PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
2557917-2	1989	The mAMSA-induced gene cleavage was found to increase with the steady-state levels of c-myc transcripts in cell lines while no cleavage could be evidenced in the other genes so far tested.	Amsacrine	4-9	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	86-91
2557917-3	1989	In mAMSA-treated N417 cells, the overall genomic DNA cleavage detected by alkaline elution was found to be about 20 times lower than the c-myc gene cleavage.	Amsacrine	3-8	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	137-142
2824033-1	1987	The effects of alpha-difluoromethylornithine (DFMO), an ornithine analogue which is an ornithine decarboxylase inhibitor, on the actions of the topoisomerase II-reactive agents 4"-(9-acridinylamino)methanesulfon-m-anisidide (m-AMSA) and etoposide (VP-16) were investigated in 2 murine L1210 leukemia lines and 2 human HL-60 leukemia lines.	Amsacrine	177-223	ornithine decarboxylase, structural 1	Mus musculus	87-110
2568172-2	1989	The MX2 cells are cross-resistant to etoposide, teniposide, bisantrene, dactinomycin, 4"-(9-acridinylamino)methanesulfon-m-anisidide, and the anthracyclines daunorubicin and doxorubicin but retain sensitivity to the Vinca alkaloids melphalan and mitomycin C.	Amsacrine	86-132	MX dynamin like GTPase 2	Homo sapiens	4-7
2539902-1	1989	Our human T-cell leukemia line, CEM/VM-1, selected for resistance to VM-26 (teniposide), is cross-resistant to several drugs that interact with topoisomerase II, including VP-16 (etoposide), 4"-(9-acridinylamino)methanesulphon-m-anisidide, daunorubicin, and mitoxantrone.	Amsacrine	191-238	host cell factor C1	Homo sapiens	172-177
2539190-1	1989	Extracts of K21 murine mastocytoma cells contain a factor that enhances formation of amsacrine-induced topoisomerase II-DNA complexes (PDCs) when added to isolated K21 nuclei.	Amsacrine	85-94	olfactory receptor family 8 subfamily B member 8	Mus musculus	12-15
2539190-1	1989	Extracts of K21 murine mastocytoma cells contain a factor that enhances formation of amsacrine-induced topoisomerase II-DNA complexes (PDCs) when added to isolated K21 nuclei.	Amsacrine	85-94	olfactory receptor family 8 subfamily B member 8	Mus musculus	164-167
2502896-1	1989	Amsacrine with high-dose cytarabine is effective therapy for Philadelphia chromosome (Ph1)-negative acute lymphoblastic leukemia (ALL).	Amsacrine	0-9	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	86-89
2825970-2	1988	Using an alkaline DNA-unwinding technique to detect drug-induced DNA strand breakage, we have shown that estrogen stimulation of T-47D human breast cancer cells enhances induction of DNA cleavage by etoposide (VP-16), 4",9-acridinylaminomethanesulfon-m-anisidide (m-AMSA), mitoxantrone, and doxorubicin, drugs known to interact with the DNA-modifying enzyme topoisomerase II.	Amsacrine	264-270	host cell factor C1	Homo sapiens	210-215
3766228-0	1986	Effect of m-AMSA on the cellular pharmacology of ara-CTP in human leukemic cells during therapy with high-dose ara-C.	Amsacrine	10-16	solute carrier family 25 member 1	Homo sapiens	53-56
3567973-0	1987	Effect of amsacrine on ara-CTP cellular pharmacology in human leukemia cells during high-dose cytarabine therapy.	Amsacrine	10-19	solute carrier family 25 member 1	Homo sapiens	27-30
6689124-1	1983	An acridine antitumor agent, 4"-(9-acridinylamino)methanesulfon-m-anisidide, has been found to be an extremely potent competitive inhibitor of aldehyde oxidase (EC 1.2.3.1).	Amsacrine	29-75	aldehyde oxidase 1	Homo sapiens	143-159
3855288-3	1985	Postinfusion amsacrine elimination was best described by a biexponential expression with a mean t1/2 alpha of 0.8 h and a terminal t1/2 beta of 5.3 h. After the third infusion there was a significant reduction (P less than 0.05) in the plasma clearance (Cl) and a prolongation of the terminal half-life (t1/2 beta) (P less than 0.01), but no change in the initial half-life (T1/2 alpha) or volume of distribution (Vd).	Amsacrine	13-22	interleukin 1 receptor like 1	Homo sapiens	96-106
3855288-3	1985	Postinfusion amsacrine elimination was best described by a biexponential expression with a mean t1/2 alpha of 0.8 h and a terminal t1/2 beta of 5.3 h. After the third infusion there was a significant reduction (P less than 0.05) in the plasma clearance (Cl) and a prolongation of the terminal half-life (t1/2 beta) (P less than 0.01), but no change in the initial half-life (T1/2 alpha) or volume of distribution (Vd).	Amsacrine	13-22	interleukin 1 receptor like 1	Homo sapiens	131-140
3855288-3	1985	Postinfusion amsacrine elimination was best described by a biexponential expression with a mean t1/2 alpha of 0.8 h and a terminal t1/2 beta of 5.3 h. After the third infusion there was a significant reduction (P less than 0.05) in the plasma clearance (Cl) and a prolongation of the terminal half-life (t1/2 beta) (P less than 0.01), but no change in the initial half-life (T1/2 alpha) or volume of distribution (Vd).	Amsacrine	13-22	interleukin 1 receptor like 1	Homo sapiens	304-314
3855288-3	1985	Postinfusion amsacrine elimination was best described by a biexponential expression with a mean t1/2 alpha of 0.8 h and a terminal t1/2 beta of 5.3 h. After the third infusion there was a significant reduction (P less than 0.05) in the plasma clearance (Cl) and a prolongation of the terminal half-life (t1/2 beta) (P less than 0.01), but no change in the initial half-life (T1/2 alpha) or volume of distribution (Vd).	Amsacrine	13-22	interleukin 1 receptor like 1	Homo sapiens	375-385
6394768-7	1984	Amsacrine at 4.0 micrograms/ml was cytotoxic to V-79 cells in the cell mutation assay, and at lower dose levels was a direct-acting mutagen for the HGPRT locus.	Amsacrine	0-9	hypoxanthine-guanine phosphoribosyltransferase	Cricetulus griseus	148-153
29913235-7	2018	Amsacrine enhanced the cytotoxicity of ABT-263 in human leukemia U937, HL-60, and Jurkat cells because of its inhibitory effect on the IKKalpha/beta-NFkappaB-mediated pathway.	Amsacrine	0-9	component of inhibitor of nuclear factor kappa B kinase complex	Homo sapiens	135-143
