The epigenetics of cancer etiology

Research output: Contribution to journalArticle

Abstract

Epigenetic dysregulation is central to cancer development and progression. This dysregulation includes hypomethylation leading to oncogene activation and chromosomal instability, hypermethylation and tumor suppressor gene silencing, and chromatin modification acting directly, and cooperatively with methylation changes, to modify gene expression. In addition, disrupted genomic imprinting appears to contribute to colorectal cancer risk, and serves as a gatekeeper in Wilms tumor. A cancer predisposing disorder, Beckwith-Wiedemann syndrome, usually arises from epigenetic errors, solidifying the causal role of epigenetics in cancer. While cancer epigenetics has been reviewed extensively elsewhere, the main focus of this review will be to present the view that epigenetics and genetics are complementary in the area of cancer etiology, the focus of this volume. I propose a hypothesis in which epigenetic alterations contribute to tumor progression, but they also increase the probability that genetic changes, when they occur, will lead to cancer initiation. This hypothesis could contribute to a new understanding of the role of environmental carcinogens that may not be fully explained through a purely genetic view or by tests, such as bacterial mutation frequency, that ignore epigenetic factors.

Original languageEnglish (US)
Pages (from-to)427-432
Number of pages6
JournalSeminars in Cancer Biology
Volume14
Issue number6
DOIs
StatePublished - Dec 2004

Keywords

  • Beckwith-Wiedemann syndrome
  • Cancer etiology
  • Epigenetic dysregulation

ASJC Scopus subject areas

  • Cancer Research

Fingerprint Dive into the research topics of 'The epigenetics of cancer etiology'. Together they form a unique fingerprint.

  • Cite this