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10.1038/ncomms6662 http://scihub22266oqcxt.onion/10.1038/ncomms6662 C4261930!4261930 !25489927     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\25489927 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Nat+Commun 2014 ; 5 (ä): 5662 Nephropedia Template TP {{tp|p=25489927 |t=2014. Resolving cancer-stroma interfacial signalling and interventions with micropatterned tumour-stromal assays |pdf=|usr=}}{{25489927 }} gab.com Text Resolving cancer-stroma interfacial signalling and interventions with micropatterned tumour-stromal assays JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=25489927 #FOAvip Tumour-stromal interactions are a determining factor in cancer progression. In vivo, the interaction interface is associated with spatially resolved distributions of cancer and stromal phenotypes. Here, we establish a micropatterned tumour-stromal assay (?TSA) with laser capture microdissection to control the location of co-cultured cells and analyse bulk and interfacial tumour-stromal signalling in driving cancer progression. ?TSA reveals a spatial distribution of phenotypes in concordance with human oestrogen receptor-positive (ER+) breast cancer samples, and heterogeneous drug activity relative to the tumour-stroma interface. Specifically, an unknown mechanism of reversine is shown in targeting tumour-stromal interfacial interactions using ER+ MCF-7 breast cancer and bone marrow-derived stromal cells. Reversine suppresses MCF-7 tumour growth and bone metastasis in vivo by reducing tumour stromalization including collagen deposition and recruitment of activated stromal cells. This study advocates ?TSA as a platform for studying tumour microenvironmental interactions and cancer field effects with applications in drug discovery and development. Twit Text FOAVip Resolving cancer-stroma interfacial signalling and interventions with micropatterned tumour-stromal assays ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=25489927 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25489927 #FOAvip English Wikipedia <ref>{{Cite pmid|25489927 }}</ref> Resolving cancer-stroma interfacial signalling and interventions with micropatterned tumour-stromal assays #MMPMID25489927 Shen K ; Luk S ; Hicks DF ; Elman JS ; Bohr S ; Iwamoto Y ; Murray R ; Pena K ; Wang F ; Seker E ; Weissleder R ; Yarmush ML ; Toner M ; Sgroi D ; Parekkadan B Nat Commun 2014[Dec]; 5 (ä): 5662 PMID25489927 show ga Tumour-stromal interactions are a determining factor in cancer progression. In vivo, the interaction interface is associated with spatially resolved distributions of cancer and stromal phenotypes. Here, we establish a micropatterned tumour-stromal assay (?TSA) with laser capture microdissection to control the location of co-cultured cells and analyse bulk and interfacial tumour-stromal signalling in driving cancer progression. ?TSA reveals a spatial distribution of phenotypes in concordance with human oestrogen receptor-positive (ER+) breast cancer samples, and heterogeneous drug activity relative to the tumour-stroma interface. Specifically, an unknown mechanism of reversine is shown in targeting tumour-stromal interfacial interactions using ER+ MCF-7 breast cancer and bone marrow-derived stromal cells. Reversine suppresses MCF-7 tumour growth and bone metastasis in vivo by reducing tumour stromalization including collagen deposition and recruitment of activated stromal cells. This study advocates ?TSA as a platform for studying tumour microenvironmental interactions and cancer field effects with applications in drug discovery and development. |*Gene Expression Regulation, Neoplastic [MESH] |Animals [MESH] |Bone Marrow Cells/metabolism [MESH] |Bone Neoplasms/pathology [MESH] |Breast Neoplasms/*pathology [MESH] |Cell Line, Tumor [MESH] |Collagen/metabolism [MESH] |Disease Progression [MESH] |Female [MESH] |Fibroblasts/metabolism [MESH] |Gene Expression Profiling [MESH] |Green Fluorescent Proteins/metabolism [MESH] |Humans [MESH] |Ki-67 Antigen/metabolism [MESH] |Mammary Neoplasms, Experimental/pathology [MESH] |Mice [MESH] |Mice, Inbred NOD [MESH] |Mice, SCID [MESH] |Microcirculation [MESH] |Morpholines/chemistry [MESH] |Neoplasm Metastasis [MESH] |Neoplasm Transplantation [MESH] |Phenotype [MESH] |Purines/chemistry [MESH] |Signal Transduction [MESH]Resolving cancer-stroma interfacial signalling and interventions with (epmc).pdf DeepDyve Pubget Overpricing