title: Epigenetic silencing of tumor suppressor genes in pancreatic cancer.
abstract: BACKGROUND
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Laboratory of Epigenetics and Chromatin Dynamics, Gastroenterology Research Unit, 10-24C Guggenheim Building, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA. lomberk.gwen@mayo.edu
authors.forename: Gwen A
authors.initials: GA
authors.lastname: Lomberk
mesh_terms: D000818:Animals; D044127:Epigenesis, Genetic / Q000502:physiology*; D015972:Gene Expression Regulation, Neoplastic / Q000502:physiology*; D020868:Gene Silencing; D016147:Genes, Tumor Suppressor / Q000502:physiology*; D006801:Humans; D010190:Pancreatic Neoplasms / Q000235:genetics*