<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Li J</submitter><funding>American Cancer Society</funding><funding>NHLBI NIH HHS</funding><funding>NCI NIH HHS</funding><funding>Welch Foundation</funding><funding>National Institutes of Health</funding><funding>Cancer Prevention and Research Institute of Texas</funding><funding>NIGMS NIH HHS</funding><pagination>81</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9241241</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>14(1)</volume><pubmed_abstract>Epigenetic abnormalities in DNA hydroxymethylation (5hmC) have been detected in patients with myeloid neoplasms, suggesting that 5hmC might act as a valuable epigenetic mark to reflect the disease status of myeloid neoplasms. Here, we report systematic genome-wide mapping of the DNA hydroxymethylomes in over 70 patients with myeloid neoplasms. Our integrative analysis leads to the identification of distinct 5hmC signatures that can sensitively discriminate patients from healthy individuals. At the molecular level, we unveiled dynamic 5hmC changes within key transcription factor (e.g., the CEBP family) binding motifs that are essential for hematopoiesis and myeloid lineage specification. 5hmC redistribution was found to alter the genome-wide binding of CEBP-α, thereby reprogramming transcri</pubmed_abstract><journal>Clinical epigenetics</journal><pubmed_title>Aberrant DNA hydroxymethylation reshapes transcription factor binding in myeloid neoplasms.</pubmed_title><pmcid>PMC9241241</pmcid><funding_grant_id>CA016672</funding_grant_id><funding_grant_id>R01HL134780</funding_grant_id><funding_grant_id>RSG-18-043-01-LIB</funding_grant_id><funding_grant_id>R01CA232017</funding_grant_id><funding_grant_id>R21 GM138824</funding_grant_id><funding_grant_id>R01 CA232017</funding_grant_id><funding_grant_id>R01 HL146852</funding_grant_id><funding_grant_id>BE-1913-20190330</funding_grant_id><funding_grant_id>RP210070</funding_grant_id><funding_grant_id>RP180131</funding_grant_id><funding_grant_id>R01 HL134780</funding_grant_id><funding_grant_id>R01 CA240258</funding_grant_id><funding_grant_id>P01 CA265748</funding_grant_id><pubmed_authors>Yang H</pubmed_authors><pubmed_authors>Class C</pubmed_authors><pubmed_authors>Li J</pubmed_authors><pubmed_authors>Lee M</pubmed_authors><pubmed_authors>He H</pubmed_authors><pubmed_authors>Siwko S</pubmed_authors><pubmed_authors>Zhou Y</pubmed_authors><pubmed_authors>Wei Y</pubmed_authors><pubmed_authors>You MJ</pubmed_authors><pubmed_authors>Garcia-Manero G</pubmed_authors><pubmed_authors>Guo L</pubmed_authors><pubmed_authors>Yang Y</pubmed_authors><pubmed_authors>Huang Y</pubmed_authors><pubmed_authors>Hong T</pubmed_authors><pubmed_authors>Wang X</pubmed_authors></additional><is_claimable>false</is_claimable><name>Aberrant DNA hydroxymethylation reshapes transcription factor binding in myeloid neoplasms.</name><description>Epigenetic abnormalities in DNA hydroxymethylation (5hmC) have been detected in patients with myeloid neoplasms, suggesting that 5hmC might act as a valuable epigenetic mark to reflect the disease status of myeloid neoplasms. Here, we report systematic genome-wide mapping of the DNA hydroxymethylomes in over 70 patients with myeloid neoplasms. Our integrative analysis leads to the identification of distinct 5hmC signatures that can sensitively discriminate patients from healthy individuals. At the molecular level, we unveiled dynamic 5hmC changes within key transcription factor (e.g., the CEBP family) binding motifs that are essential for hematopoiesis and myeloid lineage specification. 5hmC redistribution was found to alter the genome-wide binding of CEBP-α, thereby reprogramming transcri</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Jun</publication><modification>2026-07-14T16:20:42.55Z</modification><creation>2022-07-08T10:35:01.081Z</creation></dates><accession>S-EPMC9241241</accession><cross_references><pubmed>35765052</pubmed><doi>10.1186/s13148-022-01297-5</doi></cross_references></HashMap>