Cytotoxicity of cytarabine and thioguanine was significantly increased by IL-7, that of thioguanine by IL-3 as well.	Cytarabine	16-26	interleukin 7	Homo sapiens	74-78
10348147-8	1999	Cytotoxicity of cytarabine and thioguanine was significantly increased by IL-7, that of thioguanine by IL-3 as well.	Cytarabine	16-26	interleukin 3	Homo sapiens	103-107
10214872-7	1999	DT3-GM-CSF significantly improved survival of the SCID mice over Ara-C, DAB389IL-2, or control (P &lt; 0.001).	Cytarabine	65-70	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	4-10
10096557-0	1999	Dysregulation of the cyclin-dependent kinase inhibitor p21WAF1/CIP1/MDA6 increases the susceptibility of human leukemia cells (U937) to 1-beta-D-arabinofuranosylcytosine-mediated mitochondrial dysfunction and apoptosis.	Cytarabine	136-169	cyclin dependent kinase inhibitor 1A	Homo sapiens	68-72
10096557-1	1999	The effects of dysregulation of the cyclin-dependent kinase inhibitor p21WAF1/CIP1 on the apoptotic response of U937 monocytic leukemia cells to 1-beta-D-arabinofuranosylcytosine (ara-C) were examined.	Cytarabine	145-178	cyclin dependent kinase inhibitor 1A	Homo sapiens	78-82
10096557-2	1999	After a 6-h exposure to 1 microM ara-C, cells stably transfected with a p21WAF1/CIP1 antisense construct were significantly more sensitive to the induction of classic apoptotic morphology, DNA fragmentation, caspase-3 activation, poly(ADP-ribose) polymerase degradation, and underphosphorylation of the retinoblastoma protein (pRb) than their empty-vector counterparts.	Cytarabine	33-38	cyclin dependent kinase inhibitor 1A	Homo sapiens	80-84
10096557-2	1999	After a 6-h exposure to 1 microM ara-C, cells stably transfected with a p21WAF1/CIP1 antisense construct were significantly more sensitive to the induction of classic apoptotic morphology, DNA fragmentation, caspase-3 activation, poly(ADP-ribose) polymerase degradation, and underphosphorylation of the retinoblastoma protein (pRb) than their empty-vector counterparts.	Cytarabine	33-38	caspase 3	Homo sapiens	208-217
10096557-2	1999	After a 6-h exposure to 1 microM ara-C, cells stably transfected with a p21WAF1/CIP1 antisense construct were significantly more sensitive to the induction of classic apoptotic morphology, DNA fragmentation, caspase-3 activation, poly(ADP-ribose) polymerase degradation, and underphosphorylation of the retinoblastoma protein (pRb) than their empty-vector counterparts.	Cytarabine	33-38	poly(ADP-ribose) polymerase 1	Homo sapiens	230-257
10096557-2	1999	After a 6-h exposure to 1 microM ara-C, cells stably transfected with a p21WAF1/CIP1 antisense construct were significantly more sensitive to the induction of classic apoptotic morphology, DNA fragmentation, caspase-3 activation, poly(ADP-ribose) polymerase degradation, and underphosphorylation of the retinoblastoma protein (pRb) than their empty-vector counterparts.	Cytarabine	33-38	RB transcriptional corepressor 1	Homo sapiens	327-330
10096557-5	1999	Moreover, synchronization of p21 antisense-expressing cells in S-phase by aphidicolin block resulted in a further increase in ara-C-mediated apoptosis, suggesting enhanced drug sensitivity of the S-phase cell fraction.	Cytarabine	126-131	cyclin dependent kinase inhibitor 1A	Homo sapiens	29-32
10096557-6	1999	After exposure to ara-C, p21 antisense-expressing cells displayed a greater decline in mitochondrial membrane potential (deltapsi(m)) and generation of reactive oxygen species than their empty-vector counterparts, as well as early potentiation (e.g., within 2-4 h) of cytochrome c release into the cytosolic S-100 fraction.	Cytarabine	18-23	cyclin dependent kinase inhibitor 1A	Homo sapiens	25-28
10096557-7	1999	Lastly, ara-C-mediated increases in mitogen-activated protein kinase activity over basal levels were attenuated in p21 antisense-expressing cells.	Cytarabine	8-13	cyclin dependent kinase inhibitor 1A	Homo sapiens	115-118
10096557-8	1999	Collectively, these findings indicate that dysregulation of the cyclin-dependent kinase inhibitor p21WAF1/CIP1 increases the susceptibility of U937 human leukemia cells to ara-C-related lethality, and this phenomenon occurs as a relatively early event that is independent of cell cycle or pharmacodynamic factors and is associated with mitochondrial perturbations implicated in activation of the apoptotic protease cascade.	Cytarabine	172-177	cyclin dependent kinase inhibitor 1A	Homo sapiens	106-110
10355579-1	1999	BACKGROUND: Accumulation of the cytosine arabinoside (ara-C) metabolite ara-C-triphosphate (ara-CTP) in leukemic blast cells is considered to be the main determinant of ara-C cytotoxicity in vitro and in vivo.	Cytarabine	32-52	solute carrier family 25 member 1	Homo sapiens	96-99
10208551-2	1999	Treatment of mesencephalic cells with dibutyryl-cAMP (dbcAMP), 30 mM K+ (HK+), or the antimitotic ara-C not only promoted the survival of tyrosine hydroxylase expressing (TH+) neurons but also increased the proportion of these cells that were immunopositive for BDNF.	Cytarabine	98-103	brain derived neurotrophic factor	Homo sapiens	262-266
10208551-5	1999	Increases in BDNF expression resulting from K+-induced depolarization or ara-C treatment were abolished, respectively, by the L-type calcium channel blocker nifedipine and the deoxynucleotide dCTP.	Cytarabine	73-78	brain derived neurotrophic factor	Homo sapiens	13-17
10208551-7	1999	However, induction of the expression of BDNF in these neurons by dbcAMP, HK+ or ara-C was apparently not responsible for survival promotion by these factors.	Cytarabine	80-85	brain derived neurotrophic factor	Homo sapiens	40-44
10355579-1	1999	BACKGROUND: Accumulation of the cytosine arabinoside (ara-C) metabolite ara-C-triphosphate (ara-CTP) in leukemic blast cells is considered to be the main determinant of ara-C cytotoxicity in vitro and in vivo.	Cytarabine	72-77	solute carrier family 25 member 1	Homo sapiens	96-99
10355579-1	1999	BACKGROUND: Accumulation of the cytosine arabinoside (ara-C) metabolite ara-C-triphosphate (ara-CTP) in leukemic blast cells is considered to be the main determinant of ara-C cytotoxicity in vitro and in vivo.	Cytarabine	54-59	solute carrier family 25 member 1	Homo sapiens	96-99
10086731-3	1999	We report here that chemotherapeutic drugs, such as doxorubicin, cytarabine, methotrexate and 6-mercaptopurine, sensitize CD95-resistant pre-B-ALL cell lines for CD95- and lymphokine-activated killer (LAK)-induced cell death.	Cytarabine	65-75	Fas cell surface death receptor	Homo sapiens	122-126
10103100-7	1999	Here we show that Ara-C-induced death of cerebellar granule neurons is prevented by an inhibitor of cdk4, whereas inhibition of cdk1, -2 and -5 mimics the death, and non-cdk4/6 cdks are inhibited by Ara-C treatment.	Cytarabine	18-23	cyclin-dependent kinase 4	Rattus norvegicus	100-104
10037463-1	1999	Treatment with cytosine beta-D-arabinoside (AraC; 300 microM) induced a time-dependent accumulation of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) protein in nuclei purified from cultured cerebellar granule cells, with a concomitant degradation of lamin B1, a nuclear membrane protein and a substrate of CPP32/caspase-3.	Cytarabine	15-42	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	103-143
10037463-1	1999	Treatment with cytosine beta-D-arabinoside (AraC; 300 microM) induced a time-dependent accumulation of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) protein in nuclei purified from cultured cerebellar granule cells, with a concomitant degradation of lamin B1, a nuclear membrane protein and a substrate of CPP32/caspase-3.	Cytarabine	15-42	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	145-150
10037463-1	1999	Treatment with cytosine beta-D-arabinoside (AraC; 300 microM) induced a time-dependent accumulation of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) protein in nuclei purified from cultured cerebellar granule cells, with a concomitant degradation of lamin B1, a nuclear membrane protein and a substrate of CPP32/caspase-3.	Cytarabine	15-42	lamin B1	Homo sapiens	253-261
10037463-1	1999	Treatment with cytosine beta-D-arabinoside (AraC; 300 microM) induced a time-dependent accumulation of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) protein in nuclei purified from cultured cerebellar granule cells, with a concomitant degradation of lamin B1, a nuclear membrane protein and a substrate of CPP32/caspase-3.	Cytarabine	15-42	caspase 3	Homo sapiens	309-314
10037463-1	1999	Treatment with cytosine beta-D-arabinoside (AraC; 300 microM) induced a time-dependent accumulation of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) protein in nuclei purified from cultured cerebellar granule cells, with a concomitant degradation of lamin B1, a nuclear membrane protein and a substrate of CPP32/caspase-3.	Cytarabine	15-42	caspase 3	Homo sapiens	315-324
10037463-1	1999	Treatment with cytosine beta-D-arabinoside (AraC; 300 microM) induced a time-dependent accumulation of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) protein in nuclei purified from cultured cerebellar granule cells, with a concomitant degradation of lamin B1, a nuclear membrane protein and a substrate of CPP32/caspase-3.	Cytarabine	44-48	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	103-143
10037463-1	1999	Treatment with cytosine beta-D-arabinoside (AraC; 300 microM) induced a time-dependent accumulation of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) protein in nuclei purified from cultured cerebellar granule cells, with a concomitant degradation of lamin B1, a nuclear membrane protein and a substrate of CPP32/caspase-3.	Cytarabine	44-48	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	145-150
10037463-1	1999	Treatment with cytosine beta-D-arabinoside (AraC; 300 microM) induced a time-dependent accumulation of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) protein in nuclei purified from cultured cerebellar granule cells, with a concomitant degradation of lamin B1, a nuclear membrane protein and a substrate of CPP32/caspase-3.	Cytarabine	44-48	lamin B1	Homo sapiens	253-261
10037463-1	1999	Treatment with cytosine beta-D-arabinoside (AraC; 300 microM) induced a time-dependent accumulation of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) protein in nuclei purified from cultured cerebellar granule cells, with a concomitant degradation of lamin B1, a nuclear membrane protein and a substrate of CPP32/caspase-3.	Cytarabine	44-48	caspase 3	Homo sapiens	309-314
10037463-1	1999	Treatment with cytosine beta-D-arabinoside (AraC; 300 microM) induced a time-dependent accumulation of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) protein in nuclei purified from cultured cerebellar granule cells, with a concomitant degradation of lamin B1, a nuclear membrane protein and a substrate of CPP32/caspase-3.	Cytarabine	44-48	caspase 3	Homo sapiens	315-324
10037463-2	1999	Moreover, Asp-Glu-Val-Asp-fluoromethyl ketone (DEVD-fmk), a CPP32-selective antagonist, dose-dependently suppressed AraC-induced apoptosis of these neurons.	Cytarabine	116-120	caspase 3	Homo sapiens	60-65
10037463-5	1999	Six GAPDH isoforms were detected in the nuclei of AraC-treated cells.	Cytarabine	50-54	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	4-9
10086731-3	1999	We report here that chemotherapeutic drugs, such as doxorubicin, cytarabine, methotrexate and 6-mercaptopurine, sensitize CD95-resistant pre-B-ALL cell lines for CD95- and lymphokine-activated killer (LAK)-induced cell death.	Cytarabine	65-75	Fas cell surface death receptor	Homo sapiens	162-166
10500780-14	1999	Nine of the 14 pts (64%) treated with intensive anthracyclin-Ara C chemotherapy achieved complete remission, including 5/5 (100%) Pgp- cases vs 4/9 (44%) Pgp+ cases (p = 0.04) and 4/6 (67%) Rh 123- vs 4/7 (57%) Rh123+ cases (p = 0.5).	Cytarabine	61-66	ATP binding cassette subfamily B member 1	Homo sapiens	130-133
10023011-5	1999	The IC50 of cytarabine and fludarabine were significantly higher in CD34 positive cells with high Bcl-2 than in CD34 negative cells with low Bcl-2.	Cytarabine	12-22	CD34 molecule	Homo sapiens	68-72
10023011-5	1999	The IC50 of cytarabine and fludarabine were significantly higher in CD34 positive cells with high Bcl-2 than in CD34 negative cells with low Bcl-2.	Cytarabine	12-22	BCL2 apoptosis regulator	Homo sapiens	98-103
10023011-5	1999	The IC50 of cytarabine and fludarabine were significantly higher in CD34 positive cells with high Bcl-2 than in CD34 negative cells with low Bcl-2.	Cytarabine	12-22	CD34 molecule	Homo sapiens	112-116
10023011-5	1999	The IC50 of cytarabine and fludarabine were significantly higher in CD34 positive cells with high Bcl-2 than in CD34 negative cells with low Bcl-2.	Cytarabine	12-22	BCL2 apoptosis regulator	Homo sapiens	141-146
9880587-0	1999	A role for MAPK/ERK in sympathetic neuron survival: protection against a p53-dependent, JNK-independent induction of apoptosis by cytosine arabinoside.	Cytarabine	130-150	Eph receptor B1	Rattus norvegicus	16-19
9880587-0	1999	A role for MAPK/ERK in sympathetic neuron survival: protection against a p53-dependent, JNK-independent induction of apoptosis by cytosine arabinoside.	Cytarabine	130-150	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	73-76
9880587-1	1999	The antimitotic nucleoside cytosine arabinoside (araC) causes apoptosis in postmitotic neurons for which two mechanisms have been suggested: (1) araC directly inhibits a trophic factor-maintained signaling pathway required for survival, effectively mimicking trophic factor withdrawal; and (2) araC induces apoptosis by a p53-dependent mechanism distinct from trophic factor withdrawal.	Cytarabine	49-53	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	322-325
9880587-2	1999	In rat sympathetic neurons, we found that araC treatment for 12 hr induced approximately 25% apoptosis without affecting NGF-maintained signaling; there was neither reduction in the activity of mitogen activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) or protein kinase B/Akt, a kinase implicated in NGF-mediated survival, nor was there c-Jun N-terminal kinase (JNK) activation or c-Jun N-terminal phosphorylation, events implicated in apoptosis induced by NGF withdrawal.	Cytarabine	42-46	AKT serine/threonine kinase 1	Rattus norvegicus	296-299
9880587-2	1999	In rat sympathetic neurons, we found that araC treatment for 12 hr induced approximately 25% apoptosis without affecting NGF-maintained signaling; there was neither reduction in the activity of mitogen activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) or protein kinase B/Akt, a kinase implicated in NGF-mediated survival, nor was there c-Jun N-terminal kinase (JNK) activation or c-Jun N-terminal phosphorylation, events implicated in apoptosis induced by NGF withdrawal.	Cytarabine	42-46	mitogen-activated protein kinase 8	Rattus norvegicus	361-384
9880587-2	1999	In rat sympathetic neurons, we found that araC treatment for 12 hr induced approximately 25% apoptosis without affecting NGF-maintained signaling; there was neither reduction in the activity of mitogen activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) or protein kinase B/Akt, a kinase implicated in NGF-mediated survival, nor was there c-Jun N-terminal kinase (JNK) activation or c-Jun N-terminal phosphorylation, events implicated in apoptosis induced by NGF withdrawal.	Cytarabine	42-46	mitogen-activated protein kinase 8	Rattus norvegicus	386-389
9880587-3	1999	However, araC treatment, but not NGF-withdrawal, elevated expression of p53 protein before and during apoptosis.	Cytarabine	9-13	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	72-75
9880587-4	1999	Additionally, araC-induced apoptosis was suppressed in sympathetic neurons from p53 null mice.	Cytarabine	14-18	transformation related protein 53, pseudogene	Mus musculus	80-83
9880587-7	1999	Our data show that, in contrast to NGF deprivation, araC induces apoptosis via a p53-dependent, JNK-independent mechanism, against which MAPK/ERK plays a substantial protective role.	Cytarabine	52-56	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	81-84
9880587-7	1999	Our data show that, in contrast to NGF deprivation, araC induces apoptosis via a p53-dependent, JNK-independent mechanism, against which MAPK/ERK plays a substantial protective role.	Cytarabine	52-56	mitogen-activated protein kinase 8	Rattus norvegicus	96-99
9880587-7	1999	Our data show that, in contrast to NGF deprivation, araC induces apoptosis via a p53-dependent, JNK-independent mechanism, against which MAPK/ERK plays a substantial protective role.	Cytarabine	52-56	Eph receptor B1	Rattus norvegicus	142-145
10500774-2	1999	Several large cohorts of newly diagnosed AML patients treated with a classical anthracycline + standard doses of cytosine arabinoside were tested for the prognosis value of MDR1 phenotype, and demonstrated an high correlation between a significant increase of MDR1 gene expression and treatment failure (or, better, drug resistance).	Cytarabine	113-133	ATP binding cassette subfamily B member 1	Homo sapiens	260-264
10500838-6	1999	Combining Ara-C with G- or GM-CSF resulted in equal or increased LC50 (compared with LC50 of Ara-C alone) in 100% cases of AML.	Cytarabine	93-98	colony stimulating factor 2	Homo sapiens	27-33
10023011-7	1999	Both cytarabine and fludarabine have reduced Bcl-2 concentrations in both cell types.	Cytarabine	5-15	BCL2 apoptosis regulator	Homo sapiens	45-50
10029165-0	1999	Priming with G-CSF effectively enhances low-dose Ara-C-induced in vivo apoptosis in myeloid leukemia cells.	Cytarabine	49-54	colony stimulating factor 3	Homo sapiens	13-18
10029165-4	1999	In all but one patient, half killing concentration (LC50) of Ara-C was significantly reduced in the presence of G-CSF (by 400- and 1.45-fold, median: 21-fold).	Cytarabine	61-66	colony stimulating factor 3	Homo sapiens	112-117
10029165-6	1999	In vitro killing tests using a G-CSF-dependent leukemic cell line suggested that addition of G-CSF potentiates Ara-C-induced cytotoxicity through the mechanism of apoptosis.	Cytarabine	111-116	colony stimulating factor 3	Homo sapiens	31-36
10029165-6	1999	In vitro killing tests using a G-CSF-dependent leukemic cell line suggested that addition of G-CSF potentiates Ara-C-induced cytotoxicity through the mechanism of apoptosis.	Cytarabine	111-116	colony stimulating factor 3	Homo sapiens	93-98
10023703-2	1999	This study tested the efficacy and toxicity of mitoxantrone, etoposide, and intermediate dose cytarabine (MEC) with cyclosporine (CSP) as an MDR modulator in patients with recurrent and refractory acute myeloid leukemia, and also correlated P-gp expression in leukemia cells with response.	Cytarabine	94-104	C-C motif chemokine ligand 28	Homo sapiens	106-109
10077218-0	1999	Gene amplification of human cytidine deaminase proviral cDNA and increased levels of its mRNA produces enhanced drug resistance to cytosine arabinoside in retroviral-transduced murine fibroblasts.	Cytarabine	131-151	cytidine deaminase	Homo sapiens	28-46
10077218-3	1999	Human cytidine deaminase (CD) inactivates the cytosine nucleoside analogues, such as cytosine arabinoside (ARA-C), by deamination.	Cytarabine	85-105	cytidine deaminase	Homo sapiens	6-24
10077218-3	1999	Human cytidine deaminase (CD) inactivates the cytosine nucleoside analogues, such as cytosine arabinoside (ARA-C), by deamination.	Cytarabine	85-105	cytidine deaminase	Homo sapiens	26-28
10077218-3	1999	Human cytidine deaminase (CD) inactivates the cytosine nucleoside analogues, such as cytosine arabinoside (ARA-C), by deamination.	Cytarabine	107-112	cytidine deaminase	Homo sapiens	6-24
10077218-3	1999	Human cytidine deaminase (CD) inactivates the cytosine nucleoside analogues, such as cytosine arabinoside (ARA-C), by deamination.	Cytarabine	107-112	cytidine deaminase	Homo sapiens	26-28
10500808-3	1999	In this study we evaluated the relation between bcl-2 expression, spontaneous and dexamethasone (DXM) induced apoptosis, and in vitro resistance to DXM, prednisolone (PRD) and cytarabine (ARA) determined using the total cell kill colorimetric methyl-thiazol-tetrazolium salt (MTT) assay, in childhood acute lymphoblastic leukemia (ALL).	Cytarabine	176-186	BCL2 apoptosis regulator	Homo sapiens	48-53
10500809-0	1999	Comparison of BCL-2 and BAX protein expression with in vitro sensitivity to ARA-C and 6TG in AML.	Cytarabine	76-81	BCL2 apoptosis regulator	Homo sapiens	14-19
10500809-0	1999	Comparison of BCL-2 and BAX protein expression with in vitro sensitivity to ARA-C and 6TG in AML.	Cytarabine	76-81	BCL2 associated X, apoptosis regulator	Homo sapiens	24-27
10500809-5	1999	One of 7 patients (14%) whose cells were sensitive to ara-C expressed BCL-2 compared to 4/4 patients (100%) whose cells were resistant to ara-C in vitro (p = 0.05).	Cytarabine	54-59	BCL2 apoptosis regulator	Homo sapiens	70-75
10023853-0	1999	Complement receptor type 1 gene regulation: retinoic acid and cytosine arabinoside increase CR1 expression.	Cytarabine	62-82	complement C3b/C4b receptor 1 (Knops blood group)	Homo sapiens	0-26
10638491-11	1999	CONCLUSION: MINT is an active and safe regimen for relapsed/refractory NHL that have failed both an Adriamycin-containing regimen and a cytarabine/cisplatin-containing regimen.	Cytarabine	136-146	spen family transcriptional repressor	Homo sapiens	12-16
10665476-8	1999	In preclinical model systems, suppression of the cytoprotective function(s) of PKC potentiates the activity of cytotoxic agents (e.g., cytarabine) as well as ionizing radiation, and efforts to translate these findings into the clinical arena in humans are currently underway.	Cytarabine	135-145	proline rich transmembrane protein 2	Homo sapiens	79-82
10363570-1	1999	A prospective, randomized, double-blind placebo-controlled trial was designed to evaluate the impact of granulocyte/macrophage-colony-stimulating factor (GM-CSF) on the efficacy of sequential high-dose cytosine arabinoside/mitoxantrone chemotherapy (S-HAM) in adult patients with high-risk myelodysplastic syndromes (MDS).	Cytarabine	202-222	colony stimulating factor 2	Homo sapiens	104-152
10363570-1	1999	A prospective, randomized, double-blind placebo-controlled trial was designed to evaluate the impact of granulocyte/macrophage-colony-stimulating factor (GM-CSF) on the efficacy of sequential high-dose cytosine arabinoside/mitoxantrone chemotherapy (S-HAM) in adult patients with high-risk myelodysplastic syndromes (MDS).	Cytarabine	202-222	colony stimulating factor 2	Homo sapiens	154-160
10023854-2	1999	Previous work has demonstrated that Ara-C, a cytosine analogue, induces an 11-fold increase in CR1 mRNA expression in K-562 erythroleukaemia cells.	Cytarabine	36-41	complement C3b/C4b receptor 1 (Knops blood group)	Homo sapiens	95-98
10023854-5	1999	Increases in CR1 mRNA levels produced by Ara-C treatment were not a function of increased stability of the message.	Cytarabine	41-46	complement C3b/C4b receptor 1 (Knops blood group)	Homo sapiens	13-16
10023854-9	1999	These data suggest that TK, PKC and dCTP-adducted phospholipid signalling pathways may all play a role in the mechanism of Ara-C-induced CR1 transcription.	Cytarabine	123-128	TXK tyrosine kinase	Homo sapiens	24-26
10023853-0	1999	Complement receptor type 1 gene regulation: retinoic acid and cytosine arabinoside increase CR1 expression.	Cytarabine	62-82	complement C3b/C4b receptor 1 (Knops blood group)	Homo sapiens	92-95
10023854-9	1999	These data suggest that TK, PKC and dCTP-adducted phospholipid signalling pathways may all play a role in the mechanism of Ara-C-induced CR1 transcription.	Cytarabine	123-128	complement C3b/C4b receptor 1 (Knops blood group)	Homo sapiens	137-140
10023853-5	1999	Furthermore, in K-562 cells, the cytosine analogue Ara-C, an inducer of erythroid differentiation, caused the highest increases in CR1 mRNA levels as compared to untreated cells.	Cytarabine	51-56	complement C3b/C4b receptor 1 (Knops blood group)	Homo sapiens	131-134
10023853-6	1999	Ara-C also induced significant increases in CR1 message in PBCs.	Cytarabine	0-5	complement C3b/C4b receptor 1 (Knops blood group)	Homo sapiens	44-47
10023854-0	1999	Mechanism of regulation of complement receptor type 1 transcription by cytosine arabinoside in a pre-erythroid model.	Cytarabine	71-91	complement C3b/C4b receptor 1 (Knops blood group)	Homo sapiens	27-53
9916997-2	1998	Inappropriate expression of c-Myc under conditions which inhibit growth and down-regulate endogenous c-Myc expression, including serum deprivation and exposure to cytotoxic agents including the anticancer agents vinblastine, etoposide, Ara-C, and nocodazole, usually results in programmed cell death in many different cell types.	Cytarabine	236-241	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	28-33
9842975-2	1998	Here, we asked whether alterations in the p53 and RB pathways and the expression of six BCL-2 family proteins predicted acute cytotoxicity and clonogenic cell death induced by BCNU, vincristine, cytarabine, teniposide, doxorubicin, camptothecin or beta-lapachone in 12 human malignant glioma cell lines.	Cytarabine	195-205	BCL2 apoptosis regulator	Homo sapiens	88-93
9840183-8	1998	Furthermore, the protective effect of overexpression of BCL2 was more pronounced after ara-C treatment than with radiation.	Cytarabine	87-92	BCL2 apoptosis regulator	Homo sapiens	56-60
9989882-3	1998	As mobilising chemotherapy, cyclophosphamide, etoposide, doxorubicin and cytosine arabinoside were the drugs most frequently used in association with G-CSF for a total of 47 courses.	Cytarabine	73-93	colony stimulating factor 3	Homo sapiens	150-155
9886326-1	1998	Gene transfer of the cytidine deaminase (CDD) cDNA has recently been shown to induce cellular resistance to cytarabine (AraC) in vitro.	Cytarabine	108-118	cytidine deaminase	Homo sapiens	21-39
9886326-1	1998	Gene transfer of the cytidine deaminase (CDD) cDNA has recently been shown to induce cellular resistance to cytarabine (AraC) in vitro.	Cytarabine	108-118	cytidine deaminase	Homo sapiens	41-44
9845378-0	1998	Lack of cross-resistance with gemcitabine and cytarabine in cladribine-resistant HL60 cells with elevated 5"-nucleotidase activity.	Cytarabine	46-56	5'-nucleotidase ecto	Homo sapiens	106-121
9792319-4	1998	The display of LFA-3 (CD58) and DAF (CD55) by uninduced K562 was one order of magnitude lower than that of the glycophorins; following ara-C treatment there was a 50% rise in LFA-3 but a modest decrease in the level of DAF expression.	Cytarabine	135-140	CD58 molecule	Homo sapiens	15-20
9853520-0	1998	Coexpression of cytidine deaminase and mutant dihydrofolate reductase by a bicistronic retroviral vector confers resistance to cytosine arabinoside and methotrexate.	Cytarabine	127-147	cytidine deaminase	Homo sapiens	16-34
9853520-0	1998	Coexpression of cytidine deaminase and mutant dihydrofolate reductase by a bicistronic retroviral vector confers resistance to cytosine arabinoside and methotrexate.	Cytarabine	127-147	dihydrofolate reductase	Homo sapiens	46-69
9853520-7	1998	Using enzymatic assays, we observed a coordinate increase in resistance to MTX and DHFR enzyme activity following an ARA-C selection.	Cytarabine	117-122	dihydrofolate reductase	Homo sapiens	83-87
9853520-10	1998	These results demonstrate the potential of the MFG-DHFR-IRES/CD vector to confer drug resistance to both MTX and ARA-C and may have future application in chemoprotection of normal hematopoietic cells in patients with cancer.	Cytarabine	113-118	dihydrofolate reductase	Homo sapiens	51-55
9853520-10	1998	These results demonstrate the potential of the MFG-DHFR-IRES/CD vector to confer drug resistance to both MTX and ARA-C and may have future application in chemoprotection of normal hematopoietic cells in patients with cancer.	Cytarabine	113-118	cytidine deaminase	Homo sapiens	61-63
9804619-0	1998	Evidence for involvement of mitogen-activated protein kinase, rather than stress-activated protein kinase, in potentiation of 1-beta-D-arabinofuranosylcytosine-induced apoptosis by interruption of protein kinase C signaling.	Cytarabine	126-159	mitogen-activated protein kinase 9	Homo sapiens	74-105
9804619-9	1998	Moreover, acute disruption of the MAPK module by AMF, a selective inhibitor of MEK1, suppressed both basal and drug-stimulated MAPK activity and sharply increased the cytotoxicity of ara-C, suggesting the direct involvement of MAPK as a downstream antiapoptotic effector for PKC.	Cytarabine	183-188	mitogen-activated protein kinase kinase 1	Homo sapiens	79-83
9804619-12	1998	These observations collectively suggest a primary role for decreased MAPK, rather than increased SAPK, in the potentiation of ara-C cytotoxicity by interference with PKC-dependent signaling.	Cytarabine	126-131	mitogen-activated protein kinase 9	Homo sapiens	97-101
10028846-8	1998	In vitro cultures of peroxidase-negative CML blastic cells revealed that G-CSF stimulated the induction of blastic cells into the cell cycle and that blastic cell apoptosis was more pronounced in cells cultured with G-CSF plus Ara-C than with G-CSF or Ara-C alone.	Cytarabine	252-257	colony stimulating factor 3	Homo sapiens	216-221
10028846-8	1998	In vitro cultures of peroxidase-negative CML blastic cells revealed that G-CSF stimulated the induction of blastic cells into the cell cycle and that blastic cell apoptosis was more pronounced in cells cultured with G-CSF plus Ara-C than with G-CSF or Ara-C alone.	Cytarabine	252-257	colony stimulating factor 3	Homo sapiens	216-221
9930308-3	1998	CD catalyzes the deamination and pharmacological inactivation of cytosine nucleoside analogues, such as cytosine arabinoside (Ara-C).	Cytarabine	104-124	cytidine deaminase	Mus musculus	0-2
9930308-3	1998	CD catalyzes the deamination and pharmacological inactivation of cytosine nucleoside analogues, such as cytosine arabinoside (Ara-C).	Cytarabine	126-131	cytidine deaminase	Mus musculus	0-2
9792319-4	1998	The display of LFA-3 (CD58) and DAF (CD55) by uninduced K562 was one order of magnitude lower than that of the glycophorins; following ara-C treatment there was a 50% rise in LFA-3 but a modest decrease in the level of DAF expression.	Cytarabine	135-140	CD58 molecule	Homo sapiens	22-26
9792319-4	1998	The display of LFA-3 (CD58) and DAF (CD55) by uninduced K562 was one order of magnitude lower than that of the glycophorins; following ara-C treatment there was a 50% rise in LFA-3 but a modest decrease in the level of DAF expression.	Cytarabine	135-140	CD55 molecule (Cromer blood group)	Homo sapiens	37-41
9792319-4	1998	The display of LFA-3 (CD58) and DAF (CD55) by uninduced K562 was one order of magnitude lower than that of the glycophorins; following ara-C treatment there was a 50% rise in LFA-3 but a modest decrease in the level of DAF expression.	Cytarabine	135-140	CD58 molecule	Homo sapiens	175-180
9792319-11	1998	A novel hybrid Rh transcript corresponding to exons 1-4 of RHD and exons 5-10 of RHCE has been cloned and sequenced from ara-C induced K562 cells, and may have arisen by general recombination between the RHD and RHCE genes.	Cytarabine	121-126	Rh blood group D antigen	Homo sapiens	59-62
9792319-11	1998	A novel hybrid Rh transcript corresponding to exons 1-4 of RHD and exons 5-10 of RHCE has been cloned and sequenced from ara-C induced K562 cells, and may have arisen by general recombination between the RHD and RHCE genes.	Cytarabine	121-126	Rh blood group CcEe antigens	Homo sapiens	81-85
9792319-11	1998	A novel hybrid Rh transcript corresponding to exons 1-4 of RHD and exons 5-10 of RHCE has been cloned and sequenced from ara-C induced K562 cells, and may have arisen by general recombination between the RHD and RHCE genes.	Cytarabine	121-126	Rh blood group CcEe antigens	Homo sapiens	212-216
9808363-6	1998	In aracytosine-treated cultures, we observed that the numbers of NSE(+) cells as well as [35S]methionine incorporation were decreased compared with control cultures.	Cytarabine	3-14	enolase 2	Rattus norvegicus	65-68
9869205-5	1998	These results indicate that the expression of dCK gene varies in patients and suggests decreased expression of the dCK gene as one of the mechanisms responsible for clinical resistance to ara-C.	Cytarabine	188-193	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	46-49
9869205-5	1998	These results indicate that the expression of dCK gene varies in patients and suggests decreased expression of the dCK gene as one of the mechanisms responsible for clinical resistance to ara-C.	Cytarabine	188-193	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	115-118
9722302-1	1998	We investigated whether changes in iron metabolism and the transferrin receptor (TRF-R) expression were involved in the antileukaemic effects of arabinoside cytosine (ara-C).	Cytarabine	145-165	transferrin receptor	Homo sapiens	59-79
20654451-6	1998	We also demonstrate that isolated EAF hepatocytes do not respond to TGFalpha and that four different p53-inducing agents, namely DEN, taxol, doxorubicin and araC readily induce p53 in non-EAF, but not in EAF hepatocytes.	Cytarabine	157-161	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	101-104
20654451-6	1998	We also demonstrate that isolated EAF hepatocytes do not respond to TGFalpha and that four different p53-inducing agents, namely DEN, taxol, doxorubicin and araC readily induce p53 in non-EAF, but not in EAF hepatocytes.	Cytarabine	157-161	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	177-180
9797080-0	1998	Granulocyte colony-stimulating factor shortens duration of critical neutropenia and prolongs disease-free survival after sequential high-dose cytosine arabinoside and mitoxantrone (S-HAM) salvage therapy for refractory and relapsed acute myeloid leukemia.	Cytarabine	142-162	colony stimulating factor 3	Homo sapiens	0-37
9751270-1	1998	DNA methylation of the CpG-rich 5" region of the deoxycytidine kinase (dCK) gene is potentially involved in the suppression of the gene and the resistance of tumour cells to arabinosylcytosine (ara-C).	Cytarabine	174-192	deoxycytidine kinase	Homo sapiens	49-69
9751270-1	1998	DNA methylation of the CpG-rich 5" region of the deoxycytidine kinase (dCK) gene is potentially involved in the suppression of the gene and the resistance of tumour cells to arabinosylcytosine (ara-C).	Cytarabine	174-192	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	71-74
9751270-1	1998	DNA methylation of the CpG-rich 5" region of the deoxycytidine kinase (dCK) gene is potentially involved in the suppression of the gene and the resistance of tumour cells to arabinosylcytosine (ara-C).	Cytarabine	194-199	deoxycytidine kinase	Homo sapiens	49-69
9751270-1	1998	DNA methylation of the CpG-rich 5" region of the deoxycytidine kinase (dCK) gene is potentially involved in the suppression of the gene and the resistance of tumour cells to arabinosylcytosine (ara-C).	Cytarabine	194-199	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	71-74
9692399-7	1998	We report a patient with my+Ph+ALL in whom the administration of G-CSF after high-dose Cytarabin and Mitoxantrone led to a significant mobilization of leukemic cells and contamination of the stem cell harvest during cytologic marrow remission.	Cytarabine	87-96	colony stimulating factor 3	Homo sapiens	65-70
9773810-12	1998	On the other hand, DMDC as well as 1-beta-D-arabinofuranosyl-cytosine (ara-C), which is a well-known deoxycytidine analog and inhibits DNA polymerase alpha, did not inhibit RNR in LX-1 lung carcinoma at doses demonstrating antitumor activity.	Cytarabine	35-69	DNA polymerase alpha 1, catalytic subunit	Homo sapiens	135-155
9773810-12	1998	On the other hand, DMDC as well as 1-beta-D-arabinofuranosyl-cytosine (ara-C), which is a well-known deoxycytidine analog and inhibits DNA polymerase alpha, did not inhibit RNR in LX-1 lung carcinoma at doses demonstrating antitumor activity.	Cytarabine	71-76	DNA polymerase alpha 1, catalytic subunit	Homo sapiens	135-155
9789612-1	1998	BACKGROUND: BCH-4556 ((-)-2"-deoxy-3"-oxacytidine) is an L-nucleoside analogue shown to have broad preclinical anti-cancer activity, particularly against solid neoplasms such as prostate, renal, and hepatoma in vitro and in vivo, in contrast to cytosine arabinoside (ara-C) which is preferentially active against leukemia.	Cytarabine	245-265	chimerin 2	Homo sapiens	12-15
9789612-1	1998	BACKGROUND: BCH-4556 ((-)-2"-deoxy-3"-oxacytidine) is an L-nucleoside analogue shown to have broad preclinical anti-cancer activity, particularly against solid neoplasms such as prostate, renal, and hepatoma in vitro and in vivo, in contrast to cytosine arabinoside (ara-C) which is preferentially active against leukemia.	Cytarabine	267-272	chimerin 2	Homo sapiens	12-15
9716019-0	1998	Disappearance of AML1-MTG8 transcript by reverse transcriptase polymerase chain reaction in a patient in remission of acute myeloid leukemia (M2) after low-dose cytosine arabinoside.	Cytarabine	161-181	RUNX family transcription factor 1	Homo sapiens	17-21
9716019-0	1998	Disappearance of AML1-MTG8 transcript by reverse transcriptase polymerase chain reaction in a patient in remission of acute myeloid leukemia (M2) after low-dose cytosine arabinoside.	Cytarabine	161-181	RUNX1 partner transcriptional co-repressor 1	Homo sapiens	22-26
9722302-1	1998	We investigated whether changes in iron metabolism and the transferrin receptor (TRF-R) expression were involved in the antileukaemic effects of arabinoside cytosine (ara-C).	Cytarabine	145-165	transferrin receptor	Homo sapiens	81-86
9699642-1	1998	Taxol, 1-beta-D-arabinofuranosylcytosine (ara-C), and etoposide induce apoptosis in HL-60 cells that is blocked by overexpression of Bcl-2 or Bcl-xL.A 60-amino acid "loop" domain of Bcl-2 and Bcl-xL that contains phosphorylation sites is known to negatively regulate their antiapoptotic function.	Cytarabine	7-40	BCL2 apoptosis regulator	Homo sapiens	133-138
9699642-1	1998	Taxol, 1-beta-D-arabinofuranosylcytosine (ara-C), and etoposide induce apoptosis in HL-60 cells that is blocked by overexpression of Bcl-2 or Bcl-xL.A 60-amino acid "loop" domain of Bcl-2 and Bcl-xL that contains phosphorylation sites is known to negatively regulate their antiapoptotic function.	Cytarabine	7-40	BCL2 like 1	Homo sapiens	142-148
9699642-1	1998	Taxol, 1-beta-D-arabinofuranosylcytosine (ara-C), and etoposide induce apoptosis in HL-60 cells that is blocked by overexpression of Bcl-2 or Bcl-xL.A 60-amino acid "loop" domain of Bcl-2 and Bcl-xL that contains phosphorylation sites is known to negatively regulate their antiapoptotic function.	Cytarabine	7-40	BCL2 apoptosis regulator	Homo sapiens	182-187
9699642-1	1998	Taxol, 1-beta-D-arabinofuranosylcytosine (ara-C), and etoposide induce apoptosis in HL-60 cells that is blocked by overexpression of Bcl-2 or Bcl-xL.A 60-amino acid "loop" domain of Bcl-2 and Bcl-xL that contains phosphorylation sites is known to negatively regulate their antiapoptotic function.	Cytarabine	7-40	BCL2 like 1	Homo sapiens	192-198
9699642-1	1998	Taxol, 1-beta-D-arabinofuranosylcytosine (ara-C), and etoposide induce apoptosis in HL-60 cells that is blocked by overexpression of Bcl-2 or Bcl-xL.A 60-amino acid "loop" domain of Bcl-2 and Bcl-xL that contains phosphorylation sites is known to negatively regulate their antiapoptotic function.	Cytarabine	42-47	BCL2 apoptosis regulator	Homo sapiens	133-138
9722302-1	1998	We investigated whether changes in iron metabolism and the transferrin receptor (TRF-R) expression were involved in the antileukaemic effects of arabinoside cytosine (ara-C).	Cytarabine	167-172	transferrin receptor	Homo sapiens	59-79
9699642-1	1998	Taxol, 1-beta-D-arabinofuranosylcytosine (ara-C), and etoposide induce apoptosis in HL-60 cells that is blocked by overexpression of Bcl-2 or Bcl-xL.A 60-amino acid "loop" domain of Bcl-2 and Bcl-xL that contains phosphorylation sites is known to negatively regulate their antiapoptotic function.	Cytarabine	42-47	BCL2 like 1	Homo sapiens	142-148
9699642-1	1998	Taxol, 1-beta-D-arabinofuranosylcytosine (ara-C), and etoposide induce apoptosis in HL-60 cells that is blocked by overexpression of Bcl-2 or Bcl-xL.A 60-amino acid "loop" domain of Bcl-2 and Bcl-xL that contains phosphorylation sites is known to negatively regulate their antiapoptotic function.	Cytarabine	42-47	BCL2 apoptosis regulator	Homo sapiens	182-187
9699642-1	1998	Taxol, 1-beta-D-arabinofuranosylcytosine (ara-C), and etoposide induce apoptosis in HL-60 cells that is blocked by overexpression of Bcl-2 or Bcl-xL.A 60-amino acid "loop" domain of Bcl-2 and Bcl-xL that contains phosphorylation sites is known to negatively regulate their antiapoptotic function.	Cytarabine	42-47	BCL2 like 1	Homo sapiens	192-198
9699642-8	1998	Exposure to etoposide (50 microM) or ara-C (100 microM) for 4 h induced apoptosis in HL-60/neo cells, but not in HL-60/Bcl-2, HL-60/Bcl-xL, HL-60/Bcl-2delta, or HL-60/Bcl-xLdelta cells.	Cytarabine	37-42	BCL2 like 1	Homo sapiens	132-138
9722302-1	1998	We investigated whether changes in iron metabolism and the transferrin receptor (TRF-R) expression were involved in the antileukaemic effects of arabinoside cytosine (ara-C).	Cytarabine	167-172	transferrin receptor	Homo sapiens	81-86
9722302-2	1998	Treatment with 100 nM ara-C for 48h reduced thymidine uptake and increased the surface expression of the TRF-R on leukaemic blasts derived from 13/16 (81%) patients and on the HL-60 and U-937 cell lines.	Cytarabine	22-27	transferrin receptor	Homo sapiens	105-110
9744557-8	1998	By adding cytosine-1-beta-D-arabinofuranoside (Are C) and hydroxyurea (HU) 1 h prior to analysis to prevent strand break rejoining, some increase in SSB (2-3 times) was observed in the lymphocytes.	Cytarabine	10-45	small RNA binding exonuclease protection factor La	Homo sapiens	149-152
9777269-4	1998	These findings suggest the possibility of IL-3/G-CSF/cytosine arabinoside (Ara-C) combination therapy, which may be able to enhance the cytotoxic effect of Ara-C on AML progenitor cells powerfully in a wider range of patients including cases refractory for IL-3/Ara-C combination therapy.	Cytarabine	53-73	interleukin 3	Homo sapiens	42-46
9777269-4	1998	These findings suggest the possibility of IL-3/G-CSF/cytosine arabinoside (Ara-C) combination therapy, which may be able to enhance the cytotoxic effect of Ara-C on AML progenitor cells powerfully in a wider range of patients including cases refractory for IL-3/Ara-C combination therapy.	Cytarabine	53-73	colony stimulating factor 3	Homo sapiens	47-52
9777269-4	1998	These findings suggest the possibility of IL-3/G-CSF/cytosine arabinoside (Ara-C) combination therapy, which may be able to enhance the cytotoxic effect of Ara-C on AML progenitor cells powerfully in a wider range of patients including cases refractory for IL-3/Ara-C combination therapy.	Cytarabine	53-73	interleukin 3	Homo sapiens	257-261
9777269-4	1998	These findings suggest the possibility of IL-3/G-CSF/cytosine arabinoside (Ara-C) combination therapy, which may be able to enhance the cytotoxic effect of Ara-C on AML progenitor cells powerfully in a wider range of patients including cases refractory for IL-3/Ara-C combination therapy.	Cytarabine	75-80	interleukin 3	Homo sapiens	42-46
9777269-4	1998	These findings suggest the possibility of IL-3/G-CSF/cytosine arabinoside (Ara-C) combination therapy, which may be able to enhance the cytotoxic effect of Ara-C on AML progenitor cells powerfully in a wider range of patients including cases refractory for IL-3/Ara-C combination therapy.	Cytarabine	75-80	colony stimulating factor 3	Homo sapiens	47-52
9777269-4	1998	These findings suggest the possibility of IL-3/G-CSF/cytosine arabinoside (Ara-C) combination therapy, which may be able to enhance the cytotoxic effect of Ara-C on AML progenitor cells powerfully in a wider range of patients including cases refractory for IL-3/Ara-C combination therapy.	Cytarabine	75-80	interleukin 3	Homo sapiens	257-261
9777269-4	1998	These findings suggest the possibility of IL-3/G-CSF/cytosine arabinoside (Ara-C) combination therapy, which may be able to enhance the cytotoxic effect of Ara-C on AML progenitor cells powerfully in a wider range of patients including cases refractory for IL-3/Ara-C combination therapy.	Cytarabine	156-161	interleukin 3	Homo sapiens	42-46
9777269-4	1998	These findings suggest the possibility of IL-3/G-CSF/cytosine arabinoside (Ara-C) combination therapy, which may be able to enhance the cytotoxic effect of Ara-C on AML progenitor cells powerfully in a wider range of patients including cases refractory for IL-3/Ara-C combination therapy.	Cytarabine	156-161	colony stimulating factor 3	Homo sapiens	47-52
9777269-4	1998	These findings suggest the possibility of IL-3/G-CSF/cytosine arabinoside (Ara-C) combination therapy, which may be able to enhance the cytotoxic effect of Ara-C on AML progenitor cells powerfully in a wider range of patients including cases refractory for IL-3/Ara-C combination therapy.	Cytarabine	156-161	interleukin 3	Homo sapiens	257-261
9777269-4	1998	These findings suggest the possibility of IL-3/G-CSF/cytosine arabinoside (Ara-C) combination therapy, which may be able to enhance the cytotoxic effect of Ara-C on AML progenitor cells powerfully in a wider range of patients including cases refractory for IL-3/Ara-C combination therapy.	Cytarabine	156-161	interleukin 3	Homo sapiens	42-46
9777269-4	1998	These findings suggest the possibility of IL-3/G-CSF/cytosine arabinoside (Ara-C) combination therapy, which may be able to enhance the cytotoxic effect of Ara-C on AML progenitor cells powerfully in a wider range of patients including cases refractory for IL-3/Ara-C combination therapy.	Cytarabine	156-161	colony stimulating factor 3	Homo sapiens	47-52
9777269-4	1998	These findings suggest the possibility of IL-3/G-CSF/cytosine arabinoside (Ara-C) combination therapy, which may be able to enhance the cytotoxic effect of Ara-C on AML progenitor cells powerfully in a wider range of patients including cases refractory for IL-3/Ara-C combination therapy.	Cytarabine	156-161	interleukin 3	Homo sapiens	257-261
9725056-0	1998	[Low-dose oral etoposide and subcutaneous injection of low-dose cytosine arabinoside (Et-A non i.v.)	Cytarabine	64-84	endothelin receptor type A	Homo sapiens	86-90
9718275-3	1998	We report that prolonged pre-exposure of human malignant glioma cells to different cytotoxic agents, VM26, cytarabine and cisplatin, induces strong sensitization to CD95 ligand-induced apoptosis.	Cytarabine	107-117	Fas cell surface death receptor	Homo sapiens	165-169
9590144-1	1998	We sought to determine the role of granulocyte colony-stimulating factor (G-CSF) as an adjunct therapy in high-dose cytarabine-containing chemotherapy (HD C/T) for children with acute leukemia.	Cytarabine	116-126	colony stimulating factor 3	Homo sapiens	35-72
9703875-0	1998	Increased p21/WAF-1 and p53 protein levels following sequential three drug combination regimen of fludarabine, cytarabine and docetaxel induces apoptosis in human leukemia cells.	Cytarabine	111-121	cyclin dependent kinase inhibitor 1A	Homo sapiens	10-13
9703875-0	1998	Increased p21/WAF-1 and p53 protein levels following sequential three drug combination regimen of fludarabine, cytarabine and docetaxel induces apoptosis in human leukemia cells.	Cytarabine	111-121	cyclin dependent kinase inhibitor 1A	Homo sapiens	14-19
9703875-0	1998	Increased p21/WAF-1 and p53 protein levels following sequential three drug combination regimen of fludarabine, cytarabine and docetaxel induces apoptosis in human leukemia cells.	Cytarabine	111-121	tumor protein p53	Homo sapiens	24-27
10200513-0	1998	Differential p53 phosphorylation and activation of apoptosis-promoting genes Bax and Fas/APO-1 by irradiation and ara-C treatment.	Cytarabine	114-119	tumor protein p53	Homo sapiens	13-16
10200513-0	1998	Differential p53 phosphorylation and activation of apoptosis-promoting genes Bax and Fas/APO-1 by irradiation and ara-C treatment.	Cytarabine	114-119	BCL2 associated X, apoptosis regulator	Homo sapiens	77-80
10200513-0	1998	Differential p53 phosphorylation and activation of apoptosis-promoting genes Bax and Fas/APO-1 by irradiation and ara-C treatment.	Cytarabine	114-119	Fas cell surface death receptor	Homo sapiens	89-94
10200513-3	1998	Both irradiation and ara-C treatment resulted in apoptosis and induction of p53 proteins within hours.	Cytarabine	21-26	tumor protein p53	Homo sapiens	76-79
10200513-4	1998	The Bax gene was activated in irradiated and ara-C-treated BV173 cells, but Fas/APO-1 was induced only in irradiated BV173 cells.	Cytarabine	45-50	BCL2 associated X, apoptosis regulator	Homo sapiens	4-7
10200513-10	1998	Using two-dimensional gel electrophoresis, we found that the p53 proteins in irradiated and ara-C-treated BV173 cells have different isoelectric points; they converged to a single isoelectric point after in vitro treatment with phosphatase.	Cytarabine	92-97	tumor protein p53	Homo sapiens	61-64
9670853-8	1998	IFN-alpha also increases the cytotoxic effects of BCNU, teniposide and cytarabine in both cell lines, and of vincristine in LN-229 cells.	Cytarabine	71-81	interferon alpha 1	Homo sapiens	0-9
