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10.18632/oncotarget.13226 http://scihub22266oqcxt.onion/10.18632/oncotarget.13226 C5347669!5347669!27835901     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Oncotarget 2016 ; 7 (50): 81995-2012 Nephropedia Template TP {{tp|p=27835901|t=2016. Mutational activation of BRAF confers sensitivity to transforming growth factor beta inhibitors in human cancer cells |pdf=|usr=}}{{27835901}} gab.com Text Mutational activation of BRAF confers sensitivity to transforming growth factor beta inhibitors in human cancer cells JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27835901 #FOAvip Recent data implicate elevated transforming growth factor-? (TGF?) signalling in BRAF inhibitor drug-resistance mechanisms, but the potential for targeting TGF? signalling in cases of advanced melanoma has not been investigated. We show that mutant BRAFV600E confers an intrinsic dependence on TGF?/TGF? receptor 1 (TGFBR1) signalling for clonogenicity of murine melanocytes. Pharmacological inhibition of the TGFBR1 blocked the clonogenicity of human mutant BRAF melanoma cells through SMAD4-independent inhibition of mitosis, and also inhibited metastasis in xenografted zebrafish. When investigating the therapeutic potential of combining inhibitors of mutant BRAF and TGFBR1, we noted that unexpectedly, low-dose PLX-4720 (a vemurafenib analogue) promoted proliferation of drug-naïve melanoma cells. Pharmacological or pharmacogenetic inhibition of TGFBR1 blocked growth promotion and phosphorylation of SRC, which is frequently associated with vemurafenib-resistance mechanisms. Importantly, vemurafenib-resistant patient derived cells retained sensitivity to TGFBR1 inhibition, suggesting that TGFBR1 could be targeted therapeutically to combat the development of vemurafenib drug-resistance. Twit Text FOAVip Mutational activation of BRAF confers sensitivity to transforming growth factor beta inhibitors in human cancer cells ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27835901 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27835901 #FOAvip English Wikipedia <ref>{{Cite pmid|27835901}}</ref> Mutational activation of BRAF confers sensitivity to transforming growth factor beta inhibitors in human cancer cells #MMPMID27835901 Spender LC; Ferguson GJ; Liu S; Cui C; Girotti MR; Sibbet G; Higgs EB; Shuttleworth MK; Hamilton T; Lorigan P; Weller M; Vincent DF; Sansom OJ; Frame M; Dijke Pt; Marais R; Inman GJ Oncotarget 2016[Dec]; 7 (50): 81995-2012 PMID27835901show ga Recent data implicate elevated transforming growth factor-? (TGF?) signalling in BRAF inhibitor drug-resistance mechanisms, but the potential for targeting TGF? signalling in cases of advanced melanoma has not been investigated. We show that mutant BRAFV600E confers an intrinsic dependence on TGF?/TGF? receptor 1 (TGFBR1) signalling for clonogenicity of murine melanocytes. Pharmacological inhibition of the TGFBR1 blocked the clonogenicity of human mutant BRAF melanoma cells through SMAD4-independent inhibition of mitosis, and also inhibited metastasis in xenografted zebrafish. When investigating the therapeutic potential of combining inhibitors of mutant BRAF and TGFBR1, we noted that unexpectedly, low-dose PLX-4720 (a vemurafenib analogue) promoted proliferation of drug-naïve melanoma cells. Pharmacological or pharmacogenetic inhibition of TGFBR1 blocked growth promotion and phosphorylation of SRC, which is frequently associated with vemurafenib-resistance mechanisms. Importantly, vemurafenib-resistant patient derived cells retained sensitivity to TGFBR1 inhibition, suggesting that TGFBR1 could be targeted therapeutically to combat the development of vemurafenib drug-resistance. äMutational activation of BRAF confers sensitivity to transforming grow(epmc).pdf DeepDyve Pubget Overpricing