PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
28115165-0	2017	Repression of Smad3 by Stat3 and c-Ski/SnoN induces gefitinib resistance in lung adenocarcinoma.	Gefitinib	52-61	SMAD family member 3	Homo sapiens	14-19	
31331328-11	2019	Furthermore, the overexpression of PD-L1 led to primary resistance to gefitinib through the induction of EMT, which was dependent on the upregulation of Smad3 phosphorylation.	Gefitinib	70-79	SMAD family member 3	Homo sapiens	153-158	
28115165-4	2017	Here we show that signal transducer and activator of transcription (Stat)3 represses Smad3 in synergy with the potent negative regulators of TGF-beta signaling, c-Ski and SnoN, whereby renders gefitinib-sensitive HCC827 cells resistant.	Gefitinib	193-202	SMAD family member 3	Homo sapiens	85-90	
28115165-8	2017	Our results suggest that derepression of Smad3 can be a therapeutic strategy to prevent gefitinib-resistance in NSCLCs with gefitinib-sensitizing EGFR mutation.	Gefitinib	88-97	SMAD family member 3	Homo sapiens	41-46	
28115165-8	2017	Our results suggest that derepression of Smad3 can be a therapeutic strategy to prevent gefitinib-resistance in NSCLCs with gefitinib-sensitizing EGFR mutation.	Gefitinib	124-133	SMAD family member 3	Homo sapiens	41-46	
24928833-9	2014	Dual luciferase reporter assays showed gefitinib-resistant PC9/G cells transfected with SMAD3: rs11632964T allelic reporter construct showed significantly lower luciferase activities compared with cells expression C allelic reporter construct.	Gefitinib	39-48	SMAD family member 3	Homo sapiens	88-93	
24928833-11	2014	CONCLUSIONS: Among the candidate genes involved in the TGF-beta pathway, the polymorphisms of SMAD3 appear to be highly predictive of outcome of patients with lung adenocarcinoma after gefitinib treatment, especially in those with EGFR mutations.	Gefitinib	185-194	SMAD family member 3	Homo sapiens	94-99