PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
31675556-0	2019	Curcumin functions as a MEK inhibitor to induce a synthetic lethal effect on KRAS mutant colorectal cancer cells receiving targeted drug regorafenib.	regorafenib	137-148	KRAS proto-oncogene, GTPase	Homo sapiens	77-81	
34199694-14	2021	Daily practice patterns reflect the guideline recommendations in third- and fourth-line settings, with a trend toward using trifluridine-tipiracil versus regorafenib in KRAS-wildtype and KRAS-mutant tumors.	regorafenib	154-165	KRAS proto-oncogene, GTPase	Homo sapiens	169-173	
32770529-11	2020	CONCLUSIONS: Regorafenib combined with chemotherapy might be a potential alternative to conventional therapeutic options in second-line treatment of patients with metastatic colorectal cancer and could be considered as the best option for treating patients with KRAS and BRAF mutated mCRC.	regorafenib	13-24	KRAS proto-oncogene, GTPase	Homo sapiens	262-266	
31675556-4	2019	Here, we reveal that curcumin significantly enhanced the growth inhibition of regorafenib in human colorectal cancer HCT 116 cells (KRAS mutant) to a greater extent than in human colorectal cancer HT-29 cells (KRAS wild-type), producing an additive or synergistic effect in HCT 116 cells and causing an antagonistic effect in HT-29 cells.	regorafenib	78-89	KRAS proto-oncogene, GTPase	Homo sapiens	132-136	
31675556-7	2019	Our data suggest that curcumin may target one more gene other than mutant KRAS to enhance regorafenib-induced growth inhibition (synthetic lethality) in colorectal cancer HCT 116 cells, indicating a possible role of curcumin in regorafenib-treated KRAS mutant colorectal cancer.	regorafenib	90-101	KRAS proto-oncogene, GTPase	Homo sapiens	248-252	
28032528-4	2017	The results of the CORRECT study demonstrated the efficacy of regorafenib monotherapy in both KRAS wild type and mutant pretreated patients (pts).	regorafenib	62-73	KRAS proto-oncogene, GTPase	Homo sapiens	94-98	
31205516-2	2019	We evaluated the effect of regorafenib based on KRAS mutation status and the sidedness of the primary tumor in patients with metastatic colorectal cancer (mCRC).	regorafenib	27-38	KRAS proto-oncogene, GTPase	Homo sapiens	48-52	
31205516-11	2019	In a subpopulation with wild type KRAS, PFS with regorafenib was also significantly different between the LC and RC groups (2.9 months; 95% CI, 1.5 to 4.3 vs. 2.1 months; 95% CI, 0.6 to 3.6; P = 0.04).	regorafenib	49-60	KRAS proto-oncogene, GTPase	Homo sapiens	34-38	
28259999-15	2017	Moreover, the KRAS mutation declined in two patients during regorafenib monotherapy.	regorafenib	60-71	KRAS proto-oncogene, GTPase	Homo sapiens	14-18	
26640390-3	2015	Here, we detail the clinical history of an elderly woman with KRAS wild-type colon cancer who received regorafenib after prior treatment with other agents.	regorafenib	103-114	KRAS proto-oncogene, GTPase	Homo sapiens	62-66	
26489551-0	2015	[Long-Term Survival of a Patient with KRAS Mutated Colon Cancer Successfully Treated with Regorafenib].	regorafenib	90-101	KRAS proto-oncogene, GTPase	Homo sapiens	38-42	
26327919-3	2015	Regorafenib has been approved by the US Food and Drug Administration (FDA) for the treatment of metastatic colorectal cancer (mCRC) in patients who have failed treatment with fluoropyrimidine, oxaliplatin and irinotecan based chemotherapy, an anti-VEGF therapy and, if KRAS wild type, an anti-EGFR therapy.	regorafenib	0-11	KRAS proto-oncogene, GTPase	Homo sapiens	269-273	
26161928-0	2015	KRAS exon 2 mutations influence activity of regorafenib in an SW48-based disease model of colorectal cancer.	regorafenib	44-55	KRAS proto-oncogene, GTPase	Homo sapiens	0-4	
26161928-1	2015	AIM: To investigate the impact of KRAS mutation variants on the activity of regorafenib in SW48 colorectal cancer cells.	regorafenib	76-87	KRAS proto-oncogene, GTPase	Homo sapiens	34-38	
26161928-2	2015	MATERIALS & METHODS: Activity of regorafenib was evaluated in isogenic SW48 KRAS wild-type (WT) and mutant cells.	regorafenib	37-48	KRAS proto-oncogene, GTPase	Homo sapiens	80-84	
26161928-4	2015	RESULTS: Compared with KRAS WT cells, all mutant variants seemed associated with some degree of resistance to regorafenib-treatment in vitro.	regorafenib	110-121	KRAS proto-oncogene, GTPase	Homo sapiens	23-27	
26161928-6	2015	CONCLUSION: In SW48 cells, exon 2 mutations of the KRAS gene may influence antitumor effects of regorafenib.	regorafenib	96-107	KRAS proto-oncogene, GTPase	Homo sapiens	51-55	
26045027-2	2015	In 2 phase III trials, regorafenib significantly improved progression-free and overall survival in patients who had been previously treated with fluoropyrimidine-, oxaliplatin-, and irinotecan-based chemotherapy, an anti-vascular endothelial growth factor therapy, and, if (K)RAS wild type, an anti-epidermal growth factor receptor therapy.	regorafenib	23-34	KRAS proto-oncogene, GTPase	Homo sapiens	274-279	
24623990-3	2014	Thus, regorafenib is the first oral multikinase inhibitor indicated for mCRC; it currently has approval in the USA, EU, Japan, Canada, and Singapore for the treatment of mCRC patients who have been previously treated with fluoropyrimidine-, oxaliplatin-, and irinotecan-based chemotherapy, an anti-vascular endothelial growth factor therapy, and, if the tumor is KRAS wild-type, an anti-epidermal growth factor receptor therapy.	regorafenib	6-17	KRAS proto-oncogene, GTPase	Homo sapiens	363-367	
24047557-1	2013	Regorafenib, oral multi-kinase inhibitor that targets oncogenesis, tumor angiogenesis and maintenance of the tumor microenvironment, obtained its European approval, August 26, 2013 after favorable review of the European Medecines Agency in the following indication: treatment of patients with metastatic colorectal cancer who have been previously treated with fluoropyrimidine-, oxaliplatin- and irinotecan-based chemotherapy, an anti-VEGF therapy or are not considered candidates for available therapies and, if KRAS wild type, an anti-EGFR therapy.	regorafenib	0-11	KRAS proto-oncogene, GTPase	Homo sapiens	513-517