6831444-3	1983	The UV-2237-ADMR line also exhibited increased resistance to N-trifluoroacetyladriamycin-24-valerate, daunorubicin, actinomycin D, amsacrine, mitomycin C, vinblastine, and vincristine but not to bleomycin.	Amsacrine	131-140	G protein-coupled receptor 182	Mus musculus	12-16
33494466-1	2021	Amsacrine, an anticancer drug first synthesised in 1970 by Professor Cain and colleagues, showed excellent preclinical activity and underwent clinical trial in 1978 under the auspices of the US National Cancer Institute, showing activity against acute lymphoblastic leukaemia.	Amsacrine	0-9	calcineurin binding protein 1	Mus musculus	69-73
6895473-12	1981	m-AMSA-induced protein-associated SSB"s saturated at approximately 60000 per cell over a concentration range in which m-AMSA uptake by the cells was proportional to the drug concentration.	Amsacrine	2-6	Sjogren syndrome antigen B	Mus musculus	34-37
280145-1	1977	SN11841 [4"-(9-acridinylamino)-methanesulfon-m-aniside] is an antitumor compound discovered by B.F. Cain.	Amsacrine	0-7	calcineurin binding protein 1	Mus musculus	100-104
27757735-0	2017	Amsacrine-induced apoptosis of human leukemia U937 cells is mediated by the inhibition of AKT- and ERK-induced stabilization of MCL1.	Amsacrine	0-9	AKT serine/threonine kinase 1	Homo sapiens	90-93
27757735-0	2017	Amsacrine-induced apoptosis of human leukemia U937 cells is mediated by the inhibition of AKT- and ERK-induced stabilization of MCL1.	Amsacrine	0-9	mitogen-activated protein kinase 1	Homo sapiens	99-102
27757735-0	2017	Amsacrine-induced apoptosis of human leukemia U937 cells is mediated by the inhibition of AKT- and ERK-induced stabilization of MCL1.	Amsacrine	0-9	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	128-132
27757735-2	2017	However, 9-aminoacridine derivatives, which have the same structural scaffold as amsacrine, induce cancer cell apoptosis by altering the expression of BCL2 family proteins.	Amsacrine	81-90	BCL2 apoptosis regulator	Homo sapiens	151-155
27757735-3	2017	Therefore, in the present study, we assessed whether BCL2 family proteins mediated the cytotoxic effects of amsacrine on human leukemia U937 cells.	Amsacrine	108-117	BCL2 apoptosis regulator	Homo sapiens	53-57
27757735-4	2017	Amsacrine-induced apoptosis of U937 cells was characterized by caspase-9 and caspase-3 activation, increased intracellular Ca2+ concentration, mitochondrial depolarization, and MCL1 down-regulation.	Amsacrine	0-9	caspase 9	Homo sapiens	63-72
27757735-4	2017	Amsacrine-induced apoptosis of U937 cells was characterized by caspase-9 and caspase-3 activation, increased intracellular Ca2+ concentration, mitochondrial depolarization, and MCL1 down-regulation.	Amsacrine	0-9	caspase 3	Homo sapiens	77-86
27757735-4	2017	Amsacrine-induced apoptosis of U937 cells was characterized by caspase-9 and caspase-3 activation, increased intracellular Ca2+ concentration, mitochondrial depolarization, and MCL1 down-regulation.	Amsacrine	0-9	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	177-181
27757735-5	2017	Amsacrine induced MCL1 down-regulation by decreasing its stability.	Amsacrine	0-9	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	18-22
27757735-6	2017	Further, amsacrine-treated U937 cells showed AKT degradation and Ca2+-mediated ERK inactivation.	Amsacrine	9-18	AKT serine/threonine kinase 1	Homo sapiens	45-48
27757735-6	2017	Further, amsacrine-treated U937 cells showed AKT degradation and Ca2+-mediated ERK inactivation.	Amsacrine	9-18	mitogen-activated protein kinase 1	Homo sapiens	79-82
27757735-8	2017	Restoration of ERK phosphorylation and AKT expression abrogated amsacrine-induced MCL1 down-regulation.	Amsacrine	64-73	mitogen-activated protein kinase 1	Homo sapiens	15-18
27757735-8	2017	Restoration of ERK phosphorylation and AKT expression abrogated amsacrine-induced MCL1 down-regulation.	Amsacrine	64-73	AKT serine/threonine kinase 1	Homo sapiens	39-42
27757735-8	2017	Restoration of ERK phosphorylation and AKT expression abrogated amsacrine-induced MCL1 down-regulation.	Amsacrine	64-73	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	82-86
27757735-9	2017	Moreover, MCL1 over-expression inhibited amsacrine-induced depolarization of mitochondria membrane and increased the viability of amsacrine-treated cells.	Amsacrine	41-50	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	10-14
27757735-9	2017	Moreover, MCL1 over-expression inhibited amsacrine-induced depolarization of mitochondria membrane and increased the viability of amsacrine-treated cells.	Amsacrine	130-139	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	10-14
27757735-10	2017	Taken together, our data indicate that amsacrine abolishes ERK- and Pin1-mediated stabilization of MCL1 and promotes GSK3beta-mediated degradation of MCL1, leading to activate mitochondria-mediated apoptosis pathway in U937 cells.	Amsacrine	39-48	mitogen-activated protein kinase 1	Homo sapiens	59-62
27757735-10	2017	Taken together, our data indicate that amsacrine abolishes ERK- and Pin1-mediated stabilization of MCL1 and promotes GSK3beta-mediated degradation of MCL1, leading to activate mitochondria-mediated apoptosis pathway in U937 cells.	Amsacrine	39-48	peptidylprolyl cis/trans isomerase, NIMA-interacting 1	Homo sapiens	68-72
27757735-10	2017	Taken together, our data indicate that amsacrine abolishes ERK- and Pin1-mediated stabilization of MCL1 and promotes GSK3beta-mediated degradation of MCL1, leading to activate mitochondria-mediated apoptosis pathway in U937 cells.	Amsacrine	39-48	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	99-103
27757735-10	2017	Taken together, our data indicate that amsacrine abolishes ERK- and Pin1-mediated stabilization of MCL1 and promotes GSK3beta-mediated degradation of MCL1, leading to activate mitochondria-mediated apoptosis pathway in U937 cells.	Amsacrine	39-48	glycogen synthase kinase 3 beta	Homo sapiens	117-125
27757735-10	2017	Taken together, our data indicate that amsacrine abolishes ERK- and Pin1-mediated stabilization of MCL1 and promotes GSK3beta-mediated degradation of MCL1, leading to activate mitochondria-mediated apoptosis pathway in U937 cells.	Amsacrine	39-48	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	150-154
