Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1038/nature15748 http://scihub22266oqcxt.onion/10.1038/nature15748 C4662610!4662610!26560033     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       Nature 2015 ; 527 (7579): 472-6 Nephropedia Template TP {{tp|p=26560033|t=2015. EMT is not required for lung metastasis but contributes to chemoresistance |pdf=|usr=}}{{26560033}} gab.com Text EMT is not required for lung metastasis but contributes to chemoresistance JO: Nature http://www.kidney.de/pget.php?&tw=1&pmid=26560033 #FOAvip The role of epithelial to mesenchymal transition (EMT) in metastasis is a longstanding source of controversy, largely due to an inability to monitor transient and reversible EMT phenotypes in vivo. We established an EMT lineage tracing system to monitor this process, using a mesenchymal-specific Cre-mediated fluorescent marker switch system in spontaneous breast-to-lung metastasis models. We confirmed that within a predominantly epithelial primary tumor, a small portion of tumor cells undergo EMT. Strikingly, lung metastases mainly consisted of non-EMT tumor cells maintaining their epithelial phenotype. Inhibiting EMT by overexpressing miR-200 did not impact lung metastasis development. However, EMT cells significantly contribute to recurrent lung metastasis formation after chemotherapy. These cells survived cyclophosphamide treatment due to reduced proliferation, apoptotic tolerance, and elevated expression of chemoresistance-related genes. Overexpression of miR-200 abrogated this resistance. This study suggests the potential of an EMT-targeting strategy, in conjunction with conventional chemotherapies, for breast cancer treatment. Twit Text FOAVip EMT is not required for lung metastasis but contributes to chemoresistance ????Nature http://www.kidney.de/pget.php?&tw=1&pmid=26560033 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26560033 #FOAvip English Wikipedia <ref>{{Cite pmid|26560033}}</ref> EMT is not required for lung metastasis but contributes to chemoresistance #MMPMID26560033 Fischer KR; Durrans A; Lee S; Sheng J; Li F; Wong S; Choi H; El Rayes T; Ryu S; Troeger J; Schwabe RF; Vahdat LT; Altorki NK; Mittal V; Gao D Nature 2015[Nov]; 527 (7579): 472-6 PMID26560033show ga The role of epithelial to mesenchymal transition (EMT) in metastasis is a longstanding source of controversy, largely due to an inability to monitor transient and reversible EMT phenotypes in vivo. We established an EMT lineage tracing system to monitor this process, using a mesenchymal-specific Cre-mediated fluorescent marker switch system in spontaneous breast-to-lung metastasis models. We confirmed that within a predominantly epithelial primary tumor, a small portion of tumor cells undergo EMT. Strikingly, lung metastases mainly consisted of non-EMT tumor cells maintaining their epithelial phenotype. Inhibiting EMT by overexpressing miR-200 did not impact lung metastasis development. However, EMT cells significantly contribute to recurrent lung metastasis formation after chemotherapy. These cells survived cyclophosphamide treatment due to reduced proliferation, apoptotic tolerance, and elevated expression of chemoresistance-related genes. Overexpression of miR-200 abrogated this resistance. This study suggests the potential of an EMT-targeting strategy, in conjunction with conventional chemotherapies, for breast cancer treatment. äEMT is not required for lung metastasis but contributes to chemoresist(epmc).pdf DeepDyve Pubget Overpricing