PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
11879577-8	2002	The increased steroid hormone production in mutant K-ras-transfected cells was reversed by lovastatin, a pharmacologic inhibitor of p21ras function.	Lovastatin	91-101	KRAS proto-oncogene, GTPase	Homo sapiens	51-56	
8672984-4	1995	Also, agents such as perillyl alcohol and lovastatin that interfere with protein isoprenylation and, hence, inhibit oncogene activation may protect against aberrant K-ras expression.	Lovastatin	42-52	KRAS proto-oncogene, GTPase	Homo sapiens	165-170	
9472115-0	1998	Lovastatin inhibits proliferation of pancreatic cancer cell lines with mutant as well as with wild-type K-ras oncogene but has different effects on protein phosphorylation and induction of apoptosis.	Lovastatin	0-10	KRAS proto-oncogene, GTPase	Homo sapiens	104-109	
12434292-8	2002	In our previous report, we proved that lovastatin, a pharmacological inhibitor of p21(ras) function, also reversed the increase of cortisol level in mutant K-ras stably transfected human adrenocortical cells.	Lovastatin	39-49	KRAS proto-oncogene, GTPase	Homo sapiens	156-161	
16156861-5	2005	However, combinations of FTI and GGTI or lovastatin were found to synergistically inhibit MM cell proliferation, migration, K- and N-RAS processing, RAS-to-mitogen-activated protein kinase signalling and to induce apoptosis.	Lovastatin	41-51	KRAS proto-oncogene, GTPase	Homo sapiens	124-136	
34873318-0	2021	Author Correction: Autophagy inhibitors increase the susceptibility of KRAS-mutant human colorectal cancer cells to a combined treatment of 2-deoxy-D-glucose and lovastatin.	Lovastatin	162-172	KRAS proto-oncogene, GTPase	Homo sapiens	71-75	
33608672-0	2021	Autophagy inhibitors increase the susceptibility of KRAS-mutant human colorectal cancer cells to a combined treatment of 2-deoxy-D-glucose and lovastatin.	Lovastatin	143-153	KRAS proto-oncogene, GTPase	Homo sapiens	52-56	
33608672-4	2021	In this study we investigated the effect of a combination of 2-deoxy-D-glucose with lovastatin (a known inhibitor of mevalonate pathway and oxidative phosphorylation) on growth of KRAS-mutant human colorectal cancer cell lines HCT116 and LoVo.	Lovastatin	84-94	KRAS proto-oncogene, GTPase	Homo sapiens	180-184	
19760159-0	2010	Lovastatin overcomes gefitinib resistance in human non-small cell lung cancer cells with K-Ras mutations.	Lovastatin	0-10	KRAS proto-oncogene, GTPase	Homo sapiens	89-94	
19760159-11	2010	Taken together, these results suggest lovastatin can overcome gefitinib resistance, in NSCLC cells with K-Ras mutations, by down regulation of RAS protein, which leads to inhibition of both RAF/ERK and AKT pathways.	Lovastatin	38-48	KRAS proto-oncogene, GTPase	Homo sapiens	104-109