Impaired hydroxylation of 5-methylcytosine in myeloid cancers with mutant TET2

Myunggon Ko, Yun Huang, Anna M. Jankowska, Utz Pape, Mamta Tahiliani, Hozefa S. Bandukwala, Jungeun An, Edward D. Lamperti, Kian Peng Koh, Rebecca Ganetzky, X. Shirley Liu, L. Aravind, Suneet Agarwal, Jaroslaw P. Maciejewski () and Anjana Rao ()
Additional contact information
Myunggon Ko: Harvard Medical School, Immune Disease Institute and Program in Cellular and Molecular Medicine, Children’s Hospital Boston
Yun Huang: Harvard Medical School, Immune Disease Institute and Program in Cellular and Molecular Medicine, Children’s Hospital Boston
Anna M. Jankowska: Taussig Cancer Institute, Cleveland Clinic
Mamta Tahiliani: Harvard Medical School, Immune Disease Institute and Program in Cellular and Molecular Medicine, Children’s Hospital Boston
Hozefa S. Bandukwala: Harvard Medical School, Immune Disease Institute and Program in Cellular and Molecular Medicine, Children’s Hospital Boston
Jungeun An: Harvard Medical School, Immune Disease Institute and Program in Cellular and Molecular Medicine, Children’s Hospital Boston
Edward D. Lamperti: Harvard Medical School, Immune Disease Institute and Program in Cellular and Molecular Medicine, Children’s Hospital Boston
Kian Peng Koh: Harvard Medical School, Immune Disease Institute and Program in Cellular and Molecular Medicine, Children’s Hospital Boston
Rebecca Ganetzky: Taussig Cancer Institute, Cleveland Clinic
X. Shirley Liu: Dana-Farber Cancer Institute and Harvard School of Public Health
L. Aravind: National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health
Suneet Agarwal: Children's Hospital Boston and Dana-Farber Cancer Institute, Harvard Stem Cell Institute
Jaroslaw P. Maciejewski: Taussig Cancer Institute, Cleveland Clinic
Anjana Rao: Harvard Medical School, Immune Disease Institute and Program in Cellular and Molecular Medicine, Children’s Hospital Boston

Nature, 2010, vol. 468, issue 7325, 839-843

Abstract: Mutated TET in myeloid cancers Enzymes of the TET family convert 5-methylcytosine to 5-hydroxymethylcytosine (5-hmC) in DNA. Mutations in the gene encoding TET2 are common in myeloid malignancies. These disease-associated mutations are now shown to compromise TET2 catalytic activity: bone-marrow samples from patients with TET2 mutations have low levels of 5-hmC in genomic DNA, and TET2 is required for normal haematopoietic differentiation. Measurement of genomic 5-hmC levels may prove valuable as a diagnostic tool in myeloid cancers.

Date: 2010
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DOI: 10.1038/nature09586

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