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000128362 1001_ $$0P:(DE-He78)8f33377073689940e88847161b6faa77$$aSonnet, Miriam$$b0$$eFirst author$$udkfz
000128362 245__ $$aEarly aberrant DNA methylation events in a mouse model of acute myeloid leukemia.
000128362 260__ $$aLondon$$bBioMed Central$$c2014
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000128362 520__ $$aAberrant DNA methylation is frequently found in human malignancies including acute myeloid leukemia (AML). While most studies focus on later disease stages, the onset of aberrant DNA methylation events and their dynamics during leukemic progression are largely unknown.We screened genome-wide for aberrant CpG island methylation in three disease stages of a murine AML model that is driven by hypomorphic expression of the hematopoietic transcription factor PU.1. DNA methylation levels of selected genes were correlated with methylation levels of CD34+ cells and lineage negative, CD127-, c-Kit+, Sca-1+ cells; common myeloid progenitors; granulocyte-macrophage progenitors; and megakaryocyte-erythroid progenitors.We identified 1,184 hypermethylated array probes covering 762 associated genes in the preleukemic stage. During disease progression, the number of hypermethylated genes increased to 5,465 in the late leukemic disease stage. Using publicly available data, we found a significant enrichment of PU.1 binding sites in the preleukemic hypermethylated genes, suggesting that shortage of PU.1 makes PU.1 binding sites in the DNA accessible for aberrant methylation. Many known AML associated genes such as RUNX1 and HIC1 were found among the preleukemic hypermethylated genes. Nine novel hypermethylated genes, FZD5, FZD8, PRDM16, ROBO3, CXCL14, BCOR, ITPKA, HES6 and TAL1, the latter four being potential PU.1 targets, were confirmed to be hypermethylated in human normal karyotype AML patients, underscoring the relevance of the mouse model for human AML.Our study identified early aberrantly methylated genes as potential contributors to onset and progression of AML.
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000128362 7001_ $$0P:(DE-HGF)0$$aClaus, Rainer$$b1
000128362 7001_ $$0P:(DE-He78)ecb33fb615e08035fdcefcaebfdff8f0$$aBecker, Natalia$$b2$$udkfz
000128362 7001_ $$0P:(DE-HGF)0$$aZucknick, Manuela$$b3
000128362 7001_ $$0P:(DE-He78)9afda71557b3adc9663688fc0d022080$$aPetersen, Jana$$b4$$udkfz
000128362 7001_ $$0P:(DE-He78)c403a040c97f91902a7d31b93859f9fc$$aLipka, Daniel$$b5$$udkfz
000128362 7001_ $$0P:(DE-HGF)0$$aOakes, Christopher C$$b6
000128362 7001_ $$aAndrulis, Mindaugas$$b7
000128362 7001_ $$0P:(DE-He78)f2177f299ad93efd161811e331914297$$aLier, Amelie$$b8$$udkfz
000128362 7001_ $$0P:(DE-He78)7b613cadb8c16ce178713e15b85d982c$$aMilsom, Michael$$b9$$udkfz
000128362 7001_ $$0P:(DE-HGF)0$$aWitte, Tania$$b10
000128362 7001_ $$0P:(DE-HGF)0$$aGu, Lei$$b11
000128362 7001_ $$0P:(DE-HGF)0$$aKim-Wanner, Soo-Zin$$b12
000128362 7001_ $$aSchirmacher, Peter$$b13
000128362 7001_ $$aWulfert, Michael$$b14
000128362 7001_ $$aGattermann, Norbert$$b15
000128362 7001_ $$aLübbert, Michael$$b16
000128362 7001_ $$aRosenbauer, Frank$$b17
000128362 7001_ $$aRehli, Michael$$b18
000128362 7001_ $$aBullinger, Lars$$b19
000128362 7001_ $$0P:(DE-He78)ff4024f7bc236e7897d9c18ee19c451f$$aWeichenhan, Dieter$$b20$$udkfz
000128362 7001_ $$0P:(DE-He78)4301875630bc997edf491c694ae1f8a9$$aPlass, Christoph$$b21$$eLast author$$udkfz
000128362 773__ $$0PERI:(DE-600)2484394-5$$a10.1186/gm551$$gVol. 6, no. 4, p. 34 -$$n4$$p34$$tGenome medicine$$v6$$x1756-994X$$y2014
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