Cyclin D1: Polymorphism, aberrant splicing and cancer risk

K. E. Knudsen, J. Alan Diehl, C. A. Haiman, E. S. Knudsen

Research output: Contribution to journalReview article

290 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)1620-1628
Number of pages9
JournalOncogene
Volume25
Issue number11
DOIs
StatePublished - Mar 13 2006

Keywords

  • Alternative splicing
  • Cell cycle
  • Cyclin-dependent kinase
  • Nuclear localization
  • Retinoblastoma tumor suppressor

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cancer Research

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  • Cite this

    Knudsen, K. E., Alan Diehl, J., Haiman, C. A., & Knudsen, E. S. (2006). Cyclin D1: Polymorphism, aberrant splicing and cancer risk. Oncogene, 25(11), 1620-1628. https://doi.org/10.1038/sj.onc.1209371