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

Author

Listed:
  • Myunggon Ko

    (Harvard Medical School, Immune Disease Institute and Program in Cellular and Molecular Medicine, Children’s Hospital Boston
    Present address: La Jolla Institute for Allergy and Immunology, La Jolla, California 92037, USA (M.K., Y.H., J.A., A.R.).)

  • Yun Huang

    (Harvard Medical School, Immune Disease Institute and Program in Cellular and Molecular Medicine, Children’s Hospital Boston
    Present address: La Jolla Institute for Allergy and Immunology, La Jolla, California 92037, USA (M.K., Y.H., J.A., A.R.).)

  • Anna M. Jankowska

    (Taussig Cancer Institute, Cleveland Clinic)

  • Utz J. Pape

    (Harvard Medical School, Immune Disease Institute and Program in Cellular and Molecular Medicine, Children’s Hospital Boston
    Dana-Farber Cancer Institute and Harvard School of Public Health)

  • 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
    Present address: La Jolla Institute for Allergy and Immunology, La Jolla, California 92037, USA (M.K., Y.H., J.A., A.R.).)

  • 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
    Present address: La Jolla Institute for Allergy and Immunology, La Jolla, California 92037, USA (M.K., Y.H., J.A., A.R.).)

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.

Suggested Citation

  • Myunggon Ko & Yun Huang & Anna M. Jankowska & Utz J. Pape & Mamta Tahiliani & Hozefa S. Bandukwala & Jungeun An & Edward D. Lamperti & Kian Peng Koh & Rebecca Ganetzky & X. Shirley Liu & L. Aravind & , 2010. "Impaired hydroxylation of 5-methylcytosine in myeloid cancers with mutant TET2," Nature, Nature, vol. 468(7325), pages 839-843, December.
  • Handle: RePEc:nat:nature:v:468:y:2010:i:7325:d:10.1038_nature09586
    DOI: 10.1038/nature09586
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    Cited by:

    1. Morten Tulstrup & Mette Soerensen & Jakob Werner Hansen & Linn Gillberg & Maria Needhamsen & Katja Kaastrup & Kristian Helin & Kaare Christensen & Joachim Weischenfeldt & Kirsten Grønbæk, 2021. "TET2 mutations are associated with hypermethylation at key regulatory enhancers in normal and malignant hematopoiesis," Nature Communications, Nature, vol. 12(1), pages 1-10, December.

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