PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
34994624-0	2021	Divergent RET- and BRAF-Mediated Resistance to Osimertinib in EGFR-Mutant NSCLC: A Case Report.	osimertinib	47-58	ret proto-oncogene	Homo sapiens	10-13	
34203709-2	2021	Multiple receptor tyrosine kinase (RTK) pathways contribute to the resistance of NSCLC to first- and third-generation EGFR-TKIs, such as erlotinib and osimertinib.	osimertinib	151-162	ret proto-oncogene	Homo sapiens	9-33	
34344199-0	2022	Combination EGFR and RET Inhibition in Acquired Resistance to Osimertinib in EGFR-Mutant NSCLC.	osimertinib	62-73	ret proto-oncogene	Homo sapiens	21-24	
34203709-2	2021	Multiple receptor tyrosine kinase (RTK) pathways contribute to the resistance of NSCLC to first- and third-generation EGFR-TKIs, such as erlotinib and osimertinib.	osimertinib	151-162	ret proto-oncogene	Homo sapiens	35-38	
33641722-0	2021	Selpercatinib Overcomes CCDC6-RET-Mediated Resistance to Osimertinib.	osimertinib	57-68	ret proto-oncogene	Homo sapiens	30-33	
35462930-7	2022	The other patient acquired EGFR T790M and MET amplification post-dacomitinib and acquired CCDC6-RET fusion after osimertinib treatment.	osimertinib	113-124	ret proto-oncogene	Homo sapiens	96-99	
35066105-7	2022	RESULTS: Among the 45 patients included in MATCH-R who progressed on osimertinib, nine developed a second targetable alteration (n = 2 FGFR3-TACC3, n = 1 KIF5B-RET, n = 1 STRN-ALK fusions; n = 2 BRAFV600E, n = 1 KRASG12V, n = 1 KRASG12R, n = 1 KRASG12D mutations).	osimertinib	69-80	ret proto-oncogene	Homo sapiens	160-163	
33173309-5	2020	Conclusion: Our findings expanded the spectrum of RET arrangement types and provided the basis for this hypothesis: acquired RET rearrangement and EGFR exon20 p.T790M loss potentially serve an additional resistance mechanism to osimertinib in EGFR-mutated non-small-cell lung cancer (NSCLC).	osimertinib	228-239	ret proto-oncogene	Homo sapiens	50-53	
33173309-5	2020	Conclusion: Our findings expanded the spectrum of RET arrangement types and provided the basis for this hypothesis: acquired RET rearrangement and EGFR exon20 p.T790M loss potentially serve an additional resistance mechanism to osimertinib in EGFR-mutated non-small-cell lung cancer (NSCLC).	osimertinib	228-239	ret proto-oncogene	Homo sapiens	125-128	
31911548-4	2020	Nineteen percent (5/27) of patients treated with first-line osimertinib had off-target genetic resistance (2 MET amplification, 1 KRAS mutation, 1 RET fusion, and 1 BRAF fusion) whereas 4% (1/27) had an acquired EGFR mutation (EGFR G724S).	osimertinib	60-71	ret proto-oncogene	Homo sapiens	147-150