PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
34136086-6	2021	Sensitivity to nelfinavir was due to the IU-TAB-1 cell line"s gain-of function (GOF) mutation in PIK3CA and amplification of genes observed from array comparative genomic hybridization (aCGH), including AURKA, ERBB2, KIT, PDGFRA and PDGFB, that are known upregulate AKT, while resistance to everolimus was primarily driven by upregulation of downstream signaling of KIT, PDGFRA and PDGFB in the presence of mTORC1 inhibition.	Nelfinavir	15-25	platelet derived growth factor subunit B	Homo sapiens	233-238	
34136086-6	2021	Sensitivity to nelfinavir was due to the IU-TAB-1 cell line"s gain-of function (GOF) mutation in PIK3CA and amplification of genes observed from array comparative genomic hybridization (aCGH), including AURKA, ERBB2, KIT, PDGFRA and PDGFB, that are known upregulate AKT, while resistance to everolimus was primarily driven by upregulation of downstream signaling of KIT, PDGFRA and PDGFB in the presence of mTORC1 inhibition.	Nelfinavir	15-25	platelet derived growth factor subunit B	Homo sapiens	382-387