PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
31637005-5	2019	In this study, we found that EGFR TKIs, including gefitinib and AZD9291, impaired lysosome-dependent degradation of SQSTM1, thus compromising their anti-cancer efficiency.	osimertinib	64-71	sequestosome 1	Homo sapiens	116-122	
31637005-6	2019	By accumulating in the lysosome lumen, gefitinib and AZD9291 attenuated lysosomal acidification and impaired autolysosomal degradation of SQSTM1 owing to their intrinsic alkalinity.	osimertinib	53-60	sequestosome 1	Homo sapiens	138-144	
31637005-7	2019	As a result, SQSTM1 protein was stabilized in response to gefitinib and AZD9291 treatment and conferred EGFR TKI resistance.	osimertinib	72-79	sequestosome 1	Homo sapiens	13-19	
31637005-8	2019	Depleting SQSTM1 significantly increased the sensitivity of NSCLC cells to gefitinib and AZD9291 both in vitro and in vivo.	osimertinib	89-96	sequestosome 1	Homo sapiens	10-16	
32577785-7	2020	It is also noticeable that AZD9291 + ABT263 specifically caused a significantly reduced expression of p21 compared with AZD9291 or ABT263 treatment alone while AZD9291 + ABT199 specifically caused significantly reduced expressions of SQSTM1 and survivin, but increased expression of autophagosome marker LC3-II compared with AZD9291 or ABT199 treatment alone.	osimertinib	27-34	sequestosome 1	Homo sapiens	234-240