Journal Article

p16<sup>INK4a</sup> and the control of cellular proliferative life span

Lily I. Huschtscha and Roger R. Reddel

in Carcinogenesis

Volume 20, issue 6, pages 921-926
Published in print June 1999 | ISSN: 0143-3334
Published online June 1999 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/20.6.921
p16INK4a and the control of cellular proliferative life span

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Normal somatic cells have a limited proliferative capacity in vitro: after a finite number of cell divisions they eventually enter a non-proliferative state referred to as senescence. Senescence is thought to be a major tumor suppressor mechanism, and many cancers contain cells that have escaped from senescence and become immortalized. The role of telomerase activation in immortalization is currently attracting considerable attention, but immortalization is often associated with other changes including loss of normal function of the tumor suppressor locus, INK4a/ARF. Two proteins, p16INK4a and p14ARF, are encoded by this locus. Here we focus on p16INK4a and review accumulating evidence that loss of p16INK4a function may be involved in escape from the normal limits on cellular proliferative life span.

Keywords: cdk, cyclin-dependent kinase; HMEC, human mammary epithelial cells; HPV, human papillomavirus; LFS, Li–Fraumeni syndrome; MTS-1 gene, multiple tumor suppressor-1 gene; PD, population doubling; Rb, retinoblastoma; SV40, simian virus 40.

Journal Article.  5858 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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