27834128-4	2017	The aim of this study was to computationally examine the mechanisms by which genomic variations in Top2-alpha could affect its resistance to Amsacrine and Mitoxantrone as important inhibitors of the enzyme.	Amsacrine	141-150	DNA topoisomerase II alpha	Homo sapiens	99-109
28110185-4	2017	In this study, we constructed human topoisomerase II alpha (hTop2alpha) homology model docked with Amsacrine based on crystal structure of human Top2beta in complex with etoposide.	Amsacrine	99-108	DNA topoisomerase II alpha	Homo sapiens	60-70
28110185-4	2017	In this study, we constructed human topoisomerase II alpha (hTop2alpha) homology model docked with Amsacrine based on crystal structure of human Top2beta in complex with etoposide.	Amsacrine	99-108	DNA topoisomerase II beta	Homo sapiens	145-153
27834128-5	2017	RESULTS: The results showed that variants K529E, R568H, R568G and T530M could affect Top2-alpha inhibition by Amsacrine causing possible drug-resistant.	Amsacrine	110-119	DNA topoisomerase II alpha	Homo sapiens	85-95
20006932-0	2010	Assisted sonodynamic damage of bovine serum albumin by metronidazole under ultrasonic irradiation combined with photosensitive antitumor drug-Amsacrine.	Amsacrine	142-151	albumin	Homo sapiens	38-51
24122234-0	2014	Amsacrine suppresses matrix metalloproteinase-2 (MMP-2)/MMP-9 expression in human leukemia cells.	Amsacrine	0-9	matrix metallopeptidase 2	Homo sapiens	21-47
24122234-0	2014	Amsacrine suppresses matrix metalloproteinase-2 (MMP-2)/MMP-9 expression in human leukemia cells.	Amsacrine	0-9	matrix metallopeptidase 2	Homo sapiens	49-54
24122234-0	2014	Amsacrine suppresses matrix metalloproteinase-2 (MMP-2)/MMP-9 expression in human leukemia cells.	Amsacrine	0-9	matrix metallopeptidase 9	Homo sapiens	56-61
24122234-1	2014	This study explores the suppression mechanism of amsacrine (4-(9-Acridinylamino)-N-(methanesulfonyl)-m-anisidine hydrochloride) on matrix metalloproteinase-2 (MMP-2) and MMP-9 expression in human leukemia cells.	Amsacrine	49-58	matrix metallopeptidase 2	Homo sapiens	131-157
24122234-1	2014	This study explores the suppression mechanism of amsacrine (4-(9-Acridinylamino)-N-(methanesulfonyl)-m-anisidine hydrochloride) on matrix metalloproteinase-2 (MMP-2) and MMP-9 expression in human leukemia cells.	Amsacrine	49-58	matrix metallopeptidase 2	Homo sapiens	159-164
24122234-1	2014	This study explores the suppression mechanism of amsacrine (4-(9-Acridinylamino)-N-(methanesulfonyl)-m-anisidine hydrochloride) on matrix metalloproteinase-2 (MMP-2) and MMP-9 expression in human leukemia cells.	Amsacrine	49-58	matrix metallopeptidase 9	Homo sapiens	170-175
24122234-2	2014	Amsacrine attenuated cell invasion with decreased MMP-2/MMP-9 protein expression and mRNA levels in U937, Jurkat, HL-60, K562, KU812, and MEG-01 cells.	Amsacrine	0-9	matrix metallopeptidase 2	Homo sapiens	50-55
24122234-2	2014	Amsacrine attenuated cell invasion with decreased MMP-2/MMP-9 protein expression and mRNA levels in U937, Jurkat, HL-60, K562, KU812, and MEG-01 cells.	Amsacrine	0-9	matrix metallopeptidase 9	Homo sapiens	56-61
24122234-3	2014	Moreover, amsacrine reduced both MMP-2/MMP-9 promoter luciferase activity and MMP-2/MMP-9 mRNA stability in leukemia cells.	Amsacrine	10-19	matrix metallopeptidase 2	Homo sapiens	33-38
24122234-3	2014	Moreover, amsacrine reduced both MMP-2/MMP-9 promoter luciferase activity and MMP-2/MMP-9 mRNA stability in leukemia cells.	Amsacrine	10-19	matrix metallopeptidase 9	Homo sapiens	39-44
24122234-3	2014	Moreover, amsacrine reduced both MMP-2/MMP-9 promoter luciferase activity and MMP-2/MMP-9 mRNA stability in leukemia cells.	Amsacrine	10-19	matrix metallopeptidase 2	Homo sapiens	78-83
24122234-3	2014	Moreover, amsacrine reduced both MMP-2/MMP-9 promoter luciferase activity and MMP-2/MMP-9 mRNA stability in leukemia cells.	Amsacrine	10-19	matrix metallopeptidase 9	Homo sapiens	84-89
24122234-4	2014	Studies on amsacrine-treated U937 cells revealed that amsacrine-elicited ROS generation induced JNK and p38 MAPK activation but reduced the phospho-ERK level.	Amsacrine	54-63	mitogen-activated protein kinase 8	Homo sapiens	96-99
24122234-4	2014	Studies on amsacrine-treated U937 cells revealed that amsacrine-elicited ROS generation induced JNK and p38 MAPK activation but reduced the phospho-ERK level.	Amsacrine	54-63	mitogen-activated protein kinase 14	Homo sapiens	104-107
24122234-4	2014	Studies on amsacrine-treated U937 cells revealed that amsacrine-elicited ROS generation induced JNK and p38 MAPK activation but reduced the phospho-ERK level.	Amsacrine	54-63	mitogen-activated protein kinase 1	Homo sapiens	108-112
24122234-4	2014	Studies on amsacrine-treated U937 cells revealed that amsacrine-elicited ROS generation induced JNK and p38 MAPK activation but reduced the phospho-ERK level.	Amsacrine	54-63	mitogen-activated protein kinase 1	Homo sapiens	148-151
22621736-8	2012	Drugs that regulate GADD45alpha and Topoisomerase IIalpha (e.g., ethyl methanesulfomate, amsacrine and chloroquine) were shown to increase ultrasound-mediated transfection efficiency by up to 2 fold.	Amsacrine	89-98	growth arrest and DNA damage inducible alpha	Homo sapiens	20-31
24122234-5	2014	Amsacrine-induced ERK inactivation and p38 MAPK/JNK activation were demonstrated to suppress MMP-2/MMP-9 promoter luciferase activity and promote MMP-2/MMP-9 mRNA decay, respectively.	Amsacrine	0-9	mitogen-activated protein kinase 1	Homo sapiens	18-21
24122234-5	2014	Amsacrine-induced ERK inactivation and p38 MAPK/JNK activation were demonstrated to suppress MMP-2/MMP-9 promoter luciferase activity and promote MMP-2/MMP-9 mRNA decay, respectively.	Amsacrine	0-9	mitogen-activated protein kinase 14	Homo sapiens	39-42
24122234-5	2014	Amsacrine-induced ERK inactivation and p38 MAPK/JNK activation were demonstrated to suppress MMP-2/MMP-9 promoter luciferase activity and promote MMP-2/MMP-9 mRNA decay, respectively.	Amsacrine	0-9	mitogen-activated protein kinase 1	Homo sapiens	43-47