9680112-1	1998	Recent attempts to protect hematopoietic progenitor cells from cytarabine (ara-C)-induced toxicity by transfer of the cytidine deaminase (CDD) gene resulted in efficient in vitro inducibility of ara-C resistance.	Cytarabine	63-73	cytidine deaminase	Homo sapiens	118-136
9680112-1	1998	Recent attempts to protect hematopoietic progenitor cells from cytarabine (ara-C)-induced toxicity by transfer of the cytidine deaminase (CDD) gene resulted in efficient in vitro inducibility of ara-C resistance.	Cytarabine	63-73	cytidine deaminase	Homo sapiens	138-141
9680112-1	1998	Recent attempts to protect hematopoietic progenitor cells from cytarabine (ara-C)-induced toxicity by transfer of the cytidine deaminase (CDD) gene resulted in efficient in vitro inducibility of ara-C resistance.	Cytarabine	75-80	cytidine deaminase	Homo sapiens	118-136
9680112-1	1998	Recent attempts to protect hematopoietic progenitor cells from cytarabine (ara-C)-induced toxicity by transfer of the cytidine deaminase (CDD) gene resulted in efficient in vitro inducibility of ara-C resistance.	Cytarabine	75-80	cytidine deaminase	Homo sapiens	138-141
9680112-1	1998	Recent attempts to protect hematopoietic progenitor cells from cytarabine (ara-C)-induced toxicity by transfer of the cytidine deaminase (CDD) gene resulted in efficient in vitro inducibility of ara-C resistance.	Cytarabine	195-200	cytidine deaminase	Homo sapiens	118-136
9680112-1	1998	Recent attempts to protect hematopoietic progenitor cells from cytarabine (ara-C)-induced toxicity by transfer of the cytidine deaminase (CDD) gene resulted in efficient in vitro inducibility of ara-C resistance.	Cytarabine	195-200	cytidine deaminase	Homo sapiens	138-141
9590144-1	1998	We sought to determine the role of granulocyte colony-stimulating factor (G-CSF) as an adjunct therapy in high-dose cytarabine-containing chemotherapy (HD C/T) for children with acute leukemia.	Cytarabine	116-126	colony stimulating factor 3	Homo sapiens	74-79
9797704-6	1998	2-CdA, CGP 52411, tyrphostin A48, staurosporine and NDGA were active as sensitisers against ara-C in HL-60 cells, CGP 52411 and tyrphostin A48 also in HL-60/ara-C cells, and 2-CdA, staurosporine and NDGA also in U937 cells.	Cytarabine	92-97	cytidine deaminase	Homo sapiens	2-5
9797704-6	1998	2-CdA, CGP 52411, tyrphostin A48, staurosporine and NDGA were active as sensitisers against ara-C in HL-60 cells, CGP 52411 and tyrphostin A48 also in HL-60/ara-C cells, and 2-CdA, staurosporine and NDGA also in U937 cells.	Cytarabine	92-97	cytidine deaminase	Homo sapiens	176-179
9797704-6	1998	2-CdA, CGP 52411, tyrphostin A48, staurosporine and NDGA were active as sensitisers against ara-C in HL-60 cells, CGP 52411 and tyrphostin A48 also in HL-60/ara-C cells, and 2-CdA, staurosporine and NDGA also in U937 cells.	Cytarabine	157-162	cytidine deaminase	Homo sapiens	2-5
9590659-0	1998	Recombinant gene products of two natural variants of the human cytidine deaminase gene confer different deamination rates of cytarabine in vitro.	Cytarabine	125-135	cytidine deaminase	Homo sapiens	63-81
9553659-1	1998	BACKGROUND: The aim of this study was to increase disease-free survival (DFS) in AML in CR1 using a high-dose cytarabine consolidation plus G-CSF as in vivo purging and mobilization of CD34+ cells before ablative therapy and peripheral blood autograft.	Cytarabine	110-120	complement C3b/C4b receptor 1 (Knops blood group)	Homo sapiens	88-91
9590659-3	1998	These results suggest that this genetic polymorphism contributes to the different deamination phenotypes of ara-C observed in vivo, and that investigation of CDD allelotype frequencies and their correlation with ara-C resistance in patients with acute leukemia may be warranted.	Cytarabine	212-217	cytidine deaminase	Homo sapiens	158-161
9546433-6	1998	In FDCP-Mix cells expressing the ts v-abl PTK and grown at the restrictive temperature for PTK activity the cells were relatively sensitive to cytotoxic agents such as cytosine arabinoside and 5-fluorouracil but MIP-1alpha could induce growth inhibition and confer some degree of protection from these agents.	Cytarabine	168-188	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	38-41
9516378-1	1998	Macrophage Inflammatory Protein (MIP)-1alpha is myelosuppressive in vitro and in vivo for hematopoietic stem and immature subsets of myeloid progenitor cells, demonstrates some myeloprotective effects in mice treated with Ara-C and hydroxyurea, and has stem/progenitor cell mobilizing activity in mice.	Cytarabine	222-227	chemokine (C-C motif) ligand 3	Mus musculus	0-44
9502620-7	1998	In contrast, bcl-x was gradually downregulated during erythroid differentiation induced by cytosine arabinoside.	Cytarabine	91-111	BCL2 like 1	Homo sapiens	13-18
9640243-6	1998	Virus-infected cell lysates, but not control lysates, from cells grown in the presence of cytosine arabinoside also contained PKR inhibitory activity, which indicated that the inhibitory activity was associated with early viral gene expression.	Cytarabine	90-110	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	126-129
9492343-10	1998	This kinase, p56/p53lyn is rapidly induced by treatments that trigger cell cycle checkpoints (ionizing radiation, cytosine arabinoside), suggesting that this kinase may actively delay the onset of mitosis by phosphorylating Tyr15 on Cdk1.	Cytarabine	114-134	cyclin dependent kinase like 2	Homo sapiens	13-16
9492343-10	1998	This kinase, p56/p53lyn is rapidly induced by treatments that trigger cell cycle checkpoints (ionizing radiation, cytosine arabinoside), suggesting that this kinase may actively delay the onset of mitosis by phosphorylating Tyr15 on Cdk1.	Cytarabine	114-134	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	17-23
9492343-10	1998	This kinase, p56/p53lyn is rapidly induced by treatments that trigger cell cycle checkpoints (ionizing radiation, cytosine arabinoside), suggesting that this kinase may actively delay the onset of mitosis by phosphorylating Tyr15 on Cdk1.	Cytarabine	114-134	cyclin dependent kinase 1	Homo sapiens	233-237
9663763-7	1998	The release time of ara-C was between 3 days from pH EMA 0.5% and 16 days from H80/VP20/E15 gels.	Cytarabine	20-25	reticulon 4	Rattus norvegicus	83-87
9579874-9	1998	We found that AML1-ETO blocked the erythroid differentiation of K562 cells induced by low doses of Ara-C.	Cytarabine	99-104	RUNX family transcription factor 1	Homo sapiens	14-18
9579874-9	1998	We found that AML1-ETO blocked the erythroid differentiation of K562 cells induced by low doses of Ara-C.	Cytarabine	99-104	RUNX1 partner transcriptional co-repressor 1	Homo sapiens	19-22
9499413-6	1998	We propose that Ad12 infection, actinomycin D and araC all induce a similar or identical global damage arrest signal (perhaps a modification or altered conformation of p53) that preferentially interferes with metaphase condensation of the RNU1 and RNU2 loci.	Cytarabine	50-54	tumor protein p53	Homo sapiens	168-171
9499413-6	1998	We propose that Ad12 infection, actinomycin D and araC all induce a similar or identical global damage arrest signal (perhaps a modification or altered conformation of p53) that preferentially interferes with metaphase condensation of the RNU1 and RNU2 loci.	Cytarabine	50-54	RNA, U1 small nuclear 1	Homo sapiens	239-243
9499413-6	1998	We propose that Ad12 infection, actinomycin D and araC all induce a similar or identical global damage arrest signal (perhaps a modification or altered conformation of p53) that preferentially interferes with metaphase condensation of the RNU1 and RNU2 loci.	Cytarabine	50-54	RNA, U2 small nuclear 1	Homo sapiens	248-252
9569026-9	1998	Bax-K562 cells showed significantly higher fractions of apoptotic cells than pCI-neo-K562 cells when treated with ara-C, doxorubicin or SN-38.	Cytarabine	114-119	BCL2 associated X, apoptosis regulator	Homo sapiens	0-3
9548414-0	1998	Inv(16) acute myeloid leukemia cells show an increased sensitivity to cytosine arabinoside in vitro.	Cytarabine	70-90	inversin	Homo sapiens	0-3
9548414-2	1998	In particular, it has been reported that acute myeloid leukemia (AML) patients with inv(16) abnormality show a better prognosis, especially in case of treatment with high-dose Ara-C (HD Ara-C) containing regimens.	Cytarabine	176-181	inversin	Homo sapiens	84-87
9548414-2	1998	In particular, it has been reported that acute myeloid leukemia (AML) patients with inv(16) abnormality show a better prognosis, especially in case of treatment with high-dose Ara-C (HD Ara-C) containing regimens.	Cytarabine	186-191	inversin	Homo sapiens	84-87
9548414-3	1998	In this study we aimed at testing whether leukemic cells from patients showing the inv(16) were more sensitive to Ara-C in vitro, compared to AML blasts from patients with normal karyotype or chromosomal abnormalities other than t(15;17) or t(8;21).	Cytarabine	114-119	inversin	Homo sapiens	83-86
9548414-5	1998	The IC50 of Ara-C, as tested by the XTT colorimetric assay, was significantly lower in cases with inv(16) (18.5+/-15.88 micromol/l vs. 38+/-14.6 micromol/l,in cases with other abnormalities, p=0.01).	Cytarabine	12-17	inversin	Homo sapiens	98-101
9548414-7	1998	All the same, Ara-C induced apoptosis was significantly increased in cells from patients with inv(16).	Cytarabine	14-19	inversin	Homo sapiens	94-97
9548414-8	1998	Our data suggest a possible interaction between the molecular background of inv(16) and a modification of intracellular metabolism of Ara-C, and could thus provide a rationale for HD-Ara-C-based schedules for patients with inv(16) AML.	Cytarabine	134-139	inversin	Homo sapiens	223-226
9548414-8	1998	Our data suggest a possible interaction between the molecular background of inv(16) and a modification of intracellular metabolism of Ara-C, and could thus provide a rationale for HD-Ara-C-based schedules for patients with inv(16) AML.	Cytarabine	183-188	inversin	Homo sapiens	76-79
9548414-8	1998	Our data suggest a possible interaction between the molecular background of inv(16) and a modification of intracellular metabolism of Ara-C, and could thus provide a rationale for HD-Ara-C-based schedules for patients with inv(16) AML.	Cytarabine	183-188	inversin	Homo sapiens	223-226
9553659-1	1998	BACKGROUND: The aim of this study was to increase disease-free survival (DFS) in AML in CR1 using a high-dose cytarabine consolidation plus G-CSF as in vivo purging and mobilization of CD34+ cells before ablative therapy and peripheral blood autograft.	Cytarabine	110-120	CD34 molecule	Homo sapiens	185-189
9453545-0	1998	R-deprenyl and R-2-heptyl-N-methylpropargylamine prevent apoptosis in cerebellar granule neurons induced by cytosine arabinoside but not low extracellular potassium.	Cytarabine	108-128	ribonucleotide reductase regulatory subunit M2	Homo sapiens	15-18
9484842-11	1998	Finally, changes elicited through ATF2(delta1-195) also led to reduced drug resistance, as shown for MMC, araC and cisplatinum.	Cytarabine	106-110	activating transcription factor 2	Homo sapiens	34-38
10358333-0	1998	P170 (Pgp) expression in leukemic cells after therapeutic exposure to arabinosyl cytosine.	Cytarabine	70-89	phosphoglycolate phosphatase	Homo sapiens	6-9
10388104-10	1998	Cytosine arabinoside improves the therapeutic effectiveness of IFNs in CML, and IFN-&amp;agr;2b improves the prognosis, survival, and quality of life after surgery for high-risk patients with melanoma.	Cytarabine	0-20	interferon alpha 1	Homo sapiens	63-66
9338077-6	1998	The latter process is influenced by components of various signal transduction pathways (e.g., PKC) and expression of oncogenes (e.g., bcl-2, c-Jun), perturbations in which may significantly alter ara-C sensitivity.	Cytarabine	196-201	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	141-146
9338077-3	1998	First, the activity of ara-C depends on conversion to its lethal triphosphate derivative, ara-CTP, a process that is influenced by multiple factors, including nucleoside transport, phosphorylation, deamination, and levels of competing metabolites, particularly dCTP.	Cytarabine	23-28	solute carrier family 25 member 1	Homo sapiens	94-97
9338077-4	1998	Second, the antiproliferative and lethal effects of ara-C are linked to the ability of ara-CTP to interfere with one or more DNA polymerases as well as the degree to which it is incorporated into elongating DNA strands, leading to DNA fragmentation and chain termination.	Cytarabine	52-57	solute carrier family 25 member 1	Homo sapiens	91-94
9338077-6	1998	The latter process is influenced by components of various signal transduction pathways (e.g., PKC) and expression of oncogenes (e.g., bcl-2, c-Jun), perturbations in which may significantly alter ara-C sensitivity.	Cytarabine	196-201	BCL2 apoptosis regulator	Homo sapiens	134-139
9883313-6	1998	The results of the randomized trails, carried out in France, showed that the combination of IFN-alpha and cytarabine as compared with INF-alpha alone, increases the rate of major cytogenetic response and prolongs survival in the chronic phase of CML.	Cytarabine	106-116	interferon alpha 17	Homo sapiens	134-143
9771951-0	1998	Drug resistance to 5-aza-2"-deoxycytidine, 2",2"-difluorodeoxycytidine, and cytosine arabinoside conferred by retroviral-mediated transfer of human cytidine deaminase cDNA into murine cells.	Cytarabine	76-96	cytidine deaminase	Homo sapiens	148-166
9420079-0	1998	Transfection of C6 glioma cells with the bax gene and increased sensitivity to treatment with cytosine arabinoside.	Cytarabine	94-114	BCL2 associated X, apoptosis regulator	Homo sapiens	41-44
9420079-5	1998	Treatment with 1 microM cytosine arabinoside (ara-C) resulted in significantly more cells undergoing apoptosis in the cell line overexpressing bax than in the vector-only control cell line (23.57 +/- 2.6% compared with 5.3 +/- 0.7% terminal deoxynucleotidyl transferase-mediated biotinylated-deoxyuridine triphosphate nick-end labeling technique-positive cells; p = 0.007).	Cytarabine	24-44	BCL2 associated X, apoptosis regulator	Homo sapiens	143-146
9420079-5	1998	Treatment with 1 microM cytosine arabinoside (ara-C) resulted in significantly more cells undergoing apoptosis in the cell line overexpressing bax than in the vector-only control cell line (23.57 +/- 2.6% compared with 5.3 +/- 0.7% terminal deoxynucleotidyl transferase-mediated biotinylated-deoxyuridine triphosphate nick-end labeling technique-positive cells; p = 0.007).	Cytarabine	46-51	BCL2 associated X, apoptosis regulator	Homo sapiens	143-146
9420079-6	1998	Furthermore, measurements of growth curves obtained immediately after treatment with 0.5 microM ara-C demonstrated a prolonged growth arrest of at least 6 days in the cell line overexpressing bax.	Cytarabine	96-101	BCL2 associated X, apoptosis regulator	Homo sapiens	192-195
9420079-7	1998	CONCLUSIONS: These results can be used collectively to argue that overexpression of bax results in increased sensitivity of C6 cells to ara-C and that increasing bax expression may be a useful strategy, in general, for increasing the sensitivity of gliomas to antineoplastic treatments.	Cytarabine	136-141	BCL2 associated X, apoptosis regulator	Homo sapiens	84-87
9778689-0	1998	Activation of the LRP (lung resistance-related protein) gene by short-term exposure of human leukemia cells to phorbol ester and cytarabine.	Cytarabine	129-139	major vault protein	Homo sapiens	18-21
9778689-0	1998	Activation of the LRP (lung resistance-related protein) gene by short-term exposure of human leukemia cells to phorbol ester and cytarabine.	Cytarabine	129-139	major vault protein	Homo sapiens	23-54
9778689-5	1998	Among conventional chemotherapeutic drugs tested, only cytarabine (Ara C) induced the LRP mRNA expression though no increase in LRP protein was detected.	Cytarabine	55-65	major vault protein	Homo sapiens	86-89
9778689-5	1998	Among conventional chemotherapeutic drugs tested, only cytarabine (Ara C) induced the LRP mRNA expression though no increase in LRP protein was detected.	Cytarabine	67-72	major vault protein	Homo sapiens	86-89
9778689-8	1998	In HL-60 cells, the LRP activation by TPA or Ara C was sustained for at least 23 days after withdrawal of inducing agents.	Cytarabine	45-50	major vault protein	Homo sapiens	20-23
17206779-0	1997	Transfection of C6 glioma cells with the bax gene and increased sensitivity to treatment with cytosine arabinoside.	Cytarabine	94-114	BCL2 associated X, apoptosis regulator	Homo sapiens	41-44
9396780-0	1997	Agents that down-regulate or inhibit protein kinase C circumvent resistance to 1-beta-D-arabinofuranosylcytosine-induced apoptosis in human leukemia cells that overexpress Bcl-2.	Cytarabine	79-112	BCL2 apoptosis regulator	Homo sapiens	172-177
9396780-3	1997	After exposure to an equimolar concentration of ara-C (10 microM for 6 hr), HL-60/Bcl-2 cells were significantly less susceptible to apoptosis, DNA fragmentation, and loss of clonogenicity than HL-60/pCEP4 cells.	Cytarabine	48-53	BCL2 apoptosis regulator	Homo sapiens	82-87
9396780-4	1997	The protective effect of increased Bcl-2 expression was manifested by a failure of ara-C to induce activation/cleavage of the Yama protease (CPP32; caspase-3) and degradation of one of its substrates, poly(ADP-ribose)polymerase to an 85-kDa cleavage product.	Cytarabine	83-88	BCL2 apoptosis regulator	Homo sapiens	35-40
9396780-6	1997	These events were accompanied by restoration of the ability of ara-C to induce CPP32 cleavage and activation, poly(ADP-ribose) polymerase degradation, and inhibition of colony formation.	Cytarabine	63-68	caspase 3	Homo sapiens	79-84
9396780-11	1997	Collectively, these findings indicate that bryostatin 1, which down-regulates PKC, and staurosporine and UCN-01, which directly inhibit the enzyme, circumvent resistance of Bcl-2-overexpressing leukemic cells to ara-C-induced apoptosis and activation of the protease cascade.	Cytarabine	212-217	BCL2 apoptosis regulator	Homo sapiens	173-178
17206779-5	1997	Treatment with 1 microM of cytosine arabinoside (ara-C) resulted in significantly more cells undergoing apoptosis in the cell line overexpressing bax than in the vector-only control cell line (23.57 +/- 2.6% compared with 5.3 +/- 0.7% terminal deoxynucleotidyl transferase--mediated biotinylated--deoxyuridine triphosphate nick-end labeling technique-positive cells; p = 0.007).	Cytarabine	27-47	BCL2 associated X, apoptosis regulator	Homo sapiens	146-149
17206779-5	1997	Treatment with 1 microM of cytosine arabinoside (ara-C) resulted in significantly more cells undergoing apoptosis in the cell line overexpressing bax than in the vector-only control cell line (23.57 +/- 2.6% compared with 5.3 +/- 0.7% terminal deoxynucleotidyl transferase--mediated biotinylated--deoxyuridine triphosphate nick-end labeling technique-positive cells; p = 0.007).	Cytarabine	49-54	BCL2 associated X, apoptosis regulator	Homo sapiens	146-149
17206779-6	1997	Furthermore, measurements of growth curves obtained immediately after treatment with 0.5 microM ara-C demonstrated a prolonged growth arrest of at least 6 days in the cell line overexpressing bax.	Cytarabine	96-101	BCL2 associated X, apoptosis regulator	Homo sapiens	192-195
17206779-7	1997	These results can be used collectively to argue that overexpression of bax results in increased sensitivity of C6 cells to ara-C and that increasing bax expression may be a useful strategy, in general, for increasing the sensitivity of gliomas to antineoplastic treatments.	Cytarabine	123-128	BCL2 associated X, apoptosis regulator	Homo sapiens	71-74
9349524-1	1997	We have previously shown that cytosine arabinoside (AraC)-induced apoptosis of cerebellar granule cells (CGCs) results in an increase of a 38-kDa band on sodium dodecyl sulfate-polyacrylamide gel electrophoresis, identified as glyceraldehyde-3-phosphate dehydrogenase (GAPDH; EC 1.2.1.12).	Cytarabine	30-50	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	269-274
9499665-0	1997	A single high dose of idarubicin combined with high-dose ARA-C (MSKCC ALL-3 protocol) in adult and pediatric patients with acute lymphoblastic leukemia.	Cytarabine	57-62	paired box 5	Homo sapiens	70-75
9349524-0	1997	Subcellular distribution of glyceraldehyde-3-phosphate dehydrogenase in cerebellar granule cells undergoing cytosine arabinoside-induced apoptosis.	Cytarabine	108-128	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	28-68
9349524-1	1997	We have previously shown that cytosine arabinoside (AraC)-induced apoptosis of cerebellar granule cells (CGCs) results in an increase of a 38-kDa band on sodium dodecyl sulfate-polyacrylamide gel electrophoresis, identified as glyceraldehyde-3-phosphate dehydrogenase (GAPDH; EC 1.2.1.12).	Cytarabine	30-50	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	227-267
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.	Cytarabine	60-80	Myeloproliferative syndrome, transient (transient abnormal myelopoiesis)	Homo sapiens	40-43
9349524-1	1997	We have previously shown that cytosine arabinoside (AraC)-induced apoptosis of cerebellar granule cells (CGCs) results in an increase of a 38-kDa band on sodium dodecyl sulfate-polyacrylamide gel electrophoresis, identified as glyceraldehyde-3-phosphate dehydrogenase (GAPDH; EC 1.2.1.12).	Cytarabine	52-56	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	227-267
9349524-1	1997	We have previously shown that cytosine arabinoside (AraC)-induced apoptosis of cerebellar granule cells (CGCs) results in an increase of a 38-kDa band on sodium dodecyl sulfate-polyacrylamide gel electrophoresis, identified as glyceraldehyde-3-phosphate dehydrogenase (GAPDH; EC 1.2.1.12).	Cytarabine	52-56	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	269-274
9349524-2	1997	Antisense oligonucleotides to GAPDH mRNA afford acutely plated CGCs significant protection against AraC-induced apoptosis.	Cytarabine	99-103	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	30-35
9369415-4	1997	Here, we show that therapeutic concentrations of doxorubicin, methotrexate and cytarabine also induce apoptosis via activation of the CD95 system in primary leukemia cells in vivo.	Cytarabine	79-89	Fas cell surface death receptor	Homo sapiens	134-138
9376593-3	1997	Apoptosis induced in tumor cells by cytarabine, doxorubicin, and methotrexate required the activation of ICE/Ced-3 proteases (caspases), similarly to the CD95 system.	Cytarabine	36-46	caspase 1	Homo sapiens	126-134
9477124-5	1997	Low-dose therapy with cytarabine and thioguanine was given between the initial courses of histamine/IL-2.	Cytarabine	22-32	interleukin 2	Homo sapiens	100-104
9365241-0	1997	Pro-apoptotic effect of the c-Abl tyrosine kinase in the cellular response to 1-beta-D-arabinofuranosylcytosine.	Cytarabine	78-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-33
9365241-1	1997	Treatment of cells with the antimetabolite 1-beta-D-arabinofuranosylcytosine (ara-C) and other genotoxic agents is associated with activation of the c-Abl protein tyrosine kinase.	Cytarabine	78-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-154
9365241-3	1997	The present studies demonstrate that cells expressing a dominant negative, kinase-inactive c-Abl (K-R) are resistant to killing by ara-C.	Cytarabine	131-136	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	91-96
9365241-4	1997	The expression of c-Abl (K-R) blocked ara-C-induced apoptosis by a mechanism that is at least in part independent of the p53 tumor suppressor.	Cytarabine	38-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-23
9661701-0	1997	Induction of fragility at the human RNU2 locus by cytosine arabinoside is dependent upon a transcriptionally competent U2 small nuclear RNA gene and the expression of p53.	Cytarabine	50-70	RNA, U2 small nuclear 1	Homo sapiens	36-40
9661701-0	1997	Induction of fragility at the human RNU2 locus by cytosine arabinoside is dependent upon a transcriptionally competent U2 small nuclear RNA gene and the expression of p53.	Cytarabine	50-70	tumor protein p53	Homo sapiens	167-170
9661701-4	1997	In the present study we have investigated the response of the RNU2 locus to cytosine arabinoside (araC), an inhibitor of DNA polymerases and a common inducer of fragile sites.	Cytarabine	76-96	RNA, U2 small nuclear 1	Homo sapiens	62-66
9661701-4	1997	In the present study we have investigated the response of the RNU2 locus to cytosine arabinoside (araC), an inhibitor of DNA polymerases and a common inducer of fragile sites.	Cytarabine	98-102	RNA, U2 small nuclear 1	Homo sapiens	62-66
9251730-10	1997	The use of L-asparaginase, timed after high-dose Cytarabine (ARA-C) throughout therapy, might have contributed to their cure.	Cytarabine	49-59	asparaginase and isoaspartyl peptidase 1	Homo sapiens	11-25
9401275-2	1997	We conducted a clinical trial to increase the chemosensitivity of residual leukemic cells by combining G-CSF to marrow-ablative chemotherapy, including cytosine arabinoside (Ara-C), and facilitated by autologous blood cell transplantation (ABCT) for treatment of acute myelogenous leukemia (AML) in first complete remission.	Cytarabine	152-172	colony stimulating factor 3	Homo sapiens	103-108
9295281-15	1997	These data demonstrate that the stimulation of apoptosis by ara-C is self-limiting and can be enhanced by inhibition of PKC.	Cytarabine	60-65	protein kinase C alpha	Homo sapiens	120-123
9401275-3	1997	A total of 16 patients were consecutively treated with granulocyte colony-stimulating factor (G-CSF)-combined high-dose chemotherapy (busulfan, etoposide and Ara-C) followed by autotransplantation of peripheral blood progenitor cells, which had been collected after the consolidation chemotherapy.	Cytarabine	158-163	colony stimulating factor 3	Homo sapiens	94-99
9295281-7	1997	Thus, ara-C stimulates the synthesis of two second messengers with opposing effects on Bcl-2.	Cytarabine	6-11	BCL2 apoptosis regulator	Homo sapiens	87-92
9295281-8	1997	Since the effects of ara-C-induced DAG could be due to protein kinase C (PKC) activation, we determined the effects of ara-C on PKC isozymes.	Cytarabine	21-26	protein kinase C alpha	Homo sapiens	73-76
9295281-8	1997	Since the effects of ara-C-induced DAG could be due to protein kinase C (PKC) activation, we determined the effects of ara-C on PKC isozymes.	Cytarabine	119-124	protein kinase C alpha	Homo sapiens	128-131
9295281-11	1997	ET-18-OCH3 also inhibited stimulation of Bcl-2 by TPA and enhanced the decrease in Bcl-2 observed in ara-C-treated cells.	Cytarabine	101-106	BCL2 apoptosis regulator	Homo sapiens	83-88
9295281-12	1997	These data indicate that ara-C-induced apoptosis is limited by ara-C-stimulated PKCbetaII through effects on Bcl-2.	Cytarabine	25-30	BCL2 apoptosis regulator	Homo sapiens	109-114
9295281-12	1997	These data indicate that ara-C-induced apoptosis is limited by ara-C-stimulated PKCbetaII through effects on Bcl-2.	Cytarabine	63-68	BCL2 apoptosis regulator	Homo sapiens	109-114
9251730-10	1997	The use of L-asparaginase, timed after high-dose Cytarabine (ARA-C) throughout therapy, might have contributed to their cure.	Cytarabine	61-66	asparaginase and isoaspartyl peptidase 1	Homo sapiens	11-25
9264374-3	1997	The pluripotent erythroleukemic K562 and HEL cell lines express messages for a number of ETS genes, but only c-ETS-1 levels are elevated in response to treatment with hemin or cytosine arabinofuranoside (Ara-C), agents which induce erythroid differentiation.	Cytarabine	176-202	ETS proto-oncogene 1, transcription factor	Homo sapiens	109-116
9337072-0	1997	Potentiation of ara-C-induced apoptosis by the protein kinase C activator bryostatin 1 in human leukemia cells (HL-60) involves a process dependent upon c-Myc.	Cytarabine	16-21	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	153-158
9337072-1	1997	The role of the nuclear phosphoprotein c-Myc has been examined with respect to the regulation of 1-beta-D-arabinofuranosylcytosine (ara-C)-induced apoptosis in human leukemia cells exposed to bryostatin 1 and other pharmacologic protein kinase C (PKC) activators.	Cytarabine	97-130	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	39-44
9337072-1	1997	The role of the nuclear phosphoprotein c-Myc has been examined with respect to the regulation of 1-beta-D-arabinofuranosylcytosine (ara-C)-induced apoptosis in human leukemia cells exposed to bryostatin 1 and other pharmacologic protein kinase C (PKC) activators.	Cytarabine	132-137	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	39-44
9337072-3	1997	In contrast, equivalent exposure to the stage 2 tumor-promoting PKC activator mezerein (10 nM) in conjunction with ara-C reduced c-Myc levels by 87% and failed to potentiate apoptosis.	Cytarabine	115-120	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	129-134
9231747-6	1997	The effects of IL-1beta but not LPS in the mixed primary culture of diencephalon were canceled by a prior exposure to cytosine-beta-D-arabinofuranoside.	Cytarabine	118-151	interleukin 1 beta	Rattus norvegicus	15-23
9264399-4	1997	2-CdA alone and combined with cytarabine resulted in a rapid and sustained decrease in circulating eosinophils in two patients with idiopathic HES that was refractory to steroids, hydroxyurea and cytarabine.	Cytarabine	196-206	cytidine deaminase	Homo sapiens	2-5
9292531-2	1997	Ara-C metabolism was assessed by the activities of deoxycytidine kinase (DCK), deoxycytidine deaminase (DCD), DNA polymerase alpha (Poly alpha), and overall polymerase (overall Poly).	Cytarabine	0-5	deoxycytidine kinase	Homo sapiens	51-71
9292531-2	1997	Ara-C metabolism was assessed by the activities of deoxycytidine kinase (DCK), deoxycytidine deaminase (DCD), DNA polymerase alpha (Poly alpha), and overall polymerase (overall Poly).	Cytarabine	0-5	deoxycytidine kinase	Homo sapiens	73-76
9292531-2	1997	Ara-C metabolism was assessed by the activities of deoxycytidine kinase (DCK), deoxycytidine deaminase (DCD), DNA polymerase alpha (Poly alpha), and overall polymerase (overall Poly).	Cytarabine	0-5	apolipoprotein B mRNA editing enzyme catalytic subunit 3G	Homo sapiens	79-102
9292531-2	1997	Ara-C metabolism was assessed by the activities of deoxycytidine kinase (DCK), deoxycytidine deaminase (DCD), DNA polymerase alpha (Poly alpha), and overall polymerase (overall Poly).	Cytarabine	0-5	dermcidin	Homo sapiens	104-107
9292531-2	1997	Ara-C metabolism was assessed by the activities of deoxycytidine kinase (DCK), deoxycytidine deaminase (DCD), DNA polymerase alpha (Poly alpha), and overall polymerase (overall Poly).	Cytarabine	0-5	DNA polymerase alpha 1, catalytic subunit	Homo sapiens	110-130
9389365-6	1997	The rationale of the St Jude"s R4 was to optimize the schedule of the second course of ara-C at a time when the patient"s endogenous G-CSF concentration was increased and thus maximize the percent of cells captured in S phase.	Cytarabine	87-92	colony stimulating factor 3	Homo sapiens	133-138
9264374-3	1997	The pluripotent erythroleukemic K562 and HEL cell lines express messages for a number of ETS genes, but only c-ETS-1 levels are elevated in response to treatment with hemin or cytosine arabinofuranoside (Ara-C), agents which induce erythroid differentiation.	Cytarabine	204-209	ETS proto-oncogene 1, transcription factor	Homo sapiens	109-116
9264374-4	1997	Furthermore, ETS-1 antisense oligonucleotides inhibit hemoglobinization of cells treated with Ara-C or hemin, and K562 and HEL cells infected with retrovirus expressing the c-ETS-1 gene exhibit a significant increase in erythroid character (as indicated by benzidine staining for hemoglobin (Hb) and surface marker analysis), a dramatic increase in responsiveness to hemin or Ara-C, and a decreased rate of proliferation (20-40% of control rates).	Cytarabine	94-99	ETS proto-oncogene 1, transcription factor	Homo sapiens	13-18
9264374-4	1997	Furthermore, ETS-1 antisense oligonucleotides inhibit hemoglobinization of cells treated with Ara-C or hemin, and K562 and HEL cells infected with retrovirus expressing the c-ETS-1 gene exhibit a significant increase in erythroid character (as indicated by benzidine staining for hemoglobin (Hb) and surface marker analysis), a dramatic increase in responsiveness to hemin or Ara-C, and a decreased rate of proliferation (20-40% of control rates).	Cytarabine	376-381	ETS proto-oncogene 1, transcription factor	Homo sapiens	13-18
9264374-4	1997	Furthermore, ETS-1 antisense oligonucleotides inhibit hemoglobinization of cells treated with Ara-C or hemin, and K562 and HEL cells infected with retrovirus expressing the c-ETS-1 gene exhibit a significant increase in erythroid character (as indicated by benzidine staining for hemoglobin (Hb) and surface marker analysis), a dramatic increase in responsiveness to hemin or Ara-C, and a decreased rate of proliferation (20-40% of control rates).	Cytarabine	376-381	ETS proto-oncogene 1, transcription factor	Homo sapiens	173-180
9252649-3	1997	72 hours exposure of human melanoma GLL-19 cells to 1,000 nM ara-C induced growth inhibition and increased the number of EGF-R, TRF-R and nerve growth factor receptor (NGF-R) on cell surface.	Cytarabine	61-66	epidermal growth factor	Homo sapiens	121-126
9379681-6	1997	Although there is no denying the possibility that cytosine arabinoside is partly responsible, our results strongly suggest that G-CSF plays the main role in differentiation of leukemic cells into a monocyte lineage inducing apoptosis in vivo in this patient.	Cytarabine	50-70	colony stimulating factor 3	Homo sapiens	128-133
9322679-1	1997	Expression and functional activity of P-glycoprotein (P-gp) were measured in 182 acute myelogenous leukemia (AML) patients: 136 patients were treated with the AML-6 protocol (EORTC), containing daunorubicin, vincristine, and conventional-dose cytarabine (ara-C), and 21 patients received idarubicin, vepeside, and conventional-dose ara-C (ICE-AML-10 protocol/EORTC).	Cytarabine	243-253	ATP binding cassette subfamily B member 1	Homo sapiens	38-52
9322679-1	1997	Expression and functional activity of P-glycoprotein (P-gp) were measured in 182 acute myelogenous leukemia (AML) patients: 136 patients were treated with the AML-6 protocol (EORTC), containing daunorubicin, vincristine, and conventional-dose cytarabine (ara-C), and 21 patients received idarubicin, vepeside, and conventional-dose ara-C (ICE-AML-10 protocol/EORTC).	Cytarabine	255-260	ATP binding cassette subfamily B member 1	Homo sapiens	38-52
9322679-1	1997	Expression and functional activity of P-glycoprotein (P-gp) were measured in 182 acute myelogenous leukemia (AML) patients: 136 patients were treated with the AML-6 protocol (EORTC), containing daunorubicin, vincristine, and conventional-dose cytarabine (ara-C), and 21 patients received idarubicin, vepeside, and conventional-dose ara-C (ICE-AML-10 protocol/EORTC).	Cytarabine	332-337	ATP binding cassette subfamily B member 1	Homo sapiens	38-52
9252649-3	1997	72 hours exposure of human melanoma GLL-19 cells to 1,000 nM ara-C induced growth inhibition and increased the number of EGF-R, TRF-R and nerve growth factor receptor (NGF-R) on cell surface.	Cytarabine	61-66	transferrin	Homo sapiens	128-133
9252649-4	1997	Enhanced expression of beta 3 integrins CD49a, CD49c and CD49e, av integrin CD51, beta 3 integrin CD61, CD58/LFA3 and collagen IV and laminin was also detected in ara-C-treated GLL-19 cells.	Cytarabine	163-168	eukaryotic translation elongation factor 1 beta 2 pseudogene 2	Homo sapiens	23-29
9175720-4	1997	We report that preincubation of cells with TGF-beta3 for 24 hr resulted in enhanced clonogenicity following exposure to vinblastine, vincristine, etoposide, taxol, ara-C, methotrexate, or 5-FU.	Cytarabine	164-169	transforming growth factor beta 3	Homo sapiens	43-52
16465244-0	1997	Modulation of the expression of Bcl-2 and related proteins in human leukemia cells by protein kinase C activators: relationship to effects on 1-[beta-D-arabinofuranosyl]cytosine-induced apoptosis.	Cytarabine	142-177	BCL2 apoptosis regulator	Homo sapiens	32-37
16465244-11	1997	Finally, treatment of cells with bryostatin 1+/-ara-C (but not ara-C alone) resulted in a diffuse broadening of the Bcl-2 protein band, whereas exposure of cells to taxol (250 nM, 6 h) led to the appearance of a distinct Bcl-2 species with reduced mobility, phenomena compatible with protein phosphorylation.	Cytarabine	48-53	BCL2 apoptosis regulator	Homo sapiens	116-121
16465244-11	1997	Finally, treatment of cells with bryostatin 1+/-ara-C (but not ara-C alone) resulted in a diffuse broadening of the Bcl-2 protein band, whereas exposure of cells to taxol (250 nM, 6 h) led to the appearance of a distinct Bcl-2 species with reduced mobility, phenomena compatible with protein phosphorylation.	Cytarabine	48-53	BCL2 apoptosis regulator	Homo sapiens	221-226
9215616-2	1997	dCK mediating toxicity of 1-beta-D-arabinofuranosylcytosine was analyzed semiquantitatively by RT-PCR and by single-strand conformation polymorphism.	Cytarabine	26-59	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	0-3
9137794-3	1997	From 1985 to 1992 the Swiss Group for Clinical Cancer Research (SAKK) performed a randomized phase III trial to evaluate the effectiveness of one single postremission course of high-dose cytarabine (HDAC) in terms of leukaemia-free and overall survival in adults with de novo AML.	Cytarabine	187-197	histone deacetylase 9	Homo sapiens	199-203
9096690-7	1997	In contrast to the disparate responses to PMA, HL-60/AS5 and HL-60/V2 cells treated with the antimetabolite 1-beta-D-arabinofurano-sylcytosine (Ara-C; 10 microM for 6 h) displayed equal susceptibility to G1 arrest, apoptosis, and inhibition of clonogenicity, phenomena unaccompanied by p21MDA6 and p27klp1 induction, or pRB dephosphorylation.	Cytarabine	108-142	RB transcriptional corepressor 1	Homo sapiens	320-323
9096690-7	1997	In contrast to the disparate responses to PMA, HL-60/AS5 and HL-60/V2 cells treated with the antimetabolite 1-beta-D-arabinofurano-sylcytosine (Ara-C; 10 microM for 6 h) displayed equal susceptibility to G1 arrest, apoptosis, and inhibition of clonogenicity, phenomena unaccompanied by p21MDA6 and p27klp1 induction, or pRB dephosphorylation.	Cytarabine	144-149	RB transcriptional corepressor 1	Homo sapiens	320-323
9096697-0	1997	Differential effect of GM-CSF pretreatment on intracellular Ara-C metabolism in normal bone marrow mononuclear cells vs acute myeloid leukemia (AML) blasts.	Cytarabine	60-65	colony stimulating factor 2	Homo sapiens	23-29
9096697-1	1997	The effect of recombinant human granulocyte-macrophage colony-stimulating factor (GM-CSF) on the intracellular metabolism of cytosine arabinoside (Ara-C) was comparatively analyzed in normal bone marrow mononuclear cells (NBMMC) from eight healthy volunteers and in leukemic blasts from 50 patients with acute myeloid leukemia (AML).	Cytarabine	125-145	colony stimulating factor 2	Homo sapiens	32-80
9096697-1	1997	The effect of recombinant human granulocyte-macrophage colony-stimulating factor (GM-CSF) on the intracellular metabolism of cytosine arabinoside (Ara-C) was comparatively analyzed in normal bone marrow mononuclear cells (NBMMC) from eight healthy volunteers and in leukemic blasts from 50 patients with acute myeloid leukemia (AML).	Cytarabine	125-145	colony stimulating factor 2	Homo sapiens	82-88
9096697-1	1997	The effect of recombinant human granulocyte-macrophage colony-stimulating factor (GM-CSF) on the intracellular metabolism of cytosine arabinoside (Ara-C) was comparatively analyzed in normal bone marrow mononuclear cells (NBMMC) from eight healthy volunteers and in leukemic blasts from 50 patients with acute myeloid leukemia (AML).	Cytarabine	147-152	colony stimulating factor 2	Homo sapiens	32-80
9096697-1	1997	The effect of recombinant human granulocyte-macrophage colony-stimulating factor (GM-CSF) on the intracellular metabolism of cytosine arabinoside (Ara-C) was comparatively analyzed in normal bone marrow mononuclear cells (NBMMC) from eight healthy volunteers and in leukemic blasts from 50 patients with acute myeloid leukemia (AML).	Cytarabine	147-152	colony stimulating factor 2	Homo sapiens	82-88
9096697-4	1997	Median Ara-C-mediated inhibition of DNA synthesis was significantly more effective in AML blasts as compared to NBMMC (76.5 vs 55.0% at 0.05 microM and 99.0 vs 96.0% at 5.0 microM Ara-C, P &lt; 0.01) but was not influenced by GM-CSF pretreatment.	Cytarabine	7-12	colony stimulating factor 2	Homo sapiens	226-232
9096697-8	1997	At low; intermediate and high extracellular Ara-C concentrations GM-CSF pretreatment resulted in a significant enhancement of the 3H-Ara-C incorporation into the DNA in both GM-CSF responsive AML blasts and NBMMC (median of 1.3 to 2.1- and 1.4 to 1.6-fold, P &lt; 0.05).	Cytarabine	44-49	colony stimulating factor 2	Homo sapiens	65-71
9096697-8	1997	At low; intermediate and high extracellular Ara-C concentrations GM-CSF pretreatment resulted in a significant enhancement of the 3H-Ara-C incorporation into the DNA in both GM-CSF responsive AML blasts and NBMMC (median of 1.3 to 2.1- and 1.4 to 1.6-fold, P &lt; 0.05).	Cytarabine	44-49	colony stimulating factor 2	Homo sapiens	174-180
9096697-11	1997	These data reveal a different effect of GM-CSF priming on the metabolism of Ara-C in normal vs leukemic cells which may cause a preferential increase in the antileukemic cytotoxicity of Ara-C in the presence of GM-CSF.	Cytarabine	76-81	colony stimulating factor 2	Homo sapiens	40-46
9096697-11	1997	These data reveal a different effect of GM-CSF priming on the metabolism of Ara-C in normal vs leukemic cells which may cause a preferential increase in the antileukemic cytotoxicity of Ara-C in the presence of GM-CSF.	Cytarabine	76-81	colony stimulating factor 2	Homo sapiens	211-217
9096697-11	1997	These data reveal a different effect of GM-CSF priming on the metabolism of Ara-C in normal vs leukemic cells which may cause a preferential increase in the antileukemic cytotoxicity of Ara-C in the presence of GM-CSF.	Cytarabine	186-191	colony stimulating factor 2	Homo sapiens	40-46
9137794-20	1997	The results of our intensive, single course HDAC group compare favourably with less intensive, repetitive HDAC cycles, suggesting that Ara-C dose intensity may be more important than total dosage.	Cytarabine	135-140	histone deacetylase 9	Homo sapiens	44-48
9111585-3	1997	We assessed whether glioma cell killing is synergistically enhanced by cotreatment with CD95 ligand and chemotherapeutic agents, including doxorubicin, carmustine, vincristine, etoposide, teniposide, 5-fluorouracil and cytarabine.	Cytarabine	219-229	Fas cell surface death receptor	Homo sapiens	88-92
9032331-6	1997	Treatment of cells with cytosine arabinoside, which blocks the late buildup of dsRNA in vaccinia virus-infected cells, prevented induction of apoptosis by vaccinia virus with E3L deleted.	Cytarabine	24-44	double-strand RNA-binding protein	Vaccinia virus	175-178
9218105-5	1997	The use of high-dose cytosine arabinoside (HDAC 3 gm/m2) appears rational based on cytosine pharmacology.	Cytarabine	21-41	histone deacetylase 3	Homo sapiens	43-49
9052685-4	1997	Exposure of these cells to electric fields (330 or 750 mV/cm for 17 h) inhibited up-regulation of MDR1 expression by treatment with 25 microM 1-beta-D-arabinofuranosylcytosine (AraC).	Cytarabine	142-175	ATP binding cassette subfamily B member 1	Homo sapiens	98-102
9052685-4	1997	Exposure of these cells to electric fields (330 or 750 mV/cm for 17 h) inhibited up-regulation of MDR1 expression by treatment with 25 microM 1-beta-D-arabinofuranosylcytosine (AraC).	Cytarabine	177-181	ATP binding cassette subfamily B member 1	Homo sapiens	98-102
9175315-9	1997	These data provide a rationale for more extensive and more intensive testing of combinations of ara-C and F-ara in Pgp-mediated MDR acute leukemia.	Cytarabine	96-101	phosphoglycolate phosphatase	Homo sapiens	115-118
9133617-1	1997	We examined the effect of hemin, TGF-beta1 and cytosine arabinoside (Ara-C) on the levels of mRNAs for the erythroid-specific 5-aminolevulinate synthase (ALAS-E) and gamma-globin in various human myelogenous leukemia cell lines.	Cytarabine	47-67	5'-aminolevulinate synthase 2	Homo sapiens	154-160
9133617-1	1997	We examined the effect of hemin, TGF-beta1 and cytosine arabinoside (Ara-C) on the levels of mRNAs for the erythroid-specific 5-aminolevulinate synthase (ALAS-E) and gamma-globin in various human myelogenous leukemia cell lines.	Cytarabine	47-67	hemoglobin subunit gamma 1	Homo sapiens	166-178
9133617-1	1997	We examined the effect of hemin, TGF-beta1 and cytosine arabinoside (Ara-C) on the levels of mRNAs for the erythroid-specific 5-aminolevulinate synthase (ALAS-E) and gamma-globin in various human myelogenous leukemia cell lines.	Cytarabine	69-74	5'-aminolevulinate synthase 2	Homo sapiens	154-160
9133617-1	1997	We examined the effect of hemin, TGF-beta1 and cytosine arabinoside (Ara-C) on the levels of mRNAs for the erythroid-specific 5-aminolevulinate synthase (ALAS-E) and gamma-globin in various human myelogenous leukemia cell lines.	Cytarabine	69-74	hemoglobin subunit gamma 1	Homo sapiens	166-178
9028941-3	1997	In addition, the cycling status of circulating CD34+ cells, including committed clonogenic progenitor cells and the more immature LTC-IC, was determined by the cytosine arabinoside (Ara-C) suicide test and the acridine orange flow cytometric technique.	Cytarabine	160-180	CD34 molecule	Homo sapiens	47-51
9028941-11	1997	However, longer incubation with Ara-C (16 to 18 hours), in the presence of SCF, IL-3 and G-CSF, or IL-6, showed that more than 60% of LTC-IC are actually cycling, with no difference being found with BM cells.	Cytarabine	32-37	KIT ligand	Homo sapiens	75-78
8980142-2	1996	Here we report that when an HL-60 cell line resistant to cytosine arabinoside (Ara-C) was exposed to this anticancer drug, neither RB cleavage nor apoptosis was detected.	Cytarabine	79-84	RB transcriptional corepressor 1	Homo sapiens	131-133
9028941-11	1997	However, longer incubation with Ara-C (16 to 18 hours), in the presence of SCF, IL-3 and G-CSF, or IL-6, showed that more than 60% of LTC-IC are actually cycling, with no difference being found with BM cells.	Cytarabine	32-37	interleukin 3	Homo sapiens	80-84
9028941-11	1997	However, longer incubation with Ara-C (16 to 18 hours), in the presence of SCF, IL-3 and G-CSF, or IL-6, showed that more than 60% of LTC-IC are actually cycling, with no difference being found with BM cells.	Cytarabine	32-37	colony stimulating factor 3	Homo sapiens	89-94
9066648-10	1997	The amount of Fas antigen expression was slightly increased only in cells treated with a low dose of Ara-C, not in others.	Cytarabine	101-106	Fas cell surface death receptor	Homo sapiens	14-25
9639777-0	1997	Effect of concurrent use of rh-IL-3 and rh-GM-CSF on apoptosis of HL-60 cells induced by Ara-C.	Cytarabine	89-94	colony stimulating factor 2	Homo sapiens	43-49
9123849-2	1997	It is shown that transfection of K562 cells with the ASFV A179L gene protects these cells from apoptotic cell death induced by a combination of cycloheximide and actinomycin D or by treatment with cytosine arabinoside.	Cytarabine	197-217	bcl-2/bax homolog	African swine fever virus	58-63
9118972-4	1997	Inhibition of catalase and glutathione peroxidase activities also enhanced the retardation effect of nickel on the rejoining of DNA strand breaks accumulated by hydroxyurea plus cytosine-beta-D-arabinofuranoside in UV-irradiated cells.	Cytarabine	178-211	catalase	Bos taurus	14-22
8959329-10	1996	Low-dose ara-C-induced erythroid differentiation was accompanied by conversion of the retinoblastoma protein to predominantly its underphosphorylated isoform as well as by down-regulation of Myc levels in K562/Bcl-xS and K562/neo cells.	Cytarabine	9-14	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	191-194
8946931-0	1996	Constitutive overexpression of the cytidine deaminase gene confers resistance to cytosine arabinoside in vitro.	Cytarabine	81-101	cytidine deaminase	Homo sapiens	35-53
8946931-5	1996	Together, these data suggest that constitutive overexpression of the CDD gene correlates with increased ara-C resistance and thus may prove useful in considering attempts to attenuate ara-C-induced toxicity on hematopoietic progenitor cells.	Cytarabine	104-109	natriuretic peptide A	Homo sapiens	69-72
8946931-5	1996	Together, these data suggest that constitutive overexpression of the CDD gene correlates with increased ara-C resistance and thus may prove useful in considering attempts to attenuate ara-C-induced toxicity on hematopoietic progenitor cells.	Cytarabine	184-189	natriuretic peptide A	Homo sapiens	69-72
8946932-5	1996	Growth factor responsive cells are more Ara-C sensitive in G-CSF than in GM-CSF or IL-3.	Cytarabine	40-45	colony stimulating factor 3	Homo sapiens	59-64
11364014-0	1996	Cytarabine nixed for PML.	Cytarabine	0-10	PML nuclear body scaffold	Homo sapiens	21-24
8950029-3	1996	Ara-C activated SMase with 10 minutes in both Jurkat and EL4 cells, while phorbol ester (PMA) had no effect.	Cytarabine	0-5	epilepsy 4	Mus musculus	57-60
8950029-8	1996	The effects of Ara-C on JNK activity may be mediated through secondary response pathways.	Cytarabine	15-20	mitogen-activated protein kinase 8	Homo sapiens	24-27
