Implications of Genetic and Epigenetic Alterations of CDKN2A (p16INK4a) in Cancer

Ran Zhao, Bu Young Choi, Mee Hyun Lee, Ann M. Bode, Zigang Dong

Research output: Contribution to journalReview articlepeer-review

82 Scopus citations

Abstract

Aberrant gene silencing is highly associated with altered cell cycle regulation during carcinogenesis. In particular, silencing of the CDKN2A tumor suppressor gene, which encodes the p16INK4a protein, has a causal link with several different types of cancers. The p16INK4a protein plays an executional role in cell cycle and senescence through the regulation of the cyclin-dependent kinase (CDK) 4/6 and cyclin D complexes. Several genetic and epigenetic aberrations of CDKN2A lead to enhanced tumorigenesis and metastasis with recurrence of cancer and poor prognosis. In these cases, the restoration of genetic and epigenetic reactivation of CDKN2A is a practical approach for the prevention and therapy of cancer. This review highlights the genetic status of CDKN2A as a prognostic and predictive biomarker in various cancers.

Original languageEnglish (US)
Pages (from-to)30-39
Number of pages10
JournalEBioMedicine
Volume8
DOIs
StatePublished - Jun 1 2016

Bibliographical note

Funding Information:
This work was supported by grant funding from the National Institutes of Health CA166011 , CA187027 and CA196639 , The Hormel Foundation and Henan Provincial Government, China . Funders had no role in producing this manuscript.

Keywords

  • CDKN2A
  • Cancer
  • Epigenetic alterations
  • Genetic alterations
  • P16

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