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10.1136/esmoopen-2015-000023 http://scihub22266oqcxt.onion/10.1136/esmoopen-2015-000023 C5070277!5070277!27843590     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       ESMO+Open 2016 ; 1 (2): ä Nephropedia Template TP {{tp|p=27843590|t=2016. NTRK gene fusions as novel targets of cancer therapy across multiple tumour types |pdf=|usr=}}{{27843590}} gab.com Text NTRK gene fusions as novel targets of cancer therapy across multiple tumour types JO: ESMO Open http://www.kidney.de/pget.php?&tw=1&pmid=27843590 #FOAvip The tropomyosin receptor kinase (Trk) receptor family comprises 3 transmembrane proteins referred to as Trk A, B and C (TrkA, TrkB and TrkC) receptors that are encoded by the NTRK1, NTRK2 and NTRK3 genes, respectively. These receptor tyrosine kinases are expressed in human neuronal tissue and play an essential role in the physiology of development and function of the nervous system through activation by neurotrophins. Gene fusions involving NTRK genes lead to transcription of chimeric Trk proteins with constitutively activated or overexpressed kinase function conferring oncogenic potential. These genetic abnormalities have recently emerged as targets for cancer therapy, because novel compounds have been developed that are selective inhibitors of the constitutively active rearranged proteins. Developments in this field are being aided by next generation sequencing methods as tools for unbiased gene fusions discovery. In this article, we review the role of NTRK gene fusions across several tumour histologies, and the promises and challenges of targeting such genetic alterations for cancer therapy. Twit Text FOAVip NTRK gene fusions as novel targets of cancer therapy across multiple tumour types ????ESMO Open http://www.kidney.de/pget.php?&tw=1&pmid=27843590 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27843590 #FOAvip English Wikipedia <ref>{{Cite pmid|27843590}}</ref> NTRK gene fusions as novel targets of cancer therapy across multiple tumour types #MMPMID27843590 Amatu A; Sartore-Bianchi A; Siena S ESMO Open 2016[]; 1 (2): ä PMID27843590show ga The tropomyosin receptor kinase (Trk) receptor family comprises 3 transmembrane proteins referred to as Trk A, B and C (TrkA, TrkB and TrkC) receptors that are encoded by the NTRK1, NTRK2 and NTRK3 genes, respectively. These receptor tyrosine kinases are expressed in human neuronal tissue and play an essential role in the physiology of development and function of the nervous system through activation by neurotrophins. Gene fusions involving NTRK genes lead to transcription of chimeric Trk proteins with constitutively activated or overexpressed kinase function conferring oncogenic potential. These genetic abnormalities have recently emerged as targets for cancer therapy, because novel compounds have been developed that are selective inhibitors of the constitutively active rearranged proteins. Developments in this field are being aided by next generation sequencing methods as tools for unbiased gene fusions discovery. In this article, we review the role of NTRK gene fusions across several tumour histologies, and the promises and challenges of targeting such genetic alterations for cancer therapy. äNTRK gene fusions as novel targets of cancer therapy across multiple t(epmc).pdf DeepDyve Pubget Overpricing