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Telomere length and heavy-chain mutation status in familial chronic lymphocytic leukemia

  1. Author:
    Ishibe, N.
    Prieto, D. R.
    Hosack, D. A.
    Lempicki, R. A.
    Goldin, L. R.
    Raffeld, M.
    Marti, G. E.
    Caporaso, N. E.

  2. Author Address

    NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, 6120 Execut Blvd,MSC 7236, Rockville, MD 20892 USA NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Rockville, MD 20892 USA NIH, Clin Serv Program, SAIC Frederick, Frederick, MD 21702 USA NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA US FDA, Ctr Biol Res & Evaluat, Div Cell & Gene Therapies, Flow & Image Cytometry Sect, Bethesda, MD 20852 USA Ishibe N NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, 6120 Execut Blvd,MSC 7236, Rockville, MD 20892 USA
    1. Year: 2002
  2. Journal: Leukemia Research
    1. 26
    2. 9
    3. Pages: 791-794
  4. Type of Article: Article
  1. Abstract:

    We examined whether telomere lengths of peripheral blood mononuclear cells are associated with immunoglobulin gene usage in 21 familial chronic lymphocytic leukemia (CLL) patients. Subjects with unmutated V genes tended to have shorter telomeres than those with somatic mutations, especially after adjusting for age. Unlike V-H mutation status, telomere length was not predictive for survival. Our results suggest that telomere length is associated with V-H gene mutation status and provides further evidence that the biological basis of familial B-CLL is similar to that of sporadic patients. (C) 2002 Elsevier Science Ltd. All rights reserved.

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