8967975-1	1996	With the use of clonogenic survival assays, we show that wild-type p53-expressing A2780 human ovarian cell lines transfected with a dominant negative mutant p53 gene (codon 143, valine to alanine) acquired cross-resistance to ionizing radiation, cisplatin, doxorubicin, and 1-beta-D-arabinofuranosylcytosine.	Cytarabine	274-307	tumor protein p53	Homo sapiens	67-70
8967975-1	1996	With the use of clonogenic survival assays, we show that wild-type p53-expressing A2780 human ovarian cell lines transfected with a dominant negative mutant p53 gene (codon 143, valine to alanine) acquired cross-resistance to ionizing radiation, cisplatin, doxorubicin, and 1-beta-D-arabinofuranosylcytosine.	Cytarabine	274-307	tumor protein p53	Homo sapiens	157-160
9009249-0	1996	Effect of stem cell factor on leukemic progenitor cell growth and sensitivity to cytosine-arabinoside.	Cytarabine	81-101	KIT ligand	Homo sapiens	10-26
8892676-0	1996	Intracellular metabolism of Ara-C and resulting DNA fragmentation and apoptosis of human AML HL-60 cells possessing disparate levels of Bcl-2 protein.	Cytarabine	28-33	BCL2 apoptosis regulator	Homo sapiens	136-141
8892676-1	1996	We examined the effects of high intracellular levels of Bcl-2 on the metabolism and DNA incorporation of high-dose Ara-C (HIDAC) as well as on Ara-C-induced DNA strand breaks and apoptosis of human AML HL-60 cells.	Cytarabine	115-120	BCL2 apoptosis regulator	Homo sapiens	56-61
9031077-5	1996	Normal CFU-GM responded to rhG+GM-CSF or IL-3 with increased kinetic activity and sensitivity to Ara-C.	Cytarabine	97-102	colony stimulating factor 2	Homo sapiens	31-37
9009249-6	1996	Second, we tested the influence of SCF on the sensitivity to Ara-C of self-renewing leukemic cells from 18 patients with AML.	Cytarabine	61-66	KIT ligand	Homo sapiens	35-38
9031077-5	1996	Normal CFU-GM responded to rhG+GM-CSF or IL-3 with increased kinetic activity and sensitivity to Ara-C.	Cytarabine	97-102	interleukin 3	Homo sapiens	41-45
9009249-7	1996	We showed that SCF was efficient in increasing the toxicity of Ara-C on the self-renewing blast progenitors, especially with high concentrations of Ara-C.	Cytarabine	63-68	KIT ligand	Homo sapiens	15-18
9009249-7	1996	We showed that SCF was efficient in increasing the toxicity of Ara-C on the self-renewing blast progenitors, especially with high concentrations of Ara-C.	Cytarabine	148-153	KIT ligand	Homo sapiens	15-18
9009249-9	1996	These data indicate that SCF can enhance sensitivity to Ara-C of some leukemic cells with self-renewing capacity.	Cytarabine	56-61	KIT ligand	Homo sapiens	25-28
8960658-0	1996	[Successful treatment of acute non-lymphoblastic leukemia from myelodysplastic syndrome by combination of human macrophage colony-stimulating factor (M-CSF) and low dose cytosine arabinoside: M-CSF-induced proliferation and tyrosine phosphorylation in leukemic blasts].	Cytarabine	170-190	colony stimulating factor 1	Homo sapiens	192-197
8900110-7	1996	Cells lacking the c-abl gene also responded to ara-C and MMS with increases in p53 levels and induction of p21.	Cytarabine	47-52	tumor protein p53	Homo sapiens	79-82
8960658-5	1996	Based upon these findings, combined therapy with M-CSF and low dose cytosine arabinoside (ara-C) was successful.	Cytarabine	90-95	colony stimulating factor 1	Homo sapiens	49-54
8960658-7	1996	These results suggest that M-CSF could enhance the cytotoxic effect of ara-C on leukemic blasts via its intracellular signaling pathway linked to proliferation.	Cytarabine	71-76	colony stimulating factor 1	Homo sapiens	27-32
8900110-2	1996	The present studies demonstrate that the antimetabolite 1-beta-D-arabinofuranosylcytosine (ara-C) induces binding of c-Abl and p53.	Cytarabine	91-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-122
8900110-2	1996	The present studies demonstrate that the antimetabolite 1-beta-D-arabinofuranosylcytosine (ara-C) induces binding of c-Abl and p53.	Cytarabine	91-96	tumor protein p53	Homo sapiens	127-130
8900110-7	1996	Cells lacking the c-abl gene also responded to ara-C and MMS with increases in p53 levels and induction of p21.	Cytarabine	47-52	cyclin dependent kinase inhibitor 1A	Homo sapiens	107-110
8900110-3	1996	Ara-C treatment of cells that express wild type or a dominant negative, kinase-inactive c-Abl(K-R) was associated with formation of c-Abl-p53 complexes and increased expression of the cyclin-dependent kinase (Cdk) inhibitor p21.	Cytarabine	0-5	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-93
8900110-3	1996	Ara-C treatment of cells that express wild type or a dominant negative, kinase-inactive c-Abl(K-R) was associated with formation of c-Abl-p53 complexes and increased expression of the cyclin-dependent kinase (Cdk) inhibitor p21.	Cytarabine	0-5	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	132-137
8900436-0	1996	Inhibition of cytarabine-induced MDR1 (P-glycoprotein) gene activation in human tumor cells by fatty acid-polyethylene glycol-fatty acid diesters, novel inhibitors of P-glycoprotein function.	Cytarabine	14-24	ATP binding cassette subfamily B member 1	Homo sapiens	33-37
8900110-3	1996	Ara-C treatment of cells that express wild type or a dominant negative, kinase-inactive c-Abl(K-R) was associated with formation of c-Abl-p53 complexes and increased expression of the cyclin-dependent kinase (Cdk) inhibitor p21.	Cytarabine	0-5	tumor protein p53	Homo sapiens	138-141
8900110-3	1996	Ara-C treatment of cells that express wild type or a dominant negative, kinase-inactive c-Abl(K-R) was associated with formation of c-Abl-p53 complexes and increased expression of the cyclin-dependent kinase (Cdk) inhibitor p21.	Cytarabine	0-5	cyclin dependent kinase 2	Homo sapiens	209-212
8900110-3	1996	Ara-C treatment of cells that express wild type or a dominant negative, kinase-inactive c-Abl(K-R) was associated with formation of c-Abl-p53 complexes and increased expression of the cyclin-dependent kinase (Cdk) inhibitor p21.	Cytarabine	0-5	cyclin dependent kinase inhibitor 1A	Homo sapiens	224-227
8900110-4	1996	However, down-regulation of Cdk2 by ara-C was found in cells expressing wild type c-Abl and not in cells expressing c-Abl(K-R) or those deficient in p53.	Cytarabine	36-41	cyclin dependent kinase 2	Homo sapiens	28-32
8900110-4	1996	However, down-regulation of Cdk2 by ara-C was found in cells expressing wild type c-Abl and not in cells expressing c-Abl(K-R) or those deficient in p53.	Cytarabine	36-41	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-87
8900110-7	1996	Cells lacking the c-abl gene also responded to ara-C and MMS with increases in p53 levels and induction of p21.	Cytarabine	47-52	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-23
8900436-4	1996	In the present study we show that these compounds are also able to inhibit up-regulation of MDR1 gene expression caused by cytarabine (ARA-C) and doxorubicin in human tumor cell lines H9 and KB 3-1, which express minimal levels of MDR1 mRNA.	Cytarabine	123-133	ATP binding cassette subfamily B member 1	Homo sapiens	92-96
8900436-4	1996	In the present study we show that these compounds are also able to inhibit up-regulation of MDR1 gene expression caused by cytarabine (ARA-C) and doxorubicin in human tumor cell lines H9 and KB 3-1, which express minimal levels of MDR1 mRNA.	Cytarabine	135-140	ATP binding cassette subfamily B member 1	Homo sapiens	92-96
8900436-0	1996	Inhibition of cytarabine-induced MDR1 (P-glycoprotein) gene activation in human tumor cells by fatty acid-polyethylene glycol-fatty acid diesters, novel inhibitors of P-glycoprotein function.	Cytarabine	14-24	ATP binding cassette subfamily B member 1	Homo sapiens	39-53
8900436-0	1996	Inhibition of cytarabine-induced MDR1 (P-glycoprotein) gene activation in human tumor cells by fatty acid-polyethylene glycol-fatty acid diesters, novel inhibitors of P-glycoprotein function.	Cytarabine	14-24	ATP binding cassette subfamily B member 1	Homo sapiens	167-181
8806683-4	1996	The results also demonstrate that Cdk2 directly associates with the Src-like tyrosine kinase Lyn as a consequence of ara-C-treatment.	Cytarabine	117-122	cyclin dependent kinase 2	Homo sapiens	34-38
8822910-5	1996	The ara-C-induced protease activity was sensitive to overexpression of the anti-apoptotic protein Bcl-xL and the baculovirus protein p35.	Cytarabine	4-9	BCL2 like 1	Homo sapiens	98-104
8822910-5	1996	The ara-C-induced protease activity was sensitive to overexpression of the anti-apoptotic protein Bcl-xL and the baculovirus protein p35.	Cytarabine	4-9	interleukin 12A	Homo sapiens	133-136
8822910-8	1996	The results further show that ara-C induces activation of the CPP32 protease by a CrmA-insensitive and p35-sensitive mechanism.	Cytarabine	30-35	caspase 3	Homo sapiens	62-67
8822910-8	1996	The results further show that ara-C induces activation of the CPP32 protease by a CrmA-insensitive and p35-sensitive mechanism.	Cytarabine	30-35	interleukin 12A	Homo sapiens	103-106
8822910-10	1996	These findings indicate that ara-C and other DNA-damaging agents activate a CrmA-insensitive apoptotic pathway involving CPP32 and that these signals differ from those associated with apoptosis induced by the Fas receptor.	Cytarabine	29-34	caspase 3	Homo sapiens	121-126
8913519-1	1996	Deoxycytidine kinase (dCK) is a rate-limiting enzyme for the activation of ara-C.	Cytarabine	75-80	deoxycytidine kinase	Mus musculus	0-20
8913519-1	1996	Deoxycytidine kinase (dCK) is a rate-limiting enzyme for the activation of ara-C.	Cytarabine	75-80	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	22-25
8798604-3	1996	Here we show that diverse classes of DNA-damaging agents such as cisplatinum, 1-beta-D-arabinofuranosylcytosine, UV light, ionizing radiation, and methyl methanesulfonate activate p38 MAP kinase.	Cytarabine	78-111	mitogen-activated protein kinase 14	Homo sapiens	180-183
8798604-4	1996	We also demonstrate that cells deficient in c-Abl fail to activate p38 MAP kinase after treatment with cisplatinum and 1-beta-D-arabinofuranosylcytosine but not after exposure to UV and methyl methanesulfonate.	Cytarabine	119-152	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-49
8822910-0	1996	Activation of the CPP32 protease in apoptosis induced by 1-beta-D-arabinofuranosylcytosine and other DNA-damaging agents.	Cytarabine	57-90	caspase 3	Homo sapiens	18-23
8822910-2	1996	Ara-C induced apoptosis is associated with proteolytic cleavage of poly(ADP-ribose) polymerase (PARP) and protein kinase C (PKC) delta.	Cytarabine	0-5	poly(ADP-ribose) polymerase 1	Homo sapiens	67-94
8822910-2	1996	Ara-C induced apoptosis is associated with proteolytic cleavage of poly(ADP-ribose) polymerase (PARP) and protein kinase C (PKC) delta.	Cytarabine	0-5	poly(ADP-ribose) polymerase 1	Homo sapiens	96-100
8822910-2	1996	Ara-C induced apoptosis is associated with proteolytic cleavage of poly(ADP-ribose) polymerase (PARP) and protein kinase C (PKC) delta.	Cytarabine	0-5	protein kinase C delta	Homo sapiens	106-134
8822910-4	1996	The present studies show that ara-C treatment of U-937 cells is associated with induction of a protease activity that cleaves the tetrapeptides Ac-DEVD-pNA and Ac-DMOD-pNA found at the cleavage sites of PARP and PKC delta, respectively.	Cytarabine	30-35	poly(ADP-ribose) polymerase 1	Homo sapiens	203-207
8822910-4	1996	The present studies show that ara-C treatment of U-937 cells is associated with induction of a protease activity that cleaves the tetrapeptides Ac-DEVD-pNA and Ac-DMOD-pNA found at the cleavage sites of PARP and PKC delta, respectively.	Cytarabine	30-35	protein kinase C delta	Homo sapiens	212-221
8806683-0	1996	Interaction of cyclin-dependent kinase 2 and the Lyn tyrosine kinase in cells treated with 1-beta-D-arabinofuranosylcytosine.	Cytarabine	91-124	cyclin dependent kinase 2	Homo sapiens	15-40
8806683-0	1996	Interaction of cyclin-dependent kinase 2 and the Lyn tyrosine kinase in cells treated with 1-beta-D-arabinofuranosylcytosine.	Cytarabine	91-124	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	49-52
8806683-3	1996	The present studies demonstrate that treatment of U-937 cells with 1-beta-D-arabinofuranosylcytosine (ara-C) is associated with tyrosine phosphorylation of Cdk2 and inhibition of Cdk2 activity.	Cytarabine	67-100	cyclin dependent kinase 2	Homo sapiens	156-160
8806683-3	1996	The present studies demonstrate that treatment of U-937 cells with 1-beta-D-arabinofuranosylcytosine (ara-C) is associated with tyrosine phosphorylation of Cdk2 and inhibition of Cdk2 activity.	Cytarabine	67-100	cyclin dependent kinase 2	Homo sapiens	179-183
8806683-3	1996	The present studies demonstrate that treatment of U-937 cells with 1-beta-D-arabinofuranosylcytosine (ara-C) is associated with tyrosine phosphorylation of Cdk2 and inhibition of Cdk2 activity.	Cytarabine	102-107	cyclin dependent kinase 2	Homo sapiens	156-160
8806683-3	1996	The present studies demonstrate that treatment of U-937 cells with 1-beta-D-arabinofuranosylcytosine (ara-C) is associated with tyrosine phosphorylation of Cdk2 and inhibition of Cdk2 activity.	Cytarabine	102-107	cyclin dependent kinase 2	Homo sapiens	179-183
8806683-4	1996	The results also demonstrate that Cdk2 directly associates with the Src-like tyrosine kinase Lyn as a consequence of ara-C-treatment.	Cytarabine	117-122	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	93-96
8806683-8	1996	These findings suggest that the association of Lyn and Cdk2 in ara-C-treated cells may contribute to regulation of Cdk2-dependent cell cycle checkpoints.	Cytarabine	63-68	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	47-50
8806683-8	1996	These findings suggest that the association of Lyn and Cdk2 in ara-C-treated cells may contribute to regulation of Cdk2-dependent cell cycle checkpoints.	Cytarabine	63-68	cyclin dependent kinase 2	Homo sapiens	55-59
8806683-8	1996	These findings suggest that the association of Lyn and Cdk2 in ara-C-treated cells may contribute to regulation of Cdk2-dependent cell cycle checkpoints.	Cytarabine	63-68	cyclin dependent kinase 2	Homo sapiens	115-119
8826891-2	1996	The sensitivity of AML blasts to drugs such as Ara-C can be increased by the down-regulation of bcl-2 expression by antisense oligonucleotides.	Cytarabine	47-52	BCL2 apoptosis regulator	Homo sapiens	96-101
9816330-2	1996	The purpose of the present study was to explore and identify effective combinations of B43-PAP with standard chemotherapeutic drugs, including the anthracyclin doxorubicin, the epipodophyllotoxin etoposide, the nitrosurea carmustine, and the antimetabolite cytosine arabinoside.	Cytarabine	257-277	poly(A) polymerase alpha	Homo sapiens	91-94
8894252-0	1996	Resistance to cytosine arabinoside by retrovirally mediated gene transfer of human cytidine deaminase into murine fibroblast and hematopoietic cells.	Cytarabine	14-34	cytidine deaminase	Homo sapiens	83-101
8894252-3	1996	The deamination of ARA-C by cytidine deaminase results in a loss of its antineoplastic activity.	Cytarabine	19-24	cytidine deaminase	Homo sapiens	28-46
8894252-4	1996	The objective of this study was to determine if gene transfer of human cytidine deaminase into murine fibroblast and hematopoietic cells would confer drug resistance to ARA-C.	Cytarabine	169-174	cytidine deaminase	Homo sapiens	71-89
8894252-7	1996	The transfer of the human cytidine deaminase gene into murine bone marrow cells by the retroviral vector conferred a high level of drug resistance to ARA-C in clonogenic assays.	Cytarabine	150-155	cytidine deaminase	Homo sapiens	26-44
8894252-8	1996	These studies indicate that the cytidine deaminase gene could be used in cancer gene therapy by protecting normal hematopoietic cells against the cytotoxic effects of ARA-C and related cytosine nucleoside analogues.	Cytarabine	167-172	cytidine deaminase	Homo sapiens	32-50
8862446-0	1996	Forced expression of cytidine deaminase confers resistance to cytosine arabinoside and gemcitabine.	Cytarabine	62-82	cytidine deaminase	Homo sapiens	21-39
8862446-3	1996	Studies were performed to determine whether forced expression of a gene encoding the enzyme cytidine deaminase can confer resistance to cytosine arabinoside (Ara-C) and gemcitabine in vitro.	Cytarabine	136-156	cytidine deaminase	Homo sapiens	92-110
8862446-3	1996	Studies were performed to determine whether forced expression of a gene encoding the enzyme cytidine deaminase can confer resistance to cytosine arabinoside (Ara-C) and gemcitabine in vitro.	Cytarabine	158-163	cytidine deaminase	Homo sapiens	92-110
8862446-4	1996	A pooled population of NIH3T3 cells overexpressing cytidine deaminase from a retroviral construct based on the LXSN-vector (LCDSN) demonstrated a 4.5-fold increased resistance to Ara-C based on the 50% inhibitory concentration (ID50) and a 3.7-fold increased resistance to Ara-C based on the 80% inhibitory concentration (ID80) relative to cells transduced with a control vector.	Cytarabine	179-184	cytidine deaminase	Mus musculus	51-69
8862446-4	1996	A pooled population of NIH3T3 cells overexpressing cytidine deaminase from a retroviral construct based on the LXSN-vector (LCDSN) demonstrated a 4.5-fold increased resistance to Ara-C based on the 50% inhibitory concentration (ID50) and a 3.7-fold increased resistance to Ara-C based on the 80% inhibitory concentration (ID80) relative to cells transduced with a control vector.	Cytarabine	273-278	cytidine deaminase	Mus musculus	51-69
8862446-7	1996	Furthermore, Ara-C-resistance could be completely reversed in LCDSN-transduced CEM cells by a specific inhibitor of cytidine deaminase, tetrahydrouridine (THU).	Cytarabine	13-18	cytidine deaminase	Homo sapiens	116-134
8862446-9	1996	These results provide the first direct evidence that forced expression of cytidine deaminase confers cellular resistance to Ara-C and gemcitabine.	Cytarabine	124-129	cytidine deaminase	Homo sapiens	74-92
8947585-4	1996	IL-11 in combination with IL-3 and GM-CSF markedly increased CFU-C colony growth pre- and post-ARA-C or Eilatin incubation from CML and normal individual bone marrow (BM) cells.	Cytarabine	95-100	interleukin 11	Homo sapiens	0-5
8947585-4	1996	IL-11 in combination with IL-3 and GM-CSF markedly increased CFU-C colony growth pre- and post-ARA-C or Eilatin incubation from CML and normal individual bone marrow (BM) cells.	Cytarabine	95-100	interleukin 3	Homo sapiens	26-30
8947585-4	1996	IL-11 in combination with IL-3 and GM-CSF markedly increased CFU-C colony growth pre- and post-ARA-C or Eilatin incubation from CML and normal individual bone marrow (BM) cells.	Cytarabine	95-100	colony stimulating factor 2	Homo sapiens	35-41
8947585-6	1996	A decrease in BCR/ABL fusion product was observed (by FISH analysis) after incubation of BM cells from CML patients in liquid culture for 7 days with 10(-9) M ARA-C or 10(-7) M Eilatin in the presence of IL-11 alone or in combination with other cytokines.	Cytarabine	159-164	interleukin 11	Homo sapiens	204-209
11862291-4	1996	After IL-3 treatment, ara-C incorporation into the DNA was increased to 1.33 to 1.83-fold (median, 1.73-fold).	Cytarabine	22-27	interleukin 3	Homo sapiens	6-10
11862291-6	1996	These results indicate that IL-3 pretreatment increases the level of deoxycytidine kinase mRNA and ara-C incorporation into the DNA and also increases ratios of G0/G1 late-phase and S-phase subsequent to an enhancement of ara-C cytotoxicity against leukemia cells.	Cytarabine	99-104	interleukin 3	Homo sapiens	28-32
11862291-1	1996	Pretreatment of IL-3 to Kasumi-1 human acute myeloid leukemia cells enhanced 1-B-D-arabinofuranosyl cytosine (ara-C) cytotoxicity 1.2. to 1.4-fold (median 1.3).	Cytarabine	110-115	interleukin 3	Homo sapiens	16-20
11862291-2	1996	To clarify the mechanism of interleukin-3 (IL-3) on ara-C cytotoxicity, we investigated the level of deoxycytidine kinase mRNA with the competitive polymerase chain reaction method and enzyme activities, the incorporation of [(3)H] ara-C into DNA and intracellular ara-cytidine triphosphate (CTP) levels with high-performance liquid chromatography and analyzed cell cycles.	Cytarabine	52-57	interleukin 3	Homo sapiens	28-41
11862291-6	1996	These results indicate that IL-3 pretreatment increases the level of deoxycytidine kinase mRNA and ara-C incorporation into the DNA and also increases ratios of G0/G1 late-phase and S-phase subsequent to an enhancement of ara-C cytotoxicity against leukemia cells.	Cytarabine	222-227	interleukin 3	Homo sapiens	28-32
11862291-2	1996	To clarify the mechanism of interleukin-3 (IL-3) on ara-C cytotoxicity, we investigated the level of deoxycytidine kinase mRNA with the competitive polymerase chain reaction method and enzyme activities, the incorporation of [(3)H] ara-C into DNA and intracellular ara-cytidine triphosphate (CTP) levels with high-performance liquid chromatography and analyzed cell cycles.	Cytarabine	52-57	interleukin 3	Homo sapiens	43-47
8864449-7	1996	Our data suggest that the combined use of Campath 1G and anti-LFA1 was associated with an increased risk of developing BLPD, particularly children who had received a T cell-depleted BM graft, using albumen density gradient sedimentation followed by E-rosetting, and who were conditioned with Ara-C, CY and TBL.	Cytarabine	292-297	integrin subunit alpha L	Homo sapiens	62-66
8683994-13	1996	These studies complement previous work showing how regulators of AML growth affect the sensitivity of blast cells to Ara-C by changing the concentration or stability of bcl-2 protein.	Cytarabine	117-122	BCL2 apoptosis regulator	Homo sapiens	169-174
8856092-0	1996	Quantitation of resistance to cytosine arabinoside by myeloid leukemic cells expressing bcl-2.	Cytarabine	30-50	BCL2 apoptosis regulator	Homo sapiens	88-93
8856092-2	1996	The present study focuses on the quantitation of resistance to increasing doses of 1-beta-d-arabinofuranosylcytosine (Ara-C) by using hematological tumors expressing different levels of bcl-2.	Cytarabine	83-116	BCL2 apoptosis regulator	Homo sapiens	186-191
8856092-2	1996	The present study focuses on the quantitation of resistance to increasing doses of 1-beta-d-arabinofuranosylcytosine (Ara-C) by using hematological tumors expressing different levels of bcl-2.	Cytarabine	118-123	BCL2 apoptosis regulator	Homo sapiens	186-191
8856092-7	1996	Upregulation of bcl-2 by myeloid leukemic cells increased the resistance by 3 logs to Ara-C when comparing LD50 values from clonogenic assays, and decreased apoptosis by at least 3 logs when measuring dUTP positive cells by flow cytometry.	Cytarabine	86-91	BCL2 apoptosis regulator	Homo sapiens	16-21
8713072-6	1996	A variety of anti-viral and anti-cancer nucleoside drugs inhibited cNT1rat-mediated uptake of uridine by transfected COS-1 cells although to different extents (Floxidine &gt; Idoxuridine &gt; Zidovudine &gt; Zalcitabine &gt; Cytarabine &gt; Gemcitabine), suggesting that the concentrative pyrimidine-selective nucleoside transporters, of which cNT1rat is a representative, may play a role in cellular uptake of these drugs.	Cytarabine	225-235	solute carrier family 28 member 1	Rattus norvegicus	67-71
8656697-9	1996	Additionally, in refractory and late-relapsed P-gp--overexpressing AML patients treated with intermediate-dose ara-C plus amsacrine the predictive values for nonresponse were 44 and 39%, respectively, significantly (P &lt; 0.05) lower as compared to AML-6 protocol-treated refractory or late-relapsed AML patients.	Cytarabine	111-116	ATP binding cassette subfamily B member 1	Homo sapiens	46-50
8819077-0	1996	Heterogeneous effects of G-CSF and GM-CSF on cell growth and ara-C cytotoxicity in childhood leukemias which express myeloid markers.	Cytarabine	61-66	colony stimulating factor 3	Homo sapiens	25-30
8682180-6	1996	When cell proliferation was blocked by cytosine arabinoside, the beneficial effects of IGF-I and bFGF were abolished, suggesting that effects of the growth factors were mediated, at least in part, by factors associated with glia.	Cytarabine	39-59	insulin like growth factor 1	Homo sapiens	87-92
8682180-6	1996	When cell proliferation was blocked by cytosine arabinoside, the beneficial effects of IGF-I and bFGF were abolished, suggesting that effects of the growth factors were mediated, at least in part, by factors associated with glia.	Cytarabine	39-59	fibroblast growth factor 2	Homo sapiens	97-101
8819077-0	1996	Heterogeneous effects of G-CSF and GM-CSF on cell growth and ara-C cytotoxicity in childhood leukemias which express myeloid markers.	Cytarabine	61-66	colony stimulating factor 2	Homo sapiens	35-41
8926690-6	1996	As a pilot protocol intensification of treatment by idarubicine and cytarabine is scheduled one year after diagnosis for those patients not undergoing BMT and exhibiting after IFN treatment less than partial response.	Cytarabine	68-78	interferon alpha 1	Homo sapiens	176-179
8819077-7	1996	These results indicate the heterogeneous effects of G-CSF and GM-CSF on cell growth and ara-C sensitivity in childhood leukemia cells.	Cytarabine	88-93	colony stimulating factor 3	Homo sapiens	52-57
8819077-7	1996	These results indicate the heterogeneous effects of G-CSF and GM-CSF on cell growth and ara-C sensitivity in childhood leukemia cells.	Cytarabine	88-93	colony stimulating factor 2	Homo sapiens	62-68
8625309-6	1996	As a result of dCK expression, MCF-7 cells demonstrated a 2.5-fold increase in drug sensitivity to 1-beta-D-arabinofuranosylcytosine (AraC) and 2-chloro-2"-deoxyadenosine (CdA).	Cytarabine	99-132	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	15-18
8779771-2	1996	A serine protease inhibitor TPCK and an ICE-like protease inhibitor VAD-FMK prevented etoposide, camptothecin and ara-C-induced internucleosomal DNA cleavage.	Cytarabine	114-119	coagulation factor II, thrombin	Homo sapiens	2-17
8741673-3	1996	A serine protease inhibitor TPCK and an ICE-like protease inhibitor VAD-FMK prevented etoposide, camptothecin and ara-C-induced internucleosomal DNA cleavage in human myeloid leukemia HL-60 and U937 cells.	Cytarabine	114-119	coagulation factor II, thrombin	Homo sapiens	2-17
8683901-0	1996	CD7 positive acute lymphoblastic leukemia successfully treated with high dose cytosine arabinoside and mitoxantrone: a case report.	Cytarabine	78-98	CD7 molecule	Homo sapiens	0-3
8683901-6	1996	Combination chemotherapy with high dose Ara-C and mitoxantrone may be of benefit for refractory ALL with both CD7 and myeloid antigens.	Cytarabine	40-45	CD7 molecule	Homo sapiens	110-113
8625309-6	1996	As a result of dCK expression, MCF-7 cells demonstrated a 2.5-fold increase in drug sensitivity to 1-beta-D-arabinofuranosylcytosine (AraC) and 2-chloro-2"-deoxyadenosine (CdA).	Cytarabine	134-138	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	15-18
8641405-9	1996	In conclusion, FLAG is an active and tolerable combination in refractory ALL, particularly in cases with myeloid antigen expression where G-CSF appears to improve efficacy, probably increasing ara-C incorporation into the DNA of leukemic cells.	Cytarabine	193-198	colony stimulating factor 3	Homo sapiens	138-143
8791999-0	1996	Transfection of murine fibroblast cells with human cytidine deaminase cDNA confers resistance to cytosine arabinoside.	Cytarabine	97-117	cytidine deaminase	Homo sapiens	51-69
8791999-8	1996	The ability to confer drug resistance to Ara-C through gene transfer of cytidine deaminase may have the potential as a selectable marker and for the protection of the bone marrow from the toxicity produced by this analog so as to increase its effectiveness in cancer chemotherapy.	Cytarabine	41-46	cytidine deaminase	Mus musculus	72-90
8732670-9	1996	However, a significantly lower percentage of TAM67-expressing cells exposed to submicromolar concentrations of ara-C exhibited features associated with a differentiated monocytoid phenotype (i.e., increased plastic adherence and CD11b expression) compared to their parental counterparts.	Cytarabine	111-116	integrin subunit alpha M	Homo sapiens	229-234
8732670-10	1996	Lower concentrations of ara-C were also significantly less effective in decreasing the percentage of S-phase cells and in down-regulating c-myc mRNA levels in the mutant line, events associated with induction of leukemic cell differentiation.	Cytarabine	24-29	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	138-143
8732670-11	1996	Finally, ara-C-induced up-regulation of c-jun message and protein was markedly attenuated in TAM67-expressing cells, findings consistent with a c-jun dominant-negative model.	Cytarabine	9-14	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	40-45
8732670-11	1996	Finally, ara-C-induced up-regulation of c-jun message and protein was markedly attenuated in TAM67-expressing cells, findings consistent with a c-jun dominant-negative model.	Cytarabine	9-14	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	144-149
8616717-0	1996	Viral vector transduction of the human deoxycytidine kinase cDNA sensitizes glioma cells to the cytotoxic effects of cytosine arabinoside in vitro and in vivo.	Cytarabine	117-137	deoxycytidine kinase	Homo sapiens	39-59
8732670-12	1996	Collectively, these findings suggest that dysregulation of c-jun in U937 cells antagonizes low-dose ara-C-mediated cellular maturation but does not prevent higher concentration of this agent from triggering apoptosis.	Cytarabine	100-105	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	59-64
8683977-0	1996	Treatment of high risk myelodysplastic syndromes with idarubicin and cytosine arabinoside supported by granulocyte-macrophage colony-stimulating factor. (GM-CSF).	Cytarabine	69-89	colony stimulating factor 2	Homo sapiens	154-160
8616717-3	1996	The rate-limiting step in intracellular ara-C activation is phosphorylation of the prodrug by deoxycytidine kinase (dCK).	Cytarabine	40-45	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	116-119
8616717-4	1996	The present results demonstrate that both retroviral and adenoviral vector-mediated transduction of the dCK cDNA results in marked sensitization of glioma cells lines to the cytotoxic effects of ara-C in vitro.	Cytarabine	195-200	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	104-107
8616717-5	1996	We also demonstrate that ara-C treatment of established intradermal and intracerebral gliomas transduced with dCK results in significant antitumor effects in vivo.	Cytarabine	25-30	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	110-113
8616717-3	1996	The rate-limiting step in intracellular ara-C activation is phosphorylation of the prodrug by deoxycytidine kinase (dCK).	Cytarabine	40-45	deoxycytidine kinase	Homo sapiens	94-114
9816215-8	1996	Combination of F-ara-A with 1.0 and 3.0 microM ara-C also increased the incorporation of ara-CTP into DNA.	Cytarabine	47-52	solute carrier family 25 member 1	Homo sapiens	93-96
8605357-8	1996	These in vitro studies support our hypothesis that enhanced metabolism of ara-C in DS cells may be a contributing factor to the superior survival rate of DS children with AML and is possibly based on a gene dosage effect of genes localized to chromosome 21 including cystathionine-beta-synthase.	Cytarabine	74-79	cystathionine beta-synthase	Homo sapiens	267-294
8642855-9	1996	Response to Ara-C by growth factor responsive blast cells is influenced by the factor in the cultures; cells are more sensitive in cultures with G-CSF and less sensitive when GM-CSF is present.	Cytarabine	12-17	colony stimulating factor 3	Homo sapiens	145-150
8641389-3	1996	Like cytosine arabinoside (AraC), F1 and 2-CdA gain access to the cell via a specific nucleoside transporter (NST) protein.	Cytarabine	5-25	cytidine deaminase	Homo sapiens	43-46
8618470-4	1996	Nucleoside analogs such as chlorodeoxyadenosine (2-CdA) or fludarabine have shown single-agent efficacy and may be synergistic with ara-C.	Cytarabine	132-137	cytidine deaminase	Homo sapiens	51-54
8634449-2	1996	The present studies in ara-C-treated U-937 cells extend these findings by demonstrating activation of a protein kinase that phosphorylates myelin basic protein (MBP).	Cytarabine	23-28	myelin basic protein	Homo sapiens	139-159
8634449-2	1996	The present studies in ara-C-treated U-937 cells extend these findings by demonstrating activation of a protein kinase that phosphorylates myelin basic protein (MBP).	Cytarabine	23-28	myelin basic protein	Homo sapiens	161-164
8634449-7	1996	These findings support proteolytic activation of PKCdelta in the cellular response to ara-C and other DNA-damaging agents.	Cytarabine	86-91	protein kinase C delta	Homo sapiens	49-57
8613443-10	1996	Dose survival studies with use of a tetrazolium colorimetric assay showed that the MOS/ADR1 cells were cross-resistant to vincristine, vinblastine, etoposide, bleomycin, mitomycin C, and actinomycin D but not to dacarbazine, cisplatin, carboplatin, cytosine arabinoside, carmustine, cyclophosphamide, ifosfamide, methotrexate, and 5-fluorouracil.	Cytarabine	249-269	Moloney sarcoma oncogene	Mus musculus	83-86
8642855-9	1996	Response to Ara-C by growth factor responsive blast cells is influenced by the factor in the cultures; cells are more sensitive in cultures with G-CSF and less sensitive when GM-CSF is present.	Cytarabine	12-17	colony stimulating factor 2	Homo sapiens	175-181
8742032-0	1996	p53 involves cytosine arabinoside-induced apoptosis in cultured cerebellar granule neurons.	Cytarabine	13-33	transformation related protein 53, pseudogene	Mus musculus	0-3
8742366-5	1996	The present results are in line with the previous results of a negative interaction between IFN-alpha and cytarabine both in vitro in K562 human leukemia and in vivo in L1210 murine leukemia, and a synergistic cytostatic interaction between IFN-alpha and carboplatin in K562 cells.	Cytarabine	106-116	interferon alpha 1	Homo sapiens	92-101
8742366-5	1996	The present results are in line with the previous results of a negative interaction between IFN-alpha and cytarabine both in vitro in K562 human leukemia and in vivo in L1210 murine leukemia, and a synergistic cytostatic interaction between IFN-alpha and carboplatin in K562 cells.	Cytarabine	106-116	interferon alpha	Mus musculus	241-250
8742366-8	1996	On the other hand, given the negative interaction between IFN-alpha and cytarabine observed in myeloid leukemia cells, together with the inferior cytogenetic responses observed in CML patients treated with the combination of IFN-alpha and cytarabine, caution should be exercised against the continuous clinical use of the combination of IFN-alpha and cytarabine in treating CML patients.	Cytarabine	239-249	interferon alpha 1	Homo sapiens	58-67
8742366-8	1996	On the other hand, given the negative interaction between IFN-alpha and cytarabine observed in myeloid leukemia cells, together with the inferior cytogenetic responses observed in CML patients treated with the combination of IFN-alpha and cytarabine, caution should be exercised against the continuous clinical use of the combination of IFN-alpha and cytarabine in treating CML patients.	Cytarabine	239-249	interferon alpha 1	Homo sapiens	58-67
8742032-5	1996	These results indicate that p53 involves Ara C-induced apoptosis in cultured cerebellar granule neurons, in which DNA damage may initiate the apoptotic death program of the neurons.	Cytarabine	41-46	transformation related protein 53, pseudogene	Mus musculus	28-31
8599980-9	1996	G-CSF significantly enhanced the cytotoxic effect of daunorubicin, mitoxantrone, etoposide and Ara-C by 20-40%, which GM-CSF and IL-3 showed a significantly increased toxicity for Ara-C only.	Cytarabine	95-100	colony stimulating factor 3	Homo sapiens	0-5
9082756-2	1996	Deoxycytidine kinase (dCK) is one of the most important target enzymes for anti-proliferative drugs such as arabinosile-cytosine (ara-C), 2-Cl-deoxyadenosine (CdA).	Cytarabine	130-135	deoxycytidine kinase	Homo sapiens	0-20
9082756-2	1996	Deoxycytidine kinase (dCK) is one of the most important target enzymes for anti-proliferative drugs such as arabinosile-cytosine (ara-C), 2-Cl-deoxyadenosine (CdA).	Cytarabine	130-135	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	22-25
8547650-1	1996	The effectiveness of arabinosylcytosine (ara-C) for the treatment of acute myelogenous leukemia (AML) depends on the formation of its active metabolite, the triphosphate of ara-C (ara-CTP).	Cytarabine	21-39	solute carrier family 25 member 1	Homo sapiens	184-187
8547650-1	1996	The effectiveness of arabinosylcytosine (ara-C) for the treatment of acute myelogenous leukemia (AML) depends on the formation of its active metabolite, the triphosphate of ara-C (ara-CTP).	Cytarabine	41-46	solute carrier family 25 member 1	Homo sapiens	184-187
8547650-1	1996	The effectiveness of arabinosylcytosine (ara-C) for the treatment of acute myelogenous leukemia (AML) depends on the formation of its active metabolite, the triphosphate of ara-C (ara-CTP).	Cytarabine	173-178	solute carrier family 25 member 1	Homo sapiens	184-187
8547650-7	1996	To complement these studies, molecular actions of the triphosphate of ara-C and CdA on DNA extension by human DNA polymerase alpha in an in vitro model system was conducted.	Cytarabine	70-75	DNA polymerase alpha 1, catalytic subunit	Homo sapiens	110-130
8599980-9	1996	G-CSF significantly enhanced the cytotoxic effect of daunorubicin, mitoxantrone, etoposide and Ara-C by 20-40%, which GM-CSF and IL-3 showed a significantly increased toxicity for Ara-C only.	Cytarabine	95-100	colony stimulating factor 2	Homo sapiens	118-124
8599980-9	1996	G-CSF significantly enhanced the cytotoxic effect of daunorubicin, mitoxantrone, etoposide and Ara-C by 20-40%, which GM-CSF and IL-3 showed a significantly increased toxicity for Ara-C only.	Cytarabine	95-100	interleukin 3	Homo sapiens	129-133
8599980-9	1996	G-CSF significantly enhanced the cytotoxic effect of daunorubicin, mitoxantrone, etoposide and Ara-C by 20-40%, which GM-CSF and IL-3 showed a significantly increased toxicity for Ara-C only.	Cytarabine	180-185	colony stimulating factor 3	Homo sapiens	0-5
8599980-9	1996	G-CSF significantly enhanced the cytotoxic effect of daunorubicin, mitoxantrone, etoposide and Ara-C by 20-40%, which GM-CSF and IL-3 showed a significantly increased toxicity for Ara-C only.	Cytarabine	180-185	colony stimulating factor 2	Homo sapiens	118-124
8599980-9	1996	G-CSF significantly enhanced the cytotoxic effect of daunorubicin, mitoxantrone, etoposide and Ara-C by 20-40%, which GM-CSF and IL-3 showed a significantly increased toxicity for Ara-C only.	Cytarabine	180-185	interleukin 3	Homo sapiens	129-133
8530447-0	1995	c-Abl activation regulates induction of the SEK1/stress-activated protein kinase pathway in the cellular response to 1-beta-D-arabinofuranosylcytosine.	Cytarabine	117-150	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-5
8996546-3	1996	The stimulation of AraC-induced apoptosis by PKC selective inhibitor CGP 412251 and PTK-inhibitor genistein was approximately equal to that of staurosporine in HL-60/ADR cell line.	Cytarabine	19-23	protein tyrosine kinase 2 beta	Homo sapiens	84-87
8996546-3	1996	The stimulation of AraC-induced apoptosis by PKC selective inhibitor CGP 412251 and PTK-inhibitor genistein was approximately equal to that of staurosporine in HL-60/ADR cell line.	Cytarabine	19-23	aldo-keto reductase family 1 member B	Homo sapiens	166-169
8996546-4	1996	In both parental drug sensitive HL-60 cells and Pgp/p170 positive (MDR1) HL-60/VCR, staurosporine-stimulated AraC-induced apoptosis was higher than that stimulated by the PKC selective CGP 41251 inhibitor, or PTK-inhibitor genistein.	Cytarabine	109-113	phosphoglycolate phosphatase	Homo sapiens	48-51
8996546-4	1996	In both parental drug sensitive HL-60 cells and Pgp/p170 positive (MDR1) HL-60/VCR, staurosporine-stimulated AraC-induced apoptosis was higher than that stimulated by the PKC selective CGP 41251 inhibitor, or PTK-inhibitor genistein.	Cytarabine	109-113	ATP binding cassette subfamily B member 1	Homo sapiens	67-71
8996546-4	1996	In both parental drug sensitive HL-60 cells and Pgp/p170 positive (MDR1) HL-60/VCR, staurosporine-stimulated AraC-induced apoptosis was higher than that stimulated by the PKC selective CGP 41251 inhibitor, or PTK-inhibitor genistein.	Cytarabine	109-113	protein tyrosine kinase 2 beta	Homo sapiens	209-212
8996546-5	1996	These data suggest that the molecular pathway(s) for AraC-induced apoptosis can be activated and stimulated by PKC- and PTK-inhibitors in both examined drug-resistant HL-60 cell lines.	Cytarabine	53-57	protein tyrosine kinase 2 beta	Homo sapiens	120-123
9275711-9	1996	It is suggested that the histamine H2 receptor antagonist Ranit has, to some extent, potential in the treatment of myeloid leukemia, especially when combined with antineoplastic agent Ara-C at suboptimal doses.	Cytarabine	184-189	histamine receptor H2	Homo sapiens	25-46
8530447-0	1995	c-Abl activation regulates induction of the SEK1/stress-activated protein kinase pathway in the cellular response to 1-beta-D-arabinofuranosylcytosine.	Cytarabine	117-150	mitogen-activated protein kinase kinase 4	Homo sapiens	44-48
8530447-1	1995	Previous work has shown that treatment of cells with the antimetabolite 1-beta-D-arabinofuranosylcytosine (ara-C) is associated with induction of the c-jun gene.	Cytarabine	72-105	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	150-155
8530447-1	1995	Previous work has shown that treatment of cells with the antimetabolite 1-beta-D-arabinofuranosylcytosine (ara-C) is associated with induction of the c-jun gene.	Cytarabine	107-112	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	150-155
8530447-2	1995	The present studies demonstrate that ara-C activates the c-Abl non-receptor tyrosine kinase.	Cytarabine	37-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-62
8530447-3	1995	We also demonstrate that activity of the stress-activated protein kinase (SAP kinase/JNK) is increased in ara-C-treated cells.	Cytarabine	106-111	mitogen-activated protein kinase 8	Homo sapiens	85-88
8530447-4	1995	Using cells deficient in c-Abl (Abl-/-) and after introduction of the c-abl gene, we show that ara-C-induced c-Abl activity is necessary for the stimulation of SAP kinase.	Cytarabine	95-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-30
8530447-4	1995	Using cells deficient in c-Abl (Abl-/-) and after introduction of the c-abl gene, we show that ara-C-induced c-Abl activity is necessary for the stimulation of SAP kinase.	Cytarabine	95-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	27-30
8530447-4	1995	Using cells deficient in c-Abl (Abl-/-) and after introduction of the c-abl gene, we show that ara-C-induced c-Abl activity is necessary for the stimulation of SAP kinase.	Cytarabine	95-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-75
8530447-4	1995	Using cells deficient in c-Abl (Abl-/-) and after introduction of the c-abl gene, we show that ara-C-induced c-Abl activity is necessary for the stimulation of SAP kinase.	Cytarabine	95-100	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-114
8530447-5	1995	Other studies using cells transfected with a SEK1 dominant negative demonstrate that ara-C-induced SAP kinase activity is SEK1-dependent.	Cytarabine	85-90	mitogen-activated protein kinase kinase 4	Homo sapiens	45-49
8530447-5	1995	Other studies using cells transfected with a SEK1 dominant negative demonstrate that ara-C-induced SAP kinase activity is SEK1-dependent.	Cytarabine	85-90	mitogen-activated protein kinase kinase 4	Homo sapiens	122-126
8677156-3	1995	Peak total NAG, isoenzyme B and B-2-M excretion was observed on the third day after L-aspa and Ara-C injection.	Cytarabine	95-100	NBAS subunit of NRZ tethering complex	Homo sapiens	11-14
8590845-0	1995	MEC (mitoxantrone, etoposide and intermediate dose cytarabine): an effective induction regimen for previously untreated acute non-lymphocytic leukemia.	Cytarabine	51-61	C-C motif chemokine ligand 28	Homo sapiens	0-3
9019171-1	1995	The cellular response to 1-beta-D-arabinofuranosylcytosine (ara-C) includes activation of Jun/AP-1, induction of c-jun transcription, and programmed cell death.	Cytarabine	25-58	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	94-98
9019171-1	1995	The cellular response to 1-beta-D-arabinofuranosylcytosine (ara-C) includes activation of Jun/AP-1, induction of c-jun transcription, and programmed cell death.	Cytarabine	25-58	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	113-118
9019171-1	1995	The cellular response to 1-beta-D-arabinofuranosylcytosine (ara-C) includes activation of Jun/AP-1, induction of c-jun transcription, and programmed cell death.	Cytarabine	60-65	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	94-98
9019171-1	1995	The cellular response to 1-beta-D-arabinofuranosylcytosine (ara-C) includes activation of Jun/AP-1, induction of c-jun transcription, and programmed cell death.	Cytarabine	60-65	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	113-118
9019171-5	1995	The results demonstrate that ara-C also induces binding of SAP kinase to the SH2/SH3-containing adapter protein Grb2.	Cytarabine	29-34	growth factor receptor bound protein 2	Homo sapiens	112-116
8542929-9	1995	The level of BCR/ABL fusion signals detected after exposure of CD34+ cells for 16 hours to Eilatin 10(-7) M, IFN-alpha 500 U/mL, or Ara-C 10(-9) M were 54.5 +/- 5%, 63.6 +/- 5%, and 70 +/- 4%, respectively (mean +/- SE, n = 5).	Cytarabine	132-137	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20
8717185-2	1995	According to Leo Sachs proposals on the proliferation-differentiation balance impairment in malignancies we have shown various orientation for the differentiation therapy: inhibition of malignant cells using low dose of Cytosine Arabinoside in acute myeloid leukemia; suppression of the growth factor effect such as the role of interferon in hairy cell leukemia; targetted differentiation process by all trans retinoic acid in acute promyelocytic leukemia with the obtention of complete remission in all cases; differentiation of malignant and normal cells by G-CSF in acute myeloid leukemia in elderly patients.	Cytarabine	220-240	colony stimulating factor 3	Homo sapiens	560-565
7475274-8	1995	Taxol and Ara-C mediated apoptosis of CD34+, HLA-DR+ cells, and its inhibition by pIXY321, was not accompanied by any significant alteration in the intracellular p26BCL-2 levels.	Cytarabine	10-15	CD34 molecule	Homo sapiens	38-42
8748457-8	1995	In contrast, a deoxycytidine kinase-deficient cell line that was selected with arabinosylcytosine does not excrete deoxycytidine and contains high deoxycytidine deaminase activity.	Cytarabine	79-97	deoxycytidine kinase	Mus musculus	15-35
7577641-1	1995	Several studies have demonstrated that G-CSF, GM-CSF and, in particular, IL-3 can effectively recruit acute myeloid leukaemia (AML) blasts into the cell cycle, resulting in a significant increase in cytosine-arabinoside (Ara-C) mediated cytotoxicity in vitro.	Cytarabine	199-219	colony stimulating factor 3	Homo sapiens	39-44
7564507-0	1995	Direct evidence for the participation of bcl-2 in the regulation by retinoic acid of the Ara-C sensitivity of leukemic stem cells.	Cytarabine	89-94	BCL2 apoptosis regulator	Homo sapiens	41-46
7564507-6	1995	Lines with sense-oriented transfected bcl-2 were significantly less sensitive to Ara-C or H2O2 than the parental lines; the cells with anti-sense transfected genes were more sensitive than their parent but the difference did not reach statistical significance.	Cytarabine	81-86	BCL2 apoptosis regulator	Homo sapiens	38-43
7564507-10	1995	We conclude that data from the transfectants provides evidence that expression of bcl-2 is a determinant of sensitivity to Ara-C and H2O2; and that the effect of ATRA on sensitivity requires the presence of bcl-2 genes in association with regulatory elements.	Cytarabine	123-128	BCL2 apoptosis regulator	Homo sapiens	82-87
7575543-1	1995	Preexposure of HL-60 cells to a DNA-damaging agent, cytosine arabinoside (Ara-C), dramatically induced the levels of H1 kinase activities associated with cyclin E (CycE-H1K) but not cyclin A.	Cytarabine	74-79	cyclin A2	Homo sapiens	182-190
7671248-8	1995	In contrast to hydroxyurea, inhibition of DNA synthesis by 1-beta-D-arabinofuranosylcytosine produced a decrease in transferrin receptor expression.	Cytarabine	59-92	transferrin	Homo sapiens	116-127
8535214-3	1995	We used Western blotting (WB) to measure the level of expression of PCNA in peripheral blasts of 36 adult acute myelogenous leukemia (AML) patients treated with Ara-C based induction regimens.	Cytarabine	161-166	proliferating cell nuclear antigen	Homo sapiens	68-72
8535214-7	1995	We conclude that PCNA levels in this disease may be important for predicting response to Ara-C based remission induction chemotherapy.	Cytarabine	89-94	proliferating cell nuclear antigen	Homo sapiens	17-21
7577641-1	1995	Several studies have demonstrated that G-CSF, GM-CSF and, in particular, IL-3 can effectively recruit acute myeloid leukaemia (AML) blasts into the cell cycle, resulting in a significant increase in cytosine-arabinoside (Ara-C) mediated cytotoxicity in vitro.	Cytarabine	199-219	colony stimulating factor 2	Homo sapiens	46-52
