PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
32724460-2	2020	We previously showed that resistance to regorafenib, a multi-kinase inhibitor for treating colorectal cancer (CRC) patients, can be caused by mutations in the tumor suppressor FBW7, which block degradation of the pro-survival Bcl-2 family protein Mcl-1.	regorafenib	40-51	F-box and WD repeat domain containing 7	Homo sapiens	176-180	
32724460-9	2020	Importantly, Mcl-1 inhibition also sensitized FBW7-mutant PDO and PDX models to regorafenib.	regorafenib	80-91	F-box and WD repeat domain containing 7	Homo sapiens	46-50	
32724460-12	2020	FBW7 mutations might be a potential biomarker predicting for response to the regorafenib/Mcl-1 inhibitor combination.	regorafenib	77-88	F-box and WD repeat domain containing 7	Homo sapiens	0-4	
27399335-4	2017	CRC cells containing FBW7-inactivating mutations are insensitive to clinically used multi-kinase inhibitors of RAS/RAF/MEK/ERK signaling, including regorafenib and sorafenib.	regorafenib	148-159	F-box and WD repeat domain containing 7	Homo sapiens	21-25	
27399335-8	2017	CRC cells selected for regorafenib resistance have progressive enrichment of pre-existing FBW7 hotspot mutations, and are cross-resistant to other targeted drugs that induce Mcl-1 degradation.	regorafenib	23-34	F-box and WD repeat domain containing 7	Homo sapiens	90-94