Cyclin D1: polymorphism, aberrant splicing and cancer risk

Oncogene. 2006 Mar 13;25(11):1620-8. doi: 10.1038/sj.onc.1209371.

Abstract

The cyclin D1 proto-oncogene exercises powerful control over the mechanisms that regulate the mitotic cell cycle, and excessive cyclin D1 expression and/or activity is common in human cancers. Although somatic mutations of the cyclin D1 locus are rarely observed, mounting evidence demonstrates that a specific polymorphism of cyclin D1 (G/A870) and a protein product of a potentially related alternate splicing event (cyclin D1b) may influence cancer risk and outcome. Herein, we review the epidemiological and functional literatures that link these alterations of cyclin D1 to human tumor development and progression.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Alternative Splicing*
  • Cell Cycle / physiology
  • Cell Transformation, Neoplastic / genetics
  • Cyclin D1 / genetics*
  • Cyclin D1 / physiology
  • Disease Progression
  • Epidemiologic Studies
  • Humans
  • Neoplasms / epidemiology*
  • Neoplasms / genetics*
  • Neoplasms / physiopathology
  • Polymorphism, Genetic*

Substances

  • Cyclin D1