7577641-1	1995	Several studies have demonstrated that G-CSF, GM-CSF and, in particular, IL-3 can effectively recruit acute myeloid leukaemia (AML) blasts into the cell cycle, resulting in a significant increase in cytosine-arabinoside (Ara-C) mediated cytotoxicity in vitro.	Cytarabine	199-219	interleukin 3	Homo sapiens	73-77
7577641-1	1995	Several studies have demonstrated that G-CSF, GM-CSF and, in particular, IL-3 can effectively recruit acute myeloid leukaemia (AML) blasts into the cell cycle, resulting in a significant increase in cytosine-arabinoside (Ara-C) mediated cytotoxicity in vitro.	Cytarabine	221-226	colony stimulating factor 3	Homo sapiens	39-44
7577641-1	1995	Several studies have demonstrated that G-CSF, GM-CSF and, in particular, IL-3 can effectively recruit acute myeloid leukaemia (AML) blasts into the cell cycle, resulting in a significant increase in cytosine-arabinoside (Ara-C) mediated cytotoxicity in vitro.	Cytarabine	221-226	colony stimulating factor 2	Homo sapiens	46-52
7577641-1	1995	Several studies have demonstrated that G-CSF, GM-CSF and, in particular, IL-3 can effectively recruit acute myeloid leukaemia (AML) blasts into the cell cycle, resulting in a significant increase in cytosine-arabinoside (Ara-C) mediated cytotoxicity in vitro.	Cytarabine	221-226	interleukin 3	Homo sapiens	73-77
7577641-5	1995	Normal cells were not recruited, even when rhIL-3 was administered for up to 10 d. In vitro studies showed an increased Ara-C cytotoxicity on clonogenic AML cells, in particular with IL-3 plus GM-CSF, thus confirming the priming effects of IL-3 in the two responding cases.	Cytarabine	120-125	interleukin 3	Homo sapiens	45-49
7577641-5	1995	Normal cells were not recruited, even when rhIL-3 was administered for up to 10 d. In vitro studies showed an increased Ara-C cytotoxicity on clonogenic AML cells, in particular with IL-3 plus GM-CSF, thus confirming the priming effects of IL-3 in the two responding cases.	Cytarabine	120-125	colony stimulating factor 2	Homo sapiens	193-199
7577641-5	1995	Normal cells were not recruited, even when rhIL-3 was administered for up to 10 d. In vitro studies showed an increased Ara-C cytotoxicity on clonogenic AML cells, in particular with IL-3 plus GM-CSF, thus confirming the priming effects of IL-3 in the two responding cases.	Cytarabine	120-125	interleukin 3	Homo sapiens	183-187
7543292-0	1995	In vitro-induced resistance to the deoxycytidine analogues cytarabine (AraC) and 5-aza-2"-deoxycytidine (DAC) in a rat model for acute myeloid leukemia is mediated by mutations in the deoxycytidine kinase (dck) gene.	Cytarabine	59-69	deoxycytidine kinase	Rattus norvegicus	184-204
7672091-8	1995	Suppression of secondary Ph" positive clones which appeared during the previous IFN-alpha treatment was documented in 3 accelerated phase patients after ARA-C was added to their IFN-alpha treatment.	Cytarabine	153-158	interferon alpha 1	Homo sapiens	80-89
7564475-0	1995	Augmentation by aphidicolin of 1-beta-D-arabinofuranosylcytosine-induced c-jun and NF-kappa B activation in a human myeloid leukemia cell line: correlation with apoptosis.	Cytarabine	31-64	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	73-78
7564475-0	1995	Augmentation by aphidicolin of 1-beta-D-arabinofuranosylcytosine-induced c-jun and NF-kappa B activation in a human myeloid leukemia cell line: correlation with apoptosis.	Cytarabine	31-64	nuclear factor kappa B subunit 1	Homo sapiens	83-93
7564475-3	1995	Although aphidicolin itself had a marginal effect on c-jun expression, it significantly augmented ara-C induced c-jun upregulation by shortening the lag time and lowering ara-C concentrations necessary for the induction of detectable c-jun transcripts.	Cytarabine	98-103	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	112-117
7564475-3	1995	Although aphidicolin itself had a marginal effect on c-jun expression, it significantly augmented ara-C induced c-jun upregulation by shortening the lag time and lowering ara-C concentrations necessary for the induction of detectable c-jun transcripts.	Cytarabine	98-103	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	112-117
7564475-4	1995	Aphidicolin and ara-C acted synergistically to increase NF-kappa B DNA binding activity as determined by an electrophoretic mobility shift assay.	Cytarabine	16-21	nuclear factor kappa B subunit 1	Homo sapiens	56-66
7564475-6	1995	Thus, the activation of NF-kappa B and c-jun expression seems to be well correlated with the potentiation by aphidicolin of ara-C-induced apoptosis.	Cytarabine	124-129	nuclear factor kappa B subunit 1	Homo sapiens	24-34
7564475-6	1995	Thus, the activation of NF-kappa B and c-jun expression seems to be well correlated with the potentiation by aphidicolin of ara-C-induced apoptosis.	Cytarabine	124-129	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	39-44
7481845-7	1995	Cross-resistance analysis between gemcitabine and the standard drugs revealed the following rank order of correlation coefficients: ara-C &gt; doxorubicin &gt; CdA &gt; cisplatin &gt; VP-16.	Cytarabine	132-137	host cell factor C1	Homo sapiens	184-189
7654012-4	1995	These findings suggest that c-Ha-ras levels may influence therapeutic success in some tumors and may regulate metabolic pathways of drug such as ara-C.	Cytarabine	145-150	transcription factor like 5	Homo sapiens	28-32
7543292-0	1995	In vitro-induced resistance to the deoxycytidine analogues cytarabine (AraC) and 5-aza-2"-deoxycytidine (DAC) in a rat model for acute myeloid leukemia is mediated by mutations in the deoxycytidine kinase (dck) gene.	Cytarabine	59-69	deoxycytidine kinase	Rattus norvegicus	206-209
7543292-1	1995	The deoxycytidine kinase (dck) gene encodes the enzyme responsible for the metabolic activation of the antileukemic drugs cytosine arabinoside (AraC) and 5-aza-2"-deoxycytidine (decitabine, DAC).	Cytarabine	122-142	deoxycytidine kinase	Rattus norvegicus	4-24
7543292-1	1995	The deoxycytidine kinase (dck) gene encodes the enzyme responsible for the metabolic activation of the antileukemic drugs cytosine arabinoside (AraC) and 5-aza-2"-deoxycytidine (decitabine, DAC).	Cytarabine	122-142	deoxycytidine kinase	Rattus norvegicus	26-29
7543292-1	1995	The deoxycytidine kinase (dck) gene encodes the enzyme responsible for the metabolic activation of the antileukemic drugs cytosine arabinoside (AraC) and 5-aza-2"-deoxycytidine (decitabine, DAC).	Cytarabine	144-148	deoxycytidine kinase	Rattus norvegicus	4-24
7543292-1	1995	The deoxycytidine kinase (dck) gene encodes the enzyme responsible for the metabolic activation of the antileukemic drugs cytosine arabinoside (AraC) and 5-aza-2"-deoxycytidine (decitabine, DAC).	Cytarabine	144-148	deoxycytidine kinase	Rattus norvegicus	26-29
7543292-2	1995	The dck locus was analyzed at the chromosomal and the molecular level in a model of rat leukemic cell lines, in which AraC and DAC resistance was induced, that was marked by dck deficiency.	Cytarabine	118-122	deoxycytidine kinase	Rattus norvegicus	4-7
7543292-9	1995	The data demonstrate that exposure to AraC and DAC induces a resistant phenotype marked by functional dck deficiency that may be the consequence of mutations occurring in the dck gene.	Cytarabine	38-42	deoxycytidine kinase	Rattus norvegicus	102-105
7541096-0	1995	De novo induced mutations in the deoxycytidine kinase (dck) gene in rat leukemic clonal cell lines confer resistance to cytarabine (AraC) and 5-aza-2"-deoxycytidine (DAC).	Cytarabine	120-130	deoxycytidine kinase	Rattus norvegicus	33-53
7769668-6	1995	When viral DNA replication was inhibited with cytosine arabinoside, p28 was found in distinct, focal structures that may be precursors to the factories.	Cytarabine	46-66	golgi SNAP receptor complex member 1	Homo sapiens	68-71
7541096-0	1995	De novo induced mutations in the deoxycytidine kinase (dck) gene in rat leukemic clonal cell lines confer resistance to cytarabine (AraC) and 5-aza-2"-deoxycytidine (DAC).	Cytarabine	120-130	deoxycytidine kinase	Rattus norvegicus	55-58
7541096-0	1995	De novo induced mutations in the deoxycytidine kinase (dck) gene in rat leukemic clonal cell lines confer resistance to cytarabine (AraC) and 5-aza-2"-deoxycytidine (DAC).	Cytarabine	132-136	deoxycytidine kinase	Rattus norvegicus	33-53
7541096-0	1995	De novo induced mutations in the deoxycytidine kinase (dck) gene in rat leukemic clonal cell lines confer resistance to cytarabine (AraC) and 5-aza-2"-deoxycytidine (DAC).	Cytarabine	132-136	deoxycytidine kinase	Rattus norvegicus	55-58
7541096-1	1995	We have investigated whether cytarabine (AraC) or decitabine (DAC) induce deficiency of deoxycytidine kinase (DCK) through different mutations of the dck gene, related to their distinct interference with DNA replication.	Cytarabine	29-39	deoxycytidine kinase	Rattus norvegicus	88-108
7541096-1	1995	We have investigated whether cytarabine (AraC) or decitabine (DAC) induce deficiency of deoxycytidine kinase (DCK) through different mutations of the dck gene, related to their distinct interference with DNA replication.	Cytarabine	29-39	deoxycytidine kinase	Rattus norvegicus	110-113
7541096-1	1995	We have investigated whether cytarabine (AraC) or decitabine (DAC) induce deficiency of deoxycytidine kinase (DCK) through different mutations of the dck gene, related to their distinct interference with DNA replication.	Cytarabine	29-39	deoxycytidine kinase	Rattus norvegicus	150-153
7541096-1	1995	We have investigated whether cytarabine (AraC) or decitabine (DAC) induce deficiency of deoxycytidine kinase (DCK) through different mutations of the dck gene, related to their distinct interference with DNA replication.	Cytarabine	41-45	deoxycytidine kinase	Rattus norvegicus	88-108
7541096-1	1995	We have investigated whether cytarabine (AraC) or decitabine (DAC) induce deficiency of deoxycytidine kinase (DCK) through different mutations of the dck gene, related to their distinct interference with DNA replication.	Cytarabine	41-45	deoxycytidine kinase	Rattus norvegicus	110-113
7541096-7	1995	AraC induced both rearrangements and point mutations in the dck gene when administered over 140 days and 180 days, respectively.	Cytarabine	0-4	deoxycytidine kinase	Rattus norvegicus	60-63
7734320-8	1995	These results indicate that, because of the significantly increased stability, the transporter-independent uptake and the dCyd-kinase-independent cytotoxicity, NHAC might be active in ara-C-resistant cells.	Cytarabine	184-189	Cyd	Drosophila melanogaster	122-126
7543952-6	1995	Thus, G-CSF-PE40 may be useful in the selective elimination of myeloid cells expressing G-CSF receptors, especially in combination with chemotherapeutic agents like cytosine arabinoside.	Cytarabine	165-185	colony stimulating factor 3 (granulocyte)	Mus musculus	6-11
7769841-5	1995	The down-regulation could be prevented by exposing the cells to ara-C either before or after ATRA; decrease in bcl-2 protein was moderate and only obvious after 36 h of ATRA treatment.	Cytarabine	64-69	BCL2 apoptosis regulator	Homo sapiens	111-116
9816016-1	1995	Previous reports have demonstrated that a variety of anticancer drugs, e.g., 1-beta-D-arabinofuranosylcytosine (ara-C), mitoxantrone, etoposide, camptothecin, and cisplatin, induce the expression of c-jun oncogene in leukemic cells prior to producing internucleosomal DNA fragmentation and the morphological features of apoptosis.	Cytarabine	77-110	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	199-204
9816016-4	1995	First, exposure of human myeloid leukemia HL-60 cells to high-dose ara-C for 4 h produced internucleosomal DNA fragmentation preceded by c-jun induction.	Cytarabine	67-72	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	137-142
7769841-12	1995	NAC protection against ara-C killing was seen for OCI/AML-1 and 2 cells, but not for OCI/AML-5 cells.	Cytarabine	23-28	RUNX family transcription factor 1	Homo sapiens	50-59
7769841-16	1995	Left unexplained are the action of HC, which does not affect bcl-2 expression and the mechanism by which ara-C prevents down-regulation of bcl-2 by ATRA.	Cytarabine	105-110	BCL2 apoptosis regulator	Homo sapiens	139-144
9815996-3	1995	Since previous reports indicated that either overexpression of Bcl-2 protein following bcl-2 transfection into cells resulted in, or high dCTP pools contributed to, ara-C resistance in experimental cell models, both of these parameters were assessed and found not to contribute to CldAdo resistance in the murine leukemia and human B lymphoblastoid cells.	Cytarabine	165-170	B cell leukemia/lymphoma 2	Mus musculus	63-68
7718595-0	1995	1-beta-D-arabinofuranosylcytosine activates tyrosine phosphorylation of p34cdc2 and its association with the Src-like p56/p53lyn kinase in human myeloid leukemia cells.	Cytarabine	0-33	cyclin dependent kinase 1	Homo sapiens	72-79
7718595-0	1995	1-beta-D-arabinofuranosylcytosine activates tyrosine phosphorylation of p34cdc2 and its association with the Src-like p56/p53lyn kinase in human myeloid leukemia cells.	Cytarabine	0-33	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	122-128
7700081-5	1995	Ara-C caused an increase of SOD to 366%, and of catalase to 235%, while the complete Fenton reaction resulted in SOD increase to 705% and catalase decrease to 38% of the untreated control cultures.	Cytarabine	0-5	superoxide dismutase 1	Homo sapiens	28-31
7532033-0	1995	Transfection of wild-type deoxycytidine kinase (dck) cDNA into an AraC- and DAC-resistant rat leukemic cell line of clonal origin fully restores drug sensitivity.	Cytarabine	66-70	deoxycytidine kinase	Rattus norvegicus	26-46
7532033-0	1995	Transfection of wild-type deoxycytidine kinase (dck) cDNA into an AraC- and DAC-resistant rat leukemic cell line of clonal origin fully restores drug sensitivity.	Cytarabine	66-70	deoxycytidine kinase	Rattus norvegicus	48-51
7532033-1	1995	The AraC-resistant rat leukemic cell line RO/1-A has been shown to have a typical deoxycytidine kinase (DCK)-deficient phenotype and cannot metabolize the antileukemic drugs cytarabine (AraC) and decitabine (DAC).	Cytarabine	4-8	deoxycytidine kinase	Rattus norvegicus	82-102
7532033-1	1995	The AraC-resistant rat leukemic cell line RO/1-A has been shown to have a typical deoxycytidine kinase (DCK)-deficient phenotype and cannot metabolize the antileukemic drugs cytarabine (AraC) and decitabine (DAC).	Cytarabine	4-8	deoxycytidine kinase	Rattus norvegicus	104-107
7532033-5	1995	Initial rate measurements of DCK activity showed that Km values for dck were only slightly altered as a result of transfection, whereas strongly increased Vmax values were observed, resulting in a 12-fold increased phosphorylation efficiency for both dC and AraC, compared with the AraC-sensitive parental cell line RO/1 from which the RO/1-A was originally derived.	Cytarabine	258-262	deoxycytidine kinase	Rattus norvegicus	29-32
7885038-0	1995	GM-CSF and asparaginase potentiate ara-C cytotoxicity in HL-60 cells.	Cytarabine	35-40	colony stimulating factor 2	Homo sapiens	0-6
9815970-14	1995	Based on these data it could be concluded that (a) infusion of G-CSF before fludarabine augmented the rate of F-ara-ATP synthesis in circulating AML blasts during therapy, suggesting that G-CSF may benefit fludarabine therapy by biological modulation; (b) G-CSF did not increase ara-CTP accumulation, rather it may have caused it to decrease; and (c) these data imply that when G-CSF and ara-C are used in combination, administration of fludarabine prior to ara-C may maintain the ara-CTP AUC.	Cytarabine	279-284	colony stimulating factor 3	Homo sapiens	63-68
7885038-0	1995	GM-CSF and asparaginase potentiate ara-C cytotoxicity in HL-60 cells.	Cytarabine	35-40	asparaginase	Homo sapiens	11-23
7885038-8	1995	In addition, ara-C metabolism was assessed during simultaneous exposure to ara-C (10 microM x 3 h) +/- ASNase (10 U/ml the last 2 h) +/- GM-CSF (10 ng/ml beginning 24 h prior to ara-C).	Cytarabine	13-18	asparaginase	Homo sapiens	103-109
7885038-9	1995	Ara-C incorporated into DNA (P = 0.0302) and ara-CTP formation (P = 0.0084 and P = 0.0003 at 2 and 3 h timepoints, respectively) were both increased significantly by GM-CSF, with modest non-significant increases with ASNase exposures.	Cytarabine	0-5	colony stimulating factor 2	Homo sapiens	166-172
7885038-9	1995	Ara-C incorporated into DNA (P = 0.0302) and ara-CTP formation (P = 0.0084 and P = 0.0003 at 2 and 3 h timepoints, respectively) were both increased significantly by GM-CSF, with modest non-significant increases with ASNase exposures.	Cytarabine	0-5	asparaginase	Homo sapiens	217-223
7885038-11	1995	Therefore, when appropriately scheduled, both GM-CSF and ASNase may potentiate ara-C cytotoxicity.	Cytarabine	79-84	colony stimulating factor 2	Homo sapiens	46-52
7885038-11	1995	Therefore, when appropriately scheduled, both GM-CSF and ASNase may potentiate ara-C cytotoxicity.	Cytarabine	79-84	asparaginase	Homo sapiens	57-63
7745622-4	1995	After withdrawal of ARA-C, daily treatment of the cells with bFGF for 3 days induced a drastic decrease in MBP mRNA level compared to control cultures treated only with ARA-C.	Cytarabine	20-25	fibroblast growth factor 2	Rattus norvegicus	61-65
7745622-4	1995	After withdrawal of ARA-C, daily treatment of the cells with bFGF for 3 days induced a drastic decrease in MBP mRNA level compared to control cultures treated only with ARA-C.	Cytarabine	169-174	fibroblast growth factor 2	Rattus norvegicus	61-65
9815970-0	1995	Modulation of the cellular metabolism of cytarabine and fludarabine by granulocyte-colony-stimulating factor during therapy of acute myelogenous leukemia.	Cytarabine	41-51	colony stimulating factor 3	Homo sapiens	71-108
9815970-1	1995	Previous in vitro investigations demonstrated that human leukemia cells, when incubated with hematopoietic growth factors such as granulocyte-colony-stimulating factor (G-CSF), augment the accumulation of the triphosphate 1-beta-D-arabinofuranosylcytosine (ara-C cytarabine).	Cytarabine	257-262	colony stimulating factor 3	Homo sapiens	130-167
9815970-1	1995	Previous in vitro investigations demonstrated that human leukemia cells, when incubated with hematopoietic growth factors such as granulocyte-colony-stimulating factor (G-CSF), augment the accumulation of the triphosphate 1-beta-D-arabinofuranosylcytosine (ara-C cytarabine).	Cytarabine	257-262	colony stimulating factor 3	Homo sapiens	169-174
9815970-1	1995	Previous in vitro investigations demonstrated that human leukemia cells, when incubated with hematopoietic growth factors such as granulocyte-colony-stimulating factor (G-CSF), augment the accumulation of the triphosphate 1-beta-D-arabinofuranosylcytosine (ara-C cytarabine).	Cytarabine	263-273	colony stimulating factor 3	Homo sapiens	130-167
9815970-14	1995	Based on these data it could be concluded that (a) infusion of G-CSF before fludarabine augmented the rate of F-ara-ATP synthesis in circulating AML blasts during therapy, suggesting that G-CSF may benefit fludarabine therapy by biological modulation; (b) G-CSF did not increase ara-CTP accumulation, rather it may have caused it to decrease; and (c) these data imply that when G-CSF and ara-C are used in combination, administration of fludarabine prior to ara-C may maintain the ara-CTP AUC.	Cytarabine	279-284	colony stimulating factor 3	Homo sapiens	188-193
9815970-1	1995	Previous in vitro investigations demonstrated that human leukemia cells, when incubated with hematopoietic growth factors such as granulocyte-colony-stimulating factor (G-CSF), augment the accumulation of the triphosphate 1-beta-D-arabinofuranosylcytosine (ara-C cytarabine).	Cytarabine	263-273	colony stimulating factor 3	Homo sapiens	169-174
9815970-14	1995	Based on these data it could be concluded that (a) infusion of G-CSF before fludarabine augmented the rate of F-ara-ATP synthesis in circulating AML blasts during therapy, suggesting that G-CSF may benefit fludarabine therapy by biological modulation; (b) G-CSF did not increase ara-CTP accumulation, rather it may have caused it to decrease; and (c) these data imply that when G-CSF and ara-C are used in combination, administration of fludarabine prior to ara-C may maintain the ara-CTP AUC.	Cytarabine	279-284	colony stimulating factor 3	Homo sapiens	188-193
9815970-14	1995	Based on these data it could be concluded that (a) infusion of G-CSF before fludarabine augmented the rate of F-ara-ATP synthesis in circulating AML blasts during therapy, suggesting that G-CSF may benefit fludarabine therapy by biological modulation; (b) G-CSF did not increase ara-CTP accumulation, rather it may have caused it to decrease; and (c) these data imply that when G-CSF and ara-C are used in combination, administration of fludarabine prior to ara-C may maintain the ara-CTP AUC.	Cytarabine	279-284	colony stimulating factor 3	Homo sapiens	188-193
9815970-14	1995	Based on these data it could be concluded that (a) infusion of G-CSF before fludarabine augmented the rate of F-ara-ATP synthesis in circulating AML blasts during therapy, suggesting that G-CSF may benefit fludarabine therapy by biological modulation; (b) G-CSF did not increase ara-CTP accumulation, rather it may have caused it to decrease; and (c) these data imply that when G-CSF and ara-C are used in combination, administration of fludarabine prior to ara-C may maintain the ara-CTP AUC.	Cytarabine	388-393	colony stimulating factor 3	Homo sapiens	63-68
9815970-14	1995	Based on these data it could be concluded that (a) infusion of G-CSF before fludarabine augmented the rate of F-ara-ATP synthesis in circulating AML blasts during therapy, suggesting that G-CSF may benefit fludarabine therapy by biological modulation; (b) G-CSF did not increase ara-CTP accumulation, rather it may have caused it to decrease; and (c) these data imply that when G-CSF and ara-C are used in combination, administration of fludarabine prior to ara-C may maintain the ara-CTP AUC.	Cytarabine	388-393	colony stimulating factor 3	Homo sapiens	188-193
9815970-14	1995	Based on these data it could be concluded that (a) infusion of G-CSF before fludarabine augmented the rate of F-ara-ATP synthesis in circulating AML blasts during therapy, suggesting that G-CSF may benefit fludarabine therapy by biological modulation; (b) G-CSF did not increase ara-CTP accumulation, rather it may have caused it to decrease; and (c) these data imply that when G-CSF and ara-C are used in combination, administration of fludarabine prior to ara-C may maintain the ara-CTP AUC.	Cytarabine	388-393	colony stimulating factor 3	Homo sapiens	188-193
9815970-14	1995	Based on these data it could be concluded that (a) infusion of G-CSF before fludarabine augmented the rate of F-ara-ATP synthesis in circulating AML blasts during therapy, suggesting that G-CSF may benefit fludarabine therapy by biological modulation; (b) G-CSF did not increase ara-CTP accumulation, rather it may have caused it to decrease; and (c) these data imply that when G-CSF and ara-C are used in combination, administration of fludarabine prior to ara-C may maintain the ara-CTP AUC.	Cytarabine	388-393	colony stimulating factor 3	Homo sapiens	188-193
7530044-6	1995	The results further demonstrate that ara-C treatment is associated with a dose-dependent activation of p56/p53lyn and that ara-C-induced p56/p53lyn activity is blocked by the protein tyrosine inhibitors herbimycin A and genistein.	Cytarabine	123-128	cyclin dependent kinase like 2	Homo sapiens	137-140
7823945-4	1995	Exogeneous expression of c-myb in transfected cell lines abrogated erythroid differentiation induced by cadaverine or cytosine arabinoside as assessed by hemoglobin production.	Cytarabine	118-138	MYB proto-oncogene, transcription factor	Homo sapiens	25-30
7530044-0	1995	1-beta-D-arabinofuranosylcytosine activates tyrosine phosphorylation of p34cdc2 and its association with the Src-like p56/p53lyn kinase in human myeloid leukemia cells.	Cytarabine	0-33	cyclin dependent kinase 1	Homo sapiens	72-79
7530044-6	1995	The results further demonstrate that ara-C treatment is associated with a dose-dependent activation of p56/p53lyn and that ara-C-induced p56/p53lyn activity is blocked by the protein tyrosine inhibitors herbimycin A and genistein.	Cytarabine	123-128	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	107-113
7530044-0	1995	1-beta-D-arabinofuranosylcytosine activates tyrosine phosphorylation of p34cdc2 and its association with the Src-like p56/p53lyn kinase in human myeloid leukemia cells.	Cytarabine	0-33	cyclin dependent kinase like 2	Homo sapiens	118-121
7530044-6	1995	The results further demonstrate that ara-C treatment is associated with a dose-dependent activation of p56/p53lyn and that ara-C-induced p56/p53lyn activity is blocked by the protein tyrosine inhibitors herbimycin A and genistein.	Cytarabine	123-128	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	141-147
7530044-0	1995	1-beta-D-arabinofuranosylcytosine activates tyrosine phosphorylation of p34cdc2 and its association with the Src-like p56/p53lyn kinase in human myeloid leukemia cells.	Cytarabine	0-33	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	122-128
7530044-3	1995	The results of immunoprecipitation studies demonstrate that HL-60 cells respond to ara-C with tyrosine phosphorylation of the cell cycle regulatory protein p34cdc2 and a decrease in the activity of this kinase.	Cytarabine	83-88	cyclin dependent kinase 1	Homo sapiens	156-163
7530044-5	1995	Coimmunoprecipitations with anti-p34cdc2 support binding of this protein to the Src-like p56/p53lyn tyrosine kinase in ara-C-treated, but not untreated, cells.	Cytarabine	119-124	cyclin dependent kinase 1	Homo sapiens	33-40
7530044-7	1995	Studies with a glutathione S-transferase-Lyn fusion protein confirm interaction of p34cdc2 and p56/p53lyn in lysates of ara-C-treated cells.	Cytarabine	120-125	cyclin dependent kinase 1	Homo sapiens	83-90
7530044-5	1995	Coimmunoprecipitations with anti-p34cdc2 support binding of this protein to the Src-like p56/p53lyn tyrosine kinase in ara-C-treated, but not untreated, cells.	Cytarabine	119-124	cyclin dependent kinase like 2	Homo sapiens	89-92
7530044-5	1995	Coimmunoprecipitations with anti-p34cdc2 support binding of this protein to the Src-like p56/p53lyn tyrosine kinase in ara-C-treated, but not untreated, cells.	Cytarabine	119-124	tumor protein p53	Homo sapiens	93-96
7530044-7	1995	Studies with a glutathione S-transferase-Lyn fusion protein confirm interaction of p34cdc2 and p56/p53lyn in lysates of ara-C-treated cells.	Cytarabine	120-125	cyclin dependent kinase like 2	Homo sapiens	95-98
7530044-6	1995	The results further demonstrate that ara-C treatment is associated with a dose-dependent activation of p56/p53lyn and that ara-C-induced p56/p53lyn activity is blocked by the protein tyrosine inhibitors herbimycin A and genistein.	Cytarabine	37-42	cyclin dependent kinase like 2	Homo sapiens	103-106
7530044-6	1995	The results further demonstrate that ara-C treatment is associated with a dose-dependent activation of p56/p53lyn and that ara-C-induced p56/p53lyn activity is blocked by the protein tyrosine inhibitors herbimycin A and genistein.	Cytarabine	37-42	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	107-113
7530044-7	1995	Studies with a glutathione S-transferase-Lyn fusion protein confirm interaction of p34cdc2 and p56/p53lyn in lysates of ara-C-treated cells.	Cytarabine	120-125	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	99-105
7530044-6	1995	The results further demonstrate that ara-C treatment is associated with a dose-dependent activation of p56/p53lyn and that ara-C-induced p56/p53lyn activity is blocked by the protein tyrosine inhibitors herbimycin A and genistein.	Cytarabine	123-128	cyclin dependent kinase like 2	Homo sapiens	103-106
7530044-9	1995	These findings indicate that the cellular response to ara-C includes activation of p56/p53lyn and that association of p56/p53lyn with p34cdc2 may contribute to regulation of the cell cycle progression in ara-C-treated cells.	Cytarabine	54-59	cyclin dependent kinase like 2	Homo sapiens	83-86
7530044-9	1995	These findings indicate that the cellular response to ara-C includes activation of p56/p53lyn and that association of p56/p53lyn with p34cdc2 may contribute to regulation of the cell cycle progression in ara-C-treated cells.	Cytarabine	54-59	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	87-93
7530044-9	1995	These findings indicate that the cellular response to ara-C includes activation of p56/p53lyn and that association of p56/p53lyn with p34cdc2 may contribute to regulation of the cell cycle progression in ara-C-treated cells.	Cytarabine	204-209	cyclin dependent kinase like 2	Homo sapiens	83-86
7530044-9	1995	These findings indicate that the cellular response to ara-C includes activation of p56/p53lyn and that association of p56/p53lyn with p34cdc2 may contribute to regulation of the cell cycle progression in ara-C-treated cells.	Cytarabine	204-209	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	87-93
7530044-9	1995	These findings indicate that the cellular response to ara-C includes activation of p56/p53lyn and that association of p56/p53lyn with p34cdc2 may contribute to regulation of the cell cycle progression in ara-C-treated cells.	Cytarabine	204-209	cyclin dependent kinase like 2	Homo sapiens	118-121
7530044-9	1995	These findings indicate that the cellular response to ara-C includes activation of p56/p53lyn and that association of p56/p53lyn with p34cdc2 may contribute to regulation of the cell cycle progression in ara-C-treated cells.	Cytarabine	204-209	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	122-128
7530044-9	1995	These findings indicate that the cellular response to ara-C includes activation of p56/p53lyn and that association of p56/p53lyn with p34cdc2 may contribute to regulation of the cell cycle progression in ara-C-treated cells.	Cytarabine	204-209	cyclin dependent kinase 1	Homo sapiens	134-141
7805176-4	1995	To determine whether the combination leads to enhanced activity of deoxycytidine kinase (dCk), the rate-limiting enzyme in ara-C activation, we characterized the cellular dCk in CCRF/CEM/0, CCRF/CEM/ara-C/7A, and CCRF/CEM/ara-C/3A monoclonal cells before and after treatment with 6-MP.	Cytarabine	123-128	deoxycytidine kinase	Homo sapiens	67-87
7826366-2	1995	In the infected cells, Ara-CTP levels decreased to 20% of that found in uninfected H9 cells after 3 h incubation at Ara-C concentration of 1 microM, and 8.1-fold increase of cytidine deaminase activity was observed in the infected H9 cells.	Cytarabine	23-28	cytidine deaminase	Homo sapiens	174-192
7826366-3	1995	A competitive inhibitor of cytidine deaminase, 3, 4, 5, 6-tetrahydrouridine (THU), at 100 microM reversed Ara-C resistance in the infected cells.	Cytarabine	106-111	cytidine deaminase	Homo sapiens	27-45
8525773-7	1995	The increase of 2-CDA concentration to 100 or 300 nM/l in combination with ara-C and drb significantly reduced the growth of AML clonogenic cells (p &lt; 0.05).	Cytarabine	75-80	cytidine deaminase	Homo sapiens	18-21
7805176-4	1995	To determine whether the combination leads to enhanced activity of deoxycytidine kinase (dCk), the rate-limiting enzyme in ara-C activation, we characterized the cellular dCk in CCRF/CEM/0, CCRF/CEM/ara-C/7A, and CCRF/CEM/ara-C/3A monoclonal cells before and after treatment with 6-MP.	Cytarabine	123-128	sticky	Drosophila melanogaster	89-92
7536275-0	1995	[Continuation of complete remission by oral administration of cytarabine ocfosfate in a patient with M0, who achieved remission by small doses of cytosine arabinoside with G-CSF].	Cytarabine	146-166	colony stimulating factor 3	Homo sapiens	172-177
7730955-4	1995	At pH 2.0 and 37 degrees C, Ara-C was released at a slow rate, kuo (uncoated) or kco (coated), for 24 h after an initial rapid release phase that lasted for about 6 h and the ratio kuo/kco, was 1.9 and 5.7 for the DMPC:CHOL:DCP and the DPPC:CHOL:DCP compositions respectively.	Cytarabine	28-33	angiotensin I converting enzyme	Homo sapiens	214-227
7845007-7	1995	In these seven cases the decreased expression of bcl-2 was accompanied by increased apoptosis and the susceptibility of the blasts to apoptosis induced by Ara-C was increased in the presence of bcl-2 antisense.	Cytarabine	155-160	BCL2 apoptosis regulator	Homo sapiens	49-54
7845007-7	1995	In these seven cases the decreased expression of bcl-2 was accompanied by increased apoptosis and the susceptibility of the blasts to apoptosis induced by Ara-C was increased in the presence of bcl-2 antisense.	Cytarabine	155-160	BCL2 apoptosis regulator	Homo sapiens	194-199
7758997-4	1995	Experience gathered in recent years shows that idarubicin, cytosine arabinoside, and etoposide together might contribute to the modeling of an improved remission induction regimen: ICE.	Cytarabine	59-79	carboxylesterase 2	Homo sapiens	181-184
7845007-0	1995	Inhibition of bcl-2 with antisense oligonucleotides induces apoptosis and increases the sensitivity of AML blasts to Ara-C.	Cytarabine	117-122	BCL2 apoptosis regulator	Homo sapiens	14-19
7845007-4	1995	Here we have investigated the role of bcl-2 expression in mediating resistance to apoptosis induced by cytosine arabinoside in vitro.	Cytarabine	103-123	BCL2 apoptosis regulator	Homo sapiens	38-43
7528449-4	1994	In preclinical studies an enhancement of the cytotoxicity of cytosine arabinoside (AraC) on leukemic blasts could be shown by pretreatment with GM-CSF or IL-3.	Cytarabine	61-81	interleukin 3	Homo sapiens	154-158
7528449-4	1994	In preclinical studies an enhancement of the cytotoxicity of cytosine arabinoside (AraC) on leukemic blasts could be shown by pretreatment with GM-CSF or IL-3.	Cytarabine	83-87	colony stimulating factor 2	Homo sapiens	144-150
7528449-4	1994	In preclinical studies an enhancement of the cytotoxicity of cytosine arabinoside (AraC) on leukemic blasts could be shown by pretreatment with GM-CSF or IL-3.	Cytarabine	61-81	colony stimulating factor 2	Homo sapiens	144-150
7528449-4	1994	In preclinical studies an enhancement of the cytotoxicity of cytosine arabinoside (AraC) on leukemic blasts could be shown by pretreatment with GM-CSF or IL-3.	Cytarabine	83-87	interleukin 3	Homo sapiens	154-158
7528449-6	1994	The evaluation of different doses of AraC showed the most marked increase after the combination of GM-CSF with conventional rather than high doses of AraC.	Cytarabine	37-41	colony stimulating factor 2	Homo sapiens	99-105
7801145-3	1994	In in vitro experiments, preincubating leukemic cells with recombinant cytokines including GM-CSF led to a consistent, dose-dependent increase in the cytotoxicity of cytosine arabinoside (Ara-C).	Cytarabine	166-186	colony stimulating factor 2	Homo sapiens	91-97
7801145-3	1994	In in vitro experiments, preincubating leukemic cells with recombinant cytokines including GM-CSF led to a consistent, dose-dependent increase in the cytotoxicity of cytosine arabinoside (Ara-C).	Cytarabine	188-193	colony stimulating factor 2	Homo sapiens	91-97
7981228-4	1994	The inactive antimetabolite, ara-C, is activated within a cell by deoxycytidine kinase phosphorylation of the prodrug.	Cytarabine	29-34	deoxycytidine kinase	Homo sapiens	66-86
7986199-2	1994	Treatment of a human promyelocytic leukemia cell line, HL-60, with 10 micrograms/mL etoposide or 2 microM 1-beta-D-arabinofuranosylcytosine induced NF-kappa B activation within 1 hr and subsequently caused apoptosis within 3-4 hr.	Cytarabine	106-139	nuclear factor kappa B subunit 1	Homo sapiens	148-158
7981228-6	1994	Furthermore, ara-C has been shown to be metabolized to ara-CDP-choline via reversal of the cholinephosphotransferase [2] producing diglyceride, a cellular activator of protein kinase C. Thus, in situ, deoxycytidine kinase may be phosphorylated by protein kinase C with the result that self-potentiation of ara-C toxicity may occur via increased activity of deoxycytidine kinase.	Cytarabine	13-18	cut like homeobox 1	Homo sapiens	59-62
7981228-6	1994	Furthermore, ara-C has been shown to be metabolized to ara-CDP-choline via reversal of the cholinephosphotransferase [2] producing diglyceride, a cellular activator of protein kinase C. Thus, in situ, deoxycytidine kinase may be phosphorylated by protein kinase C with the result that self-potentiation of ara-C toxicity may occur via increased activity of deoxycytidine kinase.	Cytarabine	13-18	deoxycytidine kinase	Homo sapiens	201-221
7981228-6	1994	Furthermore, ara-C has been shown to be metabolized to ara-CDP-choline via reversal of the cholinephosphotransferase [2] producing diglyceride, a cellular activator of protein kinase C. Thus, in situ, deoxycytidine kinase may be phosphorylated by protein kinase C with the result that self-potentiation of ara-C toxicity may occur via increased activity of deoxycytidine kinase.	Cytarabine	13-18	deoxycytidine kinase	Homo sapiens	357-377
7961129-9	1994	In conclusion, intracellularly synthesized CDD was thought to be rapidly shed into the medium and the released CDD could play an important role in ara-C inactivation.	Cytarabine	147-152	cytidine deaminase	Mus musculus	43-46
7874002-6	1994	These concentrations of Ara-C inhibited c-myc and did not induce c-jun mRNA expression.	Cytarabine	24-29	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	40-45
7874002-7	1994	These effects of Ara-C on c-myc and c-jun expressions were not influenced by co-treatment with pIXY 321.	Cytarabine	17-22	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	26-31
7874002-7	1994	These effects of Ara-C on c-myc and c-jun expressions were not influenced by co-treatment with pIXY 321.	Cytarabine	17-22	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	36-41
7874009-0	1994	Low expression of the deoxycytidine kinase (dCK) gene in a 1-beta-D-arabinofuranosylcytosine-resistant human leukemic cell line KY-Ra.	Cytarabine	59-92	deoxycytidine kinase	Homo sapiens	22-42
7874009-0	1994	Low expression of the deoxycytidine kinase (dCK) gene in a 1-beta-D-arabinofuranosylcytosine-resistant human leukemic cell line KY-Ra.	Cytarabine	59-92	sticky	Drosophila melanogaster	44-47
7874009-1	1994	Molecular change of the deoxycytidine kinase (dCK) gene in a 1-beta-D-arabinofuranosylcytosine-resistant human leukemic cell line (KY-Ra) was investigated.	Cytarabine	61-94	deoxycytidine kinase	Homo sapiens	24-44
7874009-1	1994	Molecular change of the deoxycytidine kinase (dCK) gene in a 1-beta-D-arabinofuranosylcytosine-resistant human leukemic cell line (KY-Ra) was investigated.	Cytarabine	61-94	sticky	Drosophila melanogaster	46-49
7530135-0	1994	Idarubicin, intermediate-dose cytarabine, etoposide, and granulocyte-colony-stimulating factor are able to recruit CD34+/HLA-DR- cells during early hematopoietic recovery in accelerated and chronic phases of chronic myeloid leukemia.	Cytarabine	30-40	CD34 molecule	Homo sapiens	115-119
7523795-3	1994	Using PCR, we demonstrated GM-CSF and IL-1 expression by adherent cells taken from marrow fibroblast layers following Ara-C-induced hematopoietic damage and during marrow regeneration, while expression in control layers was not detected.	Cytarabine	118-123	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	27-33
7523795-3	1994	Using PCR, we demonstrated GM-CSF and IL-1 expression by adherent cells taken from marrow fibroblast layers following Ara-C-induced hematopoietic damage and during marrow regeneration, while expression in control layers was not detected.	Cytarabine	118-123	interleukin 1 complex	Mus musculus	38-42
7523795-4	1994	The IL-3 gene was not expressed either by layers of Ara-C-treated mice or by controls, probably due to the absence of T-lymphocytes in 2-4 week old cultures.	Cytarabine	52-57	interleukin 3	Mus musculus	4-8
7523795-7	1994	While IL-3 and GM-CSF were not present in the conditioned medium of marrow fibroblast layers either from Ara-C-treated mice or controls, IL-1 was found in low concentrations in cultures from Ara-C-treated animals.	Cytarabine	191-196	interleukin 1 complex	Mus musculus	137-141
7900157-1	1994	Effects of etoposide (VP-16) and cytosine arabinoside (Ara-C) on the cell cycle of HL-60 and THP-1 cells were studied by flow cytometry using the bromodeoxyuridine (BrdU)/DNA assay technique to investigate the efficacy of VP-16 for monocytic leukemia cells.	Cytarabine	55-60	GLI family zinc finger 2	Homo sapiens	93-98
7932594-2	1994	The structure of the modified ara-C was determined to be either beta 1-3"- or beta 1-5"-linked GlcNAc-ara-C or (GlcNAc)2-ara-C.	Cytarabine	30-35	UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2	Homo sapiens	64-72
7932594-2	1994	The structure of the modified ara-C was determined to be either beta 1-3"- or beta 1-5"-linked GlcNAc-ara-C or (GlcNAc)2-ara-C.	Cytarabine	30-35	UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2	Homo sapiens	78-86
7932594-2	1994	The structure of the modified ara-C was determined to be either beta 1-3"- or beta 1-5"-linked GlcNAc-ara-C or (GlcNAc)2-ara-C.	Cytarabine	102-107	UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2	Homo sapiens	78-86
7934168-5	1994	When the frequency of additive and synergistic interactions were calculated according to the multiplicative concept for drug interactions, the highest frequencies were observed for CdA+AraC and CdA+Dnr.	Cytarabine	185-189	cytidine deaminase	Homo sapiens	181-184
7934168-8	1994	The highest frequency of synergistic interactions was obtained for AraC+CdA, despite their cross-resistance.	Cytarabine	67-71	cytidine deaminase	Homo sapiens	72-75
7522289-8	1994	Addition of either HGF enhanced the Ara-C cytotoxicity for the relapsed samples significantly (for G-CSF p = 0.036, IL-3 p = 0.036, and for GM-CSF p = 0.036).	Cytarabine	36-41	colony stimulating factor 3	Homo sapiens	99-104
7522289-8	1994	Addition of either HGF enhanced the Ara-C cytotoxicity for the relapsed samples significantly (for G-CSF p = 0.036, IL-3 p = 0.036, and for GM-CSF p = 0.036).	Cytarabine	36-41	interleukin 3	Homo sapiens	116-120
7522289-8	1994	Addition of either HGF enhanced the Ara-C cytotoxicity for the relapsed samples significantly (for G-CSF p = 0.036, IL-3 p = 0.036, and for GM-CSF p = 0.036).	Cytarabine	36-41	colony stimulating factor 2	Homo sapiens	140-146
7522289-10	1994	However, enhancement of Ara-C cytotoxicity to AML progenitors by IL-3 or GM-CSF stimulation was significantly less in the cell specimens from AML recurrence patients as compared with the original diagnosis samples.	Cytarabine	24-29	interleukin 3	Homo sapiens	65-69
7522289-10	1994	However, enhancement of Ara-C cytotoxicity to AML progenitors by IL-3 or GM-CSF stimulation was significantly less in the cell specimens from AML recurrence patients as compared with the original diagnosis samples.	Cytarabine	24-29	colony stimulating factor 2	Homo sapiens	73-79
7522289-12	1994	IL-3 stimulation enhanced Ara-C incorporation in all samples tested.	Cytarabine	26-31	interleukin 3	Homo sapiens	0-4
7961129-9	1994	In conclusion, intracellularly synthesized CDD was thought to be rapidly shed into the medium and the released CDD could play an important role in ara-C inactivation.	Cytarabine	147-152	cytidine deaminase	Mus musculus	111-114
7961129-10	1994	6-MP interrupted some step between synthesis and shedding of CDD, resulting in a decrease of the ara-C deamination in the medium and enhancement of its antileukemic effect.	Cytarabine	97-102	cytidine deaminase	Mus musculus	61-64
7521137-5	1994	SP content and release declined to 1.5% of those found in control cultures when nonneuronal cells were suppressed with cytosine arabinoside but were partially restored (13-17% of control) by nerve growth factor.	Cytarabine	119-139	tachykinin precursor 1	Homo sapiens	0-2
8033147-6	1994	AG6000 is cross-resistant to other drug which require activation by dCK, such as 1-beta-D-arabinofuranosylcytosine, 5-aza-2"-deoxycytidine, and 2-chlorodeoxyadenosine.	Cytarabine	81-114	sticky	Drosophila melanogaster	68-71
7974627-3	1994	Since a strong correlation was found between achievement of complete remission and cellular ara-CTP levels, we propose a calculation scheme that allows steady-state adjustment of ara-CTP levels during administration of ara-C.	Cytarabine	92-97	solute carrier family 25 member 1	Homo sapiens	183-186
8057666-0	1994	Essential role of c-myc in ara-C-induced differentiation of human erythroleukemia cells.	Cytarabine	27-32	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	18-23
8057666-2	1994	We have analyzed the role of c-myc expression in ara-C-induced differentiation of K562 human erythroleukemia cells.	Cytarabine	49-54	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	29-34
8057666-6	1994	We propose that the loss of c-myc expression might be a necessary prerequisite for ara-C-induced differentiation.	Cytarabine	83-88	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	28-33
8057666-7	1994	This hypothesis was tested by transfecting a constitutive c-myc expression construct into K562 cells prior to ara-C treatment.	Cytarabine	110-115	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	58-63
8057666-8	1994	By following the differentiation parameters cell morphology, benzidine staining (hemoglobin monitored), and alkaline phosphatase activity (presence of mature red blood cell antigen monitored) in cells expressing cotransfected LacZ marker gene, it was demonstrated that the introduction of the c-myc expression plasmid blocked ara-C-induced differentiation.	Cytarabine	326-331	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	293-298
8057666-9	1994	We conclude that loss of c-myc expression mediated the differentiation found in ara-C-treated K562 cells.	Cytarabine	80-85	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	25-30
7974627-6	1994	Conversely, using the same pharmacokinetic approach, the infusion rate at which to administer ara-C in order to reach in vivo ara-CTP concentration threshold and to achieve complete remission could be calculated for each patient.	Cytarabine	94-99	solute carrier family 25 member 1	Homo sapiens	130-133
7932876-5	1994	Cytosine arabinoside (CA; doses of 0.5-8 microM) was added to the cultures on day 1 and the effectiveness in elimination of glial cells was verified on day 15 by measuring the incorporation of 3H thymidine into DNA and by immunostaining for the astrocyte marker glial fibrillary acidic protein (GFAP).	Cytarabine	0-20	glial fibrillary acidic protein	Rattus norvegicus	262-293
7950302-5	1994	Both synthetic bcl-2-As oligonucleotides and inducible expression plasmids that produce bcl-2-As transcripts induced reductions in bcl-2 expression, resulting in a marked enhancement in the sensitivity of neoplastic cells to conventional chemotherapeutic drugs such as cytosine arabinoside (ara-C) and methotrexate (MTX).	Cytarabine	269-289	BCL2 apoptosis regulator	Homo sapiens	88-93
7950302-5	1994	Both synthetic bcl-2-As oligonucleotides and inducible expression plasmids that produce bcl-2-As transcripts induced reductions in bcl-2 expression, resulting in a marked enhancement in the sensitivity of neoplastic cells to conventional chemotherapeutic drugs such as cytosine arabinoside (ara-C) and methotrexate (MTX).	Cytarabine	269-289	BCL2 apoptosis regulator	Homo sapiens	88-93
7950302-5	1994	Both synthetic bcl-2-As oligonucleotides and inducible expression plasmids that produce bcl-2-As transcripts induced reductions in bcl-2 expression, resulting in a marked enhancement in the sensitivity of neoplastic cells to conventional chemotherapeutic drugs such as cytosine arabinoside (ara-C) and methotrexate (MTX).	Cytarabine	291-296	BCL2 apoptosis regulator	Homo sapiens	88-93
7950302-5	1994	Both synthetic bcl-2-As oligonucleotides and inducible expression plasmids that produce bcl-2-As transcripts induced reductions in bcl-2 expression, resulting in a marked enhancement in the sensitivity of neoplastic cells to conventional chemotherapeutic drugs such as cytosine arabinoside (ara-C) and methotrexate (MTX).	Cytarabine	291-296	BCL2 apoptosis regulator	Homo sapiens	88-93
7932876-5	1994	Cytosine arabinoside (CA; doses of 0.5-8 microM) was added to the cultures on day 1 and the effectiveness in elimination of glial cells was verified on day 15 by measuring the incorporation of 3H thymidine into DNA and by immunostaining for the astrocyte marker glial fibrillary acidic protein (GFAP).	Cytarabine	0-20	glial fibrillary acidic protein	Rattus norvegicus	295-299
7516032-11	1994	Because the treatment choice in advanced MDS (especially between anthracycline-Ara-C or low-dose Ara-C, chemotherapy) is difficult, our preliminary therapeutic results suggest that the analysis of PGP expression could have practical importance in MDS.	Cytarabine	79-84	ATP binding cassette subfamily B member 1	Homo sapiens	197-200
8058058-0	1994	1-beta-D-arabinofuranosylcytosine activates serine/threonine protein kinases and c-jun gene expression in phorbol ester-resistant myeloid leukemia cells.	Cytarabine	0-33	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	81-86
8058058-2	1994	Recent studies have demonstrated that ara-C treatment is associated with transient induction of the c-jun early response gene.	Cytarabine	38-43	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	100-105