24122234-5	2014	Amsacrine-induced ERK inactivation and p38 MAPK/JNK activation were demonstrated to suppress MMP-2/MMP-9 promoter luciferase activity and promote MMP-2/MMP-9 mRNA decay, respectively.	Amsacrine	0-9	mitogen-activated protein kinase 8	Homo sapiens	48-51
24122234-5	2014	Amsacrine-induced ERK inactivation and p38 MAPK/JNK activation were demonstrated to suppress MMP-2/MMP-9 promoter luciferase activity and promote MMP-2/MMP-9 mRNA decay, respectively.	Amsacrine	0-9	matrix metallopeptidase 2	Homo sapiens	93-98
24122234-5	2014	Amsacrine-induced ERK inactivation and p38 MAPK/JNK activation were demonstrated to suppress MMP-2/MMP-9 promoter luciferase activity and promote MMP-2/MMP-9 mRNA decay, respectively.	Amsacrine	0-9	matrix metallopeptidase 9	Homo sapiens	99-104
24122234-5	2014	Amsacrine-induced ERK inactivation and p38 MAPK/JNK activation were demonstrated to suppress MMP-2/MMP-9 promoter luciferase activity and promote MMP-2/MMP-9 mRNA decay, respectively.	Amsacrine	0-9	matrix metallopeptidase 2	Homo sapiens	146-151
24122234-5	2014	Amsacrine-induced ERK inactivation and p38 MAPK/JNK activation were demonstrated to suppress MMP-2/MMP-9 promoter luciferase activity and promote MMP-2/MMP-9 mRNA decay, respectively.	Amsacrine	0-9	matrix metallopeptidase 9	Homo sapiens	152-157
24122234-6	2014	p38 MAPK/JNK activation led to up-regulation of protein phosphatase 2A catalytic subunit alpha (PP2Acalpha) in amsacrine-treated U937 cells.	Amsacrine	111-120	mitogen-activated protein kinase 14	Homo sapiens	0-3
24122234-6	2014	p38 MAPK/JNK activation led to up-regulation of protein phosphatase 2A catalytic subunit alpha (PP2Acalpha) in amsacrine-treated U937 cells.	Amsacrine	111-120	mitogen-activated protein kinase 1	Homo sapiens	4-8
24122234-6	2014	p38 MAPK/JNK activation led to up-regulation of protein phosphatase 2A catalytic subunit alpha (PP2Acalpha) in amsacrine-treated U937 cells.	Amsacrine	111-120	mitogen-activated protein kinase 8	Homo sapiens	9-12
24122234-7	2014	Okadaic acid (PP2A inhibitor) treatment increased MMP-2/MMP-9 mRNA stability in amsacrine-treated cells, whereas PP2Acalpha over-expression increased MMP-2/MMP-9 mRNA decay.	Amsacrine	80-89	protein phosphatase 2 phosphatase activator	Homo sapiens	14-18
24122234-7	2014	Okadaic acid (PP2A inhibitor) treatment increased MMP-2/MMP-9 mRNA stability in amsacrine-treated cells, whereas PP2Acalpha over-expression increased MMP-2/MMP-9 mRNA decay.	Amsacrine	80-89	matrix metallopeptidase 2	Homo sapiens	50-55
24122234-7	2014	Okadaic acid (PP2A inhibitor) treatment increased MMP-2/MMP-9 mRNA stability in amsacrine-treated cells, whereas PP2Acalpha over-expression increased MMP-2/MMP-9 mRNA decay.	Amsacrine	80-89	matrix metallopeptidase 9	Homo sapiens	56-61
24122234-8	2014	Amsacrine-induced MMP-2/MMP-9 down-regulation was also related to PP2Acalpha up-regulation on Jurkat, HL-60, K562, KU812, and MEG-01 cells.	Amsacrine	0-9	matrix metallopeptidase 2	Homo sapiens	18-23
24122234-8	2014	Amsacrine-induced MMP-2/MMP-9 down-regulation was also related to PP2Acalpha up-regulation on Jurkat, HL-60, K562, KU812, and MEG-01 cells.	Amsacrine	0-9	matrix metallopeptidase 9	Homo sapiens	24-29
24122234-9	2014	Collectively, our data indicate that amsacrine induces MMP-2/MMP-9 down-regulation via simultaneous suppression of genetic transcription and mRNA stability in human leukemia cells.	Amsacrine	37-46	matrix metallopeptidase 2	Homo sapiens	55-60
24122234-9	2014	Collectively, our data indicate that amsacrine induces MMP-2/MMP-9 down-regulation via simultaneous suppression of genetic transcription and mRNA stability in human leukemia cells.	Amsacrine	37-46	matrix metallopeptidase 9	Homo sapiens	61-66
24092808-9	2013	These results indicate that prolonged exposure to TKIs targeting EGFR and HER2 induce resistance to doxorubicin, etoposide, and m-AMSA through downregulation of Topo IIalpha.	Amsacrine	128-134	epidermal growth factor receptor	Homo sapiens	65-69
24092808-9	2013	These results indicate that prolonged exposure to TKIs targeting EGFR and HER2 induce resistance to doxorubicin, etoposide, and m-AMSA through downregulation of Topo IIalpha.	Amsacrine	128-134	erb-b2 receptor tyrosine kinase 2	Homo sapiens	74-78
20006932-1	2010	By research, it was found that the Amsacrine (AMSA) can interact with bovine serum albumin (BSA).	Amsacrine	35-44	albumin	Homo sapiens	77-90
20006932-1	2010	By research, it was found that the Amsacrine (AMSA) can interact with bovine serum albumin (BSA).	Amsacrine	46-50	albumin	Homo sapiens	77-90
17608728-9	2007	This prompted us to examine the effect of DNA intercalating chemotherapeutic drugs such as doxorubicin, amsacrine, and mitoxantrone on the expression of RAR-beta.	Amsacrine	104-113	retinoic acid receptor beta	Homo sapiens	153-161
17608728-12	2007	Interestingly, compounds that directly interact with the DNA (doxorubicin, amsacrine, mitoxantrone) caused a time-dependent up-regulation of the RAR-beta expression in all cell lines examined, whereas the negative control drug vincristine, which causes disruption of microtubule structures, did not stimulate RAR-beta expression.	Amsacrine	75-84	retinoic acid receptor beta	Homo sapiens	145-153
17608728-12	2007	Interestingly, compounds that directly interact with the DNA (doxorubicin, amsacrine, mitoxantrone) caused a time-dependent up-regulation of the RAR-beta expression in all cell lines examined, whereas the negative control drug vincristine, which causes disruption of microtubule structures, did not stimulate RAR-beta expression.	Amsacrine	75-84	retinoic acid receptor beta	Homo sapiens	309-317
17575151-6	2007	We show that MDM2 SNP309 rendered a panel of cancer cell lines that are homozygous for SNP309 selectively resistant (approximately 10-fold) to certain TopoII-targeting chemotherapeutic drugs (etoposide, mitoxantrone, amsacrine, and ellipticine).	Amsacrine	217-226	transformed mouse 3T3 cell double minute 2	Mus musculus	13-17
15852490-4	2005	In the immunohistochemical study, ASW markedly inhibited both cyclooxygenase-2 and OX-42 expressions in the penumbral region at 24 h after MCAo.	Amsacrine	34-37	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	62-78
