PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
18787411-3	2008	Low doses of sorafenib and vorinostat, but not the individual agents, caused an acidic sphingomyelinase and fumonisin B1-dependent increase in CD95 surface levels and CD95 association with caspase 8.	Sorafenib	13-22	caspase 8	Homo sapiens	189-198	
22843888-5	2012	Moreover, pre-treatment of Caki-1 (wild-type VHL) and 786-O (mutant VHL) with HDACIs followed by sorafenib reduced cell viability synergistically via activation of caspases and downregulation of the levels of myeloid leukemia cell differentiation protein (MCL1), phospho-extracellular signal-regulated kinase (ERK), and secreted vascular endothelial growth factor (VEGF).	Sorafenib	97-106	caspase 8	Homo sapiens	164-172	
18787411-11	2008	Thus sorafenib and vorinostat promote ceramide-dependent CD95 activation followed by induction of multiple downstream survival regulatory signals: ceramide-CD95-PERK-FADD-pro-caspase 8 (death); ceramide-CD95-PERK-eIF2alpha- downward arrowc-FLIP-s (death); ceramide-CD95-PERK-ATG5-autophagy (survival).	Sorafenib	5-14	caspase 8	Homo sapiens	175-184	
18765530-7	2008	Sorafenib and vorinostat treatment increased surface levels of CD95 and CD95 association with caspase-8.	Sorafenib	0-9	caspase 8	Homo sapiens	94-103	
29431086-5	2016	Sorafenib reduces S-nitrosation of cell death receptors and caspase-3, triggering a switch to caspase-3 from caspase-8.	Sorafenib	0-9	caspase 8	Homo sapiens	109-118	
26662956-0	2016	Synergistic effect of fisetin combined with sorafenib in human cervical cancer HeLa cells through activation of death receptor-5 mediated caspase-8/caspase-3 and the mitochondria-dependent apoptotic pathway.	Sorafenib	44-53	caspase 8	Homo sapiens	138-147	
26662956-7	2016	Our study showed that the combination of fisetin and sorafenib exerted better synergistic effects in vitro and in vivo than either agent used alone against human cervical cancer, and this synergism was based on apoptotic potential through a mitochondrial- and DR5-dependent caspase-8/caspase-3 signaling pathway.	Sorafenib	53-62	caspase 8	Homo sapiens	274-283	
17909059-4	2007	Sorafenib/TRAIL-induced cell death was accompanied by mitochondrial injury and release of cytochrome c, Smac, and AIF into the cytosol and caspase-9, caspase-3, caspase-7, and caspase-8 activation.	Sorafenib	0-9	caspase 8	Homo sapiens	176-185	
17909059-7	2007	Similarly, inhibition of the receptor-mediated apoptotic cascade with a caspase-8 dominant-negative mutant significantly blocked sorafenib/TRAIL-induced lethality but not Mcl-1 down-regulation or Bak/Bax conformational change, indicating that TRAIL-mediated receptor pathway activation is required for maximal lethality.	Sorafenib	129-138	caspase 8	Homo sapiens	72-81	
30066934-12	2018	The knockdown of cFLIP reversed the acquired sorafenib resistance by activating caspase-8 and inhibiting activated ERS in the sorafenib-resistant HCC cells.	Sorafenib	45-54	caspase 8	Homo sapiens	80-89	
28154184-6	2017	More intriguingly, we find that it is sorafenib-induced ROS accumulation that enables TRAIL to activate caspase-8 in RCC.	Sorafenib	38-47	caspase 8	Homo sapiens	104-113	
25687050-6	2015	Furthermore, sorafenib treatment resulted in the obvious increase of the Caspase-3 and Caspase-8 protein and mRNA expressions, and down-regulated the MCL-1 protein and mRNA expressions in NB4 cells.	Sorafenib	13-22	caspase 8	Homo sapiens	87-96	
25687050-7	2015	CONCLUSION: Sorafenib can inhibit proliferation and induce apopotosis of human acute promyelocytic leukemia cell NB4 through the expression of Caspase-3 and Caspase-8, and down-regulation of the expression of MCL-1.	Sorafenib	12-21	caspase 8	Homo sapiens	157-166	
24195809-6	2013	Subsequently, the expression of proteins relating to TLR3 signaling pathway, such as NF-kappaB, caspase 8 survivin, bcl-2 and PCNA affected by BM-06, sorafenib alone or in combination, was compared.	Sorafenib	150-159	caspase 8	Homo sapiens	96-105	
25738310-11	2015	Sorafenib and irinotecan sequential treatment significantly increased the levels of cleaved caspase-8, -3, and PARP in HepG2 cells.	Sorafenib	0-9	caspase 8	Homo sapiens	92-101