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10.1016/j.pharmthera.2016.01.006 http://scihub22266oqcxt.onion/10.1016/j.pharmthera.2016.01.006 C4779708!4779708!26808163     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Pharmacol+Ther 2016 ; 159 (ä): 83-92 Nephropedia Template TP {{tp|p=26808163|t=2016. Tumor cell vascular mimicry: Novel targeting opportunity in melanoma |pdf=|usr=}}{{26808163}} gab.com Text Tumor cell vascular mimicry: Novel targeting opportunity in melanoma JO: Pharmacol Ther http://www.kidney.de/pget.php?&tw=1&pmid=26808163 #FOAvip In 1999, the American Journal of Pathology published an article, entitled ?Vascular channel formation by human melanoma cells in vivo and in vitro: vasculogenic mimicry? by Maniotis and colleagues, which ignited a spirited debate for several years and earned the journal's distinction of a ?citation classic? (Maniotis et al., 1999). Tumor cell vasculogenic mimicry (VM), also known as vascular mimicry, describes the plasticity of aggressive cancer cells forming de novo vascular networks and is associated with the malignant phenotype and poor clinical outcome. The tumor cells capable of VM share the commonality of a stem cell-like, transendothelial phenotype, which may be induced by hypoxia. Since its introduction as a novel paradigm for melanoma tumor perfusion, many studies have contributed new findings illuminating the underlying molecular pathways supporting VM in a variety of tumors, including carcinomas, sarcomas, glioblastomas, astrocytomas, and melanomas. Of special significance is the lack of effectiveness of angiogenesis inhibitors on tumor cell VM, suggesting a selective resistance by this phenotype to conventional therapy. Facilitating the functional plasticity of tumor cell VM are key proteins associated with vascular, stem cell, extracellular matrix, and hypoxia-related signaling pathways -- each deserving serious consideration as potential therapeutic targets and diagnostic indicators of the aggressive, metastatic phenotype. This review highlights seminal findings pertinent to VM, including the effects of a novel, small molecular compound, CVM-1118, currently under clinical development to target VM, and illuminates important molecular pathways involved in the suppression of this plastic, aggressive phenotype, using melanoma as a model. Twit Text FOAVip Tumor cell vascular mimicry: Novel targeting opportunity in melanoma ????Pharmacol Ther http://www.kidney.de/pget.php?&tw=1&pmid=26808163 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26808163 #FOAvip English Wikipedia <ref>{{Cite pmid|26808163}}</ref> Tumor cell vascular mimicry: Novel targeting opportunity in melanoma #MMPMID26808163 Hendrix MJ; Seftor EA; Seftor RE; Chao JT; Chien DS; Chu YW Pharmacol Ther 2016[Mar]; 159 (ä): 83-92 PMID26808163show ga In 1999, the American Journal of Pathology published an article, entitled ?Vascular channel formation by human melanoma cells in vivo and in vitro: vasculogenic mimicry? by Maniotis and colleagues, which ignited a spirited debate for several years and earned the journal's distinction of a ?citation classic? (Maniotis et al., 1999). Tumor cell vasculogenic mimicry (VM), also known as vascular mimicry, describes the plasticity of aggressive cancer cells forming de novo vascular networks and is associated with the malignant phenotype and poor clinical outcome. The tumor cells capable of VM share the commonality of a stem cell-like, transendothelial phenotype, which may be induced by hypoxia. Since its introduction as a novel paradigm for melanoma tumor perfusion, many studies have contributed new findings illuminating the underlying molecular pathways supporting VM in a variety of tumors, including carcinomas, sarcomas, glioblastomas, astrocytomas, and melanomas. Of special significance is the lack of effectiveness of angiogenesis inhibitors on tumor cell VM, suggesting a selective resistance by this phenotype to conventional therapy. Facilitating the functional plasticity of tumor cell VM are key proteins associated with vascular, stem cell, extracellular matrix, and hypoxia-related signaling pathways -- each deserving serious consideration as potential therapeutic targets and diagnostic indicators of the aggressive, metastatic phenotype. This review highlights seminal findings pertinent to VM, including the effects of a novel, small molecular compound, CVM-1118, currently under clinical development to target VM, and illuminates important molecular pathways involved in the suppression of this plastic, aggressive phenotype, using melanoma as a model. äTumor cell vascular mimicry: Novel targeting opportunity in melanoma (epmc).pdf DeepDyve Pubget Overpricing