PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
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.	Etoposide	125-134	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	177-180	
11237055-8	2001	At growth inhibition levels of over 50%, STI571 + cytarabine as well as STI571 + etoposide were significantly synergistic (CI < 1, P < 0.05) in the BCR-ABL-positive cell lines evaluated.	Etoposide	81-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	158-161	
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.	Etoposide	191-200	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47	
9516141-2	1998	Apoptotic DNA fragmentation is delayed in the bcr-abl+ K562 and KCL-22 compared with the bcr-abl- U937 and HL-60 cell lines when treated with etoposide concentrations that induce similar DNA damage in the four cell lines.	Etoposide	142-151	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-53	
9516141-2	1998	Apoptotic DNA fragmentation is delayed in the bcr-abl+ K562 and KCL-22 compared with the bcr-abl- U937 and HL-60 cell lines when treated with etoposide concentrations that induce similar DNA damage in the four cell lines.	Etoposide	142-151	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	89-96	
9516141-3	1998	By the use of a cell-free system, we show that nuclei from untreated cells that express p210(bcr-abl) remain sensitive to apoptotic DNA fragmentation induced by triton-soluble extracts from p210(bcr-abl-) cells treated with etoposide.	Etoposide	224-233	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100	
9516141-3	1998	By the use of a cell-free system, we show that nuclei from untreated cells that express p210(bcr-abl) remain sensitive to apoptotic DNA fragmentation induced by triton-soluble extracts from p210(bcr-abl-) cells treated with etoposide.	Etoposide	224-233	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	195-202	
9516141-6	1998	The role of p210(bcr-abl) in this delay is confirmed by comparing the effect of etoposide on the granulocyte-macrophage colony-stimulating factor (GM-CSF)-dependent UT7 cells and the bcr-abl-transfected GM-CSF-independent UT7/9 clone.	Etoposide	80-89	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24	
9516141-7	1998	We conclude that the cytosolic pathway that leads to apoptotic DNA fragmentation in etoposide-treated leukemic cells is delayed upstream of procaspase-3-mediated events in bcr-abl+ cell lines.	Etoposide	84-93	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	172-179	
24569990-5	2014	Depletion of c-Abl or c-Src with shRNA decreased irradiation- and etoposide-induced apoptosis, suggesting that inhibitors of these kinases may be useful therapeutically.	Etoposide	66-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-18	
24260231-4	2013	In cells expressing BCR/ABL, FLT3-ITD, or Jak2-V617F, etoposide induced a sustained activation of Chk1, thus leading to the G2/M arrest of cells.	Etoposide	54-63	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	20-27	
24260231-6	2013	The PI3K inhibitor GD-0941 or the Akt inhibitor MK-2206 showed similar effects with imatinib on etoposide-treated BCR/ABL-expressing cells, including those expressing the imatinib-resistant T315I mutant, while expression of the constitutively activated Akt1-myr mutant conferred resistance to the combined treatment of etoposide and imatinib.	Etoposide	96-105	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121	
22705319-0	2012	BCR/ABL modulates protein phosphorylation associated with the etoposide-induced DNA damage response.	Etoposide	62-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7	
22705319-7	2012	BCR/ABL was shown to significantly alter the response to etoposide in many cases.	Etoposide	57-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7	
22705319-12	2012	Furthermore we found that multiple protein phosphorylation changes mediated by BCR/ABL were connected to the increased activation of NFkappaB, a key survival transcription factor, after etoposide exposure.	Etoposide	186-195	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86	
19237191-3	2009	UPR inhibition using inositol-requiring enzyme 1alpha (IRE1alpha) or activating transcription factor 6 (ATF6) dominant-negative mutants diminished the ability of Bcr-Abl to protect the cells from etoposide- and imatinib-induced apoptosis.	Etoposide	196-205	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-169	
19020542-3	2009	BCR/ABL-expressing cell lines show an increase in DNA breaks after treatment with etoposide as compared to control cells.	Etoposide	82-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7	
15978941-6	2005	Decreased expression of BCR/ABL gene was also found after cell stimulation by selectively pro-apoptotic agent etoposide and by ABL-RNAi leading to apoptosis.	Etoposide	110-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-31	
15978941-6	2005	Decreased expression of BCR/ABL gene was also found after cell stimulation by selectively pro-apoptotic agent etoposide and by ABL-RNAi leading to apoptosis.	Etoposide	110-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	28-31	
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.	Etoposide	164-173	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7	
15050919-4	2004	Furthermore, BCR/ABL increases DNA double-strand damage after etoposide treatment and leads to a defect in an intra-S phase checkpoint, causing a radioresistant DNA synthesis (RDS) phenotype.	Etoposide	62-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	13-20	
12513785-9	2002	Bcr-abl fusion gene prevented apoptosis induced by etoposide or camptothecin, but did not prevent apoptosis induced by CIK cells.	Etoposide	51-60	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7	
11937320-1	2002	Improving etoposide efficacy in BCR-ABL-positive CML cells.	Etoposide	10-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	32-39