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Volume 4, Issue 3, Pages 242-254 (June 2010)


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The epigenetics of breast cancer

Jovana Jovanovica, Jo Anders Rønnebergb, Jörg Tostc, Vessela KristensenabCorresponding Author Informationweb addressemail address

Received 14 March 2010; received in revised form 23 March 2010; accepted 2 April 2010. published online 10 May 2010.

Abstract 

Epigenetic changes can be defined as stable molecular alterations of a cellular phenotype such as the gene expression profile of a cell that are heritable during somatic cell divisions (and sometimes germ line transmissions) but do not involve changes of the DNA sequence itself. Epigenetic phenomena are mediated by several molecular mechanisms comprising histone modifications, polycomb/trithorax protein complexes, small non-coding or antisense RNAs and DNA methylation. These different modifications are closely interconnected. Epigenetic regulation is critical in normal growth and development and closely conditions the transcriptional potential of genes. Epigenetic mechanisms convey genomic adaption to an environment thereby ultimately contributing towards given phenotype. In this review we will describe the various aspects of epigenetics and in particular DNA methylation in breast carcinogenesis and their potential application for diagnosis, prognosis and treatment decision.

a Department for Clinical Molecular Biology (EpiGen), Institute for Clinical Medicine, Akershus University Hospital, University of Oslo, Norway

b Group of Cancer Genome Variation, Department of Genetics, Institute for Cancer Research, Division of Surgery and Cancer, Oslo University Hospital Radiumhospitalet, Oslo, Norway

c CEA-Institut de Génomique, Centre National de Génotypage, Laboratory for Epigenetics, 2 rue Gaston Crèmieux, 91000 Evry, France

Corresponding Author InformationCorrespondence author at: Department for Clinical Molecular Biology (EpiGen), Institute for Clinical Medicine, Akershus University Hospital, University of Oslo, Norway. Tel.: +47 22935677; fax: +47 22934440.

PII: S1574-7891(10)00024-4

doi:10.1016/j.molonc.2010.04.002


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