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JNCI Journal of the National Cancer Institute 2003 95(16):1184-1186; doi:10.1093/jnci/djg028
© 2003 by Oxford University Press
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© 2003 Oxford University Press

EDITORIAL

Walking the Telomere Plank Into Cancer

Kwok-Kin Wong, Ronald A. DePinho

Affiliations of authors: K.-K. Wong, Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA; R. A. DePinho, Department of Medical Oncology, Dana Farber Cancer Institute and Departments of Medicine and Genetics, Harvard Medical School, Boston.

Correspondence to: Ronald A. DePinho, MD, Dana-Farber Cancer Institute, Harvard Medical School, 44 Binney St., M413, Boston, MA 02115 (e-mail: ron_depinho@dfci.harvard.edu).

The first 10% of the full text of this article appears below.

Our knowledge of the basic biology of telomeres is now beginning to yield fundamental insights into the pathophysiology of complex human diseases including cancer. Telomeres cap chromosome ends and thereby prevent the ends from being recognized as free DNA double-stranded breaks, which activate p53-dependent DNA damage response systems and could produce illegitimate chromosomal fusions. Studies in model organisms, including the mouse, have demonstrated that loss of telomeric sequences results in increased chromosomal instability, activation of telomere checkpoint responses (e.g., cellular growth arrest and apoptosis), multisystem degeneration, and premature aging (1–4). The tumor suppressor p53 plays a key role in sensing and mediating the telomere checkpoint response. Analyses of the telomerase-deficient mouse system have established that p53 inactivation enhances the survival of cells with short, dysfunctional telomeres . . . [Full Text of this Article]


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