8058058-4	1994	The results demonstrate that treatment of HL-525 cells with ara-C is associated with transcriptional activation of the c-jun gene.	Cytarabine	60-65	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	119-124
8058058-10	1994	Because 12-O-tetradecanoylphorbol-13-acetate has little, if any, effect on the PKC-like and MAP kinase activities in HL-525 cells, these findings suggest that ara-C activates a distinct signaling cascade that may contribute to induction of the c-jun gene.	Cytarabine	159-164	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	244-249
8195192-5	1994	ara-C also increased expression of the transcription factor NF-kappa B which is related to the control of monocyte differentiation.	Cytarabine	0-5	nuclear factor kappa B subunit 1	Homo sapiens	60-70
7962192-4	1994	10, 184-193) showed that cytosine arabinoside, but no other arabinofuranosyl nucleoside, could induce cell death in the presence of NGF and they suggested that it may block a critical step in the NGF-signalling pathway.	Cytarabine	25-45	nerve growth factor	Rattus norvegicus	132-135
7962192-4	1994	10, 184-193) showed that cytosine arabinoside, but no other arabinofuranosyl nucleoside, could induce cell death in the presence of NGF and they suggested that it may block a critical step in the NGF-signalling pathway.	Cytarabine	25-45	nerve growth factor	Rattus norvegicus	196-199
7517190-0	1994	In vitro response of blasts to IL-3, GM-CSF, and G-CSF is different for individual AML patients: factors that stimulate leukemic clonogenic cells also enhance Ara-C cytotoxicity.	Cytarabine	159-164	interleukin 3	Homo sapiens	31-35
7517190-0	1994	In vitro response of blasts to IL-3, GM-CSF, and G-CSF is different for individual AML patients: factors that stimulate leukemic clonogenic cells also enhance Ara-C cytotoxicity.	Cytarabine	159-164	colony stimulating factor 3	Homo sapiens	49-54
7514246-0	1994	Structural analysis of the deoxycytidine kinase gene in patients with acute myeloid leukemia and resistance to cytosine arabinoside.	Cytarabine	111-131	deoxycytidine kinase	Homo sapiens	27-47
7514246-1	1994	Deficiency of deoxycytidine kinase (dCK) activity represents one possible cause of resistance to cytosine arabinoside (ara-C).	Cytarabine	97-117	deoxycytidine kinase	Homo sapiens	14-34
7514246-1	1994	Deficiency of deoxycytidine kinase (dCK) activity represents one possible cause of resistance to cytosine arabinoside (ara-C).	Cytarabine	97-117	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	36-39
7514246-1	1994	Deficiency of deoxycytidine kinase (dCK) activity represents one possible cause of resistance to cytosine arabinoside (ara-C).	Cytarabine	119-124	deoxycytidine kinase	Homo sapiens	14-34
7514246-1	1994	Deficiency of deoxycytidine kinase (dCK) activity represents one possible cause of resistance to cytosine arabinoside (ara-C).	Cytarabine	119-124	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	36-39
7514246-3	1994	In order to define the relevance of this mechanism in vivo, we analyzed the dCK gene in 16 adult patients with relapsed/refractory acute myeloid leukemia (AML) and clinical resistance to standard-dose and/or high-dose ara-C.	Cytarabine	218-223	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	76-79
7514246-9	1994	We conclude that structural alteration of the coding region of the dCK gene represents one possible mechanism for ara-C resistance in vivo, but, considering the frequency of this event, other mechanisms may play a more important role for clinical resistance to ara-C in patients with AML.	Cytarabine	114-119	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	67-70
7514246-9	1994	We conclude that structural alteration of the coding region of the dCK gene represents one possible mechanism for ara-C resistance in vivo, but, considering the frequency of this event, other mechanisms may play a more important role for clinical resistance to ara-C in patients with AML.	Cytarabine	261-266	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	67-70
21566992-2	1994	For comparison, arabinosylcytosine (Ara C), at 0.1 muM, causes the same percentage of differentiation, but cell proliferation is abolished by &gt;80%.	Cytarabine	16-34	latexin	Homo sapiens	51-54
7980770-2	1994	Deoxycytidine kinase is an enzyme required for the activation of, for example, cytarabine, the most widely used agent for the chemotherapy of haematological malignancies.	Cytarabine	79-89	deoxycytidine kinase	Homo sapiens	0-20
7980770-6	1994	Modulation of deoxycytidine kinase activity has already been shown to be an effective way to improve the effect of cytarabine and will probably be a target for new therapies.	Cytarabine	115-125	deoxycytidine kinase	Homo sapiens	14-34
21566992-2	1994	For comparison, arabinosylcytosine (Ara C), at 0.1 muM, causes the same percentage of differentiation, but cell proliferation is abolished by &gt;80%.	Cytarabine	36-41	latexin	Homo sapiens	51-54
8031880-1	1994	A lipid/peptide/drug conjugate, N4-(acylpeptidyl)-ara-C, is synthesized under mild conditions to give an ara-C prodrug protected against cytidine deaminase-catalyzed deactivation.	Cytarabine	50-55	cytidine deaminase	Homo sapiens	137-155
8152248-1	1994	Forty-five patients with untreated, de novo acute myeloid leukemia (AML) were treated with high-dose cytosine arabinoside (Ara-C) plus mitoxantrone or daunorubicin.	Cytarabine	101-121	ATP binding cassette subfamily C member 6	Homo sapiens	123-126
7515298-2	1994	By in vitro colony assay, the rhG-CSF-responsive NFS-60 leukemic cell clones are more effectively killed by Ara C in the presence of rhG-CSF than in the absence of rhG-CSF, while the killing of the rhG-CSF-unresponsive HL-60 cell clones is unaffected by rhG-CSF.	Cytarabine	108-113	colony stimulating factor 2	Homo sapiens	34-37
7515298-2	1994	By in vitro colony assay, the rhG-CSF-responsive NFS-60 leukemic cell clones are more effectively killed by Ara C in the presence of rhG-CSF than in the absence of rhG-CSF, while the killing of the rhG-CSF-unresponsive HL-60 cell clones is unaffected by rhG-CSF.	Cytarabine	108-113	colony stimulating factor 2	Homo sapiens	137-140
7509013-5	1994	Preincubation in Biorich medium with the addition of G + GM-CSF or IL-3 caused a significant enhancement of sensitivity to Ara-C across the dose curve.	Cytarabine	123-128	colony stimulating factor 2	Homo sapiens	57-63
7515298-2	1994	By in vitro colony assay, the rhG-CSF-responsive NFS-60 leukemic cell clones are more effectively killed by Ara C in the presence of rhG-CSF than in the absence of rhG-CSF, while the killing of the rhG-CSF-unresponsive HL-60 cell clones is unaffected by rhG-CSF.	Cytarabine	108-113	colony stimulating factor 2	Homo sapiens	137-140
7515298-2	1994	By in vitro colony assay, the rhG-CSF-responsive NFS-60 leukemic cell clones are more effectively killed by Ara C in the presence of rhG-CSF than in the absence of rhG-CSF, while the killing of the rhG-CSF-unresponsive HL-60 cell clones is unaffected by rhG-CSF.	Cytarabine	108-113	colony stimulating factor 2	Homo sapiens	137-140
7515298-2	1994	By in vitro colony assay, the rhG-CSF-responsive NFS-60 leukemic cell clones are more effectively killed by Ara C in the presence of rhG-CSF than in the absence of rhG-CSF, while the killing of the rhG-CSF-unresponsive HL-60 cell clones is unaffected by rhG-CSF.	Cytarabine	108-113	colony stimulating factor 2	Homo sapiens	137-140
8309245-0	1994	Modulation of intracellular metabolism of cytosine arabinoside in acute myeloid leukemia by granulocyte-macrophage colony-stimulating factor.	Cytarabine	42-62	colony stimulating factor 2	Homo sapiens	92-140
8309245-1	1994	The current study investigated the effect of granulocyte-macrophage colony-stimulating factor (GM-CSF) on the intracellular metabolism and cytotoxicity of 1-beta-D-arabinofuranosylcytosine (araC) in leukemic cells of 45 patients with acute myeloid leukemia (AML).	Cytarabine	155-188	colony stimulating factor 2	Homo sapiens	45-93
8309245-1	1994	The current study investigated the effect of granulocyte-macrophage colony-stimulating factor (GM-CSF) on the intracellular metabolism and cytotoxicity of 1-beta-D-arabinofuranosylcytosine (araC) in leukemic cells of 45 patients with acute myeloid leukemia (AML).	Cytarabine	155-188	colony stimulating factor 2	Homo sapiens	95-101
8309245-1	1994	The current study investigated the effect of granulocyte-macrophage colony-stimulating factor (GM-CSF) on the intracellular metabolism and cytotoxicity of 1-beta-D-arabinofuranosylcytosine (araC) in leukemic cells of 45 patients with acute myeloid leukemia (AML).	Cytarabine	190-194	colony stimulating factor 2	Homo sapiens	45-93
8309245-1	1994	The current study investigated the effect of granulocyte-macrophage colony-stimulating factor (GM-CSF) on the intracellular metabolism and cytotoxicity of 1-beta-D-arabinofuranosylcytosine (araC) in leukemic cells of 45 patients with acute myeloid leukemia (AML).	Cytarabine	190-194	colony stimulating factor 2	Homo sapiens	95-101
8309245-4	1994	Hence, 20 of the 23 responding patients revealed a GM-CSF induced enhancement of araC incorporation at low or conventional doses of araC (0.06-1.0 microM).	Cytarabine	81-85	colony stimulating factor 2	Homo sapiens	51-57
8309245-4	1994	Hence, 20 of the 23 responding patients revealed a GM-CSF induced enhancement of araC incorporation at low or conventional doses of araC (0.06-1.0 microM).	Cytarabine	132-136	colony stimulating factor 2	Homo sapiens	51-57
8309245-5	1994	Fourteen of the 18 cases with concomitant rises of 3H-TdR and 3H-araC incorporation into the DNA after GM-CSF had elevated DNA polymerase alpha activity (16-531%, median 72%) and in ten cases overall DNA polymerase activity was enhanced (10-70%, median 22.5%).	Cytarabine	65-69	colony stimulating factor 2	Homo sapiens	103-109
8309245-5	1994	Fourteen of the 18 cases with concomitant rises of 3H-TdR and 3H-araC incorporation into the DNA after GM-CSF had elevated DNA polymerase alpha activity (16-531%, median 72%) and in ten cases overall DNA polymerase activity was enhanced (10-70%, median 22.5%).	Cytarabine	65-69	DNA polymerase alpha 1, catalytic subunit	Homo sapiens	123-143
8309245-10	1994	Preincubation with GM-CSF increased the araC mediated cytotoxicity in ten of 13 patients by a median of 3.2-fold (range 2.2-229-fold).	Cytarabine	40-44	colony stimulating factor 2	Homo sapiens	19-25
8309250-0	1994	Resistance to cytosine arabinoside in acute leukemia: the significance of mutations in CTP synthetase.	Cytarabine	14-34	CTP synthase 1	Homo sapiens	87-101
8309250-3	1994	Mutations which cause ara-C resistance in a chinese hamster ovary (CHO) cell model have been identified as regulatory base substitutions, occurring in specific sites of the gene coding for an enzyme critical in pyrimidine metabolism, CTP synthetase (CTPs).	Cytarabine	22-27	CTP synthase 1	Cricetulus griseus	234-248
8309250-3	1994	Mutations which cause ara-C resistance in a chinese hamster ovary (CHO) cell model have been identified as regulatory base substitutions, occurring in specific sites of the gene coding for an enzyme critical in pyrimidine metabolism, CTP synthetase (CTPs).	Cytarabine	22-27	CTP synthase 1	Cricetulus griseus	250-254
7506123-0	1994	Combinations of stem cell factor with other hematopoietic growth factors enhance growth and sensitivity to cytosine arabinoside of blast progenitors in acute myelogenous leukemia.	Cytarabine	107-127	KIT ligand	Homo sapiens	16-32
7506123-2	1994	We report the effects of stem cell factor (SCF) on the growth and sensitivity to 1-beta-D-arabinofuranosylcytosine (Ara-C) of blast progenitors in acute myelogenous leukemia.	Cytarabine	81-114	KIT ligand	Homo sapiens	25-41
7506123-2	1994	We report the effects of stem cell factor (SCF) on the growth and sensitivity to 1-beta-D-arabinofuranosylcytosine (Ara-C) of blast progenitors in acute myelogenous leukemia.	Cytarabine	81-114	KIT ligand	Homo sapiens	43-46
7506123-2	1994	We report the effects of stem cell factor (SCF) on the growth and sensitivity to 1-beta-D-arabinofuranosylcytosine (Ara-C) of blast progenitors in acute myelogenous leukemia.	Cytarabine	116-121	KIT ligand	Homo sapiens	25-41
7506123-2	1994	We report the effects of stem cell factor (SCF) on the growth and sensitivity to 1-beta-D-arabinofuranosylcytosine (Ara-C) of blast progenitors in acute myelogenous leukemia.	Cytarabine	116-121	KIT ligand	Homo sapiens	43-46
7506123-5	1994	Blast cells of patients that displayed synergistic growth enhancement with SCF displayed the highest Ara-C sensitivity when HGFs were used in combination with SCF.	Cytarabine	101-106	KIT ligand	Homo sapiens	75-78
7506123-5	1994	Blast cells of patients that displayed synergistic growth enhancement with SCF displayed the highest Ara-C sensitivity when HGFs were used in combination with SCF.	Cytarabine	101-106	KIT ligand	Homo sapiens	159-162
7506123-7	1994	These data indicate that SCF enhances growth and sensitivity to Ara-C of acute myelogenous leukemia blast progenitors in a closely correlated fashion and that the cell cycle changes as well as other mechanisms are involved in the Ara-C sensitivity modulation by SCF.	Cytarabine	64-69	KIT ligand	Homo sapiens	25-28
7506123-7	1994	These data indicate that SCF enhances growth and sensitivity to Ara-C of acute myelogenous leukemia blast progenitors in a closely correlated fashion and that the cell cycle changes as well as other mechanisms are involved in the Ara-C sensitivity modulation by SCF.	Cytarabine	230-235	KIT ligand	Homo sapiens	25-28
7506123-7	1994	These data indicate that SCF enhances growth and sensitivity to Ara-C of acute myelogenous leukemia blast progenitors in a closely correlated fashion and that the cell cycle changes as well as other mechanisms are involved in the Ara-C sensitivity modulation by SCF.	Cytarabine	230-235	KIT ligand	Homo sapiens	262-265
7507861-4	1994	It was further observed that GRE prevented the antiproliferative effects of cytosine arabinoside (Ara-C) and azadeoxycytidine, suggesting that GRE contained cytidine deaminase (CDD) activity, since CDD is known to abolish the effects of these nucleoside analogs.	Cytarabine	76-96	cytidine deaminase	Homo sapiens	157-175
7507861-4	1994	It was further observed that GRE prevented the antiproliferative effects of cytosine arabinoside (Ara-C) and azadeoxycytidine, suggesting that GRE contained cytidine deaminase (CDD) activity, since CDD is known to abolish the effects of these nucleoside analogs.	Cytarabine	76-96	cytidine deaminase	Homo sapiens	177-180
7507861-4	1994	It was further observed that GRE prevented the antiproliferative effects of cytosine arabinoside (Ara-C) and azadeoxycytidine, suggesting that GRE contained cytidine deaminase (CDD) activity, since CDD is known to abolish the effects of these nucleoside analogs.	Cytarabine	98-103	cytidine deaminase	Homo sapiens	157-175
7507861-4	1994	It was further observed that GRE prevented the antiproliferative effects of cytosine arabinoside (Ara-C) and azadeoxycytidine, suggesting that GRE contained cytidine deaminase (CDD) activity, since CDD is known to abolish the effects of these nucleoside analogs.	Cytarabine	98-103	cytidine deaminase	Homo sapiens	177-180
7509013-5	1994	Preincubation in Biorich medium with the addition of G + GM-CSF or IL-3 caused a significant enhancement of sensitivity to Ara-C across the dose curve.	Cytarabine	123-128	interleukin 3	Homo sapiens	67-71
8273969-0	1994	Therapeutic manipulation of cytokines: transforming growth factor beta-1 protects mice treated with lethal doses of cytarabine.	Cytarabine	116-126	hemoglobin, beta adult major chain	Mus musculus	66-72
8273969-3	1994	Since the dose of cytotoxic chemotherapy is limited by its adverse effects on bone marrow and gut cells, we proposed that a TGF beta 1-induced block at G1/S would diminish the S phase toxicity of high dose cytarabine (ara-C).	Cytarabine	206-216	transforming growth factor, beta 1	Mus musculus	124-134
8273969-3	1994	Since the dose of cytotoxic chemotherapy is limited by its adverse effects on bone marrow and gut cells, we proposed that a TGF beta 1-induced block at G1/S would diminish the S phase toxicity of high dose cytarabine (ara-C).	Cytarabine	218-223	transforming growth factor, beta 1	Mus musculus	124-134
8273969-5	1994	Pretreatment with TGF beta 1 6-24 hours before the first dose of ara-C proved to be significantly protective; 8/9 TGF beta 1-pretreated mice survived versus 1/9 treated with TGF beta 1 for 3 hours or less or with ara-C alone (chi2 = 10.89 P = 0.001).	Cytarabine	65-70	transforming growth factor, beta 1	Mus musculus	18-28
8273969-5	1994	Pretreatment with TGF beta 1 6-24 hours before the first dose of ara-C proved to be significantly protective; 8/9 TGF beta 1-pretreated mice survived versus 1/9 treated with TGF beta 1 for 3 hours or less or with ara-C alone (chi2 = 10.89 P = 0.001).	Cytarabine	213-218	transforming growth factor, beta 1	Mus musculus	18-28
8174200-1	1994	Previous studies have demonstrated that treatment with fludarabine 4 h prior to arabinosylcytosine (ara-C) potentiates the accumulation of the active triphosphate of ara-C (ara-CTP) in leukemic lymphocytes.	Cytarabine	80-98	solute carrier family 25 member 1	Homo sapiens	177-180
7914749-10	1994	Furthermore, 11 AML patients at primary diagnosis, including five AML patients with P-gp overexpression, who were treated with idarubicin, vepesid, and cytarabine V (ara-C) showed a complete remission.	Cytarabine	166-171	ATP binding cassette subfamily B member 1	Homo sapiens	84-88
7914749-11	1994	Additionally, one daunorubicin-cytarabine-pretreated refractory AML patient was treated with the oral form of the P-gp modulator drug dexniguldipine and achieved complete remission for a duration of 7 months.	Cytarabine	31-41	ATP binding cassette subfamily B member 1	Homo sapiens	114-118
8174200-1	1994	Previous studies have demonstrated that treatment with fludarabine 4 h prior to arabinosylcytosine (ara-C) potentiates the accumulation of the active triphosphate of ara-C (ara-CTP) in leukemic lymphocytes.	Cytarabine	100-105	solute carrier family 25 member 1	Homo sapiens	177-180
8174200-1	1994	Previous studies have demonstrated that treatment with fludarabine 4 h prior to arabinosylcytosine (ara-C) potentiates the accumulation of the active triphosphate of ara-C (ara-CTP) in leukemic lymphocytes.	Cytarabine	166-171	solute carrier family 25 member 1	Homo sapiens	177-180
8132852-3	1994	That of ara-C similarly reached a maximum (102.2 +/- 39.9 mg/mL) at the end of the infusion and then declined with t1/2 alpha of 1.37 +/- 1.11 hours and t1/2 beta of 11.2 +/- 4.31 hours.	Cytarabine	8-13	CD6 molecule	Homo sapiens	115-133
7506674-8	1994	On the other hand, SCF suppressed induction of benzidine-positive cells when c-kit-positive cells were treated with hemin and Ara-C, especially at a low concentration.	Cytarabine	126-131	KIT ligand	Homo sapiens	19-22
7506674-8	1994	On the other hand, SCF suppressed induction of benzidine-positive cells when c-kit-positive cells were treated with hemin and Ara-C, especially at a low concentration.	Cytarabine	126-131	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	77-82
8399394-1	1993	Deoxycytidine kinase is a key anabolic enzyme for the activation of ara-C and other antitumor drugs, as well as normal purine and pyrimidine deoxynucleotides.	Cytarabine	68-73	deoxycytidine kinase	Homo sapiens	0-20
7906380-0	1994	Cytosine arabinoside and mitoxantrone treatment of relapsed or refractory childhood leukemia: initial response and relationship to multidrug resistance gene 1.	Cytarabine	0-20	ATP binding cassette subfamily B member 1	Homo sapiens	131-158
8231250-5	1993	In contrast, c-myc expression decreased when cells underwent terminal differentiation, either along the myelomonocytic (by 12-O-tetradecanoylphorbol-13-acetate) or erythroid (by 1-beta-D-arabinofuranosylcytosine) lineages.	Cytarabine	178-211	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	13-18
7514282-0	1993	Cell kinetic effects of granulocyte colony-stimulating factor on the sensitivity of nonlymphocytic leukemia cells to cytosine arabinoside.	Cytarabine	117-137	colony stimulating factor 3	Homo sapiens	24-61
7514282-5	1993	The number of clonogenic leukemic cells in methylcellulose was also smaller after culture with G-CSF followed by Ara-C than Ara-C alone.	Cytarabine	124-129	colony stimulating factor 3	Homo sapiens	95-100
8399394-12	1993	In contrast, phosphorylation of ara-C by deoxycytidine kinase I utilized GTP, dGTP, or ATP as a phosphate donor.	Cytarabine	32-37	deoxycytidine kinase	Homo sapiens	41-61
8399394-3	1993	Deoxycytidine kinase I utilized dCyd and ara-C as substrates, while deoxycytidine kinase II used dCyd and dThd as substrates.	Cytarabine	41-46	deoxycytidine kinase	Homo sapiens	0-20
8399394-4	1993	Deoxycytidine kinase kinase II had very low activity on ara-C as a substrate.	Cytarabine	56-61	deoxycytidine kinase	Homo sapiens	0-20
8395394-3	1993	12-O-Tetradecanoyl phorbol-13-acetate and cytosine arabinoside produced a coordinate and stable stimulation of both vimentin and A/C lamin expression in U-937 cells.	Cytarabine	42-62	vimentin	Homo sapiens	116-124
7692194-11	1993	The results obtained by the clonogenic assays showed increased cytotoxicity of Ara-C combined with G-CSF, IL-3, or GM-CSF.	Cytarabine	79-84	interleukin 3	Homo sapiens	106-110
7692194-12	1993	The median IC75 values of Ara-C decreased from 0.056 to 0.0168 microgram/ml with G-CSF (p = 0.01), from 0.108 to 0.0168 microgram/ml with IL-3 (p = 0.004) and from 0.12 to 0.0204 microgram/ml for GM-CSF (p = 0.02).	Cytarabine	26-31	colony stimulating factor 3	Homo sapiens	81-86
7692194-12	1993	The median IC75 values of Ara-C decreased from 0.056 to 0.0168 microgram/ml with G-CSF (p = 0.01), from 0.108 to 0.0168 microgram/ml with IL-3 (p = 0.004) and from 0.12 to 0.0204 microgram/ml for GM-CSF (p = 0.02).	Cytarabine	26-31	colony stimulating factor 2	Homo sapiens	196-202
7690249-0	1993	Activation of the early growth response 1 gene and nuclear pp90rsk in human myeloid leukemia cells by 1-(beta-D-arabinofuranosyl)cytosine.	Cytarabine	102-137	early growth response 1	Homo sapiens	18-41
7690249-2	1993	The present work has examined the effects of 1-(beta-D-arabinofuranosyl)cytosine (ara-C), an antileukemia agent that misincorporates into DNA, on EGR-1 expression.	Cytarabine	45-80	early growth response 1	Homo sapiens	146-151
7690249-2	1993	The present work has examined the effects of 1-(beta-D-arabinofuranosyl)cytosine (ara-C), an antileukemia agent that misincorporates into DNA, on EGR-1 expression.	Cytarabine	82-87	early growth response 1	Homo sapiens	146-151
7690249-3	1993	Treatment of HL-525 myeloid leukemia cells with ara-C was associated with transient increases in EGR-1 mRNA levels.	Cytarabine	48-53	early growth response 1	Homo sapiens	97-102
7690249-5	1993	Sequences responsive to ara-C-induced signals were determined by deletion analysis of the EGR-1 promoter.	Cytarabine	24-29	early growth response 1	Homo sapiens	90-95
8395394-3	1993	12-O-Tetradecanoyl phorbol-13-acetate and cytosine arabinoside produced a coordinate and stable stimulation of both vimentin and A/C lamin expression in U-937 cells.	Cytarabine	42-62	lamin A/C	Homo sapiens	133-138
8392910-7	1993	The enhanced EGF and transferrin binding is paralleled by a twofold increase of in vitro targeting of Ara-C-treated KB and A549 cells with anti-EGFR 108.1 mAb and anti-TrfR OKT9 mAb.	Cytarabine	102-107	transferrin	Homo sapiens	21-32
8371577-3	1993	When K562 cells were differentiated into the erythroid lineage by addition either of 1-beta-D-arabinofuranosylcytosine or hydroxyurea, an increase in ApoE mRNA and protein was detected.	Cytarabine	85-118	apolipoprotein E	Homo sapiens	150-154
8392910-7	1993	The enhanced EGF and transferrin binding is paralleled by a twofold increase of in vitro targeting of Ara-C-treated KB and A549 cells with anti-EGFR 108.1 mAb and anti-TrfR OKT9 mAb.	Cytarabine	102-107	epidermal growth factor receptor	Homo sapiens	144-148
8392910-0	1993	Cytosine arabinoside increases the binding of 125I-labelled epidermal growth factor and 125I-transferrin and enhances the in vitro targeting of human tumour cells with anti-(growth factor receptor) mAb.	Cytarabine	0-20	epidermal growth factor	Homo sapiens	60-83
8392910-0	1993	Cytosine arabinoside increases the binding of 125I-labelled epidermal growth factor and 125I-transferrin and enhances the in vitro targeting of human tumour cells with anti-(growth factor receptor) mAb.	Cytarabine	0-20	transferrin	Homo sapiens	93-104
8392910-7	1993	The enhanced EGF and transferrin binding is paralleled by a twofold increase of in vitro targeting of Ara-C-treated KB and A549 cells with anti-EGFR 108.1 mAb and anti-TrfR OKT9 mAb.	Cytarabine	102-107	transferrin receptor	Homo sapiens	168-172
8392910-2	1993	An increase in the number of epidermal growth factor and transferrin receptors (EGFR, TrfR) is induced by Ara-C on these cells.	Cytarabine	106-111	epidermal growth factor	Homo sapiens	29-52
8392910-8	1993	We propose that Ara-C could provide a new approach for the improvement of the therapeutic index of anti-EGFR and anti-TrfR immunoconjugates.	Cytarabine	16-21	epidermal growth factor receptor	Homo sapiens	104-108
8392910-2	1993	An increase in the number of epidermal growth factor and transferrin receptors (EGFR, TrfR) is induced by Ara-C on these cells.	Cytarabine	106-111	transferrin	Homo sapiens	57-68
8392910-8	1993	We propose that Ara-C could provide a new approach for the improvement of the therapeutic index of anti-EGFR and anti-TrfR immunoconjugates.	Cytarabine	16-21	transferrin receptor	Homo sapiens	118-122
8392910-2	1993	An increase in the number of epidermal growth factor and transferrin receptors (EGFR, TrfR) is induced by Ara-C on these cells.	Cytarabine	106-111	epidermal growth factor receptor	Homo sapiens	80-84
8355515-7	1993	The following gastrointestinal and hematological toxicities were attributable to Ara-C, as they had not been observed in these patients during the preceding IFN-alpha monotherapy period.	Cytarabine	81-86	interferon alpha 2	Homo sapiens	157-166
8392910-2	1993	An increase in the number of epidermal growth factor and transferrin receptors (EGFR, TrfR) is induced by Ara-C on these cells.	Cytarabine	106-111	transferrin receptor	Homo sapiens	86-90
8392910-5	1993	Two classes of EGF-binding sites with a Kd of 0.055 nM and 2.3 nM respectively, and one class of transferrin-binding sites with a Kd of about 4 nM are detected on both untreated and Ara-C-treated KB cells.	Cytarabine	182-187	transferrin	Homo sapiens	97-108
8344453-2	1993	We investigated the mitogenic effect of these growth factors on quiescent mature oligodendrocytes (OL) expressing myelin basic protein (MBP) in OL cultures that were treated for 3 days with cytosine arabinoside (ARA-C) in order to kill O-2A precursors which divide in chemically defined medium.	Cytarabine	190-210	myelin basic protein	Homo sapiens	136-139
8344453-9	1993	Conditioned medium from O-2A precursors almost halved the bFGF-induced OL proliferation after treatment with ARA-C, suggesting that O-2A progenitors control the proliferation of a subpopulation of mature OL (possibly young mature OL) via the secretion of active molecule(s).	Cytarabine	109-114	fibroblast growth factor 2	Homo sapiens	58-62
7688839-8	1993	Ara-C cytotoxicity to normal bone marrow progenitors was enhanced significantly only by G-CSF (p = 0.02 at 0.01 microM, p = 0.01 at 0.1 microM and p &lt; 0.01 at 1 microM Ara-C), and by GM-CSF at 0.1 microM Ara-C (p = 0.045).	Cytarabine	0-5	colony stimulating factor 3	Homo sapiens	88-93
7688839-8	1993	Ara-C cytotoxicity to normal bone marrow progenitors was enhanced significantly only by G-CSF (p = 0.02 at 0.01 microM, p = 0.01 at 0.1 microM and p &lt; 0.01 at 1 microM Ara-C), and by GM-CSF at 0.1 microM Ara-C (p = 0.045).	Cytarabine	0-5	colony stimulating factor 2	Homo sapiens	186-192
8407287-4	1993	In the present study, we have extended these observations by demonstrating that whole synthetic T beta 4 is more effective than the N-terminal tetrapeptide in protecting mice from the toxicity of ara-C.	Cytarabine	196-201	thymosin, beta 4, X chromosome	Mus musculus	96-104
8350628-7	1993	MEG-01/nu was evaluated for sensitivity to cytosine arabinoside, vincristine, and daunorubicin in vitro and in vivo.	Cytarabine	43-63	protein tyrosine phosphatase non-receptor type 4	Homo sapiens	0-3
8326741-0	1993	Recombinant GM-CSF modulates the metabolism of cytosine arabinoside in leukemic cells in bone marrow.	Cytarabine	47-67	colony stimulating factor 2	Homo sapiens	12-18
7686601-1	1993	Deoxycytidine kinase activity (dCk) was monitored in cell lines from a rat acute myeloid leukemia model of acquired resistance to cytosine arabinoside (AraC) and decitabine (DAC).	Cytarabine	130-150	deoxycytidine kinase	Rattus norvegicus	0-20
8326741-1	1993	The effect of human recombinant GM-CSF (rGM-CSF) on the metabolism of high dose ara-C was determined in bone marrow mononuclear cells (BMMCs) from eight normal volunteers and from seven patients with acute myelogenous leukemia (AML).	Cytarabine	80-85	colony stimulating factor 2	Homo sapiens	32-38
7686601-1	1993	Deoxycytidine kinase activity (dCk) was monitored in cell lines from a rat acute myeloid leukemia model of acquired resistance to cytosine arabinoside (AraC) and decitabine (DAC).	Cytarabine	130-150	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	31-34
8326741-1	1993	The effect of human recombinant GM-CSF (rGM-CSF) on the metabolism of high dose ara-C was determined in bone marrow mononuclear cells (BMMCs) from eight normal volunteers and from seven patients with acute myelogenous leukemia (AML).	Cytarabine	80-85	colony stimulating factor 2	Rattus norvegicus	40-47
7686601-1	1993	Deoxycytidine kinase activity (dCk) was monitored in cell lines from a rat acute myeloid leukemia model of acquired resistance to cytosine arabinoside (AraC) and decitabine (DAC).	Cytarabine	152-156	deoxycytidine kinase	Rattus norvegicus	0-20
7686601-1	1993	Deoxycytidine kinase activity (dCk) was monitored in cell lines from a rat acute myeloid leukemia model of acquired resistance to cytosine arabinoside (AraC) and decitabine (DAC).	Cytarabine	152-156	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	31-34
8326741-7	1993	Moreover, when the cells were preincubated with rGM-CSF for 16 h prior to the exposure to ara-C, leukemic blasts achieved a 7-fold higher ara-CTP/dCTP ratio as compared with normal marrow cells.	Cytarabine	90-95	colony stimulating factor 2	Rattus norvegicus	48-55
7686602-2	1993	Previous studies have shown: (i) blast cells exposed to retinoic acid before cytosine arabinoside (Ara-C) usually show increased sensitivity, but after some retinoic acid exposure times, sensitivity may be decreased; (ii) factor-sensitive or responsive blasts cultured with granulocyte colony-stimulating factor (G-CSF) are regularly more Ara-C-sensitive than when cultured with granulocyte-macrophage CSF (GM-CSF).	Cytarabine	99-104	colony stimulating factor 3	Homo sapiens	274-311
8326741-8	1993	Treatment of the cells with rGM-CSF, either simultaneously or sequentially, resulted in significantly greater amounts of ara-C incorporation into DNA in leukemic marrow cells than normal counterparts.	Cytarabine	121-126	colony stimulating factor 2	Rattus norvegicus	28-35
7686602-2	1993	Previous studies have shown: (i) blast cells exposed to retinoic acid before cytosine arabinoside (Ara-C) usually show increased sensitivity, but after some retinoic acid exposure times, sensitivity may be decreased; (ii) factor-sensitive or responsive blasts cultured with granulocyte colony-stimulating factor (G-CSF) are regularly more Ara-C-sensitive than when cultured with granulocyte-macrophage CSF (GM-CSF).	Cytarabine	99-104	colony stimulating factor 3	Homo sapiens	313-318
7686602-2	1993	Previous studies have shown: (i) blast cells exposed to retinoic acid before cytosine arabinoside (Ara-C) usually show increased sensitivity, but after some retinoic acid exposure times, sensitivity may be decreased; (ii) factor-sensitive or responsive blasts cultured with granulocyte colony-stimulating factor (G-CSF) are regularly more Ara-C-sensitive than when cultured with granulocyte-macrophage CSF (GM-CSF).	Cytarabine	99-104	colony stimulating factor 2	Homo sapiens	379-405
8326741-9	1993	The higher accumulation of ara-CTP and subsequent increased incorporation of ara-C into DNA in leukemic cells treated with rGM-CSF lead to the enhanced ara-C-mediated inhibition of DNA synthesis as compared with normal BMMCs.	Cytarabine	27-32	colony stimulating factor 2	Rattus norvegicus	123-130
7686602-2	1993	Previous studies have shown: (i) blast cells exposed to retinoic acid before cytosine arabinoside (Ara-C) usually show increased sensitivity, but after some retinoic acid exposure times, sensitivity may be decreased; (ii) factor-sensitive or responsive blasts cultured with granulocyte colony-stimulating factor (G-CSF) are regularly more Ara-C-sensitive than when cultured with granulocyte-macrophage CSF (GM-CSF).	Cytarabine	99-104	colony stimulating factor 2	Homo sapiens	407-413
8326741-9	1993	The higher accumulation of ara-CTP and subsequent increased incorporation of ara-C into DNA in leukemic cells treated with rGM-CSF lead to the enhanced ara-C-mediated inhibition of DNA synthesis as compared with normal BMMCs.	Cytarabine	77-82	colony stimulating factor 2	Rattus norvegicus	123-130
7686602-9	1993	In studies of growth factors, a single factor-dependent cell line (OCI/AML-5) was used to compare the effects of G-CSF and GM-CSF on Ara-C sensitivity.	Cytarabine	133-138	colony stimulating factor 2	Homo sapiens	123-129
7686602-11	1993	G-CSF and GM-CSF were most effective in increasing or decreasing Ara-C, respectively, when the factor under test was included in the methylcellulose cultures.	Cytarabine	65-70	colony stimulating factor 3	Homo sapiens	0-5
8326741-10	1993	The selective accumulation of ara-CTP in leukemic vs normal cells have implications for the efficacy of the treatment of AML patients with high dose ara-C and rGM-CSF.	Cytarabine	30-35	colony stimulating factor 2	Rattus norvegicus	159-166
7686602-11	1993	G-CSF and GM-CSF were most effective in increasing or decreasing Ara-C, respectively, when the factor under test was included in the methylcellulose cultures.	Cytarabine	65-70	colony stimulating factor 2	Homo sapiens	10-16
8509220-5	1993	NIH-3T3 transformants expressing H-ras were less sensitive than those expressing trk or the wild type to the indoloquinone EO9, methotrexate and arabino-furanosylcytosine.	Cytarabine	145-170	Harvey rat sarcoma virus oncogene	Mus musculus	33-38
7689660-0	1993	[Enhanced sensitivity to cytosine arabinoside by combined stimulation of steel factor and GM-CSF in a factor-dependent leukemic cell line, MO7e--in terms of a possible clinical application to AML treatment].	Cytarabine	25-45	KIT ligand	Homo sapiens	73-85
7689660-0	1993	[Enhanced sensitivity to cytosine arabinoside by combined stimulation of steel factor and GM-CSF in a factor-dependent leukemic cell line, MO7e--in terms of a possible clinical application to AML treatment].	Cytarabine	25-45	colony stimulating factor 2	Homo sapiens	90-96
7689660-8	1993	Furthermore, by combination of SLF and GM-CSF, the ara-C sensitivity was significantly wore graty enhanced than by each cytokine alone.	Cytarabine	51-56	colony stimulating factor 2	Homo sapiens	39-45
7691332-0	1993	Effects of mast cell growth factor on Ara-C mediated acute myeloid leukemia cell killing.	Cytarabine	38-43	interleukin 3	Homo sapiens	11-34
7691332-6	1993	We report in this preliminary study that MGF is able to increase proliferation in 75% of the samples studied and enhance Ara-C cytotoxicity in some of these cases.	Cytarabine	121-126	interleukin 3	Homo sapiens	41-44
8388815-6	1993	In cultures treated with RA and cytosine arabinoside, both met/HGF/SFR mRNA and protein can be localized specifically to nondividing neuronal cells.	Cytarabine	32-52	hepatocyte growth factor	Mus musculus	63-66
8509220-5	1993	NIH-3T3 transformants expressing H-ras were less sensitive than those expressing trk or the wild type to the indoloquinone EO9, methotrexate and arabino-furanosylcytosine.	Cytarabine	145-170	neurotrophic tyrosine kinase, receptor, type 1	Mus musculus	81-84
8464233-0	1993	Mitoxantrone, etoposide and intermediate-dose Ara-C (MEC): an effective regimen for poor risk acute myeloid leukemia.	Cytarabine	46-51	C-C motif chemokine ligand 28	Homo sapiens	53-56
8512587-0	1993	Activation of the jun-D gene during treatment of human myeloid leukemia cells with 1-beta-D-arabinofuranosylcytosine.	Cytarabine	83-116	JunD proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	18-23
8483318-4	1993	The DNA topoisomerase inhibitors mitoxantrone, VP-16 (etoposide), and m-AMSA (amsacrine) were more effective in inducing DNA breaks than was hydroxyurea or cytosine arabinoside (AraC).	Cytarabine	178-182	host cell factor C1	Homo sapiens	47-52
7685751-0	1993	Enhancement of cytosine arabinoside cytotoxicity by granulocyte/macrophage colony-stimulating factor and granulocyte colony-stimulating factor in a human myeloblastic leukemia cell line.	Cytarabine	15-35	colony stimulating factor 2	Homo sapiens	52-100
7685751-0	1993	Enhancement of cytosine arabinoside cytotoxicity by granulocyte/macrophage colony-stimulating factor and granulocyte colony-stimulating factor in a human myeloblastic leukemia cell line.	Cytarabine	15-35	colony stimulating factor 3	Homo sapiens	105-142
7685751-1	1993	Enhancement of the cytotoxicity of cytosine arabinoside (ara-C) by granulocyte/macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF), and the mechanisms involved, were studied in the AML-193 human leukemia cell line.	Cytarabine	35-55	colony stimulating factor 2	Homo sapiens	67-115
7685751-1	1993	Enhancement of the cytotoxicity of cytosine arabinoside (ara-C) by granulocyte/macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF), and the mechanisms involved, were studied in the AML-193 human leukemia cell line.	Cytarabine	35-55	colony stimulating factor 2	Homo sapiens	117-123
7685751-1	1993	Enhancement of the cytotoxicity of cytosine arabinoside (ara-C) by granulocyte/macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF), and the mechanisms involved, were studied in the AML-193 human leukemia cell line.	Cytarabine	35-55	colony stimulating factor 3	Homo sapiens	129-166
7685751-1	1993	Enhancement of the cytotoxicity of cytosine arabinoside (ara-C) by granulocyte/macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF), and the mechanisms involved, were studied in the AML-193 human leukemia cell line.	Cytarabine	35-55	colony stimulating factor 3	Homo sapiens	168-173
7685751-1	1993	Enhancement of the cytotoxicity of cytosine arabinoside (ara-C) by granulocyte/macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF), and the mechanisms involved, were studied in the AML-193 human leukemia cell line.	Cytarabine	57-62	colony stimulating factor 2	Homo sapiens	67-115
7685751-1	1993	Enhancement of the cytotoxicity of cytosine arabinoside (ara-C) by granulocyte/macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF), and the mechanisms involved, were studied in the AML-193 human leukemia cell line.	Cytarabine	57-62	colony stimulating factor 2	Homo sapiens	117-123
7685751-1	1993	Enhancement of the cytotoxicity of cytosine arabinoside (ara-C) by granulocyte/macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF), and the mechanisms involved, were studied in the AML-193 human leukemia cell line.	Cytarabine	57-62	colony stimulating factor 3	Homo sapiens	129-166
7685751-1	1993	Enhancement of the cytotoxicity of cytosine arabinoside (ara-C) by granulocyte/macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF), and the mechanisms involved, were studied in the AML-193 human leukemia cell line.	Cytarabine	57-62	colony stimulating factor 3	Homo sapiens	168-173
7687859-4	1993	G-CSF (5 micrograms/kg) was administered during the recovery phase in 6/14 courses with Ara-C/Etop and in 4/13 courses with Ara-C/Mit.	Cytarabine	88-93	colony stimulating factor 3	Homo sapiens	0-5
7687859-4	1993	G-CSF (5 micrograms/kg) was administered during the recovery phase in 6/14 courses with Ara-C/Etop and in 4/13 courses with Ara-C/Mit.	Cytarabine	124-129	colony stimulating factor 3	Homo sapiens	0-5
7689779-1	1993	Because recombinant human granulocyte colony-stimulating factor (G-CSF) has been reported to increase the sensitivity of acute myelogenous leukemia (AML) blast cells to cytosine arabinoside (Ara-C) in vitro, we treated a patient with refractory AML with an Ara-C-based regimen in combination with G-CSF (G-CSF/Ara-C therapy).	Cytarabine	169-189	colony stimulating factor 3	Homo sapiens	26-63
8435808-2	1993	BACKGROUND: The use of high-dose cytosine arabinoside (Ara-C) may be complicated by a characteristic form of cerebellar neurotoxicity.	Cytarabine	33-53	ATP binding cassette subfamily C member 6	Homo sapiens	55-58
8388142-4	1993	The results of experiments in which cultured cells were infected with Ad5-Luc 3 in the presence or absence of 1-beta-D-arabinofuranosyl cytosine (AraC) showed that the majority of luciferase expression was dependent on viral DNA replication.	Cytarabine	110-144	Alzheimer disease, familial, type 5	Homo sapiens	70-73
8318674-6	1993	As TNF and PAF are thought to be involved in the development of septic shock and adult respiratory distress syndrome, we hypothesize that high-dose Ara-C may be associated with cytokine release.	Cytarabine	148-153	tumor necrosis factor	Homo sapiens	3-6
8318674-6	1993	As TNF and PAF are thought to be involved in the development of septic shock and adult respiratory distress syndrome, we hypothesize that high-dose Ara-C may be associated with cytokine release.	Cytarabine	148-153	PCNA clamp associated factor	Homo sapiens	11-14
8445942-0	1993	Granulocyte-macrophage colony-stimulating factor in association to timed-sequential chemotherapy with mitoxantrone, etoposide, and cytarabine for refractory acute myelogenous leukemia.	Cytarabine	131-141	colony stimulating factor 2	Homo sapiens	0-48
8435667-2	1993	He was treated with vasopressin (DDAVP) with a good response and concurrently induced with daunorubicin and conventional doses of cytosine arabinoside.	Cytarabine	130-150	arginine vasopressin	Homo sapiens	20-31
8368048-9	1993	Actual studies focus on combinations of IFN-alpha and cytostatics, e.g. low-dose cytosine arabinoside.	Cytarabine	81-101	interferon alpha 1	Homo sapiens	40-49
7689779-1	1993	Because recombinant human granulocyte colony-stimulating factor (G-CSF) has been reported to increase the sensitivity of acute myelogenous leukemia (AML) blast cells to cytosine arabinoside (Ara-C) in vitro, we treated a patient with refractory AML with an Ara-C-based regimen in combination with G-CSF (G-CSF/Ara-C therapy).	Cytarabine	169-189	colony stimulating factor 3	Homo sapiens	65-70
7689779-1	1993	Because recombinant human granulocyte colony-stimulating factor (G-CSF) has been reported to increase the sensitivity of acute myelogenous leukemia (AML) blast cells to cytosine arabinoside (Ara-C) in vitro, we treated a patient with refractory AML with an Ara-C-based regimen in combination with G-CSF (G-CSF/Ara-C therapy).	Cytarabine	191-196	colony stimulating factor 3	Homo sapiens	26-63
7689779-1	1993	Because recombinant human granulocyte colony-stimulating factor (G-CSF) has been reported to increase the sensitivity of acute myelogenous leukemia (AML) blast cells to cytosine arabinoside (Ara-C) in vitro, we treated a patient with refractory AML with an Ara-C-based regimen in combination with G-CSF (G-CSF/Ara-C therapy).	Cytarabine	191-196	colony stimulating factor 3	Homo sapiens	65-70
7689779-1	1993	Because recombinant human granulocyte colony-stimulating factor (G-CSF) has been reported to increase the sensitivity of acute myelogenous leukemia (AML) blast cells to cytosine arabinoside (Ara-C) in vitro, we treated a patient with refractory AML with an Ara-C-based regimen in combination with G-CSF (G-CSF/Ara-C therapy).	Cytarabine	191-196	colony stimulating factor 3	Homo sapiens	297-302
7689779-1	1993	Because recombinant human granulocyte colony-stimulating factor (G-CSF) has been reported to increase the sensitivity of acute myelogenous leukemia (AML) blast cells to cytosine arabinoside (Ara-C) in vitro, we treated a patient with refractory AML with an Ara-C-based regimen in combination with G-CSF (G-CSF/Ara-C therapy).	Cytarabine	191-196	colony stimulating factor 3	Homo sapiens	297-302
7689779-1	1993	Because recombinant human granulocyte colony-stimulating factor (G-CSF) has been reported to increase the sensitivity of acute myelogenous leukemia (AML) blast cells to cytosine arabinoside (Ara-C) in vitro, we treated a patient with refractory AML with an Ara-C-based regimen in combination with G-CSF (G-CSF/Ara-C therapy).	Cytarabine	257-262	colony stimulating factor 3	Homo sapiens	26-63
7689779-1	1993	Because recombinant human granulocyte colony-stimulating factor (G-CSF) has been reported to increase the sensitivity of acute myelogenous leukemia (AML) blast cells to cytosine arabinoside (Ara-C) in vitro, we treated a patient with refractory AML with an Ara-C-based regimen in combination with G-CSF (G-CSF/Ara-C therapy).	Cytarabine	257-262	colony stimulating factor 3	Homo sapiens	65-70
7689779-1	1993	Because recombinant human granulocyte colony-stimulating factor (G-CSF) has been reported to increase the sensitivity of acute myelogenous leukemia (AML) blast cells to cytosine arabinoside (Ara-C) in vitro, we treated a patient with refractory AML with an Ara-C-based regimen in combination with G-CSF (G-CSF/Ara-C therapy).	Cytarabine	257-262	colony stimulating factor 3	Homo sapiens	26-63
7689779-1	1993	Because recombinant human granulocyte colony-stimulating factor (G-CSF) has been reported to increase the sensitivity of acute myelogenous leukemia (AML) blast cells to cytosine arabinoside (Ara-C) in vitro, we treated a patient with refractory AML with an Ara-C-based regimen in combination with G-CSF (G-CSF/Ara-C therapy).	Cytarabine	257-262	colony stimulating factor 3	Homo sapiens	65-70
8436210-2	1993	The intracellular phosphorylation of ara-C to its 5"-triphosphate (ara-CTP) is a prerequisite for its cytotoxic effects.	Cytarabine	37-42	solute carrier family 25 member 1	Homo sapiens	71-74
8462021-3	1993	In contrast, the combination of ara-C with M-CSF or with the leukemia inhibitory factor (LIF) appears to be useful in overcoming the block in differentiation of leukemic blast, while the effects of GM-CSF and IL-3 on ara-C-induced differentiation appear limited.	Cytarabine	32-37	LIF interleukin 6 family cytokine	Homo sapiens	89-92
8462021-3	1993	In contrast, the combination of ara-C with M-CSF or with the leukemia inhibitory factor (LIF) appears to be useful in overcoming the block in differentiation of leukemic blast, while the effects of GM-CSF and IL-3 on ara-C-induced differentiation appear limited.	Cytarabine	217-222	LIF interleukin 6 family cytokine	Homo sapiens	89-92
8462021-3	1993	In contrast, the combination of ara-C with M-CSF or with the leukemia inhibitory factor (LIF) appears to be useful in overcoming the block in differentiation of leukemic blast, while the effects of GM-CSF and IL-3 on ara-C-induced differentiation appear limited.	Cytarabine	217-222	colony stimulating factor 2	Homo sapiens	198-204
8462021-3	1993	In contrast, the combination of ara-C with M-CSF or with the leukemia inhibitory factor (LIF) appears to be useful in overcoming the block in differentiation of leukemic blast, while the effects of GM-CSF and IL-3 on ara-C-induced differentiation appear limited.	Cytarabine	217-222	interleukin 3	Homo sapiens	209-213
8436210-6	1993	When the cells were incubated in RPMI-1640 with ara-C (10 mumol/l) and etoposide during 2 h, the formation of ara-CTP was decreased to 71 +/- 18 (mean +/- S.D.)	Cytarabine	48-53	solute carrier family 25 member 1	Homo sapiens	114-117
8260751-0	1993	Effect of Bcl-2 on ionizing radiation and 1-beta-D-arabinofuranosylcytosine-induced internucleosomal DNA fragmentation and cell survival in human myeloid leukemia cells.	Cytarabine	42-75	BCL2 apoptosis regulator	Homo sapiens	10-15
8481660-1	1993	Analysis of different ribonucleotide reductase inhibitors to modulate arabinosylcytosine (ara-C) metabolism suggested that pretreatment with arabinosyl-2-fluoroadenine (F-ara-A) significantly potentiated the rate of ara-CTP (5"-triphosphate of ara-C) accumulation in both quiescent lymphocytes (p = 0.046) and in cycling blasts (p = 0.017).	Cytarabine	70-88	solute carrier family 25 member 1	Homo sapiens	220-223
8481660-1	1993	Analysis of different ribonucleotide reductase inhibitors to modulate arabinosylcytosine (ara-C) metabolism suggested that pretreatment with arabinosyl-2-fluoroadenine (F-ara-A) significantly potentiated the rate of ara-CTP (5"-triphosphate of ara-C) accumulation in both quiescent lymphocytes (p = 0.046) and in cycling blasts (p = 0.017).	Cytarabine	90-95	solute carrier family 25 member 1	Homo sapiens	220-223
