PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 27178121-11 2016 Dual inhibition of Ras signaling via Ral and Raf, using a combination of small-molecule inhibitor RBC8 and sorafenib, reduced the proliferation of HCC cells in culture and completely inhibited their growth as xenograft tumors in nude mice. Sorafenib 107-116 zinc fingers and homeoboxes 2 Mus musculus 45-48 29196297-5 2018 The cytotoxicity of sorafenib and aspirin was blocked by inhibition of the AMPK or ERK pathways through shRNA or via pharmacologic inhibitors of RAF (LY3009120), MEK (trametinib), or AMPK (compound C). Sorafenib 20-29 zinc fingers and homeoboxes 2 Mus musculus 145-148 29196297-7 2018 In vivo treatment of human xenografts in NSG mice with sorafenib and aspirin significantly reduced tumor volume compared with each single-agent treatment.Conclusions: Combination sorafenib and aspirin exerts cytotoxicity against RAS/RAF-mutant cells by simultaneously affecting two independent pathways and represents a promising novel strategy for the treatment of RAS-mutant cancers. Sorafenib 55-64 zinc fingers and homeoboxes 2 Mus musculus 233-236 29196297-7 2018 In vivo treatment of human xenografts in NSG mice with sorafenib and aspirin significantly reduced tumor volume compared with each single-agent treatment.Conclusions: Combination sorafenib and aspirin exerts cytotoxicity against RAS/RAF-mutant cells by simultaneously affecting two independent pathways and represents a promising novel strategy for the treatment of RAS-mutant cancers. Sorafenib 179-188 zinc fingers and homeoboxes 2 Mus musculus 233-236 29463989-3 2018 However, incomplete inhibition of RAF activity by sorafenib may also induce paradoxical activation of the mitogen-activated protein kinase (MAPK) pathway in malignant cells. Sorafenib 50-59 zinc fingers and homeoboxes 2 Mus musculus 34-37 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 zinc fingers and homeoboxes 2 Mus musculus 144-147 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 zinc fingers and homeoboxes 2 Mus musculus 192-195 20201822-5 2010 Recently, we have reported that the multi-kinase and potent Raf inhibitor sorafenib reversed memory impairment and reduced the expression of APP, Cox-2, and iNOS in the brain of the transgenic mouse model of AD, APPswe. Sorafenib 74-83 zinc fingers and homeoboxes 2 Mus musculus 60-63 15171791-13 2004 In contrast, the Raf inhibitor BAY 43-9006 did not influence adenoma formation in vivo. Sorafenib 31-42 zinc fingers and homeoboxes 2 Mus musculus 17-20 22941213-3 2013 We demonstrate that the growth of the NIH 3T3/Mdr cell line was affected in a dose-dependent manner more significantly by the pan-Raf inhibitor sorafenib than by the selective mutant B-Raf inhibitor PLX4720. Sorafenib 144-153 zinc fingers and homeoboxes 2 Mus musculus 130-133 22960170-7 2012 Sorafenib, whose targets include not only PDGFRA but also the Src downstream target Raf, was effective at inhibiting mouse and human tumor cell growth and halted progression of mouse aRMS tumors in vivo. Sorafenib 0-9 zinc fingers and homeoboxes 2 Mus musculus 84-87 21593445-13 2011 Sorafenib, a therapeutic agent targeting Raf kinases, decreases CXCL8 expression in melanoma cells through reexpression of TTP. Sorafenib 0-9 zinc fingers and homeoboxes 2 Mus musculus 41-44