PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
27121230-5	2016	The present study aimed to elucidate the anticancer effects of PI3K (BKM120) and MEK (PD1056309) inhibitors on NSCLC cell lines with KRAS or EGFR mutations.	NVP-BKM120	69-75	epidermal growth factor receptor	Homo sapiens	141-145	
27507562-1	2017	BACKGROUND: The purpose of this study was to investigate the effects of combining the phosphotidylinositol-3-kinase (PI3K) inhibitor buparlisib (BKM)120 with the anti-epidermal growth factor receptor (EGFR) agent cetuximab and radiotherapy (RT) on an orthotopic model of head and neck squamous cell carcinoma (HNSCC).	NVP-BKM120	133-143	epidermal growth factor receptor	Homo sapiens	201-205	
27121230-6	2016	Inhibition of the EGFR and KRAS downstream P13K pathway using BKM120 significantly inhibited the growth of NSCLC cell lines with either EGFR or KRAS mutations.	NVP-BKM120	62-68	epidermal growth factor receptor	Homo sapiens	136-140	
27121230-6	2016	Inhibition of the EGFR and KRAS downstream P13K pathway using BKM120 significantly inhibited the growth of NSCLC cell lines with either EGFR or KRAS mutations.	NVP-BKM120	62-68	epidermal growth factor receptor	Homo sapiens	18-22	
34178665-7	2021	An active EGFR pathway was predictive for the response to the PI3K inhibitor buparlisib (p = 6.36E-03) and an inactive EGFR and PI3K pathway was associated with efficacy of the B-cell lymphoma (BCL) inhibitor navitoclax (p = 9.26E-03).	NVP-BKM120	77-87	epidermal growth factor receptor	Homo sapiens	10-14