PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
29251327-5	2018	Significantly decreased AKT Ser473 phosphorylation in HCC cells, and conversely enhanced phosphorylation of AKT Ser473 and mTORC2 in CCC cells, were observed with sorafenib treatment.	Sorafenib	163-172	CREB regulated transcription coactivator 2	Mus musculus	123-129	
33051131-0	2020	Torin2 overcomes sorafenib resistance via suppressing mTORC2-AKT-BAD pathway in hepatocellular carcinoma cells.	Sorafenib	17-26	CREB regulated transcription coactivator 2	Mus musculus	54-60	
33051131-9	2020	Torin2 successfully suppressed the sorafenib-activated mTORC2-AKT axis, leading to the dephosphorylation of Ser136 in BAD protein, and increased the expression of total BAD, which contributed to the apoptosis in sorafenib-resistant HCC cells.	Sorafenib	35-44	CREB regulated transcription coactivator 2	Mus musculus	55-61	
33051131-10	2020	CONCLUSIONS: In this study, Torin2 and sorafenib showed synergistic cytostatic capacity in sorafenib-resistant HCC cells, via the suppression of mTORC2-AKT-BAD pathway.	Sorafenib	39-48	CREB regulated transcription coactivator 2	Mus musculus	145-151	
33051131-10	2020	CONCLUSIONS: In this study, Torin2 and sorafenib showed synergistic cytostatic capacity in sorafenib-resistant HCC cells, via the suppression of mTORC2-AKT-BAD pathway.	Sorafenib	91-100	CREB regulated transcription coactivator 2	Mus musculus	145-151	
29251327-8	2018	Simultaneous administration of everolimus to suppress activated mTORC1 in RBE cells revealed that combined everolimus and sorafenib treatment under mTORC2 disassembly could enhance growth inhibition through the suppression of both sorafenib- and everolimus-dependent AKT Ser473 phosphorylation in addition to the inhibition of mTORC1 phosphorylation.	Sorafenib	122-131	CREB regulated transcription coactivator 2	Mus musculus	148-154	
29251327-8	2018	Simultaneous administration of everolimus to suppress activated mTORC1 in RBE cells revealed that combined everolimus and sorafenib treatment under mTORC2 disassembly could enhance growth inhibition through the suppression of both sorafenib- and everolimus-dependent AKT Ser473 phosphorylation in addition to the inhibition of mTORC1 phosphorylation.	Sorafenib	231-240	CREB regulated transcription coactivator 2	Mus musculus	148-154	
29251327-9	2018	Prevention of escape by AKT/mTOR signaling from the RAF/MEK/ERK pathway in sorafenib treatment by suppressing mTORC2 activity may lead to promising new approaches in CCC therapy.	Sorafenib	75-84	CREB regulated transcription coactivator 2	Mus musculus	110-116	
27959383-4	2017	Sorafenib effectively reversed the activation status of mTORC2 induced by metformin and enhanced the suppression of the mTORC1 and MAPK pathway by metformin in HCC cells, which may be responsible for reduced proliferation upon combined treatment.	Sorafenib	0-9	CREB regulated transcription coactivator 2	Mus musculus	56-62	
27959383-5	2017	The metformin and sorafenib combination led to increased impaired proliferation and tumor inhibition of HCC in vitro and in vivo compared to single agent, which was partially bridged by disrupting the mTORC1/mTORC2 feedback loop.	Sorafenib	18-27	CREB regulated transcription coactivator 2	Mus musculus	208-214	
23434734-0	2013	The Combination of Sorafenib and Everolimus Abrogates mTORC1 and mTORC2 upregulation in osteosarcoma preclinical models.	Sorafenib	19-28	CREB regulated transcription coactivator 2	Mus musculus	65-71	
23434734-10	2013	Combining sorafenib with everolimus resulted in complete abrogation of both mTORC1 [through ROS-mediated AMP-activated kinase (AMPK) activation] and mTORC2 (through complex disassembly).	Sorafenib	10-19	CREB regulated transcription coactivator 2	Mus musculus	149-155	
23434734-12	2013	CONCLUSION: mTORC2 activation is an escape mechanism from sorafenib treatment.	Sorafenib	58-67	CREB regulated transcription coactivator 2	Mus musculus	12-18