7683227-0	1993	Effect of hemopoietic growth factors G-CSF and pIXY 321 on the activity of high dose Ara-C in human myeloid leukemia cells.	Cytarabine	85-90	colony stimulating factor 3	Homo sapiens	37-42
8260751-5	1993	Bcl-2 was capable of inhibiting 40-50% of the ara-C and ionizing radiation-induced internucleosomal DNA fragmentation at all tested concentrations.	Cytarabine	46-51	BCL2 apoptosis regulator	Homo sapiens	0-5
8260751-6	1993	However, cell survival following exposure to these agents was only increased in the bcl-2 transfectants at relatively low doses of ara-C and ionizing radiation.	Cytarabine	131-136	BCL2 apoptosis regulator	Homo sapiens	84-89
8260751-7	1993	These data demonstrate that although bcl-2 is capable of inhibiting ara-C and ionizing radiation-induced DNA fragmentation in myeloid cells, it increases cell survival only at low doses of these agents.	Cytarabine	68-73	BCL2 apoptosis regulator	Homo sapiens	37-42
1288731-11	1992	The production of interferon-gamma was stimulated 6- to 10-fold in the presence of 1-5 micrograms/ml BN 52205, BN 52211 and ARA-C.	Cytarabine	124-129	interferon gamma	Homo sapiens	18-34
1486032-0	1992	Effects of bryostatin 1 and rGM-CSF on the metabolism of 1-beta-D-arabinofuranosylcytosine in human leukaemic myeloblasts.	Cytarabine	57-90	colony stimulating factor 2	Rattus norvegicus	28-35
1486569-0	1992	Disappearance of a highly unusual clone, 46,XY,del(7)(p12),t(9;22)(q34;q11) in chronic myeloid leukemia after treatment with recombinant interferon and cytosine arabinoside.	Cytarabine	152-172	DNA polymerase epsilon 4, accessory subunit	Homo sapiens	54-57
1450413-0	1992	Granulocyte-macrophage colony-stimulating factor/interleukin-3 fusion protein (pIXY 321) enhances high-dose Ara-C-induced programmed cell death or apoptosis in human myeloid leukemia cells.	Cytarabine	108-113	colony stimulating factor 2	Homo sapiens	0-48
1292637-0	1992	IL-1 synergizes with ARA-C in aborting the development of chloroleukemia while protecting from ARA-C-induced alopecia in the rat model.	Cytarabine	95-100	interleukin 1 alpha	Homo sapiens	0-4
1394224-6	1992	The decrease in K-ras expression was greater for TPA-treated cells than for 1-beta-arabinofuranosylcytosine-treated cells.	Cytarabine	76-107	KRAS proto-oncogene, GTPase	Homo sapiens	16-21
1292637-1	1992	Recently, interleukin 1 (IL-1) was shown to protect rats from ARA-C-induced alopecia.	Cytarabine	62-67	interleukin 1 alpha	Homo sapiens	25-29
1292637-2	1992	The present study was designed to investigate the effect of combination rHu-IL-1 and ARA-C on transplantable chloroleukemia (C51) and at the same time evaluate the protective effect of IL-1 on the ARA-C-induced alopecia in the rat model.	Cytarabine	197-202	interleukin 1 alpha	Homo sapiens	185-189
1292637-7	1992	Thus, IL-1 demonstrated a double beneficial effect, synergism with ARA-C against the leukemic cells on the one hand, and protection from ARA-C-induced alopecia, on the other.	Cytarabine	67-72	interleukin 1 alpha	Homo sapiens	6-10
1292637-7	1992	Thus, IL-1 demonstrated a double beneficial effect, synergism with ARA-C against the leukemic cells on the one hand, and protection from ARA-C-induced alopecia, on the other.	Cytarabine	137-142	interleukin 1 alpha	Homo sapiens	6-10
1394146-4	1992	S49.1 and WEHI7.2 cells infected with bcl-2 but not control retrovirus also exhibited increased resistance to cell killing and DNA fragmentation induced by a wide variety of reagents, including the calcium ionophore ionomycin, the phorbol ester tetradecanoylphorbol acetate, the dihydrofolate reductase inhibitor methotrexate, the antimetabolite 1-beta-D-arabinofuranosylcytosine, and the microtubule inhibitor vincristine.	Cytarabine	346-379	B cell leukemia/lymphoma 2	Mus musculus	38-43
1413523-1	1992	African swine fever virus (ASFV) induces the synthesis of a virus-specific DNA polymerase, which is inhibited by phosphonoacetic acid and cytosine arabinoside.	Cytarabine	138-158	DNA polymerase	African swine fever virus	75-89
1426045-1	1992	A deoxycytidine kinase-deficient variant of HL60 cells (HL60-araC), isolated by its resistance to 1-beta-D-arabinofuranosyl cytosine (ara-C), shows cross-resistance to the differentiation-inducing and growth-inhibitory effects of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3).	Cytarabine	98-132	deoxycytidine kinase	Homo sapiens	2-22
1426045-1	1992	A deoxycytidine kinase-deficient variant of HL60 cells (HL60-araC), isolated by its resistance to 1-beta-D-arabinofuranosyl cytosine (ara-C), shows cross-resistance to the differentiation-inducing and growth-inhibitory effects of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3).	Cytarabine	134-139	deoxycytidine kinase	Homo sapiens	2-22
1363283-4	1992	After conventional doses of cytosine-arabinoside (Ara-C) and daunorubicin or mitoxantrone, positive P-gp cells were noted in 65% of the cases.	Cytarabine	28-48	phosphoglycolate phosphatase	Homo sapiens	100-104
1284910-6	1992	The patients treated with cytosine arabinoside following G-CSF showed hematologically good improvement.	Cytarabine	26-46	colony stimulating factor 3	Homo sapiens	57-62
1512227-5	1992	These results indicate that the induction of cytidine deaminase activity by HIV-1(IIIB) infection conferred ARA-C resistance to H9 cells.	Cytarabine	108-113	cytidine deaminase	Homo sapiens	45-63
1383642-1	1992	In vitro preincubation with recombinant granulocyte colony-stimulating factor(rhG-CSF, 100 ng/ml) enhanced the cytotoxicity of 1-beta-D-arabinofuranosylcytosine(Ara-C) in leukemic cells resistant to Ara-C from a patient with biphenotypic leukemia.	Cytarabine	127-160	colony stimulating factor 3	Homo sapiens	40-85
1383642-1	1992	In vitro preincubation with recombinant granulocyte colony-stimulating factor(rhG-CSF, 100 ng/ml) enhanced the cytotoxicity of 1-beta-D-arabinofuranosylcytosine(Ara-C) in leukemic cells resistant to Ara-C from a patient with biphenotypic leukemia.	Cytarabine	161-166	colony stimulating factor 3	Homo sapiens	40-85
1383642-1	1992	In vitro preincubation with recombinant granulocyte colony-stimulating factor(rhG-CSF, 100 ng/ml) enhanced the cytotoxicity of 1-beta-D-arabinofuranosylcytosine(Ara-C) in leukemic cells resistant to Ara-C from a patient with biphenotypic leukemia.	Cytarabine	199-204	colony stimulating factor 3	Homo sapiens	40-85
1494917-9	1992	ACM was found to increase glutamate decarboxylase activity in neuronal cultures from septum in the presence of Ara-C.	Cytarabine	111-116	glutamate-ammonia ligase	Homo sapiens	26-49
1381569-9	1992	In elderly AML patients over 60, the dose-adjustment reported by Mori, or low-dose cytarabine with G-CSF, is recommended.	Cytarabine	83-93	colony stimulating factor 3	Homo sapiens	99-104
1512227-6	1992	This conclusion was supported by the observation that a marked reversal of ARA-C resistance in the infected H9 cells occurred after treatment with the inhibitor of cytidine deaminase, 3,4,5,6-tetrahydrouridine.	Cytarabine	75-80	cytidine deaminase	Homo sapiens	164-182
1391803-0	1992	Comparative effects of G-CSF, GM-CSF and IL-3 on cytosine arabinoside- and daunorubicin-mediated cytotoxicity of acute myeloid leukemia cells and normal myeloid progenitors.	Cytarabine	49-69	interleukin 3	Homo sapiens	41-45
1391803-3	1992	On the other hand, the Ara-C- and DNR-mediated cytotoxicity of CFU-AML was not abrogated by CSF in any instance, but rather, it was significantly enhanced by all the CSF in the majority of instances.	Cytarabine	23-28	colony stimulating factor 3	Homo sapiens	166-169
1391803-5	1992	Under the same culture conditions as those for CFU-AML, all of the CSF significantly enhanced the Ara-C-mediated cytotoxicity of day 7 normal CFU-GM, although to a lesser extent than in CFU-AML.	Cytarabine	98-103	colony stimulating factor 3	Homo sapiens	67-70
1551115-1	1992	The thioether-lipid conjugate of ara-C, ara-CDP-DL-PTBA, was tested for therapeutic activity in vivo on the growth of seven different xenografts of human colorectal cancers in athymic nu/nu mice.	Cytarabine	33-38	cut like homeobox 1	Homo sapiens	44-47
1568208-9	1992	We conclude that cellular resistance to the toxicity of 1-beta-D-arabinofuranosylcytosine and dideoxycytidine in these cell lines is mediated by specific mutations within the dCK gene.	Cytarabine	56-89	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	175-178
1593908-4	1992	Exposure of normal human bone marrow mononuclear cells to identical concentrations of ara-C and byostatin 1 permitted the survival of 23% of committed myeloid progenitors (granulocyte-macrophage colony-forming units), and greater than 50% when rGM-CSF was included.	Cytarabine	86-91	colony stimulating factor 2	Rattus norvegicus	244-251
1593908-5	1992	Finally, exposure of bone marrow populations highly enriched for progenitor cells (CD34+, DR-, CD71-) to ara-C and bryostatin 1 +/- rGM-CSF for 24 h led to minimal reductions (e.g. 10-15%) in the survival of early hematopoietic progenitors (high proliferative potential colony-forming cells).	Cytarabine	105-110	CD34 molecule	Homo sapiens	83-87
1593908-5	1992	Finally, exposure of bone marrow populations highly enriched for progenitor cells (CD34+, DR-, CD71-) to ara-C and bryostatin 1 +/- rGM-CSF for 24 h led to minimal reductions (e.g. 10-15%) in the survival of early hematopoietic progenitors (high proliferative potential colony-forming cells).	Cytarabine	105-110	transferrin receptor	Homo sapiens	95-99
1326685-2	1992	In a pilot study we treated 2 patients with refractory B lymphomas with two courses of TNF alpha and consecutive aggressive chemotherapy (high dose Ara-C and mitoxantrone).	Cytarabine	148-153	tumor necrosis factor	Homo sapiens	87-96
1596909-2	1992	Unlike 1-beta-D-arabinofuranosylcytosine which is activated by deoxycytidine kinase, the enzyme responsible for the phosphorylation of CPE-C is uridine/cytidine kinase.	Cytarabine	7-40	deoxycytidine kinase	Homo sapiens	63-83
1571541-6	1992	The unadjusted Kaplan-Meier hazard rate of the ara-C + daunorubicin + GM-CSF group was not uniquely high during the initial 4 weeks after start of therapy, but was highest among the three treatment groups throughout weeks 5 to 16, suggesting that the negative effect of this treatment was not caused by acute toxicity.	Cytarabine	47-52	colony stimulating factor 2	Homo sapiens	70-76
1571541-9	1992	Our results suggest caution in the use of GM-CSF to sensitize myeloid leukemia cells to daunorubicin + ara-C chemotherapy.	Cytarabine	103-108	colony stimulating factor 2	Homo sapiens	42-48
1592362-0	1992	Effects of recombinant human interferon-alpha, beta and gamma on the antiproliferative activity of cytarabine in K562 human myeloid leukemia clonogenic cells.	Cytarabine	99-109	interferon beta 1	Homo sapiens	29-61
1601333-4	1992	2008/C13 cells expressed greater sensitivity toward Ara-C and Gemcitabine.	Cytarabine	52-57	homeobox C13	Homo sapiens	5-8
1601333-7	1992	In contrast, the metabolism and cytotoxic effects of Ara-C and dFdC in 2008 and 2008/C13 cells were not significantly altered by dCyd concentrations that are reached in the peritoneum following intravenous administration.	Cytarabine	53-58	homeobox C13	Homo sapiens	85-88
1553573-0	1992	Granulocyte-macrophage colony-stimulating factor and interleukin-3 enhance the incorporation of cytosine arabinoside into the DNA of leukemic blasts and the cytotoxic effect on clonogenic cells from patients with acute myeloid leukemia.	Cytarabine	96-116	colony stimulating factor 2	Homo sapiens	0-48
1553573-0	1992	Granulocyte-macrophage colony-stimulating factor and interleukin-3 enhance the incorporation of cytosine arabinoside into the DNA of leukemic blasts and the cytotoxic effect on clonogenic cells from patients with acute myeloid leukemia.	Cytarabine	96-116	interleukin 3	Homo sapiens	53-66
1553573-5	1992	This finding may be explained by a stimulatory effect of GM-CSF and IL-3 on ara-C phosphorylating enzymes and a more rapid incorporation of ara-CTP into the DNA of leukemic blasts.	Cytarabine	76-81	colony stimulating factor 2	Homo sapiens	57-63
1553573-5	1992	This finding may be explained by a stimulatory effect of GM-CSF and IL-3 on ara-C phosphorylating enzymes and a more rapid incorporation of ara-CTP into the DNA of leukemic blasts.	Cytarabine	76-81	interleukin 3	Homo sapiens	68-72
1553573-6	1992	These effects translated into a 2.2- to 229.0-fold increase in the cytotoxic activity of ara-C against clonogenic leukemic cells after GM-CSF or IL-3 pretreatment.	Cytarabine	89-94	colony stimulating factor 2	Homo sapiens	135-141
1553573-6	1992	These effects translated into a 2.2- to 229.0-fold increase in the cytotoxic activity of ara-C against clonogenic leukemic cells after GM-CSF or IL-3 pretreatment.	Cytarabine	89-94	interleukin 3	Homo sapiens	145-149
1553573-7	1992	Hence, GM-CSF and IL-3 enhance the intracellular metabolism of ara-C and its incorporation into the DNA of leukemic cells leading to a higher antileukemic activity of ara-C on clonogenic leukemic cells (CFU-L).	Cytarabine	63-68	colony stimulating factor 2	Homo sapiens	7-13
1553573-7	1992	Hence, GM-CSF and IL-3 enhance the intracellular metabolism of ara-C and its incorporation into the DNA of leukemic cells leading to a higher antileukemic activity of ara-C on clonogenic leukemic cells (CFU-L).	Cytarabine	63-68	interleukin 3	Homo sapiens	18-22
1553573-7	1992	Hence, GM-CSF and IL-3 enhance the intracellular metabolism of ara-C and its incorporation into the DNA of leukemic cells leading to a higher antileukemic activity of ara-C on clonogenic leukemic cells (CFU-L).	Cytarabine	167-172	colony stimulating factor 2	Homo sapiens	7-13
1553573-7	1992	Hence, GM-CSF and IL-3 enhance the intracellular metabolism of ara-C and its incorporation into the DNA of leukemic cells leading to a higher antileukemic activity of ara-C on clonogenic leukemic cells (CFU-L).	Cytarabine	167-172	interleukin 3	Homo sapiens	18-22
1592362-1	1992	The effects of recombinant human interferon-alpha, beta and gamma (IFN) on the antiproliferative activity of cytarabine (ara-C) in K562 human myeloid leukemia clonogenic cells were studied in an agar capillary microassay.	Cytarabine	109-119	interferon beta 1	Homo sapiens	33-71
1592362-1	1992	The effects of recombinant human interferon-alpha, beta and gamma (IFN) on the antiproliferative activity of cytarabine (ara-C) in K562 human myeloid leukemia clonogenic cells were studied in an agar capillary microassay.	Cytarabine	121-126	interferon beta 1	Homo sapiens	33-71
1592362-6	1992	The significant reduction of the desired antiproliferative activity of ara-C by the three interferons was reproduced in liquid suspension cultures of K562 cells on day 4 in the following order: IFN-gamma greater than IFN-beta greater than IFN-alpha.	Cytarabine	71-76	interferon gamma	Homo sapiens	194-203
1592362-6	1992	The significant reduction of the desired antiproliferative activity of ara-C by the three interferons was reproduced in liquid suspension cultures of K562 cells on day 4 in the following order: IFN-gamma greater than IFN-beta greater than IFN-alpha.	Cytarabine	71-76	interferon beta 1	Homo sapiens	217-225
1592362-6	1992	The significant reduction of the desired antiproliferative activity of ara-C by the three interferons was reproduced in liquid suspension cultures of K562 cells on day 4 in the following order: IFN-gamma greater than IFN-beta greater than IFN-alpha.	Cytarabine	71-76	interferon alpha 1	Homo sapiens	239-248
1728412-0	1992	Protection from 1-beta-D-arabinofuranosylcytosine-induced alopecia by epidermal growth factor and fibroblast growth factor in the rat model.	Cytarabine	16-49	epidermal growth factor like 1	Rattus norvegicus	70-93
1310062-12	1992	Taken together, these findings indicate that: (1) enhancement of JUN/AP-1 activity in ara-C-treated cells involves a posttranslational modification of JUN/AP-1; and (2) binding of activated JUN/AP-1 to the AP-1 site in the c-jun promoter confers ara-C inducibility of this gene.	Cytarabine	86-91	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	155-159
1310062-12	1992	Taken together, these findings indicate that: (1) enhancement of JUN/AP-1 activity in ara-C-treated cells involves a posttranslational modification of JUN/AP-1; and (2) binding of activated JUN/AP-1 to the AP-1 site in the c-jun promoter confers ara-C inducibility of this gene.	Cytarabine	86-91	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	223-228
1560255-9	1992	In cases of meningeal carcinomatosis treated by intrathecal chemotherapy with methotrexate (MTX) and cytosine arabinoside (Ara-C), CSF beta-glucuronidase reflected the neurological status better than the cell count decreased rapidly following chemotherapy and beta-glucuronidase was considered as a useful CSF marker in cases of meningeal carcinomatosis to monitor the course of the disease.	Cytarabine	101-121	colony stimulating factor 2	Homo sapiens	131-134
1560255-9	1992	In cases of meningeal carcinomatosis treated by intrathecal chemotherapy with methotrexate (MTX) and cytosine arabinoside (Ara-C), CSF beta-glucuronidase reflected the neurological status better than the cell count decreased rapidly following chemotherapy and beta-glucuronidase was considered as a useful CSF marker in cases of meningeal carcinomatosis to monitor the course of the disease.	Cytarabine	101-121	glucuronidase beta	Homo sapiens	135-153
1560255-9	1992	In cases of meningeal carcinomatosis treated by intrathecal chemotherapy with methotrexate (MTX) and cytosine arabinoside (Ara-C), CSF beta-glucuronidase reflected the neurological status better than the cell count decreased rapidly following chemotherapy and beta-glucuronidase was considered as a useful CSF marker in cases of meningeal carcinomatosis to monitor the course of the disease.	Cytarabine	123-128	glucuronidase beta	Homo sapiens	135-153
1560255-9	1992	In cases of meningeal carcinomatosis treated by intrathecal chemotherapy with methotrexate (MTX) and cytosine arabinoside (Ara-C), CSF beta-glucuronidase reflected the neurological status better than the cell count decreased rapidly following chemotherapy and beta-glucuronidase was considered as a useful CSF marker in cases of meningeal carcinomatosis to monitor the course of the disease.	Cytarabine	123-128	glucuronidase beta	Homo sapiens	260-278
1560255-9	1992	In cases of meningeal carcinomatosis treated by intrathecal chemotherapy with methotrexate (MTX) and cytosine arabinoside (Ara-C), CSF beta-glucuronidase reflected the neurological status better than the cell count decreased rapidly following chemotherapy and beta-glucuronidase was considered as a useful CSF marker in cases of meningeal carcinomatosis to monitor the course of the disease.	Cytarabine	123-128	colony stimulating factor 2	Homo sapiens	306-309
1556000-0	1992	Enhancement of the cytotoxicity of cytosine arabinoside by interleukin-3.	Cytarabine	35-55	interleukin 3	Homo sapiens	59-72
1556000-4	1992	Leukemic cells preincubated with IL-1 (10 U/ml) or IL-3 (5 U/ml) were subsequently exposed to ara-C (3 micrograms/ml) for the final 24 h and the activity of ara-C against clonogenic acute myeloid leukemia cells was evaluated in terms of the inhibition of colony formation in semisolid media.	Cytarabine	94-99	interleukin 3	Homo sapiens	51-55
1556000-5	1992	The exposure to ara-C inhibits the proliferation of a higher proportion of clonogenic cells in culture pretreated with IL-3 than in control or cells pretreated with IL-1.	Cytarabine	16-21	interleukin 3	Homo sapiens	119-123
1556000-5	1992	The exposure to ara-C inhibits the proliferation of a higher proportion of clonogenic cells in culture pretreated with IL-3 than in control or cells pretreated with IL-1.	Cytarabine	16-21	interleukin 1 alpha	Homo sapiens	165-169
1556000-6	1992	The enhanced cytotoxic effect of ara-C in the cells pretreated with IL-3 correlated with increased formation of intracellular ara-CTP.	Cytarabine	33-38	interleukin 3	Homo sapiens	68-72
1551227-0	1992	Abnormal expression of embryonic neural cell adhesion molecule (N-CAM) in the developing mouse cerebellum after neonatal administration of cytosine arabinoside.	Cytarabine	139-159	neural cell adhesion molecule 1	Mus musculus	64-69
1551227-2	1992	In the present study, the expression of neural cell adhesion molecule (N-CAM) and its distribution were examined in the mouse malformed cerebellum induced by neonatal Ara-C administration.	Cytarabine	167-172	neural cell adhesion molecule 1	Mus musculus	71-76
1551227-4	1992	On the other hand, E-N-CAM was expressed in the Ara-C treated cerebellum not only at P7 but also at P14.	Cytarabine	48-53	neural cell adhesion molecule 1	Mus musculus	19-26
1551227-4	1992	On the other hand, E-N-CAM was expressed in the Ara-C treated cerebellum not only at P7 but also at P14.	Cytarabine	48-53	S100 calcium binding protein A9 (calgranulin B)	Mus musculus	100-103
1551227-5	1992	Immunohistochemical studies revealed that E-N-CAM was observed in the area below the external granular layer (EGL) of the P7 cerebellum in both the control and Ara-C treated mice.	Cytarabine	160-165	neural cell adhesion molecule 1	Mus musculus	42-49
1551227-6	1992	In contrast, E-N-CAM immunoreactivity was found in the arrested EGL cells in the Ara-C treated cerebellum of P14 mice but not in the age-matched controls.	Cytarabine	81-86	neural cell adhesion molecule 1	Mus musculus	13-20
1551227-6	1992	In contrast, E-N-CAM immunoreactivity was found in the arrested EGL cells in the Ara-C treated cerebellum of P14 mice but not in the age-matched controls.	Cytarabine	81-86	S100 calcium binding protein A9 (calgranulin B)	Mus musculus	109-112
1310062-0	1992	Activation of the AP-1 transcription factor by arabinofuranosylcytosine in myeloid leukemia cells.	Cytarabine	47-71	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	18-22
1310062-1	1992	Previous studies have shown that 1-beta-D-arabinofuranosylcytosine (ara-C) induces transcription of the c-jun immediate early response gene in human myeloid leukemia cells.	Cytarabine	33-66	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	104-109
1310062-1	1992	Previous studies have shown that 1-beta-D-arabinofuranosylcytosine (ara-C) induces transcription of the c-jun immediate early response gene in human myeloid leukemia cells.	Cytarabine	68-73	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	104-109
1310062-4	1992	The results demonstrate that ara-C-induced c-jun transcription is mediated by an element between positions -74 and -20 upstream to the start site.	Cytarabine	29-34	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	43-48
1310062-6	1992	Competition with an oligonucleotide containing the AP-1 consensus sequence indicated that ara-C stimulates binding of nuclear proteins at the AP-1 site in the c-jun promoter.	Cytarabine	90-95	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	51-55
1310062-6	1992	Competition with an oligonucleotide containing the AP-1 consensus sequence indicated that ara-C stimulates binding of nuclear proteins at the AP-1 site in the c-jun promoter.	Cytarabine	90-95	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	142-146
1310062-6	1992	Competition with an oligonucleotide containing the AP-1 consensus sequence indicated that ara-C stimulates binding of nuclear proteins at the AP-1 site in the c-jun promoter.	Cytarabine	90-95	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	159-164
1310062-8	1992	The binding of JUN/AP-1 was maximal at 1 hour of ara-C treatment and decreased to baseline levels at 12 hours.	Cytarabine	49-54	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	19-23
1310062-9	1992	The finding that ara-C induces AP-1 binding in the absence of protein synthesis indicated that this agent activates already synthesized JUN/AP-1.	Cytarabine	17-22	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	31-35
1310062-9	1992	The finding that ara-C induces AP-1 binding in the absence of protein synthesis indicated that this agent activates already synthesized JUN/AP-1.	Cytarabine	17-22	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	140-144
1310062-11	1992	The results show that AP-1 enhances SV40 promoter activity in ara-C-treated cells.	Cytarabine	62-67	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	22-26
1310062-12	1992	Taken together, these findings indicate that: (1) enhancement of JUN/AP-1 activity in ara-C-treated cells involves a posttranslational modification of JUN/AP-1; and (2) binding of activated JUN/AP-1 to the AP-1 site in the c-jun promoter confers ara-C inducibility of this gene.	Cytarabine	86-91	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	69-73
1310062-12	1992	Taken together, these findings indicate that: (1) enhancement of JUN/AP-1 activity in ara-C-treated cells involves a posttranslational modification of JUN/AP-1; and (2) binding of activated JUN/AP-1 to the AP-1 site in the c-jun promoter confers ara-C inducibility of this gene.	Cytarabine	86-91	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	155-159
1310062-12	1992	Taken together, these findings indicate that: (1) enhancement of JUN/AP-1 activity in ara-C-treated cells involves a posttranslational modification of JUN/AP-1; and (2) binding of activated JUN/AP-1 to the AP-1 site in the c-jun promoter confers ara-C inducibility of this gene.	Cytarabine	86-91	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	155-159
1729409-6	1992	Aggregate cultures deprived of glial cells, i.e., neuron-enriched cultures prepared by treating early cultures with the antimitotic drug cytosine arabinoside, exhibited pronounced deficits in M-NF, H-NF, MAP 2, MAP 1, synapsin I, and brain spectrin, with increased levels of a 145-kDa brain spectrin breakdown product.	Cytarabine	137-157	microtubule-associated protein 2	Rattus norvegicus	204-209
1728412-1	1992	The present study was designed to examine the effect of epidermal growth factor (EGF) and fibroblast growth factor (FGF) on 1-beta-D-arabinofuranosylcytosine (ARA-C)- and cyclophosphamide-induced alopecia in the young rat model.	Cytarabine	124-157	epidermal growth factor like 1	Rattus norvegicus	56-79
1728412-1	1992	The present study was designed to examine the effect of epidermal growth factor (EGF) and fibroblast growth factor (FGF) on 1-beta-D-arabinofuranosylcytosine (ARA-C)- and cyclophosphamide-induced alopecia in the young rat model.	Cytarabine	124-157	epidermal growth factor like 1	Rattus norvegicus	81-84
1728412-1	1992	The present study was designed to examine the effect of epidermal growth factor (EGF) and fibroblast growth factor (FGF) on 1-beta-D-arabinofuranosylcytosine (ARA-C)- and cyclophosphamide-induced alopecia in the young rat model.	Cytarabine	159-164	epidermal growth factor like 1	Rattus norvegicus	56-79
1728412-1	1992	The present study was designed to examine the effect of epidermal growth factor (EGF) and fibroblast growth factor (FGF) on 1-beta-D-arabinofuranosylcytosine (ARA-C)- and cyclophosphamide-induced alopecia in the young rat model.	Cytarabine	159-164	epidermal growth factor like 1	Rattus norvegicus	81-84
1728412-4	1992	Both human and murine EGF protected rats from ARA-C-induced alopecia.	Cytarabine	46-51	epidermal growth factor	Mus musculus	22-25
1728412-6	1992	In other experiments the administration of acidic FGF (aFGF) with ARA-C resulted in protection from alopecia limited to the site of FGF injection.	Cytarabine	66-71	fibroblast growth factor 1	Rattus norvegicus	43-53
1728412-6	1992	In other experiments the administration of acidic FGF (aFGF) with ARA-C resulted in protection from alopecia limited to the site of FGF injection.	Cytarabine	66-71	fibroblast growth factor 1	Rattus norvegicus	55-59
1728412-8	1992	It is concluded that both EGF and FGF are effective in protecting against ARA-C-induced alopecia in the rat model.	Cytarabine	74-79	epidermal growth factor like 1	Rattus norvegicus	26-29
1375134-0	1992	Potent inhibitors for the deamination of cytosine arabinoside and 5-aza-2"-deoxycytidine by human cytidine deaminase.	Cytarabine	41-61	cytidine deaminase	Homo sapiens	98-116
1309827-11	1992	When the cells were treated with bFGF and 10(-6) M ARA-C together, the proliferation was completely blocked and CST activity decreased by 72% below control values, whereas CNP activity was not significantly decreased.	Cytarabine	51-56	2',3'-cyclic nucleotide 3' phosphodiesterase	Rattus norvegicus	172-175
1552225-10	1992	Ara-C exposure reduced CFU-GM numbers generated with nac from GM-CSF LTBMCs to 10% of GM-CSF controls (week 1).	Cytarabine	0-5	colony stimulating factor 2	Homo sapiens	62-68
1552225-10	1992	Ara-C exposure reduced CFU-GM numbers generated with nac from GM-CSF LTBMCs to 10% of GM-CSF controls (week 1).	Cytarabine	0-5	colony stimulating factor 2	Homo sapiens	86-92
1552225-11	1992	However, CFU-GM numbers grown with nac from Ara-C exposed GM-CSF-dependent LTBMCs recovered above control levels after week 3.	Cytarabine	44-49	colony stimulating factor 2	Homo sapiens	58-64
1286578-1	1992	Deamination of cytosine arabinoside (ara-C) by cytidine deaminase is the main mode of inactivation of this drug which can be responsible for ara-C resistance.	Cytarabine	15-35	cytidine deaminase	Homo sapiens	47-65
1286578-1	1992	Deamination of cytosine arabinoside (ara-C) by cytidine deaminase is the main mode of inactivation of this drug which can be responsible for ara-C resistance.	Cytarabine	37-42	cytidine deaminase	Homo sapiens	47-65
1286578-1	1992	Deamination of cytosine arabinoside (ara-C) by cytidine deaminase is the main mode of inactivation of this drug which can be responsible for ara-C resistance.	Cytarabine	141-146	cytidine deaminase	Homo sapiens	47-65
1286578-2	1992	The present study was undertaken to determine the effect of tetrahydrouridine (THU; a potent inhibitor of cytidine deaminase) on ara-C transport and metabolism in human cells.	Cytarabine	129-134	cytidine deaminase	Homo sapiens	106-124
1583063-0	1992	Recombinant human interferons alpha, beta and gamma reduce the antiproliferative action of cytarabine in K562 human myeloid leukaemia clonogenic cells.	Cytarabine	91-101	interferon beta 1	Homo sapiens	18-51
1583063-1	1992	The effects of recombinant human interferons alpha, beta and gamma (IFN) on the antiproliferative activity of cytarabine in K562 human myeloid leukaemia clonogenic cells were studied in an agar capillary microassay.	Cytarabine	110-120	interferon beta 1	Homo sapiens	33-72
1801688-8	1991	The cell biological effects of GM-CSF in vivo include an immediate increase of leukemic blasts and of normal myeloid cells in the peripheral blood with a median of 2.0, an increase of cells in the S-phase of the cell cycle in bone marrow biopsies, an increase in DNA polymerase activity, an increase in Ara-C cytotoxicity and immunophenotypic changes compatible with differentiation of leukemic blasts along the pathway of normal myeloid progenitors.	Cytarabine	303-308	colony stimulating factor 2	Homo sapiens	31-37
1374492-5	1992	Simultaneous continuous infusions of ara-C and VP-16 (cycle 1) given at individualized doses to achieve drug plasma concentrations of 1 microM and 30 microM, respectively, produced complete remission (CR) in 26 of 61 patients (43%); an additional 17 patients entered CR after Dauno/ara-C (cycle 2), and one patient required 4 cycles of chemotherapy to achieve CR (total CR rate = 72%).	Cytarabine	282-287	host cell factor C1	Homo sapiens	47-52
1374493-3	1992	VAPA and 80-035 used an anthracycline with standard dose cytosine arabinoside (ara-c) for remission induction followed by twelve to fourteen months of intensive sequential chemotherapy.	Cytarabine	57-77	VAMP associated protein A	Homo sapiens	0-4
1374493-3	1992	VAPA and 80-035 used an anthracycline with standard dose cytosine arabinoside (ara-c) for remission induction followed by twelve to fourteen months of intensive sequential chemotherapy.	Cytarabine	79-84	VAMP associated protein A	Homo sapiens	0-4
1732723-1	1992	The present studies have examined the effects of 1-beta-D-arabinofuranosylcytosine (ara-C) on activation of the transcription factor kappa B (NF-kappa B).	Cytarabine	49-82	nuclear factor kappa B subunit 1	Homo sapiens	142-152
1732723-1	1992	The present studies have examined the effects of 1-beta-D-arabinofuranosylcytosine (ara-C) on activation of the transcription factor kappa B (NF-kappa B).	Cytarabine	84-89	nuclear factor kappa B subunit 1	Homo sapiens	142-152
1732723-2	1992	The results demonstrate that treatment of human KG-1 myeloid leukemia cells with ara-C is associated with induction of protein binding to the NF-kappa B consensus sequence.	Cytarabine	81-86	nuclear factor kappa B subunit 1	Homo sapiens	142-152
1732723-3	1992	NF-kappa B binding was activated at 30 min and reached maximal levels of binding at 1-2 hr of ara-C treatment.	Cytarabine	94-99	nuclear factor kappa B subunit 1	Homo sapiens	0-10
1732723-4	1992	The NF-kappa B consensus sequence was ligated to the heterologous thymidine kinase (TK) promoter and the human growth hormone (GH) reporter gene to determine whether ara-C-induced NF-kappa B activity includes an enhancer function.	Cytarabine	166-171	nuclear factor kappa B subunit 1	Homo sapiens	180-190
1732723-5	1992	Ara-C treatment had little effect on transient expression of pTKGH in KG-1 cells but increased transcription of the p (NF-kappa B) TKGH vector by 8-fold.	Cytarabine	0-5	nuclear factor kappa B subunit 1	Homo sapiens	119-129
1732723-6	1992	The results also demonstrate that ara-C transiently increases NF-kappa B mRNA levels.	Cytarabine	34-39	nuclear factor kappa B subunit 1	Homo sapiens	62-72
1732723-7	1992	However, the finding that ara-C-induced binding of NF-kappa B to DNA occurs in the presence of cycloheximide indicates that this agent activates preexisting NF-kappa B protein.	Cytarabine	26-31	nuclear factor kappa B subunit 1	Homo sapiens	51-61
1732723-7	1992	However, the finding that ara-C-induced binding of NF-kappa B to DNA occurs in the presence of cycloheximide indicates that this agent activates preexisting NF-kappa B protein.	Cytarabine	26-31	nuclear factor kappa B subunit 1	Homo sapiens	157-167
1732723-8	1992	These results suggest that ara-C induces a cytoplasmic pathway that transduces signals to the nucleus by activation of NF-kappa B.	Cytarabine	27-32	nuclear factor kappa B subunit 1	Homo sapiens	119-129
1732724-1	1992	Recent studies have demonstrated that 1-beta-D-arabinofuranosylcytosine (ara-C) activates the transcription of the jun/fos early response genes in human myeloid leukemia cells.	Cytarabine	38-71	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	119-122
1732724-1	1992	Recent studies have demonstrated that 1-beta-D-arabinofuranosylcytosine (ara-C) activates the transcription of the jun/fos early response genes in human myeloid leukemia cells.	Cytarabine	73-78	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	119-122
1435087-4	1992	Stimulation of neurite outgrowth was abolished by exposure to cytosine arabinofuranoside, an agent toxic to non-neuronal cells, implying that trophic effects of insulin or insulin-like growth factors require the presence of non-neuronal elements in culture.	Cytarabine	62-88	insulin	Cavia porcellus	161-168
1435087-4	1992	Stimulation of neurite outgrowth was abolished by exposure to cytosine arabinofuranoside, an agent toxic to non-neuronal cells, implying that trophic effects of insulin or insulin-like growth factors require the presence of non-neuronal elements in culture.	Cytarabine	62-88	insulin	Cavia porcellus	172-179
1893953-0	1991	Differential effect of interleukin 3 on the metabolism of high-dose cytosine arabinoside in normal versus leukemic human bone marrow cells.	Cytarabine	68-88	interleukin 3	Homo sapiens	23-36
1769096-1	1991	Treatment of septal cultures prepared from 17-day-old embryos with two different antimitotic agents, cytosine arabinoside (ara C) and 5"-fluoro-2"-deoxyuridine (FUdR), caused a 2-fold increase in the level of choline acetyltransferase (CAT) activity and no change in the glutamic acid decarboxylase (GAD) activity.	Cytarabine	101-121	choline O-acetyltransferase	Rattus norvegicus	209-234
1769096-1	1991	Treatment of septal cultures prepared from 17-day-old embryos with two different antimitotic agents, cytosine arabinoside (ara C) and 5"-fluoro-2"-deoxyuridine (FUdR), caused a 2-fold increase in the level of choline acetyltransferase (CAT) activity and no change in the glutamic acid decarboxylase (GAD) activity.	Cytarabine	101-121	choline O-acetyltransferase	Rattus norvegicus	236-239
1804392-1	1991	5"-Chloro-5"-deoxyarabinosylcytosine (5"-chloro-araC), a lipophilic and cytidine-deaminase resistant analog of the cytotoxic agent arabinosylcytosine (araC) was evaluated in terms of bioactivation, transformation and its cytotoxic activity in vitro.	Cytarabine	18-36	cytidine deaminase	Mus musculus	72-90
1804392-1	1991	5"-Chloro-5"-deoxyarabinosylcytosine (5"-chloro-araC), a lipophilic and cytidine-deaminase resistant analog of the cytotoxic agent arabinosylcytosine (araC) was evaluated in terms of bioactivation, transformation and its cytotoxic activity in vitro.	Cytarabine	48-52	cytidine deaminase	Mus musculus	72-90
1873797-0	1991	Hemin enhances the sensitivity of erythroleukemia cells to 1-beta-D-arabinofuranosylcytosine by both activation of deoxycytidine kinase and reduction of cytidine deaminase activity.	Cytarabine	59-92	cytidine deaminase	Homo sapiens	153-171
1907849-0	1991	Regulation of c-jun gene expression in HL-60 leukemia cells by 1-beta-D-arabinofuranosylcytosine.	Cytarabine	63-96	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	14-19
1907849-3	1991	Recent work has demonstrated that ara-C transiently induces expression of the c-jun immediate early response gene.	Cytarabine	34-39	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	78-83
1907849-4	1991	The present studies in HL-60 myeloid leukemia cells extend these findings by demonstrating that the increase in c-jun mRNA levels at 6 h of ara-C treatment is regulated by a transcriptional mechanism.	Cytarabine	140-145	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	112-117
1907849-6	1991	Previous work in phorbol ester treated cells has indicated that c-jun expression is regulated by the activation of protein kinase C. The present results demonstrate that protein kinase C activity is increased in ara-C-treated cells.	Cytarabine	212-217	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	64-69
1907849-8	1991	Moreover, the induction of c-jun transcripts by ara-C was inhibited by the isoquinolinesulfonamide derivative H7, but not by HA1004, suggesting that this effect is mediated by protein kinase C. Ara-C-induced c-jun expression was also inhibited by staurosporine, another inhibitor of protein kinase C. Taken together, these results indicate that the cellular response to ara-C includes the activation of protein kinase C and that ara-C potentially induces c-jun transcription by a protein kinase C dependent signaling mechanism.	Cytarabine	48-53	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	27-32
1907849-8	1991	Moreover, the induction of c-jun transcripts by ara-C was inhibited by the isoquinolinesulfonamide derivative H7, but not by HA1004, suggesting that this effect is mediated by protein kinase C. Ara-C-induced c-jun expression was also inhibited by staurosporine, another inhibitor of protein kinase C. Taken together, these results indicate that the cellular response to ara-C includes the activation of protein kinase C and that ara-C potentially induces c-jun transcription by a protein kinase C dependent signaling mechanism.	Cytarabine	48-53	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	208-213
1907849-8	1991	Moreover, the induction of c-jun transcripts by ara-C was inhibited by the isoquinolinesulfonamide derivative H7, but not by HA1004, suggesting that this effect is mediated by protein kinase C. Ara-C-induced c-jun expression was also inhibited by staurosporine, another inhibitor of protein kinase C. Taken together, these results indicate that the cellular response to ara-C includes the activation of protein kinase C and that ara-C potentially induces c-jun transcription by a protein kinase C dependent signaling mechanism.	Cytarabine	48-53	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	208-213
1907849-8	1991	Moreover, the induction of c-jun transcripts by ara-C was inhibited by the isoquinolinesulfonamide derivative H7, but not by HA1004, suggesting that this effect is mediated by protein kinase C. Ara-C-induced c-jun expression was also inhibited by staurosporine, another inhibitor of protein kinase C. Taken together, these results indicate that the cellular response to ara-C includes the activation of protein kinase C and that ara-C potentially induces c-jun transcription by a protein kinase C dependent signaling mechanism.	Cytarabine	194-199	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	27-32
1907849-8	1991	Moreover, the induction of c-jun transcripts by ara-C was inhibited by the isoquinolinesulfonamide derivative H7, but not by HA1004, suggesting that this effect is mediated by protein kinase C. Ara-C-induced c-jun expression was also inhibited by staurosporine, another inhibitor of protein kinase C. Taken together, these results indicate that the cellular response to ara-C includes the activation of protein kinase C and that ara-C potentially induces c-jun transcription by a protein kinase C dependent signaling mechanism.	Cytarabine	194-199	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	208-213
1907849-8	1991	Moreover, the induction of c-jun transcripts by ara-C was inhibited by the isoquinolinesulfonamide derivative H7, but not by HA1004, suggesting that this effect is mediated by protein kinase C. Ara-C-induced c-jun expression was also inhibited by staurosporine, another inhibitor of protein kinase C. Taken together, these results indicate that the cellular response to ara-C includes the activation of protein kinase C and that ara-C potentially induces c-jun transcription by a protein kinase C dependent signaling mechanism.	Cytarabine	194-199	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	208-213
1907849-8	1991	Moreover, the induction of c-jun transcripts by ara-C was inhibited by the isoquinolinesulfonamide derivative H7, but not by HA1004, suggesting that this effect is mediated by protein kinase C. Ara-C-induced c-jun expression was also inhibited by staurosporine, another inhibitor of protein kinase C. Taken together, these results indicate that the cellular response to ara-C includes the activation of protein kinase C and that ara-C potentially induces c-jun transcription by a protein kinase C dependent signaling mechanism.	Cytarabine	370-375	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	27-32
1907849-8	1991	Moreover, the induction of c-jun transcripts by ara-C was inhibited by the isoquinolinesulfonamide derivative H7, but not by HA1004, suggesting that this effect is mediated by protein kinase C. Ara-C-induced c-jun expression was also inhibited by staurosporine, another inhibitor of protein kinase C. Taken together, these results indicate that the cellular response to ara-C includes the activation of protein kinase C and that ara-C potentially induces c-jun transcription by a protein kinase C dependent signaling mechanism.	Cytarabine	370-375	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	27-32
1893953-1	1991	We have examined the effect of recombinant interleukin 3 (rIL-3) on the metabolism of high-dose cytosine arabinoside (Ara-C), an S-phase-specific agent, in normal human bone marrow mononuclear cells (BMMC) and leukemic blasts from patients with acute myeloid leukemia (AML).	Cytarabine	96-116	interleukin 3	Homo sapiens	43-56
1893953-1	1991	We have examined the effect of recombinant interleukin 3 (rIL-3) on the metabolism of high-dose cytosine arabinoside (Ara-C), an S-phase-specific agent, in normal human bone marrow mononuclear cells (BMMC) and leukemic blasts from patients with acute myeloid leukemia (AML).	Cytarabine	96-116	interleukin 3	Rattus norvegicus	58-63
1893953-1	1991	We have examined the effect of recombinant interleukin 3 (rIL-3) on the metabolism of high-dose cytosine arabinoside (Ara-C), an S-phase-specific agent, in normal human bone marrow mononuclear cells (BMMC) and leukemic blasts from patients with acute myeloid leukemia (AML).	Cytarabine	118-123	interleukin 3	Homo sapiens	43-56
1893953-1	1991	We have examined the effect of recombinant interleukin 3 (rIL-3) on the metabolism of high-dose cytosine arabinoside (Ara-C), an S-phase-specific agent, in normal human bone marrow mononuclear cells (BMMC) and leukemic blasts from patients with acute myeloid leukemia (AML).	Cytarabine	118-123	interleukin 3	Rattus norvegicus	58-63
1893953-4	1991	Compared to treatment with Ara-C (10 mumol/liter) alone, prior and coadministration of rIL-3 with Ara-C increased Ara-CTP levels in leukemic blasts.	Cytarabine	27-32	interleukin 3	Rattus norvegicus	87-92
1893953-4	1991	Compared to treatment with Ara-C (10 mumol/liter) alone, prior and coadministration of rIL-3 with Ara-C increased Ara-CTP levels in leukemic blasts.	Cytarabine	98-103	interleukin 3	Rattus norvegicus	87-92
1893953-6	1991	Following treatment with Ara-C plus rIL-3 versus Ara-C alone, the alteration in Ara-C DNA incorporation corresponded with the change in Ara-CTP to dCTP ratio observed in normal BMMC and AML blasts.	Cytarabine	49-54	interleukin 3	Rattus norvegicus	36-41
1893953-6	1991	Following treatment with Ara-C plus rIL-3 versus Ara-C alone, the alteration in Ara-C DNA incorporation corresponded with the change in Ara-CTP to dCTP ratio observed in normal BMMC and AML blasts.	Cytarabine	49-54	interleukin 3	Rattus norvegicus	36-41
1893953-7	1991	The differential effect of rIL-3 on the metabolism of high-dose Ara-C in normal versus leukemic cells may indicate a role for rIL-3 in enhancing the selectivity of Ara-C toward leukemic myeloblasts.	Cytarabine	64-69	interleukin 3	Rattus norvegicus	27-32
1893953-7	1991	The differential effect of rIL-3 on the metabolism of high-dose Ara-C in normal versus leukemic cells may indicate a role for rIL-3 in enhancing the selectivity of Ara-C toward leukemic myeloblasts.	Cytarabine	64-69	interleukin 3	Rattus norvegicus	126-131
1893953-7	1991	The differential effect of rIL-3 on the metabolism of high-dose Ara-C in normal versus leukemic cells may indicate a role for rIL-3 in enhancing the selectivity of Ara-C toward leukemic myeloblasts.	Cytarabine	164-169	interleukin 3	Rattus norvegicus	27-32
1893953-7	1991	The differential effect of rIL-3 on the metabolism of high-dose Ara-C in normal versus leukemic cells may indicate a role for rIL-3 in enhancing the selectivity of Ara-C toward leukemic myeloblasts.	Cytarabine	164-169	interleukin 3	Rattus norvegicus	126-131
1819747-2	1991	The 1-beta-D-arabinofuranosylcytosine (ara-C) conjugates 1-O-alkyl (ether) and 1-S-alkyl (thioether) phospholipids, being analogues of ara-CDP-sn-1,2-O-dipalmitoylglycerol (1), showed significant antitumor activity against L1210 and P388 leukemia in vivo.	Cytarabine	4-37	cut-like homeobox 1	Mus musculus	139-142
1819747-2	1991	The 1-beta-D-arabinofuranosylcytosine (ara-C) conjugates 1-O-alkyl (ether) and 1-S-alkyl (thioether) phospholipids, being analogues of ara-CDP-sn-1,2-O-dipalmitoylglycerol (1), showed significant antitumor activity against L1210 and P388 leukemia in vivo.	Cytarabine	39-44	cut-like homeobox 1	Mus musculus	139-142
1766538-10	1991	In 2 cases of meningeal carcinomatosis treated by intrathecal chemotherapy with MTX and Ara-C, CSF beta--glucuronidase and CEA showed clinical condition better than the cell count in CSF decreased rapidly following chemotherapy.	Cytarabine	88-93	glucuronidase beta	Homo sapiens	99-118
1824260-0	1991	Treatment with interleukin-3 plus granulocyte-macrophage colony-stimulating factors improves the selectivity of Ara-C in vitro against acute myeloid leukemia blasts.	Cytarabine	112-117	interleukin 3	Homo sapiens	15-28
1824260-1	1991	Hematopoietic growth factors (HGFs) interleukin-3 (IL-3) and granulocyte-macrophage colony-stimulating factor (GM-CSF) individually have been shown to increase the percentage of acute myeloid leukemia (AML) blasts in S phase and enhance the cytotoxic effects of Ara-C against these blasts in culture.	Cytarabine	262-267	interleukin 3	Homo sapiens	51-55
1824260-1	1991	Hematopoietic growth factors (HGFs) interleukin-3 (IL-3) and granulocyte-macrophage colony-stimulating factor (GM-CSF) individually have been shown to increase the percentage of acute myeloid leukemia (AML) blasts in S phase and enhance the cytotoxic effects of Ara-C against these blasts in culture.	Cytarabine	262-267	colony stimulating factor 2	Homo sapiens	61-109
1824260-1	1991	Hematopoietic growth factors (HGFs) interleukin-3 (IL-3) and granulocyte-macrophage colony-stimulating factor (GM-CSF) individually have been shown to increase the percentage of acute myeloid leukemia (AML) blasts in S phase and enhance the cytotoxic effects of Ara-C against these blasts in culture.	Cytarabine	262-267	colony stimulating factor 2	Homo sapiens	111-117
1824260-2	1991	We compared in vitro the effects of a combined treatment with GM-CSF (10 ng/mL) plus IL-3 (10 ng/mL) on the metabolism and cytotoxicity of Ara-C in normal bone marrow mononuclear cells (NBMMC) and AML blasts.	Cytarabine	139-144	colony stimulating factor 2	Homo sapiens	62-68
