PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
2879622-3	1987	Following removal of extracellular vinblastine, the elevation of cell VP-16 was maintained through an additional 55-min incubation period.	Vinblastine	35-46	host cell factor C1	Homo sapiens	70-75	
9446803-6	1998	Furthermore, when PC3 cells were treated with a panel of apoptosis-inducing agents, it was found that camptothecin, bleomycin, VP16 and TNF-alpha induced varying amounts of cytosolic accumulation of cytochrome c either prior to or concurrent with PARP cleavage while vinblastine and BHPP did not.	Vinblastine	267-278	host cell factor C1	Homo sapiens	127-131	
8940082-4	1996	Treatment with vinblastine or etoposide (VP-16) also activated JNK, with maximum increases of 6.5- and 4.3-fold, respectively.	Vinblastine	15-26	host cell factor C1	Homo sapiens	41-46	
2536292-1	1989	We optimized the modulation of drug resistance by the irreversible augmentation of cytotoxicity of coincubating vinblastine (VNB) with VP-16 and the reversible increase in cytotoxicity of coincubation of verapamil (VPL) with VNB and VP-16.	Vinblastine	112-123	host cell factor C1	Homo sapiens	135-140	
2536292-1	1989	We optimized the modulation of drug resistance by the irreversible augmentation of cytotoxicity of coincubating vinblastine (VNB) with VP-16 and the reversible increase in cytotoxicity of coincubation of verapamil (VPL) with VNB and VP-16.	Vinblastine	125-128	host cell factor C1	Homo sapiens	135-140	
12907245-7	2003	Vinblastine caused inactivation of ERK whereas ERK was unaffected in cells exposed to doxorubicin or VP-16.	Vinblastine	0-11	host cell factor C1	Homo sapiens	101-106	
1972771-7	1990	In contrast, nonradioactive VP-16 was 100- to 500-fold less potent than vinblastine in competing with P-gp photolabeling, suggesting that VP-16 has significantly lower affinity for P-gp than Vinca alkaloids have.	Vinblastine	72-83	host cell factor C1	Homo sapiens	138-143	
2879622-2	1987	At concentrations of 0.05-20 microM, vinblastine, vincristine, and maytansine similarly increased the steady-state cell concentration of VP-16 (2.5 microM) up to 2-fold.	Vinblastine	37-48	host cell factor C1	Homo sapiens	137-142	
2438232-3	1987	Subsequent studies demonstrated that: post PVB, surgery can cure patients; vinblastine dosage can be lowered from 0.4 to 0.3 mg/kg without sacrificing cure potential; maintenance vinblastine is not necessary; VP-16 can be substituted for vinblastine with equivalent cure rates and decreased neuromuscular toxicity.	Vinblastine	75-86	host cell factor C1	Homo sapiens	209-214	
2879622-6	1987	At vinblastine concentrations of 0.05-0.2 microM, the increase in cell VP-16 was due to a progressive increase in nonexchangeable VP-16.	Vinblastine	3-14	host cell factor C1	Homo sapiens	71-76	
2879622-6	1987	At vinblastine concentrations of 0.05-0.2 microM, the increase in cell VP-16 was due to a progressive increase in nonexchangeable VP-16.	Vinblastine	3-14	host cell factor C1	Homo sapiens	130-135	
2879622-9	1987	Elevation of exchangeable VP-16 in the presence of vinblastine was due to inhibition of the unidirectional efflux of this epipodophyllotoxin with a 69% decline in the rate constant for efflux.	Vinblastine	51-62	host cell factor C1	Homo sapiens	26-31	
2879622-12	1987	VP-16-induced DNA damage was enhanced by vinblastine concentrations above 0.5 microM, concentrations that elevated exchangeable VP-16, with a maximum doubling of radiation equivalent single-strand break frequency observed with 20 microM vinblastine, consistent with the maximum elevation of cell VP-16 with 20 microM Vinca alkaloid.	Vinblastine	41-52	host cell factor C1	Homo sapiens	0-5	
2879622-12	1987	VP-16-induced DNA damage was enhanced by vinblastine concentrations above 0.5 microM, concentrations that elevated exchangeable VP-16, with a maximum doubling of radiation equivalent single-strand break frequency observed with 20 microM vinblastine, consistent with the maximum elevation of cell VP-16 with 20 microM Vinca alkaloid.	Vinblastine	237-248	host cell factor C1	Homo sapiens	0-5	
2879622-13	1987	These results indicate that vinblastine and other microtubule inhibitors elevate cell VP-16 by inhibition of the efflux of exchangeable drug and by increasing the level of nonexchangeable drug.	Vinblastine	28-39	host cell factor C1	Homo sapiens	86-91	
2579442-8	1985	Among patients who have multiple resistance to drugs such as vinblastine, bleomycin, and cis-platinum, 50% have achieved remission when treated with the EP/OMB schedule (VP-16 and cis-platinum alternated with vincristine, methotrexate, and bleomycin) repeated at short intervals.	Vinblastine	61-72	host cell factor C1	Homo sapiens	170-175	
6177438-8	1982	This case suggest that VP16-213 combined with bleomycin + cis-platinum has great activity against NSGCT of the testis and may have a different spectrum of activity from vinblastine, bleomycin, and cis-platinum, making it a valuable addition to the drugs available for the management of these tumours.	Vinblastine	169-180	host cell factor C1	Homo sapiens	23-27