16600179-5	2006	Additionally, introduction of anti-nucleolin antibody sensitized cells to death induced by the topoisomerase II inhibitor, amsacrine.	Amsacrine	123-132	nucleolin	Homo sapiens	35-44
16600179-6	2006	Introduction of anti-Rad51 antibody also reduced intra-plasmid homologous recombination activity and induced hypersensitivity to amsacrine-induced cell death.	Amsacrine	129-138	RAD51 recombinase	Homo sapiens	21-26
16239602-1	2006	The anti cancer drug methyl N-(4"-(9-acridinylamino)-3-methoxy-phenyl) methane sulfonamide (mAMSA) targets human DNA topoisomerase IIbeta.	Amsacrine	92-97	DNA topoisomerase II beta	Homo sapiens	113-137
16239602-3	2006	Random mutagenesis of human DNA topoisomerase IIbeta cDNA, followed by selection in yeast for resistance to mAMSA, identified betaP732L.	Amsacrine	108-113	DNA topoisomerase II beta	Homo sapiens	28-52
16818498-10	2006	To confirm that the increase in sensitivity was not solely due to the elevated expression of TOP2 or due to specific effects of the drug-hypersensitive TOP2 alleles, we also found that deletion of genes required for NHEJ increased the sensitivity of rad52 deletions to both etoposide and mAMSA.	Amsacrine	288-293	recombinase RAD52	Saccharomyces cerevisiae S288C	250-255
16177561-4	2005	We also found that several randomly chosen acridine derivatives, including 9-aminoacridine, amsacrine, quinacrine and acridine orange, induced p53 transcriptional activity.	Amsacrine	92-101	tumor protein p53	Homo sapiens	143-146
16177561-8	2005	In addition, in vivo delivery of quinacrine and amsacrine induced p53 transcriptional activity in tumor xenografts.	Amsacrine	48-57	tumor protein p53	Homo sapiens	66-69
15148258-0	2004	Inhibition of cardiac HERG currents by the DNA topoisomerase II inhibitor amsacrine: mode of action.	Amsacrine	74-83	potassium voltage-gated channel subfamily H member 2	Homo sapiens	22-26
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.	Amsacrine	114-123	ETS variant transcription factor 6	Homo sapiens	4-8
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.	Amsacrine	114-123	RUNX family transcription factor 1	Homo sapiens	9-14
15258255-9	2004	Disruption of p53 and p21 had minor influence on the cytotoxicity of doxorubicin, whereas p53 but not p21 disruption was associated with increased resistance to amsacrine.	Amsacrine	161-170	tumor protein p53	Homo sapiens	90-93
15148258-5	2004	3 Amsacrine blocked HERG currents in HEK 293 cells and Xenopus oocytes in a concentration-dependent manner, with IC50 values of 209.4 nm and 2.0 microm, respectively.	Amsacrine	2-11	potassium voltage-gated channel subfamily H member 2	Homo sapiens	20-24
15148258-8	2004	HERG current block by amsacrine was not frequency dependent.	Amsacrine	22-31	potassium voltage-gated channel subfamily H member 2	Homo sapiens	0-4
15148258-9	2004	5 The S6 domain mutations Y652A and F656A attenuated (Y652A) or abolished (F656A, Y652A/F656A) HERG current blockade, indicating that amsacrine binding requires a common drug receptor within the pore-S6 region.	Amsacrine	134-143	potassium voltage-gated channel subfamily H member 2	Homo sapiens	95-99
15148258-10	2004	6 In conclusion, these data demonstrate that the anticancer drug amsacrine is an antagonist of cloned HERG potassium channels, providing a molecular mechanism for the previously reported QTc interval prolongation during clinical administration of amsacrine.	Amsacrine	65-74	potassium voltage-gated channel subfamily H member 2	Homo sapiens	102-106
15148258-10	2004	6 In conclusion, these data demonstrate that the anticancer drug amsacrine is an antagonist of cloned HERG potassium channels, providing a molecular mechanism for the previously reported QTc interval prolongation during clinical administration of amsacrine.	Amsacrine	247-256	potassium voltage-gated channel subfamily H member 2	Homo sapiens	102-106
12683237-0	2003	[Effect of etoposide and amsacrine on mitotic progression of GM-130 and Hep-2 cell lines.	Amsacrine	25-34	golgin A2	Homo sapiens	61-67
12547280-4	2003	Using the alkaline comet assay, we showed that amsacrine at concentrations from the range 0.01 to 10 microM induced DNA damage in normal human lymphocytes, human promyelocytic leukemia HL-60 cells lacking the p53 gene and murine pro-B lymphoid cells BaF3 expressing BCR/ABL oncogene measured as the increase in percentage tail DNA.	Amsacrine	47-56	tumor protein p53	Homo sapiens	209-212
12547280-4	2003	Using the alkaline comet assay, we showed that amsacrine at concentrations from the range 0.01 to 10 microM induced DNA damage in normal human lymphocytes, human promyelocytic leukemia HL-60 cells lacking the p53 gene and murine pro-B lymphoid cells BaF3 expressing BCR/ABL oncogene measured as the increase in percentage tail DNA.	Amsacrine	47-56	BCR activator of RhoGEF and GTPase	Mus musculus	266-273
12930926-4	2003	Idarubicin and amsacrin were given at the end of a cycle to allow the cell-cycle-dependent cytotoxicity of cytarabine in the context of G-CSF to have a greater effect.	Amsacrine	15-23	colony stimulating factor 3	Homo sapiens	136-141
12683237-2	2003	It has been shown that inhibitors of topoisomerase II (topo II) etoposide and amsacrine results in accumulation of GM-130 and Hep-2 cells with 4c DNA amount.	Amsacrine	78-87	golgin A2	Homo sapiens	115-121
12683237-5	2003	GM-130 and Hep-2 cells that were first blocked and then washed from nocodazole, and after that treated with 50 microM etoposide or 20 microM amsacrine, were shown to enter pseudo-G1 with 4c DNA amount per cell.	Amsacrine	141-150	golgin A2	Homo sapiens	0-6
12683237-6	2003	In the presence of nocodazole, 4 and 40 microM amsacrine evoked transition of all mitotic cells to pseudo-G1 within 1 h. 15 or 30 minutes pulse treatments of GM-130 cells with 40 microM amsacrine in the presence of nocodazole, followed by incubation in drug-free medium, resulted in the similar transition of cells to pseudo-G1.	Amsacrine	47-56	golgin A2	Homo sapiens	158-164
12683237-6	2003	In the presence of nocodazole, 4 and 40 microM amsacrine evoked transition of all mitotic cells to pseudo-G1 within 1 h. 15 or 30 minutes pulse treatments of GM-130 cells with 40 microM amsacrine in the presence of nocodazole, followed by incubation in drug-free medium, resulted in the similar transition of cells to pseudo-G1.	Amsacrine	186-195	golgin A2	Homo sapiens	158-164
