Supplementary Table 2 from Progressive Chromatin Repression and Promoter Methylation of CTNNA1 Associated with Advanced Myeloid Malignancies

Ye, Ying; McDevitt, Michael A.; Guo, Mingzhou; Zhang, Wei; Galm, Oliver; Gore, Steven D.; Karp, Judith E.; Maciejewski, Jaroslaw P.; Kowalski, Jeanne; Tsai, Hua-Ling; Gondek, Lukasz P.; Tsai, Hsing-Chen; Wang, Xiaofei; Hooker, Craig; Smith, B. Douglas; Carraway, Hetty E.; Herman, James G.

doi:10.1158/0008-5472.22381053.v1

Supplementary Table 2 from Progressive Chromatin Repression and Promoter Methylation of CTNNA1 Associated with Advanced Myeloid Malignancies

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posted on 2023-03-30, 19:10 authored by Ying Ye, Michael A. McDevitt, Mingzhou Guo, Wei Zhang, Oliver Galm, Steven D. Gore, Judith E. Karp, Jaroslaw P. Maciejewski, Jeanne Kowalski, Hua-Ling Tsai, Lukasz P. Gondek, Hsing-Chen Tsai, Xiaofei Wang, Craig Hooker, B. Douglas Smith, Hetty E. Carraway, James G. Herman

Supplementary Table 2 from Progressive Chromatin Repression and Promoter Methylation of CTNNA1 Associated with Advanced Myeloid Malignancies

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ARTICLE ABSTRACT

Complete loss or deletion of the long arm of chromosome 5 is frequent in myelodysplastic syndrome (MDS) and acute myelogenous leukemia (AML). The putative gene(s) deleted and responsible for the pathogenesis of these poor prognosis hematologic disorders remain controversial. This study is a comprehensive analysis of previously implicated and novel genes for epigenetic inactivation in AML and MDS. In 146 AML cases, methylation of CTNNA1 was frequent, and more common in AML patients with 5q deletion (31%) than those without 5q deletion (14%), whereas no methylation of other 5q genes was observed. In 31 MDS cases, CTNNA1 methylation was only found in high-risk MDS (≥RAEB2), but not in low-risk MDS (

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Epigenetics Genome Biology Silencing and reactivation of gene expression Structural genomics Hematological Cancers Leukemias

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Supplementary Table 2 from Progressive Chromatin Repression and Promoter Methylation of CTNNA1 Associated with Advanced Myeloid Malignancies

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