Faculty Collaboration Database

Epigenetic silencing of tumor suppressor genes in pancreatic cancer. J Gastrointest Cancer 2011 Jun;42(2):93-9

Date

02/15/2011

Pubmed ID

21318291

DOI

10.1007/s12029-011-9256-2

Scopus ID

2-s2.0-79956201806 (requires institutional sign-in at Scopus site)   17 Citations

Abstract

INTRODUCTION: Without any alteration of DNA sequence, heritable changes in gene expression, caused by epigenetic pathways, are gaining a spotlight in research of diseases, and in particular, cancer. Although the dominant paradigm in cancer research, proposed by Vogelstein, suggested that cancer progression was caused by a sequential accumulation of genetic aberrations, basic science studies in epigenetics have now advanced our knowledge enough to apply its concepts and methodology to the study of cancer. In fact, chromatin dynamics and small RNAs are altered far more prevalently in cancer than genetic alterations and most important, can be reversible, lending themselves as attractive therapeutic targets.

CONCLUDING REMARKS: In the current review, the inactivation of p16 will be utilized as the most prominent example of epigenetic silencing of a tumor suppressor gene in pancreatic cancer. In addition, fundamental insight will be given into why and how epigenetics can be targeted for therapeutic purposes. This knowledge will help the reader in determining the breadth and depth of this field of study with potentially high impact to oncology.

Author List

Lomberk GA

Author

Gwen Lomberk PhD Professor in the Surgery department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

Animals
Epigenesis, Genetic
Gene Expression Regulation, Neoplastic
Gene Silencing
Genes, Tumor Suppressor
Humans
Pancreatic Neoplasms