11585056-1	2001	The topoisomerase II inhibitors teniposide (VM-26), doxorubicin, and amsacrine (m-AMSA), as well as ionizing radiation, induce a transient suppression of c-myc mRNA, which correlates with growth inhibition of MCF-7 breast tumor cells.	Amsacrine	69-78	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	154-159
11585056-1	2001	The topoisomerase II inhibitors teniposide (VM-26), doxorubicin, and amsacrine (m-AMSA), as well as ionizing radiation, induce a transient suppression of c-myc mRNA, which correlates with growth inhibition of MCF-7 breast tumor cells.	Amsacrine	80-86	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	154-159
10570059-5	1999	These results show that both topo IIalpha and beta are in vivo targets for etoposide, mitoxantrone, and amsacrine (mAMSA) in topo IIbeta +/+ cells.	Amsacrine	104-113	ATPase, class II, type 9B	Mus musculus	130-136
11459812-7	2001	Among the compounds tested, two inhibitors of topo II, amsacrine and etoposide, attenuated the formation of osteoclast-like cells via reciprocal regulation of the expression of mRNAs for RANKL and OPG in ST2 cells, acting similarly to genistein.	Amsacrine	55-64	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	187-192
11459812-7	2001	Among the compounds tested, two inhibitors of topo II, amsacrine and etoposide, attenuated the formation of osteoclast-like cells via reciprocal regulation of the expression of mRNAs for RANKL and OPG in ST2 cells, acting similarly to genistein.	Amsacrine	55-64	tumor necrosis factor receptor superfamily, member 11b (osteoprotegerin)	Mus musculus	197-200
11108797-7	2000	In addition, there was an effect of amsacrine on the expression of bcl-x(L) in the resistant cell line only, but at concentrations higher than the IC(50) of this drug.	Amsacrine	36-45	BCL2 like 1	Homo sapiens	67-75
11206712-1	2000	Avene spa water (ASW) inhibits the histamine release induced in mast cells by substance P; the inhibition is reversed by EDTA and by EGTA.	Amsacrine	17-20	surfactant protein A2	Homo sapiens	6-9
11470519-3	2001	In this work, we showed these mutants are also resistant against doxorubicin and mAMSA in vivo in the yeast strain ISE2, rad52, top2-4 at the non-permissive temperature.	Amsacrine	81-86	recombinase RAD52	Saccharomyces cerevisiae S288C	121-126
11464106-8	2001	Conversely, ASW-containing medium induced a decrease in IL-4 production by normal peripheral blood lymphocytes.	Amsacrine	12-15	interleukin 4	Homo sapiens	56-60
10570059-5	1999	These results show that both topo IIalpha and beta are in vivo targets for etoposide, mitoxantrone, and amsacrine (mAMSA) in topo IIbeta +/+ cells.	Amsacrine	115-120	ATPase, class II, type 9A	Mus musculus	34-41
10570059-5	1999	These results show that both topo IIalpha and beta are in vivo targets for etoposide, mitoxantrone, and amsacrine (mAMSA) in topo IIbeta +/+ cells.	Amsacrine	115-120	ATPase, class II, type 9B	Mus musculus	130-136
10570059-8	1999	Increased survival of topo IIbeta -/- cells compared with topo IIbeta +/+ cells was observed after treatment with amsacrine (mAMSA), methyl N-(4"-[9-acridinylamino]-2-methoxyphenyl) carbamate hydrochloride (AMCA), methyl N-(4"-[9-acridinylamino]-2-methoxyphenyl)carbamate hydrochloride (mAMCA), mitoxantrone, and etoposide.	Amsacrine	114-123	ATPase, class II, type 9B	Mus musculus	27-33
10570059-8	1999	Increased survival of topo IIbeta -/- cells compared with topo IIbeta +/+ cells was observed after treatment with amsacrine (mAMSA), methyl N-(4"-[9-acridinylamino]-2-methoxyphenyl) carbamate hydrochloride (AMCA), methyl N-(4"-[9-acridinylamino]-2-methoxyphenyl)carbamate hydrochloride (mAMCA), mitoxantrone, and etoposide.	Amsacrine	114-123	ATPase, class II, type 9B	Mus musculus	63-69
10570059-8	1999	Increased survival of topo IIbeta -/- cells compared with topo IIbeta +/+ cells was observed after treatment with amsacrine (mAMSA), methyl N-(4"-[9-acridinylamino]-2-methoxyphenyl) carbamate hydrochloride (AMCA), methyl N-(4"-[9-acridinylamino]-2-methoxyphenyl)carbamate hydrochloride (mAMCA), mitoxantrone, and etoposide.	Amsacrine	125-130	ATPase, class II, type 9B	Mus musculus	27-33
10570059-8	1999	Increased survival of topo IIbeta -/- cells compared with topo IIbeta +/+ cells was observed after treatment with amsacrine (mAMSA), methyl N-(4"-[9-acridinylamino]-2-methoxyphenyl) carbamate hydrochloride (AMCA), methyl N-(4"-[9-acridinylamino]-2-methoxyphenyl)carbamate hydrochloride (mAMCA), mitoxantrone, and etoposide.	Amsacrine	125-130	ATPase, class II, type 9B	Mus musculus	63-69
10570059-9	1999	These studies showed that topo IIbeta -/- cells were significantly more resistant to mAMSA, AMCA, mAMCA, and mitoxantrone, than topo IIbeta +/+ cells, indicating that topo IIbeta is an important target for the cytotoxic effects of these compounds.	Amsacrine	85-90	ATPase, class II, type 9B	Mus musculus	31-37
9709006-9	1998	Analysis of the beta 2m status of other drug-resistant MCF-7 sublines revealed that deregulation of beta 2m is not limited to DOX resistance, but can also be detected in cells selected for resistance to mAMSA and DOX-verapamil.	Amsacrine	203-208	beta-2-microglobulin	Homo sapiens	100-107
10570059-5	1999	These results show that both topo IIalpha and beta are in vivo targets for etoposide, mitoxantrone, and amsacrine (mAMSA) in topo IIbeta +/+ cells.	Amsacrine	104-113	ATPase, class II, type 9A	Mus musculus	34-41
9709006-11	1998	Furthermore, we provide evidence that the partial inhibition of beta 2m by antisense RNA results in 2-3-fold decreased sensitivity of MCF-7 cells to DOX and mAMSA.	Amsacrine	157-162	beta-2-microglobulin	Homo sapiens	64-71
9046036-7	1997	The Ca2+ activated DNA fragmentation was significantly prevented by the presence of etoposide, genistein and amsacrine with the concentrations of 10(-5) and 10(-4) M in the reaction mixture, although ATA (10(-5) and 10(-4) M) had no effect.	Amsacrine	109-118	carbonic anhydrase 2	Rattus norvegicus	4-7
