PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
30412912-0	2019	Enhancing the Radiation Response in KRAS Mutant Colorectal Cancers Using the c-Met Inhibitor Crizotinib.	Crizotinib	93-103	KRAS proto-oncogene, GTPase	Homo sapiens	36-40	
30352902-6	2019	In one patient, the KRAS mutation was acquired post-crizotinib, while the remaining 4 METex14 patients harbored the KRAS mutation prior to MET TKI therapy.	Crizotinib	52-62	KRAS proto-oncogene, GTPase	Homo sapiens	20-24	
30412912-10	2019	KRAS mutant cell lines LoVo, HCT116, and DLD1 were resistant to cetuximab but sensitive to crizotinib.	Crizotinib	91-101	KRAS proto-oncogene, GTPase	Homo sapiens	0-4	
30412912-15	2019	CONCLUSIONS: Inhibition of c-Met with crizotinib effectively sensitizes cetuximab-resistant KRAS mutant colorectal cancer cell lines to radiation.	Crizotinib	38-48	KRAS proto-oncogene, GTPase	Homo sapiens	92-96	
30412912-2	2019	In this study, we used a small molecule inhibitor of c-Met, crizotinib, in cetuximab-resistant, mutant KRAS-driven colorectal cancer cell lines and assessed radiosensitization.	Crizotinib	60-70	KRAS proto-oncogene, GTPase	Homo sapiens	103-107	
30072474-0	2018	Amplification of Wild-type KRAS Imparts Resistance to Crizotinib in MET Exon 14 Mutant Non-Small Cell Lung Cancer.	Crizotinib	54-64	KRAS proto-oncogene, GTPase	Homo sapiens	27-31	
30072474-3	2018	In this study, we characterize acquired amplification of wild-type (WT) KRAS as a molecular mechanism behind crizotinib resistance in three cases of METex14-mutant NSCLC and propose a combination therapy to target it.	Crizotinib	109-119	KRAS proto-oncogene, GTPase	Homo sapiens	72-76	
30072474-8	2018	RESULTS: KRAS amplification is a recurrent genetic event in crizotinib-resistant METex14-mutant NSCLC.	Crizotinib	60-70	KRAS proto-oncogene, GTPase	Homo sapiens	9-13	
30072474-10	2018	CONCLUSIONS: Using patient-derived cell line and xenografts, we characterize the mechanism of crizotinib resistance mediated by KRAS amplification in METex14-mutant NSCLC and demonstrate the superior efficacy of the dual MET/PI3K inhibition as a therapeutic strategy addressing this resistance mechanism.	Crizotinib	94-104	KRAS proto-oncogene, GTPase	Homo sapiens	128-132	
26381283-13	2016	The 2 KRAS-mutant DP patients experienced opposite responses to crizotinib.	Crizotinib	64-74	KRAS proto-oncogene, GTPase	Homo sapiens	6-10	
28601386-0	2017	Detection of ALK and KRAS Mutations in Circulating Tumor DNA of Patients With Advanced ALK-Positive NSCLC With Disease Progression During Crizotinib Treatment.	Crizotinib	138-148	KRAS proto-oncogene, GTPase	Homo sapiens	21-25	
28601386-9	2017	CONCLUSION: ALK and KRAS mutations are associated with acquired resistance to crizotinib in ALK-positive NSCLC.	Crizotinib	78-88	KRAS proto-oncogene, GTPase	Homo sapiens	20-24	
28007627-6	2017	Six of seven patients with ALK/KRAS co-alterations (86%) were primary refractory to crizotinib.	Crizotinib	84-94	KRAS proto-oncogene, GTPase	Homo sapiens	31-35	
27040858-3	2016	At the first line therapy, the patient was treated with crizotinib because of the KRAS mutation that is a known resistant factor of EGFR-TKI resistance, but no responsive.	Crizotinib	56-66	KRAS proto-oncogene, GTPase	Homo sapiens	82-86	
26898615-0	2016	K-RAS mutations indicating primary resistance to crizotinib in ALK-rearranged adenocarcinomas of the lung: Report of two cases and review of the literature.	Crizotinib	49-59	KRAS proto-oncogene, GTPase	Homo sapiens	0-5	
26898615-4	2016	Search for similar cases in the literature reveals that concomitant K-RAS mutations and ALK rearrangement occur in a subset of NSCLC and seems to lead to resistance to crizotinib.	Crizotinib	168-178	KRAS proto-oncogene, GTPase	Homo sapiens	68-73	
34568053-3	2021	We present a 34-year-old young man with ALK rearrangement-positive and KRAS-wild pancreatic cancer who had a remarkable response to crizotinib after resistance to prior chemotherapy and re-response to alectinib after brain metastases developed.	Crizotinib	132-142	KRAS proto-oncogene, GTPase	Homo sapiens	71-75	
25691052-5	2015	Interestingly, we identified focal KRAS amplification in a biopsy of a tumor from a patient that had become resistant to crizotinib treatment.Altogether our data suggest that the activation of members of the RAS family can confer resistance to ROS1 inhibitors.	Crizotinib	121-131	KRAS proto-oncogene, GTPase	Homo sapiens	35-39	
26517679-2	2015	Although the inhibitor crizotinib, as it blocks the kinase activity of the resulting EML4-ALK fusion protein, displays remarkable initial responses, a fraction of NSCLC cases eventually become resistant to crizotinib by acquiring mutations in the ALK domain or activating bypass pathways via EGFR, KIT, or KRAS.	Crizotinib	23-33	KRAS proto-oncogene, GTPase	Homo sapiens	306-310	
25232318-0	2014	Durable Response to Crizotinib in a MET-Amplified, KRAS-Mutated Carcinoma of Unknown Primary.	Crizotinib	20-30	KRAS proto-oncogene, GTPase	Homo sapiens	51-55