PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
31619257-0	2019	Phloretin attenuates STAT-3 activity and overcomes sorafenib resistance targeting SHP-1-mediated inhibition of STAT3 and Akt/VEGFR2 pathway in hepatocellular carcinoma.	Sorafenib	51-60	nuclear receptor subfamily 0 group B member 2	Homo sapiens	82-87	
25047655-10	2014	These results demonstrate that inactivation of RFX/SHP-1 induced by sustained sorafenib treatment confers sorafenib resistance to HCC through p-STAT3 up-regulation.	Sorafenib	78-87	nuclear receptor subfamily 0 group B member 2	Homo sapiens	51-56	
28077164-0	2017	Erratum to: Novel sorafenib analogues induce apoptosis through SHP-1 dependent STAT3 inactivation in human breast cancer cells.	Sorafenib	18-27	nuclear receptor subfamily 0 group B member 2	Homo sapiens	63-68	
29113744-0	2018	Corrigendum to "Blockade of STAT3 activation by sorafenib derivatives through enhancing SHP-1 phosphatase activity" [Eur.	Sorafenib	48-57	nuclear receptor subfamily 0 group B member 2	Homo sapiens	88-93	
26206949-0	2015	Sorafenib Action in Hepatitis B Virus X-Activated Oncogenic Androgen Pathway in Liver through SHP-1.	Sorafenib	0-9	nuclear receptor subfamily 0 group B member 2	Homo sapiens	94-99	
26206949-10	2015	Sorafenib markedly inhibited the HBx-enhanced AR activity through activating the SHP-1 phosphatase, which antagonized the activation of Akt/GSK3beta and c-Src by HBx.	Sorafenib	0-9	nuclear receptor subfamily 0 group B member 2	Homo sapiens	81-86	
26206949-11	2015	Moreover, SHP-1 protein level was much higher in the liver than in testis, which enabled sorafenib to inhibit aberrant AR activity in the HBx-expressing liver, while not affecting the physiological AR function in normal liver or testis.	Sorafenib	89-98	nuclear receptor subfamily 0 group B member 2	Homo sapiens	10-15	
25047655-10	2014	These results demonstrate that inactivation of RFX/SHP-1 induced by sustained sorafenib treatment confers sorafenib resistance to HCC through p-STAT3 up-regulation.	Sorafenib	106-115	nuclear receptor subfamily 0 group B member 2	Homo sapiens	51-56	
24418169-7	2014	Combination of sorafenib and YC-1 significantly inhibited the expression of p-STAT3 (Y705) (S727), p-ERK1/2, cyclin D1 and survivin and SHP-1 activity compared with sorafenib or YC-1 used alone in all tested HCC cell lines.	Sorafenib	15-24	nuclear receptor subfamily 0 group B member 2	Homo sapiens	136-141	
22180308-11	2012	In conclusion, dovitinib induces significant apoptosis in HCC cells and sorafenib-resistant cells via SHP-1-mediated inhibition of STAT3.	Sorafenib	72-81	nuclear receptor subfamily 0 group B member 2	Homo sapiens	102-107	
23392173-5	2013	Silencing of SHP-1 by small interference RNA (siRNA) reduced the effect of sorafenib on P-STAT3 and autophagy.	Sorafenib	75-84	nuclear receptor subfamily 0 group B member 2	Homo sapiens	13-18	
23392173-10	2013	Furthermore, our in vivo data showed that both sorafenib and SC-59 inhibited tumor growth, downregulated P-STAT3, enhanced the activity of SHP-1 and induced autophagy in PLC5 tumors, suggesting that sorafenib and SC-59 activate autophagy in HCC.	Sorafenib	47-56	nuclear receptor subfamily 0 group B member 2	Homo sapiens	139-144	
23392173-10	2013	Furthermore, our in vivo data showed that both sorafenib and SC-59 inhibited tumor growth, downregulated P-STAT3, enhanced the activity of SHP-1 and induced autophagy in PLC5 tumors, suggesting that sorafenib and SC-59 activate autophagy in HCC.	Sorafenib	199-208	nuclear receptor subfamily 0 group B member 2	Homo sapiens	139-144	
23392173-11	2013	In conclusion, sorafenib and SC-59 induce autophagy in HCC through a SHP-1-STAT3-Mcl-1-Beclin 1 pathway.	Sorafenib	15-24	nuclear receptor subfamily 0 group B member 2	Homo sapiens	69-74	
22978563-10	2013	CONCLUSIONS AND IMPLICATIONS: Sorafenib and its derivative SC-49 sensitize HCC cells to the antitumour effects of CS-1008 through SHP-1-dependent inactivation of STAT3.	Sorafenib	30-39	nuclear receptor subfamily 0 group B member 2	Homo sapiens	130-135