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10.1126/scitranslmed.aaa5731 http://scihub22266oqcxt.onion/10.1126/scitranslmed.aaa5731 C4644635!4644635!26062848     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       Sci+Transl+Med 2015 ; 7 (291): 291ra96 Nephropedia Template TP {{tp|p=26062848|t=2015. Integration of Hedgehog and mutant FLT3 signaling in myeloid leukemia |pdf=|usr=}}{{26062848}} gab.com Text Integration of Hedgehog and mutant FLT3 signaling in myeloid leukemia JO: Sci Transl Med http://www.kidney.de/pget.php?&tw=1&pmid=26062848 #FOAvip FLT3 internal tandem duplication (ITD) mutations resulting in constitutive kinase activity are common in acute myeloid leukemia (AML) and carry a poor prognosis. Several agents targeting FLT3 have been developed, but their limited clinical activity suggests that the inhibition of other factors contributing to the malignant phenotype is required. We examined gene expression data sets as well as primary specimens and found that the expression of GLI2, a major effector of the Hedgehog (Hh) signaling pathway, was increased in FLT3-ITD compared to wild type FLT3 AML. To examine the functional role of the Hh pathway, we studied mice in which Flt3-ITD expression results in an indolent myeloproliferative state and found that constitutive Hh signaling accelerated the development of AML by enhancing STAT5 signaling and the proliferation of bone marrow myeloid progenitors. Furthermore, combined FLT3 and Hh pathway inhibition limited leukemic growth in vitro and in vivo, and this approach may serve as a therapeutic strategy for FLT3-ITD AML. Twit Text FOAVip Integration of Hedgehog and mutant FLT3 signaling in myeloid leukemia ????Sci Transl Med http://www.kidney.de/pget.php?&tw=1&pmid=26062848 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26062848 #FOAvip English Wikipedia <ref>{{Cite pmid|26062848}}</ref> Integration of Hedgehog and mutant FLT3 signaling in myeloid leukemia #MMPMID26062848 Lim Y; Gondek L; Li L; Wang Q; Ma H; Chang E; Huso DL; Foerster S; Marchionni L; McGovern K; Watkins DN; Peacock CD; Levis M; Smith BD; Merchant AA; Small D; Matsui W Sci Transl Med 2015[Jun]; 7 (291): 291ra96 PMID26062848show ga FLT3 internal tandem duplication (ITD) mutations resulting in constitutive kinase activity are common in acute myeloid leukemia (AML) and carry a poor prognosis. Several agents targeting FLT3 have been developed, but their limited clinical activity suggests that the inhibition of other factors contributing to the malignant phenotype is required. We examined gene expression data sets as well as primary specimens and found that the expression of GLI2, a major effector of the Hedgehog (Hh) signaling pathway, was increased in FLT3-ITD compared to wild type FLT3 AML. To examine the functional role of the Hh pathway, we studied mice in which Flt3-ITD expression results in an indolent myeloproliferative state and found that constitutive Hh signaling accelerated the development of AML by enhancing STAT5 signaling and the proliferation of bone marrow myeloid progenitors. Furthermore, combined FLT3 and Hh pathway inhibition limited leukemic growth in vitro and in vivo, and this approach may serve as a therapeutic strategy for FLT3-ITD AML. äIntegration of Hedgehog and mutant FLT3 signaling in myeloid leukemia (epmc).pdf DeepDyve Pubget Overpricing