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10.1158/1541-7786.MCR-14-0709 http://scihub22266oqcxt.onion/10.1158/1541-7786.MCR-14-0709 C4433420!4433420!25724428     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Mol+Cancer+Res 2015 ; 13 (5): 863-9 Nephropedia Template TP {{tp|p=25724428|t=2015. Detection of Tumor Suppressor Genes in Cancer Development by a Novel shRNA-based method |pdf=|usr=}}{{25724428}} gab.com Text Detection of Tumor Suppressor Genes in Cancer Development by a Novel shRNA-based method JO: Mol Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=25724428 #FOAvip Pancreatic cancer is one of the deadliest cancers with poor survival rates and limited therapeutic options. To improve the understanding of this disease's biology, a prerequisite for the generation of novel therapeutics, new platforms for rapid and efficient genetic and therapeutic screening are needed. Therefore, a combined in vitro/in vivo hybrid shRNA-assay was developed using isolated murine primary pancreatic ductal cells (PDCs), in which oncogenic KrasG12D could be activated in vitro by genomic recombination through 4OH-tamoxifen-induced nuclear translocation of Cre-ERT2 expressed under control of the ROSA26 promoter. Further genetic manipulation was achieved through selective and stable RNA interference (RNAi) against the tumor suppressors p16Ink4a (CDKN2A) or p53 (TP53) using lentiviral gene delivery. Treatment of PDCs with 4OH-tamoxifen increased phosphorylation of extracelluar signal-regulated kinase (ERK) downstream of KRAS, and subsequent lentiviral transduction resulted in sustained target gene repression. Double-mutant PDCs were then re-introduced into the pancreata of NOD-SCID-gamma (NSG) mice and monitored for tumor growth. Orthotopic implantation of PDCs carrying the activated KrasG12D-allele and shRNA against p16Ink4a or p53 resulted in tumor growth, metastasis and reduced survival of NSG mice. In contrast, KrasG12D alone was not sufficient to induce tumor growth. Implications: The combinatory in vitro/in vivo approach described in this study allows for rapid and efficient identification of genes involved in carcinogenesis and opens new avenues for the development of therapeutic strategies to improve cancer treatment. Twit Text FOAVip Detection of Tumor Suppressor Genes in Cancer Development by a Novel shRNA-based method ????Mol Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=25724428 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25724428 #FOAvip English Wikipedia <ref>{{Cite pmid|25724428}}</ref> Detection of Tumor Suppressor Genes in Cancer Development by a Novel shRNA-based method #MMPMID25724428 von Burstin J; Diersch S; Schneider G; Reichert M; Rustgi AK; Schmid RM Mol Cancer Res 2015[May]; 13 (5): 863-9 PMID25724428show ga Pancreatic cancer is one of the deadliest cancers with poor survival rates and limited therapeutic options. To improve the understanding of this disease's biology, a prerequisite for the generation of novel therapeutics, new platforms for rapid and efficient genetic and therapeutic screening are needed. Therefore, a combined in vitro/in vivo hybrid shRNA-assay was developed using isolated murine primary pancreatic ductal cells (PDCs), in which oncogenic KrasG12D could be activated in vitro by genomic recombination through 4OH-tamoxifen-induced nuclear translocation of Cre-ERT2 expressed under control of the ROSA26 promoter. Further genetic manipulation was achieved through selective and stable RNA interference (RNAi) against the tumor suppressors p16Ink4a (CDKN2A) or p53 (TP53) using lentiviral gene delivery. Treatment of PDCs with 4OH-tamoxifen increased phosphorylation of extracelluar signal-regulated kinase (ERK) downstream of KRAS, and subsequent lentiviral transduction resulted in sustained target gene repression. Double-mutant PDCs were then re-introduced into the pancreata of NOD-SCID-gamma (NSG) mice and monitored for tumor growth. Orthotopic implantation of PDCs carrying the activated KrasG12D-allele and shRNA against p16Ink4a or p53 resulted in tumor growth, metastasis and reduced survival of NSG mice. In contrast, KrasG12D alone was not sufficient to induce tumor growth. Implications: The combinatory in vitro/in vivo approach described in this study allows for rapid and efficient identification of genes involved in carcinogenesis and opens new avenues for the development of therapeutic strategies to improve cancer treatment. äDetection of Tumor Suppressor Genes in Cancer Development by a Novel s(epmc).pdf DeepDyve Pubget Overpricing