PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
30154433-4	2018	In this study, we investigated the effect of SASP-related p16/IL6 axis on sorafenib resistance in HCC.	Sorafenib	74-83	cyclin dependent kinase inhibitor 2A	Homo sapiens	58-61	
30154433-0	2018	ID1-induced p16/IL6 axis activation contributes to the resistant of hepatocellular carcinoma cells to sorafenib.	Sorafenib	102-111	cyclin dependent kinase inhibitor 2A	Homo sapiens	12-15	
30154433-5	2018	Initially, we noticed that HCC cells with a high level of p16/IL6 axis exhibited a low sensitivity to sorafenib.	Sorafenib	102-111	cyclin dependent kinase inhibitor 2A	Homo sapiens	58-61	
30154433-8	2018	Moreover, SASP-related p16/IL6 axis contributed to the formation of acquired resistance in cells received long-term exposure to sorafenib.	Sorafenib	128-137	cyclin dependent kinase inhibitor 2A	Homo sapiens	23-26	
30154433-9	2018	In acquired sorafenib-resistant cells, ID1 low expression, p16/IL6 axis up-regulation, and AKT phosphorylation activation were observed.	Sorafenib	12-21	cyclin dependent kinase inhibitor 2A	Homo sapiens	59-62	
30154433-12	2018	Our study reveals that SASP-related p16/IL6 axis activation is responsible for sorafenib resistance, which will be a novel strategy to prevent the drug resistance.	Sorafenib	79-88	cyclin dependent kinase inhibitor 2A	Homo sapiens	36-39	
23724131-12	2013	KRAS transfection of urothelial carcinoma cells led to upregulation of p16(INK4a) and uPA accompanied by loss of E-cadherin that could be inhibited by application of the kinase-inhibitor Sorafenib.	Sorafenib	187-196	cyclin dependent kinase inhibitor 2A	Homo sapiens	71-74	
25862847-20	2015	On the contrary, p16-positive CERV196 showed increased susceptibility to sorafenib and sunitinib concerning suppression of AREG expression.	Sorafenib	73-82	cyclin dependent kinase inhibitor 2A	Homo sapiens	17-20	
23724131-12	2013	KRAS transfection of urothelial carcinoma cells led to upregulation of p16(INK4a) and uPA accompanied by loss of E-cadherin that could be inhibited by application of the kinase-inhibitor Sorafenib.	Sorafenib	187-196	cyclin dependent kinase inhibitor 2A	Homo sapiens	75-80	
23724131-13	2013	CONCLUSIONS: Our results show that overexpression of p16(INK4a) in UCIS is neither associated with HPV infection nor p16(INK4a) gene amplification but is a consequence of enhanced RAS/MAPK signalling that promotes EMT, possibly due to Sorafenib-sensitive paracrine secretion of the EMT activator uPA.	Sorafenib	235-244	cyclin dependent kinase inhibitor 2A	Homo sapiens	53-56	
23724131-13	2013	CONCLUSIONS: Our results show that overexpression of p16(INK4a) in UCIS is neither associated with HPV infection nor p16(INK4a) gene amplification but is a consequence of enhanced RAS/MAPK signalling that promotes EMT, possibly due to Sorafenib-sensitive paracrine secretion of the EMT activator uPA.	Sorafenib	235-244	cyclin dependent kinase inhibitor 2A	Homo sapiens	57-62