PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
32005746-1	2020	PURPOSE: Concurrent inhibition of mTOR and PI3K led to improved efficacy in preclinical models and provided the rationale for this phase I study of everolimus and buparlisib (BKM120) in patients with advanced solid tumor.	NVP-BKM120	163-173	mechanistic target of rapamycin kinase	Homo sapiens	34-38	
32898555-7	2020	In this study we demonstrate the effects of PI3K/Akt/mTOR pathway inhibition by buparlisib on PD-L1 expression in HNSCC cell lines.	NVP-BKM120	80-90	mechanistic target of rapamycin kinase	Homo sapiens	53-57	
33471836-8	2021	The triple combination treatment of mTOR inhibitor AZD2014 and BKM120 or AZD2014 and BYL719 with radiation showed a significantly enhanced inhibitory effect on radioresistant OML1-R cells.	NVP-BKM120	63-69	mechanistic target of rapamycin kinase	Homo sapiens	36-40	
30982255-0	2019	[NVP-BKM120 in combination with letrozole inhibit human breast cancer stem cells via PI3K/mTOR pathway].	NVP-BKM120	5-11	mechanistic target of rapamycin kinase	Homo sapiens	90-94	
22159814-7	2012	NVP-BKM120 demonstrated             anti-proliferative activity in 11 human gastric cancer cell lines by decreasing             mTOR downstream signaling.	NVP-BKM120	4-10	mechanistic target of rapamycin kinase	Homo sapiens	128-132	
28662162-7	2017	BKM120 exhibited cytotoxicity in MB cells in a dose and time-dependent manner by inhibiting activation of downstream signaling molecules AKT and mTOR, and activating caspase-mediated apoptotic pathways.	NVP-BKM120	0-6	mechanistic target of rapamycin kinase	Homo sapiens	145-149	
27986714-1	2017	Data from the BELLE-3 trial suggest that adding the investigational PI3K inhibitor buparlisib to endocrine therapy may improve outcomes for patients with hormone receptor-positive advanced breast cancer whose tumors become resistant to mTOR inhibition.	NVP-BKM120	83-93	mechanistic target of rapamycin kinase	Homo sapiens	236-240	
27507562-4	2017	The highest inhibitory effect of treatments on cell proliferation, mitogen-activated protein kinase (MAPK) and PI3K/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathways were found with the BKM120-cetuximab association.	NVP-BKM120	215-221	mechanistic target of rapamycin kinase	Homo sapiens	139-168	
27507562-4	2017	The highest inhibitory effect of treatments on cell proliferation, mitogen-activated protein kinase (MAPK) and PI3K/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathways were found with the BKM120-cetuximab association.	NVP-BKM120	215-221	mechanistic target of rapamycin kinase	Homo sapiens	170-174	
27531477-15	2016	The immunohistochemical analysis showed that BKM120 inhibited mTOR activity, and the enhanced WNT/beta-catenin activity reversed the phenotype of inhibitory mTOR induced by BKM120.	NVP-BKM120	45-51	mechanistic target of rapamycin kinase	Homo sapiens	62-66	
27531477-15	2016	The immunohistochemical analysis showed that BKM120 inhibited mTOR activity, and the enhanced WNT/beta-catenin activity reversed the phenotype of inhibitory mTOR induced by BKM120.	NVP-BKM120	173-179	mechanistic target of rapamycin kinase	Homo sapiens	157-161	
26402468-5	2015	Buparlisib inhibited activation of Akt and signaling molecules downstream of mTORC1 (mTOR complex 1) in Ewing sarcoma, osteosarcoma, and rhabdomyosarcoma cell lines.	NVP-BKM120	0-10	mechanistic target of rapamycin kinase	Homo sapiens	77-81