PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
29932973-10	2018	All of that provided possibility to overcome the intolerance of sorafenib by drug compatibility through protection against mitochondria damage, inhibition of anaerobic glycolysis and suppression of lipid synthesis based on PI3K/Akt/mTOR pathway.	Sorafenib	64-73	mechanistic target of rapamycin kinase	Mus musculus	232-236	
33675613-6	2021	In addition, the combination of sorafenib and SSRIs synergistically inhibited the effects of the AKT/mTOR pathway.	Sorafenib	32-41	mechanistic target of rapamycin kinase	Mus musculus	101-105	
32547320-13	2020	In conclusion, epalrestat heightens sorafenib"s anti-cancer effects via blocking the mTOR pathway, thus inducing cell cycle arrest, apoptosis, and autophagy.	Sorafenib	36-45	mechanistic target of rapamycin kinase	Mus musculus	85-89	
25952930-8	2015	Sorafenib and everolimus combination was effective in mTOR and ERM blockade; exerted synergistic effects on the inhibition of MPM cell proliferation; triggered ROS production and consequent AMPK-p38 mediated-apoptosis.	Sorafenib	0-9	mechanistic target of rapamycin kinase	Mus musculus	54-58	
28903416-9	2017	Using a mouse xenograft model we can show that a combination therapy with tocilizumab and low dosage of sorafenib suppresses 786-O tumor growth, reduces AKT-mTOR pathway and inhibits angiogenesis in vivo more efficient than sorafenib alone.	Sorafenib	104-113	mechanistic target of rapamycin kinase	Mus musculus	157-161	
25952930-10	2015	CONCLUSIONS: ERM and mTOR pathways are activated in MPM and "druggable" by a combination of sorafenib and everolimus.	Sorafenib	92-101	mechanistic target of rapamycin kinase	Mus musculus	21-25	
25953027-8	2015	RESULTS: Pharmacodynamic analysis revealed that a single dose of sorafenib decreased activation of the PI3K/AKT/mTOR signaling axis at doses of 30-60 mg/kg, but activated JAK/STAT3 signaling.	Sorafenib	65-74	mechanistic target of rapamycin kinase	Mus musculus	112-116	
25953027-16	2015	CONCLUSIONS: In summary, we provide insights into the molecular responses of sorafenib therapy in a clinically relevant model of prostate cancer and present preclinical evidence for the development of targeted treatment strategies based on the use of multikinase inhibitors in combination with mTOR inhibitors for the treatment of advanced prostate cancer.	Sorafenib	77-86	mechanistic target of rapamycin kinase	Mus musculus	294-298	
23434734-9	2013	RESULTS: After sorafenib treatment, mTORC1 signaling was reduced (downstream target P-S6), whereas mTORC2 was increased (phospho-mTOR Ser2481) in MNNG-HOS xenografts compared with vehicle-treated mice.	Sorafenib	15-24	mechanistic target of rapamycin kinase	Mus musculus	36-40	
23434734-13	2013	When sorafenib is combined with everolimus, its antitumor activity is increased by complete inhibition of the mTOR pathway in the preclinical setting.	Sorafenib	5-14	mechanistic target of rapamycin kinase	Mus musculus	110-114	
22753710-9	2012	Sorafenib and PI-103 as single agents differentially inhibited or activated key enzymes (MEK, ERK, AKT, mTOR, and S6K) in PI3K/AKT/mTOR and RAS/RAF/MAPK signaling pathways.	Sorafenib	0-9	mechanistic target of rapamycin kinase	Mus musculus	104-108	
22753710-9	2012	Sorafenib and PI-103 as single agents differentially inhibited or activated key enzymes (MEK, ERK, AKT, mTOR, and S6K) in PI3K/AKT/mTOR and RAS/RAF/MAPK signaling pathways.	Sorafenib	0-9	mechanistic target of rapamycin kinase	Mus musculus	131-135	
22753710-13	2012	CONCLUSION: The combination of PI-103 and sorafenib has the advantage over mono-drug therapy on inhibition of HCC cell proliferation and tumorigenesis by inhibiting both PI3K/AKT/mTOR and RAS/RAF/MAPK signaling pathways.	Sorafenib	42-51	mechanistic target of rapamycin kinase	Mus musculus	179-183