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Hypermethylation of the Ink4b locus in murine myeloid leukemia and increased susceptibility to leukemia in p15(Ink4b)- defficient mice

  1. Author:
    Wolff, L.
    Garin, M. T.
    Koller, R.
    Bies, J.
    Liao, W.
    Malumbres, M.
    Tessarollo, L.
    Powell, D.
    Perella, C.

  2. Author Address

    NCI, Ctr Canc Res, NIH, Bldg 37,Room 4124A,37 Convent Dr MSC 4255, Bethesda, MD 20892 USA NCI, Ctr Canc Res, NIH, Bethesda, MD 20892 USA Ctr Nacl Invest Oncol, E-28029 Madrid, Spain NCI, SAIC Frederick, Bethesda, MD 20892 USA NCI, Data Management Serv, Frederick, MD 21701 USA Wolff L NCI, Ctr Canc Res, NIH, Bldg 37,Room 4124A,37 Convent Dr MSC 4255, Bethesda, MD 20892 USA
    1. Year: 2003
  2. Journal: Oncogene
    1. 22
    2. 58
    3. Pages: 9265-9274
  4. Type of Article: Article
  1. Abstract:

    The Ink4b gene (Cdkn2b) encodes p15(Ink4b), a cyclin-dependent kinase inhibitor. It has been implicated in playing a role in the development of acute myeloid leukemia (AML) in man, since it is hypermethylated with high frequency. We provide evidence that the gene is a tumor suppressor for myeloid leukemia in mice. The evidence is twofold: (1) retrovirus-induced myeloid leukemias of the myelomonocytic phenotype were found to have hypermethylation of the 5' CpG island of the Ink4b gene, and this could be correlated with reduced mRNA expression, as demonstrated by TaqMan real-time PCR. p15(Ink4b) mRNA expression in a leukemia cell line, with hypermethylation at the locus, was induced following treatment with 5-aza-2'- deoxycytidine.(2) Targeted deletion of one allele in mice by removal of exon 2 increases their susceptibility to retrovirus- induced myeloid leukemia. Mice deficient in both alleles were not more susceptible to myeloid disease than those deficient in one allele, raising the possibility that there are opposing forces related to the development of myeloid leukemia in Ink4b null mice.

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