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10.1016/j.phrs.2016.03.013 http://scihub22266oqcxt.onion/10.1016/j.phrs.2016.03.013 C4876767!4876767 !26995304     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26995304 &cmd=llinks): Failed to open stream: HTTP request failed! 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SRPK1 inhibition in prostate cancer: A novel anti-angiogenic treatment through modulation of VEGF alternative splicing |pdf=|usr=}}{{26995304 }} gab.com Text SRPK1 inhibition in prostate cancer: A novel anti-angiogenic treatment through modulation of VEGF alternative splicing JO: Pharmacol Res http://www.kidney.de/pget.php?&tw=1&pmid=26995304 #FOAvip Prostate cancer remains one of the leading causes of cancer death in men around the world, regardless of intense research and development of novel therapies in the last 10 years. One of the new avenues that has been tested - inhibition of angiogenesis - has been disappointing so far in clinical studies in spite of strong evidence that determinants of angiogenesis (e.g. vascular endothelial growth factor) are strongly associated with disease progression. One of the reasons for these outcomes may be our poor understanding of the biology of angiogenesis in prostate cancer (and probably other cancers as well) resulting in inhibition of both detrimental and favourable molecules. We discuss here novel targeted and more specific approaches to inhibit angiogenesis in prostate cancer as well as a completely new therapeutic modality to do this - modulation of alternative splicing - that may be applicable to other molecules/biological processes as well. Twit Text FOAVip SRPK1 inhibition in prostate cancer: A novel anti-angiogenic treatment through modulation of VEGF alternative splicing ????Pharmacol Res http://www.kidney.de/pget.php?&tw=1&pmid=26995304 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26995304 #FOAvip English Wikipedia <ref>{{Cite pmid|26995304 }}</ref> SRPK1 inhibition in prostate cancer: A novel anti-angiogenic treatment through modulation of VEGF alternative splicing #MMPMID26995304 Mavrou A ; Oltean S Pharmacol Res 2016[May]; 107 (ä): 276-281 PMID26995304 show ga Prostate cancer remains one of the leading causes of cancer death in men around the world, regardless of intense research and development of novel therapies in the last 10 years. One of the new avenues that has been tested - inhibition of angiogenesis - has been disappointing so far in clinical studies in spite of strong evidence that determinants of angiogenesis (e.g. vascular endothelial growth factor) are strongly associated with disease progression. One of the reasons for these outcomes may be our poor understanding of the biology of angiogenesis in prostate cancer (and probably other cancers as well) resulting in inhibition of both detrimental and favourable molecules. We discuss here novel targeted and more specific approaches to inhibit angiogenesis in prostate cancer as well as a completely new therapeutic modality to do this - modulation of alternative splicing - that may be applicable to other molecules/biological processes as well. |Alternative Splicing [MESH] |Angiogenesis Inhibitors/pharmacology/*therapeutic use [MESH] |Animals [MESH] |Humans [MESH] |Male [MESH] |Prostatic Neoplasms/*drug therapy/genetics/metabolism [MESH] |Protein Serine-Threonine Kinases/*antagonists & inhibitors [MESH]SRPK1 inhibition in prostate cancer: A novel anti-angiogenic treatment(epmc).pdf DeepDyve Pubget Overpricing