1824260-2	1991	We compared in vitro the effects of a combined treatment with GM-CSF (10 ng/mL) plus IL-3 (10 ng/mL) on the metabolism and cytotoxicity of Ara-C in normal bone marrow mononuclear cells (NBMMC) and AML blasts.	Cytarabine	139-144	interleukin 3	Homo sapiens	85-89
1824260-8	1991	These in vitro studies indicate that a combined treatment with IL-3 plus GM-CSF may improve the selectivity of Ara-C against AML blasts.	Cytarabine	111-116	interleukin 3	Homo sapiens	63-67
1824260-8	1991	These in vitro studies indicate that a combined treatment with IL-3 plus GM-CSF may improve the selectivity of Ara-C against AML blasts.	Cytarabine	111-116	colony stimulating factor 2	Homo sapiens	73-79
1719308-10	1991	It was concluded that exposure to GM-CSF or IL-3 decreased ara-C sensitivity in blasts that were actively making DNA.	Cytarabine	59-64	colony stimulating factor 2	Homo sapiens	34-40
1719308-10	1991	It was concluded that exposure to GM-CSF or IL-3 decreased ara-C sensitivity in blasts that were actively making DNA.	Cytarabine	59-64	interleukin 3	Homo sapiens	44-48
1715961-7	1991	The cells are more ara-C sensitive in MGF or G-CSF than in IL-3 or GM-CSF.	Cytarabine	19-24	interleukin 3	Homo sapiens	38-41
1715961-7	1991	The cells are more ara-C sensitive in MGF or G-CSF than in IL-3 or GM-CSF.	Cytarabine	19-24	colony stimulating factor 3	Homo sapiens	45-50
1907257-4	1991	Combinations containing inhibitors of DNA polymerase (ara-C, aphidicolin) or these inhibitors and hydroxyurea inhibited DNA repair in A2780/PAM and A549 cells.	Cytarabine	54-59	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	140-143
1780751-0	1991	To overcome pharmacologic and cytokinetic resistance to cytarabine in the treatment of acute myelogenous leukemia by using recombinant interleukin-3?	Cytarabine	56-66	interleukin 3	Homo sapiens	135-148
2065892-3	1991	In the present study, using the young rat model, recombinant human IL 1 beta produced excellent protection from cytosine arabinoside-induced alopecia.	Cytarabine	112-132	interleukin 1 beta	Homo sapiens	67-76
1840161-2	1991	The patient was treated with high doses of cytarabine followed by intravenous anti-CD10 monoclonal antibody (J5) in an effort to prevent the recovery of the leukemic CD10 positive clone following the bone marrow hypoplasia resulting from the chemotherapy.	Cytarabine	43-53	membrane metalloendopeptidase	Homo sapiens	166-170
1672790-1	1991	We report a case of a patient who developed a fatal adult respiratory distress syndrome (ARDS) during treatment with rh granulocyte-macrophage colony stimulating factor (rhGM-CSF) (250 mcg/m2/day s.c.) and low-dose cytosine-arabinoside (Ara-C) (20 mg/m2/day s.c.).	Cytarabine	237-242	colony stimulating factor 2	Homo sapiens	120-168
1849032-7	1991	The mRNA for 1,25(OH)2D3 receptor (VDR) was detected in K562 cells, and was downregulated by a 96-hour exposure to 1,25(OH)2D3 or a 48-hour exposure to Ara-C.	Cytarabine	152-157	vitamin D receptor	Homo sapiens	35-38
1996082-0	1991	Induction of c-jun expression in the myeloid leukemia cell line KG-1 by 1-beta-D-arabinofuranosylcytosine.	Cytarabine	72-105	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	13-18
1826536-2	1991	We have previously shown that entry of myeloid leukemic cells into S phase can be accelerated in vitro through the use of recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF), resulting in enhancement of ara-C-mediated cytotoxicity.	Cytarabine	229-234	colony stimulating factor 2	Homo sapiens	140-188
1828375-6	1991	Clinical trials are currently being conducted in an attempt to determine whether GM-CSF is able to overcome kinetic resistance of leukemic myeloblasts to cell cycle-specific agents such as cytarabine in the treatment of patients with acute myeloid leukemia.	Cytarabine	189-199	colony stimulating factor 2	Homo sapiens	81-87
1996082-8	1991	Moreover, nuclear run-on analysis disclosed that c-jun induction by Ara-C in KG-1 cells took place at a transcriptional level.	Cytarabine	68-73	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	49-54
1996082-2	1991	We show that c-Jun/AP-1 is inducible as well as coordinately regulated, in the human acute myelogenous leukemia cell line KG-1, by the cytostatic drug 1-beta-D-arabinofuranosylcytosine (Ara-C).	Cytarabine	151-184	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	13-18
1996082-9	1991	Taken together, these findings indicate that c-jun mRNA, unlike its rapid (within minutes) induction by serum in fibroblasts, is induced by Ara-C in KG-1 cells following a much more prolonged time course and is regulated essentially at a transcriptional level.	Cytarabine	140-145	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	45-50
1996082-2	1991	We show that c-Jun/AP-1 is inducible as well as coordinately regulated, in the human acute myelogenous leukemia cell line KG-1, by the cytostatic drug 1-beta-D-arabinofuranosylcytosine (Ara-C).	Cytarabine	186-191	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	13-18
1996082-4	1991	Whereas KG-1 cells displayed only barely detectable amounts of c-jun transcripts when cultured in the presence of serum, Ara-C at concentrations of 1 to 50 microM induced c-jun transcripts in a dose-dependent fashion.	Cytarabine	121-126	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	171-176
1996082-5	1991	Time course studies showed that 10 microM Ara-C induced c-jun transcripts 6 hr after initiation of culture.	Cytarabine	42-47	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	56-61
2018385-3	1991	Recombinant human GM-CSF significantly enhanced the cytostatic effect of hydroxyurea and cytarabine, and consequently reduced their ED90 concentrations.	Cytarabine	89-99	colony stimulating factor 2	Homo sapiens	18-24
1988185-7	1991	The cytosine analog 1-beta-D-arabinofuranosyl-cytosine completely inhibited SSB disappearance, indicating that the removal of the repairable ENU-induced SSBs involves excision repair events.	Cytarabine	20-54	small RNA binding exonuclease protection factor La	Homo sapiens	76-79
1760944-4	1991	GM-CSF and to a lesser extent IL-3 enhanced the antiproliferative effect of cytarabine in K562 cells, whereas the three interferons reduced it.	Cytarabine	76-86	colony stimulating factor 2	Homo sapiens	0-6
1760944-4	1991	GM-CSF and to a lesser extent IL-3 enhanced the antiproliferative effect of cytarabine in K562 cells, whereas the three interferons reduced it.	Cytarabine	76-86	interleukin 3	Homo sapiens	30-34
1760944-5	1991	The efficacy of cytarabine in inhibiting the growth of K562 cells was doubled by its combination with GM-CSF or IL-3 but was halved by its combination with interferons.	Cytarabine	16-26	colony stimulating factor 2	Homo sapiens	102-108
1760944-5	1991	The efficacy of cytarabine in inhibiting the growth of K562 cells was doubled by its combination with GM-CSF or IL-3 but was halved by its combination with interferons.	Cytarabine	16-26	interleukin 3	Homo sapiens	112-116
1845130-3	1991	Other studies have indicated that IL-3 may enhance the ability of ara-C to kill leukemic cells by cytokinetic and pharmacologic mechanisms.	Cytarabine	66-71	interleukin 3	Homo sapiens	34-38
1845130-5	1991	On the basis of in vitro studies, clinical trials with ara-C are underway that are examining the usefulness of GM-CSF and IL-3 in cell cycle recruitment of leukemic myeloblasts.	Cytarabine	55-60	colony stimulating factor 2	Homo sapiens	111-117
1884247-1	1991	In this study, the relationship between the dCTP/ara-CTP ratio and the cytotoxic effect of cytosine arabinoside (ara-C) was investigated.	Cytarabine	91-111	solute carrier family 25 member 1	Homo sapiens	45-48
2169922-14	1990	In the presence of cytosine arabinoside, which induces erythroid differentiation, K562 cells down-regulated expression of TCII receptors.	Cytarabine	19-39	transcobalamin 2	Homo sapiens	122-126
2050130-10	1991	We propose that both the increase in Mf and the increase in the incidence of hprt gene structural alterations are due to the accumulation of strand breaks in repairing regions of DNA under these conditions of ara-C induced inhibition of repair.	Cytarabine	209-214	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	77-81
2030604-2	1991	Murine leukemia cells resistant to cytosine arabinoside (ara-C) due to a deletion of deoxycytidine kinase are collaterally sensitive to DAUrd, which inhibits the de novo production of CTP and hence results in dCTP depletion.	Cytarabine	35-55	deoxycytidine kinase	Mus musculus	85-105
2030604-2	1991	Murine leukemia cells resistant to cytosine arabinoside (ara-C) due to a deletion of deoxycytidine kinase are collaterally sensitive to DAUrd, which inhibits the de novo production of CTP and hence results in dCTP depletion.	Cytarabine	57-62	deoxycytidine kinase	Mus musculus	85-105
2046385-8	1991	Moreover, leukemic mice administered both GM-CSF and ara-C had a lower marrow leukemic load than mice treated with ara-C only.	Cytarabine	115-120	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	42-48
2046385-10	1991	Leukemic mice treated with GM-CSF and ara-C had a longer life expectancy and a smaller leukemic load than mice administered ara-C only.	Cytarabine	124-129	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	27-33
1705960-5	1990	The survival of normal CFU-GM was significantly increased if cells were treated with IFN 1 h before 3 h of Ara-C exposure.	Cytarabine	107-112	IFN1@	Homo sapiens	85-90
2122980-0	1990	Transcriptional regulation of c-jun gene expression by arabinofuranosylcytosine in human myeloid leukemia cells.	Cytarabine	55-79	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	30-35
2122980-3	1990	This work examines the effects of ara-C on c-jun gene expression in human KG-1 myeloid leukemia cells.	Cytarabine	34-39	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	43-48
2122980-5	1990	Ara-C treatment was also associated with increases in c-jun transcripts in U-937, THP-1, and HL-60 myeloid leukemia cells.	Cytarabine	0-5	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	54-59
2122980-5	1990	Ara-C treatment was also associated with increases in c-jun transcripts in U-937, THP-1, and HL-60 myeloid leukemia cells.	Cytarabine	0-5	GLI family zinc finger 2	Homo sapiens	82-87
2122980-8	1990	Moreover, the half-life of c-jun transcripts in ara-C-treated KG-1 cells was 42 min.	Cytarabine	48-53	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	27-32
2393720-7	1990	T beta 4 messenger RNA increased in MOLT-3 during differentiation by 12-O-tetradecanoylphorbol-13-acetate (TPA), in HL60 cells induced by TPA or dimethylsulfoxide and K562 cells stimulated by cytosine arabinoside or hemin.	Cytarabine	192-212	thymosin beta 4 X-linked	Homo sapiens	0-8
2122229-0	1990	Regulation of jun-B gene expression by 1-beta-D-arabinofuranosyl-cytosine in human myeloid leukemia cells.	Cytarabine	39-73	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	14-19
2122229-5	1990	Nuclear run-on assays demonstrated that ara-C treatment is associated with an increased rate of jun-B gene transcription.	Cytarabine	40-45	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	96-101
1696204-0	1990	Effect of interleukin 3 on cytosine arabinoside-mediated cytotoxicity of leukemic myeloblasts.	Cytarabine	27-47	interleukin 3	Homo sapiens	10-23
2223644-5	1990	The results showed that, in those cases which were good responders to IL-3 in the 3H-TdR uptake assay (19 out of 24), Ara-C exposure eliminated a greater proportion of clonogenic cells if pretreated with IL-3 than if untreated (P less than 0.001), while in cases unresponsive to IL-3 this effect was not significant.	Cytarabine	118-123	interleukin 3	Homo sapiens	70-74
2223644-5	1990	The results showed that, in those cases which were good responders to IL-3 in the 3H-TdR uptake assay (19 out of 24), Ara-C exposure eliminated a greater proportion of clonogenic cells if pretreated with IL-3 than if untreated (P less than 0.001), while in cases unresponsive to IL-3 this effect was not significant.	Cytarabine	118-123	interleukin 3	Homo sapiens	204-208
2223644-5	1990	The results showed that, in those cases which were good responders to IL-3 in the 3H-TdR uptake assay (19 out of 24), Ara-C exposure eliminated a greater proportion of clonogenic cells if pretreated with IL-3 than if untreated (P less than 0.001), while in cases unresponsive to IL-3 this effect was not significant.	Cytarabine	118-123	interleukin 3	Homo sapiens	204-208
2223644-7	1990	Finally IL-3 pretreatment was also able to increase the cytotoxic effect of Ara-C on leukaemic cells co-cultured, to simulate clinical AML remission, with normal bone marrow cells.	Cytarabine	76-81	interleukin 3	Homo sapiens	8-12
1696204-3	1990	Because cytosine arabinoside (Ara-C), which targets only cells in S-phase of the mitotic cell cycle, is included in most chemotherapeutic regimens for the treatment of acute myelogenous leukemia, we explored the hypothesis that the recruitment of quiescent immature leukemic blasts into the cell cycle by the early acting growth factor interleukin 3 (IL-3) can increase the efficacy of Ara-C for kill of leukemic stem cells.	Cytarabine	8-28	interleukin 3	Homo sapiens	322-355
1696204-3	1990	Because cytosine arabinoside (Ara-C), which targets only cells in S-phase of the mitotic cell cycle, is included in most chemotherapeutic regimens for the treatment of acute myelogenous leukemia, we explored the hypothesis that the recruitment of quiescent immature leukemic blasts into the cell cycle by the early acting growth factor interleukin 3 (IL-3) can increase the efficacy of Ara-C for kill of leukemic stem cells.	Cytarabine	30-35	interleukin 3	Homo sapiens	322-355
2117685-5	1990	Consistent with this interpretation, we observed a decrease in ara-C sensitivity in LiF treated cultures.	Cytarabine	63-68	LIF interleukin 6 family cytokine	Homo sapiens	84-87
2364392-1	1990	1-beta-D-Arabinofuranosylcytosine 5"-diphosphate-rac-1-S-octadecyl-2-O- palmitoyl-1-thioglycerol (ara-CDP-DL-PTBA) is an effective stable 1-beta-D-arabinofuranosylcytosine (ara-C) conjugate of thioether phospholipid against a variety of transplantable tumors in mice.	Cytarabine	138-171	Rac family small GTPase 1	Mus musculus	49-54
2212834-6	1990	2) Conversion of ara-C to the active form, ara-CTP, was also rapid.	Cytarabine	17-22	solute carrier family 25 member 1	Homo sapiens	47-50
2212834-9	1990	The production of ara-CTP occurred in such a way that, when the extracellular ara-C concentration was lower than 10 microM, more than 90% of the uptake of ara-C was converted to ara-CTP, while at concentrations above 10 microM the efficiency at production (the ratio of total ara-C to ara-CTP production) was decreased.	Cytarabine	18-23	solute carrier family 25 member 1	Homo sapiens	182-185
2212834-9	1990	The production of ara-CTP occurred in such a way that, when the extracellular ara-C concentration was lower than 10 microM, more than 90% of the uptake of ara-C was converted to ara-CTP, while at concentrations above 10 microM the efficiency at production (the ratio of total ara-C to ara-CTP production) was decreased.	Cytarabine	18-23	solute carrier family 25 member 1	Homo sapiens	182-185
2212834-9	1990	The production of ara-CTP occurred in such a way that, when the extracellular ara-C concentration was lower than 10 microM, more than 90% of the uptake of ara-C was converted to ara-CTP, while at concentrations above 10 microM the efficiency at production (the ratio of total ara-C to ara-CTP production) was decreased.	Cytarabine	78-83	solute carrier family 25 member 1	Homo sapiens	22-25
2212834-9	1990	The production of ara-CTP occurred in such a way that, when the extracellular ara-C concentration was lower than 10 microM, more than 90% of the uptake of ara-C was converted to ara-CTP, while at concentrations above 10 microM the efficiency at production (the ratio of total ara-C to ara-CTP production) was decreased.	Cytarabine	78-83	solute carrier family 25 member 1	Homo sapiens	182-185
2212834-9	1990	The production of ara-CTP occurred in such a way that, when the extracellular ara-C concentration was lower than 10 microM, more than 90% of the uptake of ara-C was converted to ara-CTP, while at concentrations above 10 microM the efficiency at production (the ratio of total ara-C to ara-CTP production) was decreased.	Cytarabine	78-83	solute carrier family 25 member 1	Homo sapiens	182-185
2212834-9	1990	The production of ara-CTP occurred in such a way that, when the extracellular ara-C concentration was lower than 10 microM, more than 90% of the uptake of ara-C was converted to ara-CTP, while at concentrations above 10 microM the efficiency at production (the ratio of total ara-C to ara-CTP production) was decreased.	Cytarabine	78-83	solute carrier family 25 member 1	Homo sapiens	22-25
2212834-9	1990	The production of ara-CTP occurred in such a way that, when the extracellular ara-C concentration was lower than 10 microM, more than 90% of the uptake of ara-C was converted to ara-CTP, while at concentrations above 10 microM the efficiency at production (the ratio of total ara-C to ara-CTP production) was decreased.	Cytarabine	78-83	solute carrier family 25 member 1	Homo sapiens	182-185
2212834-9	1990	The production of ara-CTP occurred in such a way that, when the extracellular ara-C concentration was lower than 10 microM, more than 90% of the uptake of ara-C was converted to ara-CTP, while at concentrations above 10 microM the efficiency at production (the ratio of total ara-C to ara-CTP production) was decreased.	Cytarabine	78-83	solute carrier family 25 member 1	Homo sapiens	182-185
2201833-6	1990	These data demonstrate that GM-CSF acts similarly to HSA as an active stimulator of leukemic cell proliferation and net intracellular ara-C metabolism in vitro, and support clinical trials designed to examine the role of rhGM-CSF in enhancing ara-C cytotoxicity by increasing the growth fraction of drug-responsive target cells in vivo.	Cytarabine	134-139	colony stimulating factor 2	Homo sapiens	28-34
2201833-6	1990	These data demonstrate that GM-CSF acts similarly to HSA as an active stimulator of leukemic cell proliferation and net intracellular ara-C metabolism in vitro, and support clinical trials designed to examine the role of rhGM-CSF in enhancing ara-C cytotoxicity by increasing the growth fraction of drug-responsive target cells in vivo.	Cytarabine	243-248	colony stimulating factor 2	Homo sapiens	28-34
2369709-2	1990	The authors saw four patients who developed acute tumor lysis syndrome when treated for advanced-stage, refractory chronic lymphocytic leukemia (CLL) with an initial cycle of cytosine arabinoside (Ara-C) 2 g/m2 every 12 hours x 4, cisplatin 35 mg/m2 every 24 hours x 2, and etoposide 100 mg/m2 every 24 hours x 2 (ACE).	Cytarabine	197-202	angiotensin I converting enzyme	Homo sapiens	314-317
2364392-1	1990	1-beta-D-Arabinofuranosylcytosine 5"-diphosphate-rac-1-S-octadecyl-2-O- palmitoyl-1-thioglycerol (ara-CDP-DL-PTBA) is an effective stable 1-beta-D-arabinofuranosylcytosine (ara-C) conjugate of thioether phospholipid against a variety of transplantable tumors in mice.	Cytarabine	138-171	cut-like homeobox 1	Mus musculus	102-105
2364392-1	1990	1-beta-D-Arabinofuranosylcytosine 5"-diphosphate-rac-1-S-octadecyl-2-O- palmitoyl-1-thioglycerol (ara-CDP-DL-PTBA) is an effective stable 1-beta-D-arabinofuranosylcytosine (ara-C) conjugate of thioether phospholipid against a variety of transplantable tumors in mice.	Cytarabine	98-103	Rac family small GTPase 1	Mus musculus	49-54
2340464-2	1990	The effectiveness and toxicities of high-dose cytosine arabinoside with L-asparaginase (HiDAC-ASNase) were evaluated in 41 patients with "poor risk" acute nonlymphocytic leukemia (ANLL).	Cytarabine	46-66	asparaginase and isoaspartyl peptidase 1	Homo sapiens	72-86
2184901-2	1990	GM-CSF began 3 days after completion of induction chemotherapy (ara-C 1.5 g/m2 d x 4 days by continuous IV infusion after a 3 g/m2 bolus).	Cytarabine	64-69	colony stimulating factor 2	Homo sapiens	0-6
2146451-6	1990	After treatment with low dose cytosine arabinoside, a clinical, analytical and histological remission was achieved, with a return of BTG and PF4 values to the normal range.	Cytarabine	30-50	platelet factor 4	Homo sapiens	141-144
2328788-5	1990	After treatment with high-dose Ara-C, Hb declined, and serum EPO increased markedly in everyone.	Cytarabine	31-36	erythropoietin	Homo sapiens	61-64
2304361-2	1990	Following high-dose bolus ara-C therapy patients with INV [16] or del [16q] had long remissions despite low AUC and peak values while patients with -5, del [5q], -7, or del [7q] were frequently resistant despite average AUC and peak values.	Cytarabine	26-31	inversin	Homo sapiens	54-57
2307989-2	1990	In addition, the records of all pediatric oncology patients who received high-dose cytarabine (HDAC) chemotherapy were reviewed.	Cytarabine	83-93	histone deacetylase 9	Homo sapiens	95-99
2105564-5	1990	We have shown that BU and Ara-C suppressed the colony formation induced by interleukin-3 (IL-3) more effectively than that by granulocyte colony-stimulating factor (G-CSF).	Cytarabine	26-31	interleukin 3	Homo sapiens	75-88
2186322-13	1990	In summary, GM-CSF +/- Ara-C in MDS results in objective remission with manageable toxicity.	Cytarabine	23-28	colony stimulating factor 2	Homo sapiens	12-18
2105564-5	1990	We have shown that BU and Ara-C suppressed the colony formation induced by interleukin-3 (IL-3) more effectively than that by granulocyte colony-stimulating factor (G-CSF).	Cytarabine	26-31	interleukin 3	Homo sapiens	90-94
2304422-1	1990	Concentrations of ara-CTP in leukemic cells isolated from CSF and of ara-C in lumbar CSF were measured following intraventricular ara-C administration in two girls with refractory meningeal leukemia.	Cytarabine	69-74	colony stimulating factor 2	Homo sapiens	85-88
2249330-7	1990	The Km and Vmax values of ara-C for deoxycytidine kinase and the feedback inhibition of this enzyme by ara-CTP in the different leukemic cell lines could not explain the differences in metabolism of this analogue in these cells.	Cytarabine	26-31	deoxycytidine kinase	Homo sapiens	36-56
2232847-1	1990	We studied the effect of preincubation with recombinant GM-CSF on the activity of cytarabine and doxorubicin against clonogenic acute myeloid leukemia cells (CFU-AML).	Cytarabine	82-92	colony stimulating factor 2	Homo sapiens	56-62
2232847-4	1990	Leukemia cells preincubated with GM-CSF for 6-48 h were exposed to cytarabine (2-200 micrograms/ml) or doxorubicin (0.01-0.1 microgram/ml) for 3 h and CFU-AML assayed.	Cytarabine	67-77	colony stimulating factor 2	Homo sapiens	33-39
2124813-0	1990	Induction of c-fos gene expression by arabinofuranosylcytosine in human KG-1 leukemia cells.	Cytarabine	38-62	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	13-18
2124813-2	1990	The present results demonstrate that exposure of human KG-1 myeloid leukemic cells to 1-beta-D-arabinofuranosylcytosine (ara-C) was associated with increases in c-fos gene expression.	Cytarabine	86-119	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	161-166
2124813-2	1990	The present results demonstrate that exposure of human KG-1 myeloid leukemic cells to 1-beta-D-arabinofuranosylcytosine (ara-C) was associated with increases in c-fos gene expression.	Cytarabine	121-126	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	161-166
2124813-4	1990	The level of c-fos transcripts was maximal after 6 hr of exposure to 5 x 10(-6) M ara-C and subsequently declined to that in untreated cells.	Cytarabine	82-87	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	13-18
2124813-8	1990	These combined results demonstrate that ara-C increased c-fos mRNA levels in KG-1 cells and that this effect was associated with transcriptional activation of the c-fos gene.	Cytarabine	40-45	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	56-61
2124813-8	1990	These combined results demonstrate that ara-C increased c-fos mRNA levels in KG-1 cells and that this effect was associated with transcriptional activation of the c-fos gene.	Cytarabine	40-45	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	163-168
2298268-4	1990	In addition, exposure of leukemic myeloblasts to Ara-C and dCyd for 96 h in culture medium lacking PHA-LCM eliminated the secondary plating efficiency (PE2) of leukemic colonies in 11 of 13 samples assayed and reduced values dramatically in the remaining 2.	Cytarabine	49-54	ETS2 repressor factor	Homo sapiens	152-155
2338846-0	1990	Modulation of the effect of 1-beta-D-arabinofuranosylcytosine based on changes of cytidine deaminase activity in HL60 cells.	Cytarabine	28-61	cytidine deaminase	Homo sapiens	82-100
2338846-1	1990	The effect of changes in cytidine deaminase activity on the growth inhibitory effect of 1-beta-D-arabinofuranosylcytosine (Ara-C) has been investigated in the human promyelocytic cell line, HL60.	Cytarabine	88-121	cytidine deaminase	Homo sapiens	25-43
2338846-1	1990	The effect of changes in cytidine deaminase activity on the growth inhibitory effect of 1-beta-D-arabinofuranosylcytosine (Ara-C) has been investigated in the human promyelocytic cell line, HL60.	Cytarabine	123-128	cytidine deaminase	Homo sapiens	25-43
2338846-4	1990	These results show that it is possible to modulate the effect of Ara-C by changing the activity of cytidine deaminase.	Cytarabine	65-70	cytidine deaminase	Homo sapiens	99-117
33788972-8	2021	In addition, the RNAi prodrug-induced decrease in PLK1 can be used to potentiate the effect of cytarabine.	Cytarabine	95-105	polo like kinase 1	Homo sapiens	50-54
33236384-3	2021	We report the frequencies of LCH-related PCs in paediatric patients (n = 317) treated by the JLSG-96/02 AraC-containing regimens.	Cytarabine	104-108	LCH	Homo sapiens	29-32
33811007-1	2021	BACKGROUND: FLAG +- Ida (fludarabine, cytarabine, granulocyte colony-stimulating factor, and idarubicin), is a salvage chemotherapy regimen for relapsed or refractory (R/R) acute myeloid leukemia (AML), with complete remission (CR) rates historically ranging from 52% to 63%.	Cytarabine	38-48	alpha-L-iduronidase	Homo sapiens	20-23
34953799-0	2022	Overexpressed mitogen-and stress-activated protein kinase 1 promotes the resistance of cytarabine in acute myeloid leukemia through brahma related gene 1-mediated upregulation of heme oxygenase-1.	Cytarabine	87-97	SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4	Homo sapiens	132-153
8761380-8	1996	In U937 spheroids, cultured by the fibrin clot technique, we found an accumulation in the S-phase too as well as an increase of the transferrin receptor expression after Ara-C preincubation.	Cytarabine	170-175	transferrin receptor	Homo sapiens	132-152
34953799-0	2022	Overexpressed mitogen-and stress-activated protein kinase 1 promotes the resistance of cytarabine in acute myeloid leukemia through brahma related gene 1-mediated upregulation of heme oxygenase-1.	Cytarabine	87-97	heme oxygenase 1	Homo sapiens	179-195
34953799-7	2022	In vitro experiments revealed that the sensitivity of AML cell lines THP-1 and U937 to cytarabine (Ara-C) significantly decreased after overexpression of MSK1.	Cytarabine	87-97	ribosomal protein S6 kinase A5	Homo sapiens	154-158
34953799-7	2022	In vitro experiments revealed that the sensitivity of AML cell lines THP-1 and U937 to cytarabine (Ara-C) significantly decreased after overexpression of MSK1.	Cytarabine	99-104	ribosomal protein S6 kinase A5	Homo sapiens	154-158
34953799-8	2022	Meanwhile, downregulation of MSK1 by siRNA transfection or treatment of pharmacological inhibitor SB-747651A in AML cell lines and primary AML cells enhanced the sensitivity to Ara-C.	Cytarabine	177-182	ribosomal protein S6 kinase A5	Homo sapiens	29-33
34953799-13	2022	Downregulation of MSK1 enhanced the sensitivity of AML cells to Ara-C.	Cytarabine	64-69	ribosomal protein S6 kinase A5	Homo sapiens	18-22
34872003-0	2022	Coculture in vitro with endothelial cells induces cytarabine resistance of acute myeloid leukemia cells in a VEGF-A/VEGFR-2 signaling-independent manner.	Cytarabine	50-60	vascular endothelial growth factor A	Homo sapiens	109-115
34872003-0	2022	Coculture in vitro with endothelial cells induces cytarabine resistance of acute myeloid leukemia cells in a VEGF-A/VEGFR-2 signaling-independent manner.	Cytarabine	50-60	kinase insert domain receptor	Homo sapiens	116-123
34872003-7	2022	When VEGFR-2 was knocked out in EA.hy926 cells using the CRISPR-Cas9 system, the cytarabine-induced apoptosis of AML cells did not significantly change compared with that of wild-type cells.	Cytarabine	81-91	kinase insert domain receptor	Homo sapiens	5-12
34958665-9	2022	Lama4-/- MSCs displayed increased anti-oxidant activities and promoted AML stem cell proliferation and chemoresistance to cytarabine, which was accompanied by increased mitochondrial transfer from the MSCs to AML cells and reduced reactive oxygen species in AML cells in vitro.	Cytarabine	122-132	laminin, alpha 4	Mus musculus	0-5
34847435-3	2022	This 13.4 nm T22-GFP-H6-Ara-C nanoconjugate selectively eliminates CXCR4+ AML cells, which are protected by its anchoring to the bone marrow (BM) niche, being involved in AML progression and chemotherapy resistance.	Cytarabine	24-29	chemokine (C-X-C motif) receptor 4	Mus musculus	67-72
34847435-5	2022	Moreover, repeated T22-GFP-H6-Ara-C administration selectively eliminates CXCR4+ leukemic cells in BM, spleen and liver.	Cytarabine	30-35	chemokine (C-X-C motif) receptor 4	Mus musculus	74-79
34792179-8	2022	KIF2A siRNA inhibited proliferation but enhanced apoptosis and chemosensitivity to ADR and AraC in KG-1 and Kasumi-1 cells, which also inactivated PI3K/AKT and RhoA/ROCK pathways.	Cytarabine	91-95	kinesin family member 2A	Homo sapiens	0-5
34792179-8	2022	KIF2A siRNA inhibited proliferation but enhanced apoptosis and chemosensitivity to ADR and AraC in KG-1 and Kasumi-1 cells, which also inactivated PI3K/AKT and RhoA/ROCK pathways.	Cytarabine	91-95	AKT serine/threonine kinase 1	Homo sapiens	152-155
34792179-8	2022	KIF2A siRNA inhibited proliferation but enhanced apoptosis and chemosensitivity to ADR and AraC in KG-1 and Kasumi-1 cells, which also inactivated PI3K/AKT and RhoA/ROCK pathways.	Cytarabine	91-95	ras homolog family member A	Homo sapiens	160-164
34958665-10	2022	Similarly, we detected lower levels of reactive oxygen species in AML cells from Lama4-/- mice post-cytarabine treatment.	Cytarabine	100-110	laminin, alpha 4	Mus musculus	81-86
34976810-3	2021	SAMHD1 was also reported as a barrier to cytarabine, a common chemotherapy drug for mantle cell lymphoma (MCL), and as a biomarker of grim prognosis for acute myelocytic leukemia (AML) patients.	Cytarabine	41-51	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	0-6
34976810-11	2021	The MCL cell line with SAMHD1 knockdown showed lower Ki-67 proliferation index, higher caspase-3, and higher sensitivity to cytarabine.	Cytarabine	124-134	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	23-29
34836965-7	2021	Introduction of Cdc42 Activity Specific Inhibitor, CASIN, enhances the eradication of ALL leukemia stem cells by AraC+QC and prolongs the survival of both primary and secondary transplanted recipients without affecting normal long-term human hematopoiesis.	Cytarabine	113-117	cell division cycle 42	Homo sapiens	16-21
34857808-4	2021	Suppression of the chemokine CXCL12 ranked highly among the candidates of the cytarabine group.	Cytarabine	78-88	C-X-C motif chemokine ligand 12	Homo sapiens	29-35
34678222-9	2021	DFF40 deficient cells show chemoresistance to antimetabolites (e.g. methotrexate, 6-mercaptopurine and cytarabine) and surprisingly, they are more sensitive to TOP2 inhibitors (e.g. etoposide and teniposide).	Cytarabine	103-113	DNA fragmentation factor subunit beta	Homo sapiens	0-5
34678222-10	2021	DFF40 deficient cells exposed to cytarabine present lower phosphatidylserine translocation levels to the outer cell membrane layer.	Cytarabine	33-43	DNA fragmentation factor subunit beta	Homo sapiens	0-5
34678222-12	2021	The abolition of DFF40 expression in Jurkat cells significantly impairs histone H2AX phosphorylation following etoposide and cytarabine treatments.	Cytarabine	125-135	DNA fragmentation factor subunit beta	Homo sapiens	17-22
34181204-1	2021	BACKGROUND AND OBJECTIVE: The phase III ALFA-0701 study demonstrated the efficacy and safety of gemtuzumab ozogamicin (GO) versus standard of care (SOC) chemotherapy (daunorubicin and cytarabine) for the treatment of adult patients with de novo CD33+ acute myeloid leukaemia (AML).	Cytarabine	184-194	CD33 molecule	Homo sapiens	245-249
34496224-8	2021	Lastly, the KO of mitoNEET was associated with decreased proliferation as compared to control cells when exposed to the standard of care agent cytarabine (Ara-C).	Cytarabine	143-153	CDGSH iron sulfur domain 1	Homo sapiens	18-26
34868981-3	2021	In our in vitro studies, knockdown of CENPE expression resulted in the suppression of proliferation of myeloid leukemia cells and reversal of cytarabine (Ara-C) chemoresistance.	Cytarabine	142-152	centromere protein E	Homo sapiens	38-43
34738194-1	2022	SAMHD1 is a deoxynucleoside triphosphate triphosphohydrolase (dNTPase) that restricts viral replication in infected cells and limits the sensitivity to cytarabine by hydrolysing its active metabolite, as recently shown in acute myeloid leukemia.	Cytarabine	152-162	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	0-6
34738194-7	2022	We hypothesized that expression of SAMHD1 could predict short time to progression in patients treated with Cytarabine as part of high-dose chemotherapy.	Cytarabine	107-117	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	35-41
34868981-3	2021	In our in vitro studies, knockdown of CENPE expression resulted in the suppression of proliferation of myeloid leukemia cells and reversal of cytarabine (Ara-C) chemoresistance.	Cytarabine	154-159	centromere protein E	Homo sapiens	38-43
34868981-5	2021	Overexpression of LIN28A promoted the proliferation and Ara-C chemoresistance of leukemic cells.	Cytarabine	56-61	lin-28 homolog A	Homo sapiens	18-24
34868981-7	2021	In addition, the impacts of LIN28A on cell growth, apoptosis, cell cycle progression, and Ara-C chemoresistance were reverted by the knockdown of CENPE.	Cytarabine	90-95	lin-28 homolog A	Homo sapiens	28-34
34868981-7	2021	In addition, the impacts of LIN28A on cell growth, apoptosis, cell cycle progression, and Ara-C chemoresistance were reverted by the knockdown of CENPE.	Cytarabine	90-95	centromere protein E	Homo sapiens	146-151
34732236-3	2021	Glasdegib, the small-molecule inhibitor of smoothened (SMO), also showed improved overall survival in patients not eligible for intensive chemotherapy when combined with low-dose cytarabine compared to low-dose cytarabine alone.	Cytarabine	179-189	smoothened, frizzled class receptor	Homo sapiens	55-58
34732236-3	2021	Glasdegib, the small-molecule inhibitor of smoothened (SMO), also showed improved overall survival in patients not eligible for intensive chemotherapy when combined with low-dose cytarabine compared to low-dose cytarabine alone.	Cytarabine	211-221	smoothened, frizzled class receptor	Homo sapiens	55-58
34496224-8	2021	Lastly, the KO of mitoNEET was associated with decreased proliferation as compared to control cells when exposed to the standard of care agent cytarabine (Ara-C).	Cytarabine	155-160	CDGSH iron sulfur domain 1	Homo sapiens	18-26
34816103-6	2021	In vivo, the combination of tigecycline and cytarabine reduced leukemia progression in the AML-PDX model with high CDK6-AS1 levels, supporting the concept of a mitochondrial vulnerability.	Cytarabine	44-54	cyclin dependent kinase 6	Homo sapiens	115-119
34539849-0	2021	Pan-RAF inhibitor LY3009120 is highly synergistic with low-dose cytarabine, but not azacitidine, in acute myeloid leukemia with RAS mutations.	Cytarabine	64-74	zinc fingers and homeoboxes 2	Homo sapiens	4-7
34539849-6	2021	We found that the combination of low-dose cytarabine and LY3009120 showed a synergistic effect in NRAS-mutated HL-60 cells and KRAS-mutated NB4 cells.	Cytarabine	42-52	NRAS proto-oncogene, GTPase	Homo sapiens	98-102
34539849-6	2021	We found that the combination of low-dose cytarabine and LY3009120 showed a synergistic effect in NRAS-mutated HL-60 cells and KRAS-mutated NB4 cells.	Cytarabine	42-52	KRAS proto-oncogene, GTPase	Homo sapiens	127-131
34539849-9	2021	Our findings indicate that combination therapy with pan-RAF inhibitor LY3009120 and low-dose cytarabine may be a promising treatment strategy for RAS-mutated AML.	Cytarabine	93-103	zinc fingers and homeoboxes 2	Homo sapiens	56-59
34716195-7	2022	Pulse-chase double-labeling experiments with EdU and BrdU after cytarabine wash-out demonstrated a higher rate of fork collapse in DNMT3A(mut)-expressing cells.	Cytarabine	64-74	DNA methyltransferase 3A	Mus musculus	131-137
34707185-0	2021	CD157 signaling promotes survival of acute myeloid leukemia cells and modulates sensitivity to cytarabine through regulation of anti-apoptotic Mcl-1.	Cytarabine	95-105	bone marrow stromal cell antigen 1	Homo sapiens	0-5
34707185-0	2021	CD157 signaling promotes survival of acute myeloid leukemia cells and modulates sensitivity to cytarabine through regulation of anti-apoptotic Mcl-1.	Cytarabine	95-105	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	143-148
34707185-4	2021	CD157-targeting antibodies enhanced survival, decreased apoptosis and reduced AraC toxicity in AML blasts and cell lines.	Cytarabine	78-82	bone marrow stromal cell antigen 1	Homo sapiens	0-5
34707185-7	2021	Indeed, the Mcl-1-specific inhibitor S63845 restored apoptosis by disrupting the interaction of Mcl-1 with Bim and Bak and significantly increased AraC toxicity in CD157-high but not in CD157-low AML cells.	Cytarabine	147-151	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	12-17
34718324-0	2021	A prospective biomarker analysis of alvocidib followed by cytarabine and mitoxantrone in MCL-1-dependent relapsed/refractory acute myeloid leukemia.	Cytarabine	58-68	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	89-94
34816103-6	2021	In vivo, the combination of tigecycline and cytarabine reduced leukemia progression in the AML-PDX model with high CDK6-AS1 levels, supporting the concept of a mitochondrial vulnerability.	Cytarabine	44-54	prostaglandin D2 receptor	Homo sapiens	120-123
34681817-3	2021	We showed that under acute myeloid leukemia (AML) conditions, alone and in combination with cytarabine (CYT), there was significant damage in the histology of seminiferous tubules, a significant increase in apoptotic cells of the seminiferous tubules, and a reduction in spermatogonial cells (SALL and PLZF) and in meiotic (CREM) and post-meiotic (ACROSIN) cells.	Cytarabine	92-102	zinc finger and BTB domain containing 16	Mus musculus	302-306
34492683-7	2021	Interestingly, IKZF1 knockout and IK6 knock-in cells both have significantly increased sensitivity to cytarabine, likely owing to marked downregulation of SAMHD1 after IKZF1 knockout.	Cytarabine	102-112	IKAROS family zinc finger 1	Homo sapiens	15-20
34492683-7	2021	Interestingly, IKZF1 knockout and IK6 knock-in cells both have significantly increased sensitivity to cytarabine, likely owing to marked downregulation of SAMHD1 after IKZF1 knockout.	Cytarabine	102-112	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	155-161
34492683-7	2021	Interestingly, IKZF1 knockout and IK6 knock-in cells both have significantly increased sensitivity to cytarabine, likely owing to marked downregulation of SAMHD1 after IKZF1 knockout.	Cytarabine	102-112	IKAROS family zinc finger 1	Homo sapiens	168-173
34681817-3	2021	We showed that under acute myeloid leukemia (AML) conditions, alone and in combination with cytarabine (CYT), there was significant damage in the histology of seminiferous tubules, a significant increase in apoptotic cells of the seminiferous tubules, and a reduction in spermatogonial cells (SALL and PLZF) and in meiotic (CREM) and post-meiotic (ACROSIN) cells.	Cytarabine	92-102	cAMP responsive element modulator	Mus musculus	324-328
34681817-3	2021	We showed that under acute myeloid leukemia (AML) conditions, alone and in combination with cytarabine (CYT), there was significant damage in the histology of seminiferous tubules, a significant increase in apoptotic cells of the seminiferous tubules, and a reduction in spermatogonial cells (SALL and PLZF) and in meiotic (CREM) and post-meiotic (ACROSIN) cells.	Cytarabine	92-102	acrosin prepropeptide	Mus musculus	348-355
34681817-3	2021	We showed that under acute myeloid leukemia (AML) conditions, alone and in combination with cytarabine (CYT), there was significant damage in the histology of seminiferous tubules, a significant increase in apoptotic cells of the seminiferous tubules, and a reduction in spermatogonial cells (SALL and PLZF) and in meiotic (CREM) and post-meiotic (ACROSIN) cells.	Cytarabine	104-107	zinc finger and BTB domain containing 16	Mus musculus	302-306
34681817-3	2021	We showed that under acute myeloid leukemia (AML) conditions, alone and in combination with cytarabine (CYT), there was significant damage in the histology of seminiferous tubules, a significant increase in apoptotic cells of the seminiferous tubules, and a reduction in spermatogonial cells (SALL and PLZF) and in meiotic (CREM) and post-meiotic (ACROSIN) cells.	Cytarabine	104-107	cAMP responsive element modulator	Mus musculus	324-328
34681817-3	2021	We showed that under acute myeloid leukemia (AML) conditions, alone and in combination with cytarabine (CYT), there was significant damage in the histology of seminiferous tubules, a significant increase in apoptotic cells of the seminiferous tubules, and a reduction in spermatogonial cells (SALL and PLZF) and in meiotic (CREM) and post-meiotic (ACROSIN) cells.	Cytarabine	104-107	acrosin prepropeptide	Mus musculus	348-355
34681817-9	2021	We showed that GCSF injection in combination with AML and cytarabine (AML + CYT + GCSF) extended the survival of mice for a week (from 6.5 weeks to 7.5 weeks) compared to (AML + CYT).	Cytarabine	58-68	colony stimulating factor 3 (granulocyte)	Mus musculus	82-86
34681817-9	2021	We showed that GCSF injection in combination with AML and cytarabine (AML + CYT + GCSF) extended the survival of mice for a week (from 6.5 weeks to 7.5 weeks) compared to (AML + CYT).	Cytarabine	76-79	colony stimulating factor 3 (granulocyte)	Mus musculus	15-19
34641952-1	2021	BACKGROUND: SAMHD1 mediates resistance to anti-cancer nucleoside analogues, including cytarabine, decitabine, and nelarabine that are commonly used for the treatment of leukaemia, through cleavage of their triphosphorylated forms.	Cytarabine	86-96	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	12-18
34681817-11	2021	GCSF significantly improved the spermatogonial niche expressed by increased the expression levels of testicular GDNF, SCF and MCSF growth factors in AML-treated mice and (AML + CYT)-treated mice compared to those groups without GCSF.	Cytarabine	177-180	colony stimulating factor 3	Homo sapiens	0-4
34681817-13	2021	Our results show for the first time the capacity of post injection of GCSF into AML- and CYT-treated mice to improve the cellular and biomolecular mechanisms that lead to improve/restore spermatogenesis and male fertility.	Cytarabine	89-92	colony stimulating factor 3	Homo sapiens	70-74
34641952-15	2021	CNDAC-adapted sublines displayed cross-resistance only to other DCK substrates (e.g. cytarabine, decitabine).	Cytarabine	85-95	deoxycytidine kinase	Homo sapiens	64-67
34416320-2	2021	To what extent differences in cytidine deaminase (CDA) activity, the enzyme that catabolizes free cytarabine in the liver, can affect the pharmacokinetics of liposomal cytarabine as well, is unknown.	Cytarabine	98-108	cytidine deaminase	Homo sapiens	30-48
34641952-17	2021	In cytarabine-adapted AML cells, increased SAMHD1 and reduced DCK levels contributed to cytarabine and CNDAC resistance.	Cytarabine	3-13	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	43-49
34641952-17	2021	In cytarabine-adapted AML cells, increased SAMHD1 and reduced DCK levels contributed to cytarabine and CNDAC resistance.	Cytarabine	3-13	deoxycytidine kinase	Homo sapiens	62-65
34641952-17	2021	In cytarabine-adapted AML cells, increased SAMHD1 and reduced DCK levels contributed to cytarabine and CNDAC resistance.	Cytarabine	88-98	SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1	Homo sapiens	43-49
34641952-17	2021	In cytarabine-adapted AML cells, increased SAMHD1 and reduced DCK levels contributed to cytarabine and CNDAC resistance.	Cytarabine	88-98	deoxycytidine kinase	Homo sapiens	62-65
34416320-2	2021	To what extent differences in cytidine deaminase (CDA) activity, the enzyme that catabolizes free cytarabine in the liver, can affect the pharmacokinetics of liposomal cytarabine as well, is unknown.	Cytarabine	98-108	cytidine deaminase	Homo sapiens	50-53
34416320-2	2021	To what extent differences in cytidine deaminase (CDA) activity, the enzyme that catabolizes free cytarabine in the liver, can affect the pharmacokinetics of liposomal cytarabine as well, is unknown.	Cytarabine	168-178	cytidine deaminase	Homo sapiens	30-48
34416320-2	2021	To what extent differences in cytidine deaminase (CDA) activity, the enzyme that catabolizes free cytarabine in the liver, can affect the pharmacokinetics of liposomal cytarabine as well, is unknown.	Cytarabine	168-178	cytidine deaminase	Homo sapiens	50-53
34416320-12	2021	This proof-of-concept study suggests that CDA status has a major impact on cytarabine PK and possibly safety in AML patients even when administered as a liposome.	Cytarabine	75-85	cytidine deaminase	Homo sapiens	42-45
34112534-7	2021	Mechanistically, synergistic anti-tumor effect of Ara-C/Brusatol in AML cells is mediated by attenuating Nrf2 expression.	Cytarabine	50-55	NFE2 like bZIP transcription factor 2	Homo sapiens	105-109
34358965-4	2021	These results indicate that the anticancer effects of Ara-C not only include the commonly known antimetabolic effects, but also the induction of cell death by nuclear transfer of GAPDH through interaction with POP.	Cytarabine	54-59	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	179-184
34358965-4	2021	These results indicate that the anticancer effects of Ara-C not only include the commonly known antimetabolic effects, but also the induction of cell death by nuclear transfer of GAPDH through interaction with POP.	Cytarabine	54-59	prolyl endopeptidase	Homo sapiens	210-213
34358965-0	2021	Prolyl oligopeptidase participates in the cytosine arabinoside-induced nuclear translocation of glyceraldehyde 3-phosphate dehydrogenase in a human neuroblastoma cell line.	Cytarabine	42-62	prolyl endopeptidase	Homo sapiens	0-21
34358965-0	2021	Prolyl oligopeptidase participates in the cytosine arabinoside-induced nuclear translocation of glyceraldehyde 3-phosphate dehydrogenase in a human neuroblastoma cell line.	Cytarabine	42-62	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	96-136
34358965-1	2021	Previously, we reported that glyceraldehyde 3-phosphate dehydrogenase (GAPDH) is a binding partner of prolyl oligopeptidase (POP) in neuroblastoma NB-1 cells and that the POP inhibitor, SUAM-14746, inhibits cytosine arabinoside (Ara-C)-induced nuclear translocation of GAPDH and protects against Ara-C cytotoxicity.	Cytarabine	207-227	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	29-69
34358965-1	2021	Previously, we reported that glyceraldehyde 3-phosphate dehydrogenase (GAPDH) is a binding partner of prolyl oligopeptidase (POP) in neuroblastoma NB-1 cells and that the POP inhibitor, SUAM-14746, inhibits cytosine arabinoside (Ara-C)-induced nuclear translocation of GAPDH and protects against Ara-C cytotoxicity.	Cytarabine	207-227	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	71-76
34358965-1	2021	Previously, we reported that glyceraldehyde 3-phosphate dehydrogenase (GAPDH) is a binding partner of prolyl oligopeptidase (POP) in neuroblastoma NB-1 cells and that the POP inhibitor, SUAM-14746, inhibits cytosine arabinoside (Ara-C)-induced nuclear translocation of GAPDH and protects against Ara-C cytotoxicity.	Cytarabine	207-227	prolyl endopeptidase	Homo sapiens	102-123
34358965-1	2021	Previously, we reported that glyceraldehyde 3-phosphate dehydrogenase (GAPDH) is a binding partner of prolyl oligopeptidase (POP) in neuroblastoma NB-1 cells and that the POP inhibitor, SUAM-14746, inhibits cytosine arabinoside (Ara-C)-induced nuclear translocation of GAPDH and protects against Ara-C cytotoxicity.	Cytarabine	207-227	prolyl endopeptidase	Homo sapiens	171-174
34358965-1	2021	Previously, we reported that glyceraldehyde 3-phosphate dehydrogenase (GAPDH) is a binding partner of prolyl oligopeptidase (POP) in neuroblastoma NB-1 cells and that the POP inhibitor, SUAM-14746, inhibits cytosine arabinoside (Ara-C)-induced nuclear translocation of GAPDH and protects against Ara-C cytotoxicity.	Cytarabine	207-227	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	269-274