9625435-0	1998	Transcriptional down-regulation of c-myc expression in an erythroleukemic cell line, K562, and its doxorubicin-resistant variant by two topoisomerase II inhibitors, doxorubicin and amsacrine.	Amsacrine	181-190	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	35-40
9625435-5	1998	We have shown that Topo II-mediated breaks induced by amsacrine are probably responsible for the down-regulation of c-myc in the resistant line.	Amsacrine	54-63	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	116-121
10021886-8	1998	Pgp is responsible for cell resistance to cytotoxic compounds of natural origin, such as anthracyclines, vinca alkaloids, epipodophyllotoxins, taxanes, colchicine and amsacrine.	Amsacrine	167-176	ATP binding cassette subfamily B member 1	Homo sapiens	0-3
9422071-0	1997	[Expression of DNA topoisomerases (I, II alpha, II beta) mRNA in etoposide- and mAMSA-resistant cell lines].	Amsacrine	80-85	DNA topoisomerase II beta	Homo sapiens	15-55
9371511-1	1997	We have shown previously that NAD/poly(ADP-ribose) polymerase-deficient cells that overexpress Mr 78,000 glucose-regulated stress protein (GRP78) are resistant to topoisomerase II inhibitors, such as etoposide, m-amsacrine, and doxorubicin.	Amsacrine	211-222	poly [ADP-ribose] polymerase 1	Cricetulus griseus	34-61
9371511-1	1997	We have shown previously that NAD/poly(ADP-ribose) polymerase-deficient cells that overexpress Mr 78,000 glucose-regulated stress protein (GRP78) are resistant to topoisomerase II inhibitors, such as etoposide, m-amsacrine, and doxorubicin.	Amsacrine	211-222	endoplasmic reticulum chaperone BiP	Cricetulus griseus	139-144
9331091-7	1997	This work demonstrates that topoisomerase II beta is a pharmacological target for 9-OH-ellipticine, etoposide, or 4"-(9-acridinylamino)methanesulfon-m-anisidide and plays a role in the cytotoxicity of these agents.	Amsacrine	114-160	DNA topoisomerase II beta	Homo sapiens	28-49
9331091-8	1997	Furthermore, topoisomerase II beta is the preferential target for 4"-(9-acridinylamino)methanesulfon-m-anisidide.	Amsacrine	66-112	DNA topoisomerase II beta	Homo sapiens	13-34
9389932-8	1997	Both m-AMCA and amsacrine induced p53 protein expression in proliferating but not in non-proliferating H460 cells, and induced p21WAF1 regardless of proliferation status.	Amsacrine	16-25	tumor protein p53	Homo sapiens	34-37
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 < 0.05) lower as compared to AML-6 protocol-treated refractory or late-relapsed AML patients.	Amsacrine	122-131	ATP binding cassette subfamily B member 1	Homo sapiens	46-50
8986129-3	1996	Here we report the first high-resolution study of amsacrine (mAMSA) induced DNA breakage by human topoisomerase II beta (overexpressed and purified from yeast) and a direct comparison with the recombinant alpha isoform.	Amsacrine	50-59	DNA topoisomerase II beta	Homo sapiens	98-119
8986129-3	1996	Here we report the first high-resolution study of amsacrine (mAMSA) induced DNA breakage by human topoisomerase II beta (overexpressed and purified from yeast) and a direct comparison with the recombinant alpha isoform.	Amsacrine	61-66	DNA topoisomerase II beta	Homo sapiens	98-119
8980384-0	1996	Differential expression of DNA topoisomerase II alpha and -beta in P-gp and MRP-negative VM26, mAMSA and mitoxantrone-resistant sublines of the human SCLC cell line GLC4.	Amsacrine	95-100	DNA topoisomerase II beta	Homo sapiens	27-63
8823806-6	1996	Following cell exposure to dexamethasone, DNA-protein cleavable complex formation and cytotoxicity induced by etoposide, doxorubicin, and amsacrine were increased in the MDA-VP-hTOP2MAM cells compared with MDA-VP-MAM cells.	Amsacrine	138-147	sarcoglycan gamma	Homo sapiens	182-185
8831577-11	1996	Treatment with DX or AMSA caused similar effects, suggesting that p53-induced changes in cyclin, cdk, and cdk inhibitors after DNA damage are not responsible for the marked reduction in the cytotoxicity of DX we observed in wt p53-expressing cells.	Amsacrine	21-25	tumor protein p53	Homo sapiens	66-69
8068039-5	1994	In contrast, amsacrine stimulated the levels of c-jun mRNA only 3-fold in both cell lines, and its c-jun stimulatory effects were decreased at concentrations greater than 50 microM.	Amsacrine	13-22	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	48-53
7688089-2	1993	The Topo II inhibitor m-AMSA induced fewer SCE in EM9 than in AA8, mainly when given during the first S period.	Amsacrine	22-28	ERCC excision repair 2, TFIIH core complex helicase subunit	Homo sapiens	50-53
8243649-1	1993	We have investigated the effect of mAMSA, a potent topoisomerase II inhibitor, on the c-myc proto-oncogene of the acute promyelocytic leukemia HL60 cell line during its differentiation.	Amsacrine	35-40	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	86-91
8243649-5	1993	In HL60 cells treated with both mAMSA and DMSO, the sites in the c-myc gene at which mAMSA had induced cleavage were not altered.	Amsacrine	32-37	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	65-70
8243649-6	1993	However, a DNA cleavage site located at the end of the first c-myc exon (position +3100), was strongly stimulated by mAMSA and DMSO treatment.	Amsacrine	117-122	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	61-66
8313366-3	1994	By contrast, amsacrine induction of the HPRT- phenotype in AL cells is at least two decades less frequent and is not concentration dependent.	Amsacrine	13-22	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	40-44
8243480-2	1993	The covalent binding of topoisomerase II to the LTR was strongly stimulated by different inhibitors of the enzyme 4"-demethylepipodophyllotoxin-9-(4,6-O-2-ethylidene-beta-D-glucopy ranoside (VP-16), 4"-(9-acridinylamino)methanesulfon-m-anisidine) (m-AMSA) and an ellipticine derivative.	Amsacrine	248-254	Topoisomerase 2	Drosophila melanogaster	24-40
8518026-3	1993	A substantial (14- to 39-fold) enhancement of vinblastine toxicity to highly multidrug-resistant (MCF-7Adr) cells expressing P-glycoprotein was also observed in the presence of tamoxifen, toremifene and their metabolites, while m-amsacrine, cisplatin and melphalan toxicity was unaffected.	Amsacrine	228-239	ATP binding cassette subfamily B member 1	Homo sapiens	125-139
