Molecular Oncology
Volume 2, Issue 1 , Pages 33-40, June 2008

Epigenetics and cancer, 2nd IARC meeting, Lyon, France, 6 and 7 December 2007

Epigenetics Group, International Agency for Research on Cancer (IARC), 150 Cours Albert Thomas, 69008 Lyon, France

Received 28 February 2008; received in revised form 14 March 2008; accepted 17 March 2008. published online 23 April 2008.

Abstract 

It is becoming widely accepted that epigenetic alterations are universally present in human malignancies and that cancer is as much a disease of abnormal epigenetics as it is a genetic disease. The potential utility of epigenetics and epigenomics in cancer research and cancer control is highlighted by the fact that many funding agencies put cancer epigenetics on the priority list. The goal of this meeting, held at the offices of the International Agency for Research on Cancer in Lyon, France, 6 and 7 December 2007, was to discuss recent conceptual and technological advances in cancer epigenetics and epigenomics, the future research needs in the field, and their implications for early detection, risk assessment and prevention of cancer.

While epigenetics has been historically linked to phenomena that do not follow normal genetic principles of heritability, recent mechanistic advances have begun to change our understanding of complex diseases including cancer, traditionally viewed as genetic in origin. It is now known that epigenetic mechanisms play critical roles in regulation of many cellular functions and their deregulation may disrupt the control of fundamental processes leading to tumour formation. A flurry of screening and functional studies revealed that most key processes found in cancer cells, such as silencing of tumour suppressor genes, activation of oncogenes, aberrant cell cycle processes, defects in DNA repair, and deregulation of cell death, can be triggered by epigenetic deregulation. Two important features that distinguish epigenetic changes from genetic alterations are the gradual appearance and reversibility of epigenetic events. These features make epigenetic alterations an attractive target for therapeutic intervention and the development of preventive strategies. For example, aberrant patterns of DNA methylation and histone acetylation and methylation can be targeted by drugs aiming to re-activate epigenetically silenced genes. Until now, most studies on epigenetic changes in cancer were generally focused on specific genes. However, this meeting also stressed the need to take advantage of recent progress in epigenomics and emergence of powerful technologies for detection of epigenetic changes in high throughput and genome-wide settings. This may further advance our capacity to evaluate the contribution of epigenetic changes induced by environmental epimutagens to human cancer. This information may prove critical for the design of efficient strategies for early diagnosis, therapy, and prevention of cancer.

Keywords: Epigenetic changes, Epigenomics, DNA methylation, Histone modifications, Cancer, Environment, Molecular epidemiology

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 Meeting participants: Stephan Beck (UCL Cancer Institute, University College London, UK), Haim J. Bendayan (Hôpital Pitié Salpêtrière, Paris, France), Manon van Engeland (Maastricht University, the Netherlands), Robert Feil (Institute of Molecular Genetics, University of Montpellier, France), Zdenko Herceg (International Agency for Research on Cancer, France), Triantafillos Liloglou (University of Liverpool, UK), Gerd Pfeifer (City of Hope National Medical Center, USA), Dirk Schübeler (Friedrich Miescher Institute, Switzerland), Minoru Toyota (Sapporo Medical University, Japan), Benjamin Tycko (Columbia University, USA), Mukesh Verma (National Cancer Institute, NIH, USA), Robyn Ward (University of Sydney, Australia).

PII: S1574-7891(08)00038-0

doi:10.1016/j.molonc.2008.03.005

Molecular Oncology
Volume 2, Issue 1 , Pages 33-40, June 2008