<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Griffiths EA</submitter><funding>NCI NIH HHS</funding><pagination>590-600</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3052845</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>5(7)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Methylation of tumor suppression genes (TSGs) is common in myeloid malignancies. However, application of this as a molecular marker for risk stratification in patients with AML is limited.&lt;h4>Design and methods&lt;/h4>To elucidate the impact of patterns of TSG methylation on outcome in cytogenetically normal patients, 106 samples from patients with having normal cytogenetic AML were evaluated for methylation of 12 genes by MSP. For sake of comparison, samples from patients with AML and abnormal cytogenetics (n = 63) were also evaluated.&lt;h4>Results&lt;/h4>Methylation frequencies in the whole group (n = 169) were similar to previous reports for CDH1 (31%), ER (31%), FHIT (9%), p15 (INK4b) (44%), p73 (25%), and SOCS1 (75%). Methylation of CTNNA1 was observed in 10%, CEBP-α in16%,</pubmed_abstract><journal>Epigenetics</journal><pubmed_title>Epigenetic differences in cytogenetically normal versus abnormal acute myeloid leukemia.</pubmed_title><pmcid>PMC3052845</pmcid><funding_grant_id>K24 CA111717</funding_grant_id><funding_grant_id>CA06793</funding_grant_id><pubmed_authors>McDevitt MA</pubmed_authors><pubmed_authors>Karp JE</pubmed_authors><pubmed_authors>Hooker CM</pubmed_authors><pubmed_authors>Mohammad HP</pubmed_authors><pubmed_authors>Smith BD</pubmed_authors><pubmed_authors>Carraway HE</pubmed_authors><pubmed_authors>Herman JG</pubmed_authors><pubmed_authors>Griffiths EA</pubmed_authors><pubmed_authors>Gore SD</pubmed_authors></additional><is_claimable>false</is_claimable><name>Epigenetic differences in cytogenetically normal versus abnormal acute myeloid leukemia.</name><description>&lt;h4>Background&lt;/h4>Methylation of tumor suppression genes (TSGs) is common in myeloid malignancies. However, application of this as a molecular marker for risk stratification in patients with AML is limited.&lt;h4>Design and methods&lt;/h4>To elucidate the impact of patterns of TSG methylation on outcome in cytogenetically normal patients, 106 samples from patients with having normal cytogenetic AML were evaluated for methylation of 12 genes by MSP. For sake of comparison, samples from patients with AML and abnormal cytogenetics (n = 63) were also evaluated.&lt;h4>Results&lt;/h4>Methylation frequencies in the whole group (n = 169) were similar to previous reports for CDH1 (31%), ER (31%), FHIT (9%), p15 (INK4b) (44%), p73 (25%), and SOCS1 (75%). Methylation of CTNNA1 was observed in 10%, CEBP-α in16%,</description><dates><release>2010-01-01T00:00:00Z</release><publication>2010 Oct</publication><modification>2025-04-04T01:33:58.991Z</modification><creation>2019-03-27T00:39:30Z</creation></dates><accession>S-EPMC3052845</accession><cross_references><pubmed>20671427</pubmed><doi>10.4161/epi.5.7.12558</doi></cross_references></HashMap>