PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
10785598-2	2000	We studied 5-FU- and ZD1694-induced TS inhibition in relation to the expression of p53, p21, Bcl-2 and Bax in six colon carcinoma cell lines, two with a wild-type (wt) p53 (Lovo, LS174T) and four with a mutant (mt) p53 (WiDr, WiDr/F, HT29 and SW948) phenotype.	raltitrexed	21-27	BCL2 associated X, apoptosis regulator	Homo sapiens	103-106	
10690558-5	2000	Compared to A253/Vec, A253/Bax cells exhibited 9.5- and 13.5-fold increases in sensitivity to raltitrexed and SN-38, respectively.	raltitrexed	94-105	BCL2 associated X, apoptosis regulator	Homo sapiens	27-30	
10690558-12	2000	In contrast, both raltitrexed and irinotecan were significantly more active against A253/Bax xenografts than against A253/Vec xenografts; the yield for complete tumor regression (cure) was 40% and 100% with raltitrexed and irinotecan, respectively, with no significant toxicity.	raltitrexed	18-29	BCL2 associated X, apoptosis regulator	Homo sapiens	89-92	
10489165-3	1999	A253/Bax cells exhibited a significant increase in in vitro sensitivity to various anticancer drugs, including tomudex (9.5-fold), SN-38 (13.8-fold), doxorubicin (7.9-fold), taxol (3.1-fold), 5-FU (2.7-fold), and 5-FU/LV (4.5-fold).	raltitrexed	111-118	BCL2 associated X, apoptosis regulator	Homo sapiens	5-8	
10489165-6	1999	Treatment with tomudex induced the formation of Bax dimer in a drug concentration-dependent manner.	raltitrexed	15-22	BCL2 associated X, apoptosis regulator	Homo sapiens	48-51	
10489165-8	1999	Low level of Bax dimerization was also detected in parental A253 cells following tomudex exposure.	raltitrexed	81-88	BCL2 associated X, apoptosis regulator	Homo sapiens	13-16