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10.1016/j.leukres.2016.07.002 http://scihub22266oqcxt.onion/10.1016/j.leukres.2016.07.002 C5266616!5266616!27486062     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27486062&cmd=llinks): Failed to open stream: HTTP request failed! 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TLE4 regulation of wnt-mediated inflammation underlies its role as a tumor suppressor in myeloid leukemia |pdf=|usr=}}{{27486062}} gab.com Text TLE4 regulation of wnt-mediated inflammation underlies its role as a tumor suppressor in myeloid leukemia JO: Leuk Res http://www.kidney.de/pget.php?&tw=1&pmid=27486062 #FOAvip The presence of AML1-ETO (RUNX1-CBF2T1), a fusion oncoprotein resulting from a t(8;21) chromosomal translocation, has been implicated as a necessary but insufficient event in the development of a subset of acute myeloid leukemias (AML). While AML1-ETO prolongs survival and inhibits differentiation of hematopoietic stem cells (HSC), other contributory events are needed for cell proliferation and leuke-mogenesis. We have postulated that specific tumor suppressor genes keep the leukemic potential of AML1-ETO in check. In studying del(9q), one of the most common concomitant chromosomal abnormalities with t(8;21), we identified the loss of an apparent tumor suppressor, TLE4, that appears to cooperate with AML1-ETO to confer a leukemic phenotype. This study sought to identify the molecular basis of this cooperation. We show that the loss of TLE4 confers proliferative advantage to leukemic cells, simultaneous with an upregulation of a pro-inflammatory signature mediated through aberrant increases in Wnt signaling activity. We further demonstrate that inhibition of cyclooxygenase (COX) activity partly reverses the pro-leukemic phenotype due to TLE4 knockdown, pointing towards a novel therapeutic approach for myeloid leukemia. Twit Text FOAVip TLE4 regulation of wnt-mediated inflammation underlies its role as a tumor suppressor in myeloid leukemia ????Leuk Res http://www.kidney.de/pget.php?&tw=1&pmid=27486062 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27486062 #FOAvip English Wikipedia <ref>{{Cite pmid|27486062}}</ref> TLE4 regulation of wnt-mediated inflammation underlies its role as a tumor suppressor in myeloid leukemia #MMPMID27486062 Shin TH; Brynczka C; Dayyani F; Rivera MN; Sweetser DA Leuk Res 2016[Sep]; 48 (ä): 46-56 PMID27486062show ga The presence of AML1-ETO (RUNX1-CBF2T1), a fusion oncoprotein resulting from a t(8;21) chromosomal translocation, has been implicated as a necessary but insufficient event in the development of a subset of acute myeloid leukemias (AML). While AML1-ETO prolongs survival and inhibits differentiation of hematopoietic stem cells (HSC), other contributory events are needed for cell proliferation and leuke-mogenesis. We have postulated that specific tumor suppressor genes keep the leukemic potential of AML1-ETO in check. In studying del(9q), one of the most common concomitant chromosomal abnormalities with t(8;21), we identified the loss of an apparent tumor suppressor, TLE4, that appears to cooperate with AML1-ETO to confer a leukemic phenotype. This study sought to identify the molecular basis of this cooperation. We show that the loss of TLE4 confers proliferative advantage to leukemic cells, simultaneous with an upregulation of a pro-inflammatory signature mediated through aberrant increases in Wnt signaling activity. We further demonstrate that inhibition of cyclooxygenase (COX) activity partly reverses the pro-leukemic phenotype due to TLE4 knockdown, pointing towards a novel therapeutic approach for myeloid leukemia. äTLE4 regulation of wnt-mediated inflammation underlies its role as a t(epmc).pdf DeepDyve Pubget Overpricing