1317259-0	1992	Differential effects of amsacrine and epipodophyllotoxins on topoisomerase II cleavage in the human c-myc protooncogene.	Amsacrine	24-33	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	100-105
1333205-0	1992	Oxidative metabolism of amsacrine by the neutrophil enzyme myeloperoxidase.	Amsacrine	24-33	myeloperoxidase	Homo sapiens	59-74
1333205-3	1992	A potential candidate, that may be relevant to the metabolism of amsacrine in blood and its action in myeloid leukaemias and myelosuppression, is the haem enzyme myeloperoxidase.	Amsacrine	65-74	myeloperoxidase	Homo sapiens	162-177
1333205-6	1992	Detailed studies of the mechanism by which myeloperoxidase oxidizes amsacrine revealed that the semiquinone imine free radical is a likely intermediate in this reaction.	Amsacrine	68-77	myeloperoxidase	Homo sapiens	43-58
1333205-7	1992	Oxidation of amsacrine analogues indicated that factors other than their reduction potential determine how readily they are metabolized by myeloperoxidase.	Amsacrine	13-22	myeloperoxidase	Homo sapiens	139-154
1333205-8	1992	Both amsacrine and CI-921 inhibited production of hypochlorous acid by myeloperoxidase.	Amsacrine	5-14	myeloperoxidase	Homo sapiens	71-86
1333205-10	1992	Amsacrine inhibited by a different mechanism that may involve conversion of myeloperoxidase to compound III, which is also unable to oxidize Cl-.	Amsacrine	0-9	myeloperoxidase	Homo sapiens	76-91
1333205-11	1992	The susceptibility of amsacrine to oxidation by myeloperoxidase indicates that this reaction may contribute to the cytotoxicity of amsacrine toward neutrophils, monocytes and their precursors.	Amsacrine	22-31	myeloperoxidase	Homo sapiens	48-63
1333205-11	1992	The susceptibility of amsacrine to oxidation by myeloperoxidase indicates that this reaction may contribute to the cytotoxicity of amsacrine toward neutrophils, monocytes and their precursors.	Amsacrine	131-140	myeloperoxidase	Homo sapiens	48-63
1336489-1	1992	Recombinant human tumor necrosis factor (rHuTNF) synergistically potentiates the cytotoxicity of the topoisomerase I inhibitor camptothecin, and the topoisomerase II inhibitors epidoxorubicin, etoposide, mitoxantrone, ellipticine, actinomycin D and 4"-(9-acridinylamino)methanesulfon-m-anisidide on A2780 human ovarian cancer cell line.	Amsacrine	249-295	tumor necrosis factor	Homo sapiens	18-39
1602973-0	1992	Micronucleus induction by camptothecin and amsacrine in bone marrow of male and female CD-1 mice.	Amsacrine	43-52	CD1 antigen complex	Mus musculus	87-91
1850089-2	1991	Under these conditions, m-AMSA and VP-16 induce the differentiation of the cells efficiently, as proved both by an increase in the production of reactive oxygen species and by the activation of the surface expression of CD11b and CD11c, two differentiation-specific antigens.	Amsacrine	24-30	integrin subunit alpha M	Homo sapiens	220-225
1363724-0	1992	Structure-activity studies of amsacrine analogs in drug resistant human leukemia cell lines expressing either altered DNA topoisomerase II or P-glycoprotein.	Amsacrine	30-39	ATP binding cassette subfamily B member 1	Homo sapiens	142-156
1850089-2	1991	Under these conditions, m-AMSA and VP-16 induce the differentiation of the cells efficiently, as proved both by an increase in the production of reactive oxygen species and by the activation of the surface expression of CD11b and CD11c, two differentiation-specific antigens.	Amsacrine	24-30	integrin subunit alpha X	Homo sapiens	230-235
2158396-1	1990	A combination of tumor necrosis factor (TNF) and the topoisomerase I inhibitor, camptothecin, or the topoisomerase II inhibitors, teniposide and amsacrine, produced dose-dependent synergistic cytotoxicity against the murine L929 fibrosarcoma cells.	Amsacrine	145-154	tumor necrosis factor	Mus musculus	17-38
1976136-5	1990	Following treatment with AMSA, etoposide, and 5-iminodaunorubicin, topoisomerase II-mediated DNA cleavage in DR4 cells and nuclei was reduced compared with cleavage in HT1080 parent cells and nuclei.	Amsacrine	25-29	major histocompatibility complex, class II, DR beta 4	Homo sapiens	109-112
2158396-1	1990	A combination of tumor necrosis factor (TNF) and the topoisomerase I inhibitor, camptothecin, or the topoisomerase II inhibitors, teniposide and amsacrine, produced dose-dependent synergistic cytotoxicity against the murine L929 fibrosarcoma cells.	Amsacrine	145-154	tumor necrosis factor	Mus musculus	40-43
2159323-0	1990	Stabilization of the topoisomerase II-DNA cleavage complex by antineoplastic drugs: inhibition of enzyme-mediated DNA religation by 4"-(9-acridinylamino)methanesulfon-m-anisidide.	Amsacrine	132-178	Topoisomerase 2	Drosophila melanogaster	21-37
2159323-1	1990	In order to elucidate the mechanism by which the intercalative antineoplastic drug 4"-(9-acridinylamino)methanesulfon-m-anisidide (m-AMSA) stabilizes the covalent topoisomerase II-DNA cleavage complex, the effect of the drug on the DNA cleavage/religation reaction of the type II enzyme from Drosophila melanogaster was examined.	Amsacrine	83-129	Topoisomerase 2	Drosophila melanogaster	163-179
1967551-6	1990	LU-49888 labeling of Pgp was also inhibited by actinomycin D (45%), podophyllotoxin (47%), and amsacrine (82%), marginally by doxorubicin (25%), colchicine (22%), daunorubicin (18%), and etoposide (14%), but not by teniposide.	Amsacrine	95-104	ATP binding cassette subfamily B member 1	Homo sapiens	21-24
1967222-3	1990	GLC4/ADR expressed cross-resistance to teniposide, etoposide, 4"-(9-acridinylamino)methanesulfon-m-anisidide (m-AMSA), and mitoxantrone.	Amsacrine	62-108	aldo-keto reductase family 1 member B	Homo sapiens	5-8
1967222-3	1990	GLC4/ADR expressed cross-resistance to teniposide, etoposide, 4"-(9-acridinylamino)methanesulfon-m-anisidide (m-AMSA), and mitoxantrone.	Amsacrine	110-116	aldo-keto reductase family 1 member B	Homo sapiens	5-8
1967222-7	1990	Etoposide and m-AMSA-induced DNA cleavage was 5-fold reduced in cellular extracts from GLC4/ADR.	Amsacrine	14-20	aldo-keto reductase family 1 member B	Homo sapiens	92-95