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10.1371/journal.pbio.1002537 http://scihub22266oqcxt.onion/10.1371/journal.pbio.1002537 C5008749!5008749!27584724     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       PLoS+Biol 2016 ; 14 (9): ä Nephropedia Template TP {{tp|p=27584724|t=2016. Epithelial Tumors Originate in Tumor Hotspots, a Tissue-Intrinsic Microenvironment |pdf=|usr=}}{{27584724}} gab.com Text Epithelial Tumors Originate in Tumor Hotspots, a Tissue-Intrinsic Microenvironment JO: PLoS Biol http://www.kidney.de/pget.php?&tw=1&pmid=27584724 #FOAvip Malignant tumors are caused by uncontrolled proliferation of transformed mutant cells that have lost the ability to maintain tissue integrity. Although a number of causative genetic backgrounds for tumor development have been discovered, the initial steps mutant cells take to escape tissue integrity and trigger tumorigenesis remain elusive. Here, we show through analysis of conserved neoplastic tumor-suppressor genes (nTSGs) in Drosophila wing imaginal disc epithelia that tumor initiation depends on tissue-intrinsic local cytoarchitectures, causing tumors to consistently originate in a specific region of the tissue. In this ?tumor hotspot? where cells constitute a network of robust structures on their basal side, nTSG-deficient cells delaminate from the apical side of the epithelium and begin tumorigenic overgrowth by exploiting endogenous Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling activity. Conversely, in other regions, the ?tumor coldspot? nTSG-deficient cells are extruded toward the basal side and undergo apoptosis. When the direction of delamination is reversed through suppression of RhoGEF2, an activator of the Rho family small GTPases, and JAK/STAT is activated ectopically in these coldspot nTSG-deficient cells, tumorigenesis is induced. These data indicate that two independent processes, apical delamination and JAK/STAT activation, are concurrently required for the initiation of nTSG-deficient-induced tumorigenesis. Given the conservation of the epithelial cytoarchitecture, tumorigenesis may be generally initiated from tumor hotspots by a similar mechanism. Twit Text FOAVip Epithelial Tumors Originate in Tumor Hotspots, a Tissue-Intrinsic Microenvironment ????PLoS Biol http://www.kidney.de/pget.php?&tw=1&pmid=27584724 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27584724 #FOAvip English Wikipedia <ref>{{Cite pmid|27584724}}</ref> Epithelial Tumors Originate in Tumor Hotspots, a Tissue-Intrinsic Microenvironment #MMPMID27584724 Tamori Y; Suzuki E; Deng WM PLoS Biol 2016[Sep]; 14 (9): ä PMID27584724show ga Malignant tumors are caused by uncontrolled proliferation of transformed mutant cells that have lost the ability to maintain tissue integrity. Although a number of causative genetic backgrounds for tumor development have been discovered, the initial steps mutant cells take to escape tissue integrity and trigger tumorigenesis remain elusive. Here, we show through analysis of conserved neoplastic tumor-suppressor genes (nTSGs) in Drosophila wing imaginal disc epithelia that tumor initiation depends on tissue-intrinsic local cytoarchitectures, causing tumors to consistently originate in a specific region of the tissue. In this ?tumor hotspot? where cells constitute a network of robust structures on their basal side, nTSG-deficient cells delaminate from the apical side of the epithelium and begin tumorigenic overgrowth by exploiting endogenous Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling activity. Conversely, in other regions, the ?tumor coldspot? nTSG-deficient cells are extruded toward the basal side and undergo apoptosis. When the direction of delamination is reversed through suppression of RhoGEF2, an activator of the Rho family small GTPases, and JAK/STAT is activated ectopically in these coldspot nTSG-deficient cells, tumorigenesis is induced. These data indicate that two independent processes, apical delamination and JAK/STAT activation, are concurrently required for the initiation of nTSG-deficient-induced tumorigenesis. Given the conservation of the epithelial cytoarchitecture, tumorigenesis may be generally initiated from tumor hotspots by a similar mechanism. äEpithelial Tumors Originate in Tumor Hotspots, a Tissue-Intrinsic Micr(epmc).pdf DeepDyve Pubget Overpricing