34358965-1	2021	Previously, we reported that glyceraldehyde 3-phosphate dehydrogenase (GAPDH) is a binding partner of prolyl oligopeptidase (POP) in neuroblastoma NB-1 cells and that the POP inhibitor, SUAM-14746, inhibits cytosine arabinoside (Ara-C)-induced nuclear translocation of GAPDH and protects against Ara-C cytotoxicity.	Cytarabine	229-234	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	29-69
34358965-1	2021	Previously, we reported that glyceraldehyde 3-phosphate dehydrogenase (GAPDH) is a binding partner of prolyl oligopeptidase (POP) in neuroblastoma NB-1 cells and that the POP inhibitor, SUAM-14746, inhibits cytosine arabinoside (Ara-C)-induced nuclear translocation of GAPDH and protects against Ara-C cytotoxicity.	Cytarabine	229-234	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	71-76
34358965-1	2021	Previously, we reported that glyceraldehyde 3-phosphate dehydrogenase (GAPDH) is a binding partner of prolyl oligopeptidase (POP) in neuroblastoma NB-1 cells and that the POP inhibitor, SUAM-14746, inhibits cytosine arabinoside (Ara-C)-induced nuclear translocation of GAPDH and protects against Ara-C cytotoxicity.	Cytarabine	229-234	prolyl endopeptidase	Homo sapiens	102-123
34358965-1	2021	Previously, we reported that glyceraldehyde 3-phosphate dehydrogenase (GAPDH) is a binding partner of prolyl oligopeptidase (POP) in neuroblastoma NB-1 cells and that the POP inhibitor, SUAM-14746, inhibits cytosine arabinoside (Ara-C)-induced nuclear translocation of GAPDH and protects against Ara-C cytotoxicity.	Cytarabine	229-234	prolyl endopeptidase	Homo sapiens	125-128
34358965-1	2021	Previously, we reported that glyceraldehyde 3-phosphate dehydrogenase (GAPDH) is a binding partner of prolyl oligopeptidase (POP) in neuroblastoma NB-1 cells and that the POP inhibitor, SUAM-14746, inhibits cytosine arabinoside (Ara-C)-induced nuclear translocation of GAPDH and protects against Ara-C cytotoxicity.	Cytarabine	229-234	prolyl endopeptidase	Homo sapiens	171-174
34358965-1	2021	Previously, we reported that glyceraldehyde 3-phosphate dehydrogenase (GAPDH) is a binding partner of prolyl oligopeptidase (POP) in neuroblastoma NB-1 cells and that the POP inhibitor, SUAM-14746, inhibits cytosine arabinoside (Ara-C)-induced nuclear translocation of GAPDH and protects against Ara-C cytotoxicity.	Cytarabine	229-234	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	269-274
34358965-2	2021	To carry out a more in-depth analysis of the interaction between POP and GAPDH, we generated POP-KO NB-1 cells and compared the nuclear translocation of GAPDH after Ara-C with or without SUAM-14746 treatment to wild-type NB-1 cells by western blotting and fluorescence immunostaining.	Cytarabine	165-170	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	153-158
34112534-9	2021	The activation of Nrf2 by Sulforaphane (SFP) could reverse the chemotherapeutic effect and changes of glycolysis of concomitant of Ara-C with Brusatol in AML cell lines.	Cytarabine	131-136	NFE2 like bZIP transcription factor 2	Homo sapiens	18-22
34112534-10	2021	Additionally, Ara-C/Brusatol co-treatment decreased Glucose-6-phosphate dehydrogenase (G6PD) protein expression and increased the sensitivity of Ara-C.	Cytarabine	14-19	glucose-6-phosphate dehydrogenase	Homo sapiens	87-91
34417161-0	2021	Efficacy and Safety of Azacytidine in Combination With Fludarabine and High-Dose Cytarabine With G-CSF (FLAG) in Relapsed/Refractory Acute Myeloid Leukemia: A Nonrandomized, Open-Label, Phase II Study.	Cytarabine	81-91	colony stimulating factor 3	Homo sapiens	97-102
34236556-1	2021	BACKGROUND: Addition of cytarabine to high-dose methotrexate (HD-MTX) chemotherapy improves outcome of primary CNS lymphoma (PCNSL); however, the combination therapy increases toxicity.	Cytarabine	24-34	metaxin 1	Homo sapiens	65-68
34131282-7	2021	In vivo, LONA overexpression acts as an oncogenic lncRNA reducing the survival of mice transplanted with AML cells and rendering AML tumors more resistant to AraC chemotherapy.These data indicate that mutation-dependent nuclear export of NPM1 leads to nuclear retention and consequent oncogenic functions of the overexpressed lncRNA LONA, thus uncovering a novel NPM1 mutation-dependent pathway in AML pathogenesis.	Cytarabine	158-162	nucleophosmin 1	Mus musculus	238-242
34627417-11	2021	CONCLUSION: Cytarabine-resistant ALL cell lines are successfully established by using low concentration continuous induction method, and its drug-resistant mechanism may be related to the deficiencies of DCK and cyclinB1.	Cytarabine	12-22	deoxycytidine kinase	Homo sapiens	204-207
34271301-0	2021	Cytarabine and EIP co-administration synergistically reduces viability of acute lymphoblastic leukemia cells with high ERG expression.	Cytarabine	0-10	ETS transcription factor ERG	Homo sapiens	119-122
34627417-11	2021	CONCLUSION: Cytarabine-resistant ALL cell lines are successfully established by using low concentration continuous induction method, and its drug-resistant mechanism may be related to the deficiencies of DCK and cyclinB1.	Cytarabine	12-22	cyclin B1	Homo sapiens	212-220
34627412-11	2021	Experimental treatment was carried out on the leukemia mouse model transplanted with MLL-AF9 spleen cells, and it was found that the traditional chemotherapy drug cytarabine could delay the onset of leukemia and prolong the survival time of the mouse model.	Cytarabine	163-173	lysine (K)-specific methyltransferase 2A	Mus musculus	85-88
34298712-7	2021	Furthermore, we showed that while AraC induced an immune response regulation by increasing CD39 expression and by reinforcing the interferon-gamma/PD-L1 axis, EVT-701 reduced CD39 and PD-L1 expression in vitro in a panel of both murine and human AML cell lines, especially upon AraC treatment.	Cytarabine	34-38	ectonucleoside triphosphate diphosphohydrolase 1	Mus musculus	91-95
34627412-11	2021	Experimental treatment was carried out on the leukemia mouse model transplanted with MLL-AF9 spleen cells, and it was found that the traditional chemotherapy drug cytarabine could delay the onset of leukemia and prolong the survival time of the mouse model.	Cytarabine	163-173	myeloid/lymphoid or mixed-lineage leukemia; translocated to, 3	Mus musculus	89-92
34572794-3	2021	In the last years, the therapeutic options have rapidly changed, with the approval of innovative compounds that provide new opportunities, together with new challenges for clinicians: among them, on 1 September, 2017 the Food and Drug Administration granted approval for Gemtuzumab Ozogamicin (GO) in combination with daunorubicin and cytarabine for the treatment of adult patients affected by newly diagnosed CD33+ AML.	Cytarabine	335-345	CD33 molecule	Homo sapiens	410-414
34394903-2	2021	In this study, we aimed to investigate the molecular mechanism of KDM4C-dependent MALAT1/miR-328-3p/CCND2 axis in cytarabine (Ara-C) resistance in the context of AML.	Cytarabine	126-131	microRNA 328	Mus musculus	89-96
34394903-2	2021	In this study, we aimed to investigate the molecular mechanism of KDM4C-dependent MALAT1/miR-328-3p/CCND2 axis in cytarabine (Ara-C) resistance in the context of AML.	Cytarabine	126-131	cyclin D2	Mus musculus	100-105
34394903-5	2021	After conducting gain- and loss-of-function assays, we investigated the effect of KDM4C on cell Ara-C resistance.	Cytarabine	96-101	lysine (K)-specific demethylase 4C	Mus musculus	82-87
34394903-6	2021	A NOD/SCID mouse model was established to further investigate the roles of KDM4C/MALAT1/miR-328-3p/CCND2 in Ara-C resistant AML cells.	Cytarabine	108-113	cyclin D2	Mus musculus	99-104
34394903-8	2021	KDM4C upregulation promoted the demethylation in the promoter region of MALAT1 to increase its expression, MALAT1 targeted and inhibited miR-328-3p expression, enhancing the Ara-C resistance of HL-60/A.	Cytarabine	174-179	lysine (K)-specific demethylase 4C	Mus musculus	0-5
34394903-8	2021	KDM4C upregulation promoted the demethylation in the promoter region of MALAT1 to increase its expression, MALAT1 targeted and inhibited miR-328-3p expression, enhancing the Ara-C resistance of HL-60/A.	Cytarabine	174-179	metastasis associated lung adenocarcinoma transcript 1 (non-coding RNA)	Mus musculus	72-78
34394903-8	2021	KDM4C upregulation promoted the demethylation in the promoter region of MALAT1 to increase its expression, MALAT1 targeted and inhibited miR-328-3p expression, enhancing the Ara-C resistance of HL-60/A.	Cytarabine	174-179	metastasis associated lung adenocarcinoma transcript 1 (non-coding RNA)	Mus musculus	107-113
34394903-9	2021	miR-328-3p targeted and suppressed the expression of CCND2 in HL-60/A to inhibit the Ara-C resistance.	Cytarabine	85-90	cyclin D2	Mus musculus	53-58
34394903-10	2021	Mechanistically, KDM4C regulated miR-328-3p/CCND2 through MALAT1, resulting in Ara-C resistance in AML.	Cytarabine	79-84	lysine (K)-specific demethylase 4C	Mus musculus	17-22
34394903-10	2021	Mechanistically, KDM4C regulated miR-328-3p/CCND2 through MALAT1, resulting in Ara-C resistance in AML.	Cytarabine	79-84	cyclin D2	Mus musculus	44-49
34394903-10	2021	Mechanistically, KDM4C regulated miR-328-3p/CCND2 through MALAT1, resulting in Ara-C resistance in AML.	Cytarabine	79-84	metastasis associated lung adenocarcinoma transcript 1 (non-coding RNA)	Mus musculus	58-64
34394903-11	2021	Findings in an in vivo xenograft NOD/SCID mouse model further confirmed the contribution of KDM4C/MALAT1/miR-328-3p/CCND2 in the Ara-C resistant AML.	Cytarabine	129-134	lysine (K)-specific demethylase 4C	Mus musculus	92-97
34394903-11	2021	Findings in an in vivo xenograft NOD/SCID mouse model further confirmed the contribution of KDM4C/MALAT1/miR-328-3p/CCND2 in the Ara-C resistant AML.	Cytarabine	129-134	metastasis associated lung adenocarcinoma transcript 1 (non-coding RNA)	Mus musculus	98-104
34394903-11	2021	Findings in an in vivo xenograft NOD/SCID mouse model further confirmed the contribution of KDM4C/MALAT1/miR-328-3p/CCND2 in the Ara-C resistant AML.	Cytarabine	129-134	microRNA 328	Mus musculus	105-112
34394903-11	2021	Findings in an in vivo xenograft NOD/SCID mouse model further confirmed the contribution of KDM4C/MALAT1/miR-328-3p/CCND2 in the Ara-C resistant AML.	Cytarabine	129-134	cyclin D2	Mus musculus	116-121
34394903-13	2021	The downregulation of miR-328-3p increased the level of CCND2, which induced the Ara-C resistance in AML.	Cytarabine	81-86	cyclin D2	Mus musculus	56-61
34109436-0	2021	Curcumin induces apoptosis by inhibiting BCAT1 expression and mTOR signaling in cytarabine-resistant myeloid leukemia cells.	Cytarabine	80-90	mechanistic target of rapamycin kinase	Homo sapiens	62-66
34109436-9	2021	The results demonstrated that curcumin inhibited BCAT1 expression in Kasumi-1, KG-1, HL60, cytarabine-resistant HL60, and cytarabine-resistant primary myeloid leukemia cells.	Cytarabine	91-101	branched chain amino acid transaminase 1	Homo sapiens	49-54
34109436-11	2021	Furthermore, BCAT1 and mTOR signaling may modulate each other in cytarabine-resistant HL60 cells.	Cytarabine	65-75	branched chain amino acid transaminase 1	Homo sapiens	13-18
34109436-11	2021	Furthermore, BCAT1 and mTOR signaling may modulate each other in cytarabine-resistant HL60 cells.	Cytarabine	65-75	mechanistic target of rapamycin kinase	Homo sapiens	23-27
34251414-3	2021	In a phase 1 study of AML patients treated with G3139, cytarabine, and daunorubicin induction with cytarabine consolidation, no antisense-related toxicity was reported, and BCL2 downregulation occurred in patients achieving complete remission.	Cytarabine	55-65	BCL2 apoptosis regulator	Homo sapiens	173-177
34216770-6	2021	This report is the first demonstrating that Ara-C combined with DS can modulate immune responses and revert immunosuppression as evidenced by increased IFN-gamma and IL-12p40 without changes in IL-10 in peripheral blood mononuclear cells, and increased CD80 and decreased CD163 on immunosuppressive macrophages.	Cytarabine	44-49	interferon gamma	Homo sapiens	152-161
34216770-6	2021	This report is the first demonstrating that Ara-C combined with DS can modulate immune responses and revert immunosuppression as evidenced by increased IFN-gamma and IL-12p40 without changes in IL-10 in peripheral blood mononuclear cells, and increased CD80 and decreased CD163 on immunosuppressive macrophages.	Cytarabine	44-49	interleukin 10	Homo sapiens	194-199
34216770-6	2021	This report is the first demonstrating that Ara-C combined with DS can modulate immune responses and revert immunosuppression as evidenced by increased IFN-gamma and IL-12p40 without changes in IL-10 in peripheral blood mononuclear cells, and increased CD80 and decreased CD163 on immunosuppressive macrophages.	Cytarabine	44-49	CD80 molecule	Homo sapiens	253-257
34216770-6	2021	This report is the first demonstrating that Ara-C combined with DS can modulate immune responses and revert immunosuppression as evidenced by increased IFN-gamma and IL-12p40 without changes in IL-10 in peripheral blood mononuclear cells, and increased CD80 and decreased CD163 on immunosuppressive macrophages.	Cytarabine	44-49	CD163 molecule	Homo sapiens	272-277
34216770-7	2021	Furthermore, Ara-C/DS increased MHC class I expression on cancer cells while increasing the production of antigen-specific IFN-gamma+ CD8+ T cells in viral peptide-challenged lymphocytes from both humans and vaccinated mice.	Cytarabine	13-18	interferon gamma	Homo sapiens	123-132
34196511-16	2021	Indeed, doxorubicin plus cytarabine (DA), the standard chemotherapeutic regimen used in AML treatment, could specifically kill c-Kit+ B220+ Mac-1- cells, but it hardly affected c-Kit+ B220+ Mac-1+ cells.	Cytarabine	25-35	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	127-132
34196511-16	2021	Indeed, doxorubicin plus cytarabine (DA), the standard chemotherapeutic regimen used in AML treatment, could specifically kill c-Kit+ B220+ Mac-1- cells, but it hardly affected c-Kit+ B220+ Mac-1+ cells.	Cytarabine	25-35	protein tyrosine phosphatase, receptor type, C	Mus musculus	134-138
34196511-16	2021	Indeed, doxorubicin plus cytarabine (DA), the standard chemotherapeutic regimen used in AML treatment, could specifically kill c-Kit+ B220+ Mac-1- cells, but it hardly affected c-Kit+ B220+ Mac-1+ cells.	Cytarabine	25-35	integrin alpha M	Mus musculus	140-145
34252711-4	2021	Loss of function studies demonstrated that silencing of GILT in AML cells sensitized them to Ara-C treatment both in vitro and in vivo.	Cytarabine	93-98	IFI30 lysosomal thiol reductase	Homo sapiens	56-60
34252711-5	2021	Further mechanistic findings revealed that the ROS-mediated mitochondrial damage plays a pivotal role in inducing apoptosis of GILT-inhibited AML cells after Ara-C treatment.	Cytarabine	158-163	IFI30 lysosomal thiol reductase	Homo sapiens	127-131
34394903-0	2021	KDM4C contributes to cytarabine resistance in acute myeloid leukemia via regulating the miR-328-3p/CCND2 axis through MALAT1.	Cytarabine	21-31	lysine (K)-specific demethylase 4C	Mus musculus	0-5
34394903-0	2021	KDM4C contributes to cytarabine resistance in acute myeloid leukemia via regulating the miR-328-3p/CCND2 axis through MALAT1.	Cytarabine	21-31	microRNA 328	Mus musculus	88-95
34394903-0	2021	KDM4C contributes to cytarabine resistance in acute myeloid leukemia via regulating the miR-328-3p/CCND2 axis through MALAT1.	Cytarabine	21-31	cyclin D2	Mus musculus	99-104
34394903-0	2021	KDM4C contributes to cytarabine resistance in acute myeloid leukemia via regulating the miR-328-3p/CCND2 axis through MALAT1.	Cytarabine	21-31	metastasis associated lung adenocarcinoma transcript 1 (non-coding RNA)	Mus musculus	118-124
34394903-2	2021	In this study, we aimed to investigate the molecular mechanism of KDM4C-dependent MALAT1/miR-328-3p/CCND2 axis in cytarabine (Ara-C) resistance in the context of AML.	Cytarabine	114-124	lysine (K)-specific demethylase 4C	Mus musculus	66-71
34394903-2	2021	In this study, we aimed to investigate the molecular mechanism of KDM4C-dependent MALAT1/miR-328-3p/CCND2 axis in cytarabine (Ara-C) resistance in the context of AML.	Cytarabine	114-124	metastasis associated lung adenocarcinoma transcript 1 (non-coding RNA)	Mus musculus	82-88
34394903-2	2021	In this study, we aimed to investigate the molecular mechanism of KDM4C-dependent MALAT1/miR-328-3p/CCND2 axis in cytarabine (Ara-C) resistance in the context of AML.	Cytarabine	114-124	microRNA 328	Mus musculus	89-96
34394903-2	2021	In this study, we aimed to investigate the molecular mechanism of KDM4C-dependent MALAT1/miR-328-3p/CCND2 axis in cytarabine (Ara-C) resistance in the context of AML.	Cytarabine	114-124	cyclin D2	Mus musculus	100-105
34394903-2	2021	In this study, we aimed to investigate the molecular mechanism of KDM4C-dependent MALAT1/miR-328-3p/CCND2 axis in cytarabine (Ara-C) resistance in the context of AML.	Cytarabine	126-131	lysine (K)-specific demethylase 4C	Mus musculus	66-71
34394903-2	2021	In this study, we aimed to investigate the molecular mechanism of KDM4C-dependent MALAT1/miR-328-3p/CCND2 axis in cytarabine (Ara-C) resistance in the context of AML.	Cytarabine	126-131	metastasis associated lung adenocarcinoma transcript 1 (non-coding RNA)	Mus musculus	82-88
34298712-7	2021	Furthermore, we showed that while AraC induced an immune response regulation by increasing CD39 expression and by reinforcing the interferon-gamma/PD-L1 axis, EVT-701 reduced CD39 and PD-L1 expression in vitro in a panel of both murine and human AML cell lines, especially upon AraC treatment.	Cytarabine	34-38	interferon gamma	Mus musculus	130-146
34298712-7	2021	Furthermore, we showed that while AraC induced an immune response regulation by increasing CD39 expression and by reinforcing the interferon-gamma/PD-L1 axis, EVT-701 reduced CD39 and PD-L1 expression in vitro in a panel of both murine and human AML cell lines, especially upon AraC treatment.	Cytarabine	34-38	CD274 antigen	Mus musculus	147-152
34080665-0	2021	HOXA11 plays critical roles in disease progression and response to cytarabine in AML.	Cytarabine	67-77	homeobox A11	Mus musculus	0-6
34095945-4	2021	Then, zwitterionic sulfobetaine (ZS) and CXCR4 antagonist peptide E5 were modified onto the surface of the nanoparticles via covalent bonding to fabricate a nanoplatform (denoted as HMPBs(DNR + AraC)@PEI-ZS-E5).	Cytarabine	194-198	C-X-C motif chemokine receptor 4	Homo sapiens	41-46
34307420-0	2021	Case Report: PD-1 Blockade Combined Autologous Hematopoietic Stem Cell Transplantation With Modified BEAM Regimen Containing High-Dose Cytarabine to Treat R/R Hodgkin"s Lymphoma.	Cytarabine	135-145	programmed cell death 1	Homo sapiens	13-17
34080665-2	2021	Previous findings with a mouse model showed that cooperation of MLL/AF10 with tyrosine-protein phosphatase non-receptor type 11 (PTPN11)G503A accelerated leukemia development, but increased cytarabine (Ara-C) sensitivity of leukemia cells.	Cytarabine	190-200	lysine (K)-specific methyltransferase 2A	Mus musculus	64-67
34080665-2	2021	Previous findings with a mouse model showed that cooperation of MLL/AF10 with tyrosine-protein phosphatase non-receptor type 11 (PTPN11)G503A accelerated leukemia development, but increased cytarabine (Ara-C) sensitivity of leukemia cells.	Cytarabine	190-200	myeloid/lymphoid or mixed-lineage leukemia; translocated to, 10	Mus musculus	68-72
34080665-2	2021	Previous findings with a mouse model showed that cooperation of MLL/AF10 with tyrosine-protein phosphatase non-receptor type 11 (PTPN11)G503A accelerated leukemia development, but increased cytarabine (Ara-C) sensitivity of leukemia cells.	Cytarabine	190-200	protein tyrosine phosphatase, non-receptor type 11	Mus musculus	78-127
34080665-2	2021	Previous findings with a mouse model showed that cooperation of MLL/AF10 with tyrosine-protein phosphatase non-receptor type 11 (PTPN11)G503A accelerated leukemia development, but increased cytarabine (Ara-C) sensitivity of leukemia cells.	Cytarabine	190-200	protein tyrosine phosphatase, non-receptor type 11	Mus musculus	129-135
34080665-2	2021	Previous findings with a mouse model showed that cooperation of MLL/AF10 with tyrosine-protein phosphatase non-receptor type 11 (PTPN11)G503A accelerated leukemia development, but increased cytarabine (Ara-C) sensitivity of leukemia cells.	Cytarabine	202-207	lysine (K)-specific methyltransferase 2A	Mus musculus	64-67
34080665-2	2021	Previous findings with a mouse model showed that cooperation of MLL/AF10 with tyrosine-protein phosphatase non-receptor type 11 (PTPN11)G503A accelerated leukemia development, but increased cytarabine (Ara-C) sensitivity of leukemia cells.	Cytarabine	202-207	myeloid/lymphoid or mixed-lineage leukemia; translocated to, 10	Mus musculus	68-72
34080665-2	2021	Previous findings with a mouse model showed that cooperation of MLL/AF10 with tyrosine-protein phosphatase non-receptor type 11 (PTPN11)G503A accelerated leukemia development, but increased cytarabine (Ara-C) sensitivity of leukemia cells.	Cytarabine	202-207	protein tyrosine phosphatase, non-receptor type 11	Mus musculus	78-127
34080665-2	2021	Previous findings with a mouse model showed that cooperation of MLL/AF10 with tyrosine-protein phosphatase non-receptor type 11 (PTPN11)G503A accelerated leukemia development, but increased cytarabine (Ara-C) sensitivity of leukemia cells.	Cytarabine	202-207	protein tyrosine phosphatase, non-receptor type 11	Mus musculus	129-135
34080665-8	2021	Functional studies of Hoxa11 knockdown or overexpression in MLL/AF10(OM-LZ) cells revealed that Hoxa11 expression levels were associated with survival in vivo and Ara-C sensitivity/apoptosis in vitro.	Cytarabine	163-168	homeobox A11	Mus musculus	22-28
34080665-11	2021	These results indicated that the expression of HOXA11 increased cell apoptosis and predicted an improved response to Ara-C in AML.	Cytarabine	117-122	homeobox A11	Mus musculus	47-53
34327076-0	2021	CD5+ Diffuse Large B-Cell Lymphoma With Leukemic Transformation: A Rare Case With Central Nervous System Involvement, Treated With R-CHOP and Intrathecal Methotrexate/Cytarabine.	Cytarabine	167-177	CD5 molecule	Homo sapiens	0-3
34143546-2	2021	An ATP-competitive small molecular PLK1 inhibitor, volasertib, has reached phase III in clinical trials in patients with refractory acute myeloid leukemia as a combination treatment with cytarabine.	Cytarabine	187-197	polo like kinase 1	Homo sapiens	35-39
34327076-9	2021	To our knowledge, this is the first such case of CD5+ DLBCL with leukemic transformation treated with dose-reduced R-CHOP and IT MTX/cytarabine.	Cytarabine	133-143	CD5 molecule	Homo sapiens	49-52
34108527-8	2021	Further, combined with the fixed-ratio liposomal formulation of daunorubicin and cytarabine, CPX-351, M3814 enhanced the efficacy against leukemia cells in vitro and in vivo without increasing hematopoietic toxicity, suggesting that DNA-PK inhibition could offer a novel clinical strategy for harnessing the anticancer potential of p53 in AML therapy.	Cytarabine	81-91	protein kinase, DNA-activated, catalytic subunit	Homo sapiens	233-239
34130695-3	2021	Focusing on the overexpression of human equilibrative nucleoside transporter 1 (ENT1) on the membrane of choriocarcinoma cells (JEG-3), cytarabine (Cy, a substrate of ENT1)-grafted liposomes (Cy-Lipo) were introduced for the targeted delivery of methotrexate (Cy-Lipo@MTX) for choriocarcinoma therapy in this study.	Cytarabine	136-146	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	167-171
34130695-3	2021	Focusing on the overexpression of human equilibrative nucleoside transporter 1 (ENT1) on the membrane of choriocarcinoma cells (JEG-3), cytarabine (Cy, a substrate of ENT1)-grafted liposomes (Cy-Lipo) were introduced for the targeted delivery of methotrexate (Cy-Lipo@MTX) for choriocarcinoma therapy in this study.	Cytarabine	148-150	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	167-171
34130695-4	2021	ENT1 has a high affinity for Cy-Lipo and can mediate the endocytosis of the designed nanovehicles into JEG-3 cells.	Cytarabine	29-31	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	0-4
34108527-8	2021	Further, combined with the fixed-ratio liposomal formulation of daunorubicin and cytarabine, CPX-351, M3814 enhanced the efficacy against leukemia cells in vitro and in vivo without increasing hematopoietic toxicity, suggesting that DNA-PK inhibition could offer a novel clinical strategy for harnessing the anticancer potential of p53 in AML therapy.	Cytarabine	81-91	tumor protein p53	Homo sapiens	332-335
35321842-4	2022	AMPK knock out cells demonstrated significant resistance to cytarabine and doxorubicin both in vitro and in vivo.	Cytarabine	60-70	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	0-4
34466208-0	2021	Comparison of Long-Acting G-CSF (PD-Lasta) with Short-Acting G-CSF (PD-Grastim) in Neutrophil Recovery Following Consolidation Chemotherapy with High-Dose Cytarabine in Acute Myeloid Leukemia: A Randomized Clinical Trial.	Cytarabine	155-165	colony stimulating factor 3	Homo sapiens	26-31
34466208-0	2021	Comparison of Long-Acting G-CSF (PD-Lasta) with Short-Acting G-CSF (PD-Grastim) in Neutrophil Recovery Following Consolidation Chemotherapy with High-Dose Cytarabine in Acute Myeloid Leukemia: A Randomized Clinical Trial.	Cytarabine	155-165	colony stimulating factor 3	Homo sapiens	61-66
35628366-0	2022	Involvement of ORAI1/SOCE in Human AML Cell Lines and Primary Cells According to ABCB1 Activity, LSC Compartment and Potential Resistance to Ara-C Exposure.	Cytarabine	141-146	ORAI calcium release-activated calcium modulator 1	Homo sapiens	15-20
35306047-3	2022	We have previously found that mutations in DNMT3A, one of the most commonly mutated genes in acute myeloid leukemia and associated with poor prognosis, predisposed cells to DNA damage and cell killing by cytarabine, cladribine, and other nucleoside analogs, which coincided with PARP1 dysfunction and DNA repair defect (Venugopal et al, 2021).	Cytarabine	204-214	DNA methyltransferase 3 alpha	Homo sapiens	43-49
35306047-3	2022	We have previously found that mutations in DNMT3A, one of the most commonly mutated genes in acute myeloid leukemia and associated with poor prognosis, predisposed cells to DNA damage and cell killing by cytarabine, cladribine, and other nucleoside analogs, which coincided with PARP1 dysfunction and DNA repair defect (Venugopal et al, 2021).	Cytarabine	204-214	poly(ADP-ribose) polymerase 1	Homo sapiens	279-284
35306047-5	2022	Next, we discuss PARP inhibition as a rational strategy to increase cytarabine efficacy in cells without DNMT3A mutations, while considering the implications of PARP inhibitor resistance for promoting clonal hematopoiesis.	Cytarabine	68-78	poly(ADP-ribose) polymerase 1	Homo sapiens	17-21
35306047-6	2022	Finally, we examine the utility of p53 potentiators to boost leukemia cell killing by cytarabine in the context of mutant DNMT3A.	Cytarabine	86-96	tumor protein p53	Homo sapiens	35-38
35580565-3	2022	Here, we present the case of a 69-year-old woman with therapy-related nucleophosmin-1 (NPM1) and FLT3-internal tandem duplication (FLT3-ITD) positive acute myeloid leukemia treated with induction and consolidation with CPX-351 (liposomal daunorubicin plus cytarabine) followed by off-label azacitidine maintenance who obtained a complete remission (CR) with persistent measurable residual disease.	Cytarabine	256-266	fms related receptor tyrosine kinase 3	Homo sapiens	97-101
35580565-3	2022	Here, we present the case of a 69-year-old woman with therapy-related nucleophosmin-1 (NPM1) and FLT3-internal tandem duplication (FLT3-ITD) positive acute myeloid leukemia treated with induction and consolidation with CPX-351 (liposomal daunorubicin plus cytarabine) followed by off-label azacitidine maintenance who obtained a complete remission (CR) with persistent measurable residual disease.	Cytarabine	256-266	fms related receptor tyrosine kinase 3	Homo sapiens	131-135
35628366-8	2022	Finally, we present evidence that ORAI1 expression and SOCE amplitude are modulated during the establishment of an apoptosis resistance phenotype elicited by the chemotherapeutic drug Ara-C.	Cytarabine	184-189	ORAI calcium release-activated calcium modulator 1	Homo sapiens	34-39
35400362-0	2022	(Influence of Serum TGF-beta1 and EGFR Levels on the Therapeutic Effect of High-Dose AraC in Patients with Acute Myeloid Leukemia Based on the Decision Curve).	Cytarabine	85-89	transforming growth factor beta 1	Homo sapiens	20-29
35615150-0	2022	Transfer of IGF2BP3 Through Ara-C-Induced Apoptotic Bodies Promotes Survival of Recipient Cells.	Cytarabine	28-33	insulin like growth factor 2 mRNA binding protein 3	Homo sapiens	12-19
35615150-7	2022	Proteomics analysis in combination with mass spectrometry revealed that Ara-C-induced ABs carried numerous RNA-binding proteins, notably including insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3).	Cytarabine	72-77	insulin like growth factor 2 mRNA binding protein 3	Homo sapiens	147-198
35615150-7	2022	Proteomics analysis in combination with mass spectrometry revealed that Ara-C-induced ABs carried numerous RNA-binding proteins, notably including insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3).	Cytarabine	72-77	insulin like growth factor 2 mRNA binding protein 3	Homo sapiens	200-207
35615150-10	2022	Our findings demonstrate that AB-derived IGF2BP3 plays an essential role in acquired Ara-C resistance in MDS/AML patients, and is a potential therapeutic target for suppression of Ara-C resistance.	Cytarabine	85-90	insulin like growth factor 2 mRNA binding protein 3	Homo sapiens	41-48
35615150-10	2022	Our findings demonstrate that AB-derived IGF2BP3 plays an essential role in acquired Ara-C resistance in MDS/AML patients, and is a potential therapeutic target for suppression of Ara-C resistance.	Cytarabine	180-185	insulin like growth factor 2 mRNA binding protein 3	Homo sapiens	41-48
35247918-3	2022	We demonstrate that MTH1 is a potential druggable target expressed by the majority of AML patients and the inv(16)/KITD816Y AML mouse model mimicking the genetics of AML patients exhibiting poor response to standard chemotherapy (i.e. anthracycline & cytarabine).	Cytarabine	251-261	nudix hydrolase 1	Homo sapiens	20-24
35519003-0	2022	The Nuclear Proteins TP73 and CUL4A Confer Resistance to Cytarabine by Induction of Translesion DNA Synthesis via Mono-ubiquitination of PCNA.	Cytarabine	57-67	tumor protein p73	Homo sapiens	21-25
35519003-0	2022	The Nuclear Proteins TP73 and CUL4A Confer Resistance to Cytarabine by Induction of Translesion DNA Synthesis via Mono-ubiquitination of PCNA.	Cytarabine	57-67	cullin 4A	Homo sapiens	30-35
35519003-0	2022	The Nuclear Proteins TP73 and CUL4A Confer Resistance to Cytarabine by Induction of Translesion DNA Synthesis via Mono-ubiquitination of PCNA.	Cytarabine	57-67	proliferating cell nuclear antigen	Homo sapiens	137-141
35519003-6	2022	P73 confers resistance to cytarabine therapy by transactivation of REV3L, encoding the catalytic subunit of translesion DNA polymerase zeta, and CUL4A probably by influencing proliferating cell nuclear antigen (PCNA) and the polymerase switch towards error-prone translesion DNA polymerases.	Cytarabine	26-36	tumor protein p73	Homo sapiens	0-3
35519003-6	2022	P73 confers resistance to cytarabine therapy by transactivation of REV3L, encoding the catalytic subunit of translesion DNA polymerase zeta, and CUL4A probably by influencing proliferating cell nuclear antigen (PCNA) and the polymerase switch towards error-prone translesion DNA polymerases.	Cytarabine	26-36	REV3 like, DNA directed polymerase zeta catalytic subunit	Homo sapiens	67-72
35519003-6	2022	P73 confers resistance to cytarabine therapy by transactivation of REV3L, encoding the catalytic subunit of translesion DNA polymerase zeta, and CUL4A probably by influencing proliferating cell nuclear antigen (PCNA) and the polymerase switch towards error-prone translesion DNA polymerases.	Cytarabine	26-36	cullin 4A	Homo sapiens	145-150
35519003-6	2022	P73 confers resistance to cytarabine therapy by transactivation of REV3L, encoding the catalytic subunit of translesion DNA polymerase zeta, and CUL4A probably by influencing proliferating cell nuclear antigen (PCNA) and the polymerase switch towards error-prone translesion DNA polymerases.	Cytarabine	26-36	proliferating cell nuclear antigen	Homo sapiens	175-209
35519003-6	2022	P73 confers resistance to cytarabine therapy by transactivation of REV3L, encoding the catalytic subunit of translesion DNA polymerase zeta, and CUL4A probably by influencing proliferating cell nuclear antigen (PCNA) and the polymerase switch towards error-prone translesion DNA polymerases.	Cytarabine	26-36	proliferating cell nuclear antigen	Homo sapiens	211-215
35519003-8	2022	As CUL4A needs to be activated by neddylation to facilitate the degradation of several proteins including PCNA, we propose a novel explanation for the synergism between cytarabine and the neddylation inhibitor pevonedistat by inhibition of translesion synthesis.	Cytarabine	169-179	cullin 4A	Homo sapiens	3-8
35519003-8	2022	As CUL4A needs to be activated by neddylation to facilitate the degradation of several proteins including PCNA, we propose a novel explanation for the synergism between cytarabine and the neddylation inhibitor pevonedistat by inhibition of translesion synthesis.	Cytarabine	169-179	proliferating cell nuclear antigen	Homo sapiens	106-110
35519003-9	2022	In keeping with this, in AML patients treated with cytarabine, we found high expression of CUL4A and TP73 to be associated with poor prognosis.	Cytarabine	51-61	cullin 4A	Homo sapiens	91-96
35519003-9	2022	In keeping with this, in AML patients treated with cytarabine, we found high expression of CUL4A and TP73 to be associated with poor prognosis.	Cytarabine	51-61	tumor protein p73	Homo sapiens	101-105
35443722-9	2022	Artesunate serves as a bridge for venetoclax and cytarabine combination by Noxa and Bim-mediated apoptosis and Mcl-1 reduction.	Cytarabine	49-59	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	75-79
35443722-9	2022	Artesunate serves as a bridge for venetoclax and cytarabine combination by Noxa and Bim-mediated apoptosis and Mcl-1 reduction.	Cytarabine	49-59	BCL2 like 11	Homo sapiens	84-87
35443722-9	2022	Artesunate serves as a bridge for venetoclax and cytarabine combination by Noxa and Bim-mediated apoptosis and Mcl-1 reduction.	Cytarabine	49-59	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	111-116
35443722-10	2022	We provide a new triple combination for AML treatment by targeting the Noxa/Mcl-1/Bim axis to reverse Mcl-1/p-Chk1 resistance of cytarabine therapy.	Cytarabine	129-139	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	71-75
35443722-10	2022	We provide a new triple combination for AML treatment by targeting the Noxa/Mcl-1/Bim axis to reverse Mcl-1/p-Chk1 resistance of cytarabine therapy.	Cytarabine	129-139	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	76-81
35443722-10	2022	We provide a new triple combination for AML treatment by targeting the Noxa/Mcl-1/Bim axis to reverse Mcl-1/p-Chk1 resistance of cytarabine therapy.	Cytarabine	129-139	BCL2 like 11	Homo sapiens	82-85
35443722-10	2022	We provide a new triple combination for AML treatment by targeting the Noxa/Mcl-1/Bim axis to reverse Mcl-1/p-Chk1 resistance of cytarabine therapy.	Cytarabine	129-139	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	102-107
35443722-10	2022	We provide a new triple combination for AML treatment by targeting the Noxa/Mcl-1/Bim axis to reverse Mcl-1/p-Chk1 resistance of cytarabine therapy.	Cytarabine	129-139	checkpoint kinase 1	Homo sapiens	110-114
35456712-7	2022	Polymorphisms of SLC29A1, responsible for cytarabine uptake, demonstrated significant associations with survival and response in Asian populations.	Cytarabine	42-52	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	17-24
35413116-1	2022	The phase III MIRROS trial (NCT02545283) evaluated the efficacy and safety of the small-molecule MDM2 antagonist idasanutlin plus cytarabine in patients with relapsed/refractory acute myeloid leukemia (R/R AML).	Cytarabine	130-140	MDM2 proto-oncogene	Homo sapiens	97-101
35486629-8	2022	A combination of 3 subclones (expressing or not expressing WT1) was found to lead to prolonged mouse survival after Ara-c treatment (as long as 150 days).	Cytarabine	116-121	WT1 transcription factor	Mus musculus	59-62
35443722-0	2022	Artesunate improves venetoclax plus cytarabine AML cell targeting by regulating the Noxa/Bim/Mcl-1/p-Chk1 axis.	Cytarabine	36-46	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	84-88
35443722-0	2022	Artesunate improves venetoclax plus cytarabine AML cell targeting by regulating the Noxa/Bim/Mcl-1/p-Chk1 axis.	Cytarabine	36-46	BCL2 like 11	Homo sapiens	89-92
35443722-0	2022	Artesunate improves venetoclax plus cytarabine AML cell targeting by regulating the Noxa/Bim/Mcl-1/p-Chk1 axis.	Cytarabine	36-46	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	93-98
35443722-0	2022	Artesunate improves venetoclax plus cytarabine AML cell targeting by regulating the Noxa/Bim/Mcl-1/p-Chk1 axis.	Cytarabine	36-46	checkpoint kinase 1	Homo sapiens	101-105
35443722-3	2022	Cytarabine induces S phase arrest-mediated DNA damage with activation of DNA replication checkpoint kinase 1 (Chk1) through phosphorylation, while venetoclax induces B cell lymphoma 2 (Bcl-2)-interacting mediator of cell death (Bim)-mediated apoptotic DNA damage.	Cytarabine	0-10	checkpoint kinase 1	Homo sapiens	89-108
35443722-3	2022	Cytarabine induces S phase arrest-mediated DNA damage with activation of DNA replication checkpoint kinase 1 (Chk1) through phosphorylation, while venetoclax induces B cell lymphoma 2 (Bcl-2)-interacting mediator of cell death (Bim)-mediated apoptotic DNA damage.	Cytarabine	0-10	checkpoint kinase 1	Homo sapiens	110-114
35443722-3	2022	Cytarabine induces S phase arrest-mediated DNA damage with activation of DNA replication checkpoint kinase 1 (Chk1) through phosphorylation, while venetoclax induces B cell lymphoma 2 (Bcl-2)-interacting mediator of cell death (Bim)-mediated apoptotic DNA damage.	Cytarabine	0-10	BCL2 like 11	Homo sapiens	228-231
35443722-7	2022	Silencing Mcl-1 or adding venetoclax/artesunate diminishes the cytarabine resistance pathway p-Chk1.	Cytarabine	63-73	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	10-15
35443722-7	2022	Silencing Mcl-1 or adding venetoclax/artesunate diminishes the cytarabine resistance pathway p-Chk1.	Cytarabine	63-73	checkpoint kinase 1	Homo sapiens	95-99
35395971-0	2022	(Influence of Serum TGF-beta1 and EGFR Levels on the Therapeutic Effect of High-Dose AraC in Patients with Acute Myeloid Leukemia Based on the Decision Curve).	Cytarabine	85-89	transforming growth factor beta 1	Homo sapiens	20-29
35395971-0	2022	(Influence of Serum TGF-beta1 and EGFR Levels on the Therapeutic Effect of High-Dose AraC in Patients with Acute Myeloid Leukemia Based on the Decision Curve).	Cytarabine	85-89	epidermal growth factor receptor	Homo sapiens	34-38
35395971-1	2022	OBJECTIVE: To analyze the influence of serum levels of transforming growth factor-beta1 (TGF-beta1) and epidermal growth factor receptor (EGFR) on the therapeutic effect of high-dose cytarabine (HD-AraC) in patients with acute myeloid leukemia (AML).	Cytarabine	183-193	transforming growth factor beta 1	Homo sapiens	55-87
35395971-1	2022	OBJECTIVE: To analyze the influence of serum levels of transforming growth factor-beta1 (TGF-beta1) and epidermal growth factor receptor (EGFR) on the therapeutic effect of high-dose cytarabine (HD-AraC) in patients with acute myeloid leukemia (AML).	Cytarabine	183-193	transforming growth factor beta 1	Homo sapiens	89-98
35395971-1	2022	OBJECTIVE: To analyze the influence of serum levels of transforming growth factor-beta1 (TGF-beta1) and epidermal growth factor receptor (EGFR) on the therapeutic effect of high-dose cytarabine (HD-AraC) in patients with acute myeloid leukemia (AML).	Cytarabine	183-193	epidermal growth factor receptor	Homo sapiens	104-136
35395971-1	2022	OBJECTIVE: To analyze the influence of serum levels of transforming growth factor-beta1 (TGF-beta1) and epidermal growth factor receptor (EGFR) on the therapeutic effect of high-dose cytarabine (HD-AraC) in patients with acute myeloid leukemia (AML).	Cytarabine	183-193	epidermal growth factor receptor	Homo sapiens	138-142
35395973-1	2022	OBJECTIVE: To investigate the mechanism of miR-155 promoting drug resistance of children B-ALL to Ara-C by regulating Wnt/beta-Catenin signaling pathway.	Cytarabine	98-103	microRNA 155	Homo sapiens	43-50
35395973-1	2022	OBJECTIVE: To investigate the mechanism of miR-155 promoting drug resistance of children B-ALL to Ara-C by regulating Wnt/beta-Catenin signaling pathway.	Cytarabine	98-103	catenin beta 1	Homo sapiens	122-134
35395973-4	2022	REH/ Ara-C cells were transfected with miR-155 inhibitor.	Cytarabine	5-10	microRNA 155	Homo sapiens	39-46
35400362-0	2022	(Influence of Serum TGF-beta1 and EGFR Levels on the Therapeutic Effect of High-Dose AraC in Patients with Acute Myeloid Leukemia Based on the Decision Curve).	Cytarabine	85-89	epidermal growth factor receptor	Homo sapiens	34-38
35033530-2	2022	Hydrophilic cytarabine (Cyt) is first loaded into the mesopores of the aminated MSN (NH2-MSN), which is encapsulated by the hydrogel of HA and cystamine (Cys) crosslinked via amidation.	Cytarabine	12-22	moesin	Homo sapiens	80-83
35400362-1	2022	OBJECTIVE: To analyze the influence of serum levels of transforming growth factor-beta1 (TGF-beta1) and epidermal growth factor receptor (EGFR) on the therapeutic effect of high-dose cytarabine (HD-AraC) in patients with acute myeloid leukemia (AML).	Cytarabine	183-193	transforming growth factor beta 1	Homo sapiens	55-87
35033530-2	2022	Hydrophilic cytarabine (Cyt) is first loaded into the mesopores of the aminated MSN (NH2-MSN), which is encapsulated by the hydrogel of HA and cystamine (Cys) crosslinked via amidation.	Cytarabine	12-22	moesin	Homo sapiens	85-92
35033530-2	2022	Hydrophilic cytarabine (Cyt) is first loaded into the mesopores of the aminated MSN (NH2-MSN), which is encapsulated by the hydrogel of HA and cystamine (Cys) crosslinked via amidation.	Cytarabine	24-27	moesin	Homo sapiens	80-83
35400362-1	2022	OBJECTIVE: To analyze the influence of serum levels of transforming growth factor-beta1 (TGF-beta1) and epidermal growth factor receptor (EGFR) on the therapeutic effect of high-dose cytarabine (HD-AraC) in patients with acute myeloid leukemia (AML).	Cytarabine	183-193	transforming growth factor beta 1	Homo sapiens	89-98
35033530-2	2022	Hydrophilic cytarabine (Cyt) is first loaded into the mesopores of the aminated MSN (NH2-MSN), which is encapsulated by the hydrogel of HA and cystamine (Cys) crosslinked via amidation.	Cytarabine	24-27	moesin	Homo sapiens	85-92
35400362-1	2022	OBJECTIVE: To analyze the influence of serum levels of transforming growth factor-beta1 (TGF-beta1) and epidermal growth factor receptor (EGFR) on the therapeutic effect of high-dose cytarabine (HD-AraC) in patients with acute myeloid leukemia (AML).	Cytarabine	183-193	epidermal growth factor receptor	Homo sapiens	104-136
35400362-1	2022	OBJECTIVE: To analyze the influence of serum levels of transforming growth factor-beta1 (TGF-beta1) and epidermal growth factor receptor (EGFR) on the therapeutic effect of high-dose cytarabine (HD-AraC) in patients with acute myeloid leukemia (AML).	Cytarabine	183-193	epidermal growth factor receptor	Homo sapiens	138-142
35184394-11	2022	We further screened the US FDA-approved antitumour drug library and identified cytarabine as a potential clinically applicable EEF2K inhibitor that could synergise with BET inhibitors in melanoma treatment.	Cytarabine	79-89	eukaryotic elongation factor 2 kinase	Homo sapiens	127-132
35066694-9	2022	Further study proved that Curcumin treatment resulted in inhibition of SQLE, a key enzyme of cholesterol biosynthesis, to increase sensitivity to Ara-C.	Cytarabine	146-151	squalene epoxidase	Mus musculus	71-75
34966123-1	2022	PURPOSE OF REVIEW: Venetoclax is a BCL-2 inhibitor that was approved in combination therapy with hypomethylating agents or low dose cytarabine for newly diagnosed acute myeloid leukemia (AML).	Cytarabine	132-142	BCL2 apoptosis regulator	Homo sapiens	35-40
35242129-8	2022	Furthermore, cyclophosphamide restrained the differentiation of alloreactive CD4+Foxp3- conventional T cells at both days +7 and +21, whereas methotrexate and cytarabine only restrained differentiation at day +7.	Cytarabine	159-169	CD4 antigen	Mus musculus	77-80
35242129-8	2022	Furthermore, cyclophosphamide restrained the differentiation of alloreactive CD4+Foxp3- conventional T cells at both days +7 and +21, whereas methotrexate and cytarabine only restrained differentiation at day +7.	Cytarabine	159-169	forkhead box P3	Mus musculus	81-86
35228900-4	2022	Upregulation of lncNBAT1 reduced the sensitivity of DLBCL cells to chemotherapeutic agents (methotrexate (MTX) or cytarabine (Ara-C)) that induced S phase arrest, whereas knockdown of lncNBAT1 significantly relieved the chemoresistance of HBX-expressing DLBCLs.	Cytarabine	114-124	X protein	Hepatitis B virus	239-242
35045423-2	2022	METHODS: We retrospectively reviewed the charts of adult AML patients in first complete remission (CR1) who underwent consolidation chemotherapy with high-dose cytarabine.	Cytarabine	160-170	complement C3b/C4b receptor 1 (Knops blood group)	Homo sapiens	99-102
35039904-6	2022	iHCK-37 plus 5-Azacytidine or Cytarabine treatment was able to reduce the activation of oncogenic pathways, MAPK/ERK and PI3K/AKT, leading to reduction of ERK and AKT phosphorylation, and increased BAX and decreased BCL-XL protein expression.	Cytarabine	30-40	mitogen-activated protein kinase 1	Homo sapiens	108-112
35039904-6	2022	iHCK-37 plus 5-Azacytidine or Cytarabine treatment was able to reduce the activation of oncogenic pathways, MAPK/ERK and PI3K/AKT, leading to reduction of ERK and AKT phosphorylation, and increased BAX and decreased BCL-XL protein expression.	Cytarabine	30-40	mitogen-activated protein kinase 1	Homo sapiens	113-116
35039904-6	2022	iHCK-37 plus 5-Azacytidine or Cytarabine treatment was able to reduce the activation of oncogenic pathways, MAPK/ERK and PI3K/AKT, leading to reduction of ERK and AKT phosphorylation, and increased BAX and decreased BCL-XL protein expression.	Cytarabine	30-40	AKT serine/threonine kinase 1	Homo sapiens	126-129
35039904-6	2022	iHCK-37 plus 5-Azacytidine or Cytarabine treatment was able to reduce the activation of oncogenic pathways, MAPK/ERK and PI3K/AKT, leading to reduction of ERK and AKT phosphorylation, and increased BAX and decreased BCL-XL protein expression.	Cytarabine	30-40	mitogen-activated protein kinase 1	Homo sapiens	155-158
35039904-6	2022	iHCK-37 plus 5-Azacytidine or Cytarabine treatment was able to reduce the activation of oncogenic pathways, MAPK/ERK and PI3K/AKT, leading to reduction of ERK and AKT phosphorylation, and increased BAX and decreased BCL-XL protein expression.	Cytarabine	30-40	AKT serine/threonine kinase 1	Homo sapiens	163-166
35039904-6	2022	iHCK-37 plus 5-Azacytidine or Cytarabine treatment was able to reduce the activation of oncogenic pathways, MAPK/ERK and PI3K/AKT, leading to reduction of ERK and AKT phosphorylation, and increased BAX and decreased BCL-XL protein expression.	Cytarabine	30-40	BCL2 associated X, apoptosis regulator	Homo sapiens	198-201
35039904-6	2022	iHCK-37 plus 5-Azacytidine or Cytarabine treatment was able to reduce the activation of oncogenic pathways, MAPK/ERK and PI3K/AKT, leading to reduction of ERK and AKT phosphorylation, and increased BAX and decreased BCL-XL protein expression.	Cytarabine	30-40	BCL2 like 1	Homo sapiens	216-222
35080912-8	2022	In combination with the chemotherapeutic agent Ara-C (cytosine arabinoside), restoration of miR-31-5p using G7 poly (amidoamine) nanosized dendriplex encapsulating miR-31-5p eliminated LSCs and inhibited acute myeloid leukemia (AML) progression in patient-derived xenograft mouse models.	Cytarabine	47-52	microRNA 31	Homo sapiens	92-98
35080912-8	2022	In combination with the chemotherapeutic agent Ara-C (cytosine arabinoside), restoration of miR-31-5p using G7 poly (amidoamine) nanosized dendriplex encapsulating miR-31-5p eliminated LSCs and inhibited acute myeloid leukemia (AML) progression in patient-derived xenograft mouse models.	Cytarabine	47-52	microRNA 31	Homo sapiens	164-170
35080912-8	2022	In combination with the chemotherapeutic agent Ara-C (cytosine arabinoside), restoration of miR-31-5p using G7 poly (amidoamine) nanosized dendriplex encapsulating miR-31-5p eliminated LSCs and inhibited acute myeloid leukemia (AML) progression in patient-derived xenograft mouse models.	Cytarabine	54-74	microRNA 31	Homo sapiens	92-98
35080912-8	2022	In combination with the chemotherapeutic agent Ara-C (cytosine arabinoside), restoration of miR-31-5p using G7 poly (amidoamine) nanosized dendriplex encapsulating miR-31-5p eliminated LSCs and inhibited acute myeloid leukemia (AML) progression in patient-derived xenograft mouse models.	Cytarabine	54-74	microRNA 31	Homo sapiens	164-170