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cancer & methylation

Cancer, oncogenes and methylation


Event description:

DNA methylation represents an epigenetic means of inheritance without associated DNA sequence alterations. Though the function of DNA methylation is still not completely understood, roles have been proposed for control of gene _expression, chromosomal integrity, and recombinational events. DNA methylation is particularly important in CpG islands within promoter regions as methylation is associated with transcriptional repression of the associated gene. Though DNA methylation patterns change during embryogenesis and development, they are thought to be relatively stable in the adult.

Aberrant CpG island methylation has been associated with changes observed in aging and neoplastic cells. A growing list of genes, including known tumor-suppressor genes, have been shown to have aberrant CpG island methylation in cancer. This webcast addressed the growing evidence for a pivotal role of DNA methylation in oncogenesis as well as the methods being employed in this field of research.  Dr Charles Cantor will summarize the state of the work being done and a panel of thought leaders will discuss their work and ideas around where this field is headed. 

The webcast of the conference at http://www.bio.com/newsfeatures/infocus.jhtml?infocusId=1100001&realmId


DNA Methylation, Cancer Susceptibility, and Nutrient Interactions

Cindy D. Davis*,1 and Eric O. Uthus

* National Institutes of Health, National Cancer Institute, Nutritional Sciences Research Group, Rockville, Maryland 20892–7328; and United States Department of Agriculture, Grand Forks Human Nutrition Research Center, Grand Forks, North Dakota 58202–9034

To whom requests for reprints should be addressed at 1 Nutritional Sciences Research Group, Division of Cancer Prevention, National Cancer Institute, 6130 Executive Boulevard, Suite 3159, Rockville, MD 20892–7328. E-mail: davisci@mail.nih.gov

DNA methylation is an important epigenetic mechanism of transcriptional control. DNA methylation plays an essential role in maintaining cellular function, and changes in methylation patterns may contribute to the development of cancer. Aberrant methylation of DNA (global hypomethylation accompanied by region-specific hypermethylation) is frequently found in tumor cells. Global hypomethylation can result in chromosome instability, and hypermethylation has been associated with the inaction of tumor suppressor genes. Preclinical and clinical studies suggest that part of the cancer-protective effects associated with several bioactive food components may relate to DNA methylation patterns. Dietary factors that are involved in one-carbon metabolism provide the most compelling data for the interaction of nutrients and DNA methylation because they influence the supply of methyl groups, and therefore the biochemical pathways of methylation processes. These nutrients include folate, vitamin B12, vitamin B6, methionine, and choline. However, looking at individual nutrients may be too simplistic. Dietary methyl (folate, choline, and methionine) deficiency in combination causes decreased tissue S-adeno-sylmethionine, global DNA hypomethylation, hepatic steatosis, cirrhosis, and ultimately hepatic tumorigenesis in rodents in the absence of carcinogen treatment. Other dietary components such as vitamin B12, alcohol, and selenium may modify the response to inadequate dietary folate.

Key Words: DNA methylation • cancer • folate • selenium • epigenetics



Endocrine-Related Cancer 13 (2) 357-3

Copyright 2006 by the Society for Endocrinology.

The emerging roles of DNA methylation in the clinical management of prostate cancer


Antoinette S Perry, Ruth Foley, Karen Woodson1 and Mark Lawler

Institute of Molecular Medicine, Trinity College Dublin, Ireland
1 Center for Cancer Research, National Cancer Institute,
6116 Executive Blvd, Bethesda, MD 20892, USA

(Requests for offprints should be addressed to A S Perry; Email: perryan@tcd.ie )

Aberrant DNA methylation is one of the hallmarks of carcinogenesis and has been recognized in cancer cells for more than 20 years. The role of DNA methylation in malignant transformation of the prostate has been intensely studied, from its contribution to the early stages of tumour development to the advanced stages of androgen independence. The most significant advances have involved the discovery of numerous targets such as GSTP1, Ras-association domain family 1A (RASSF1A) and retinoic acid receptor 2 (RAR2) that become inactivated through promoter hypermethylation during the course of disease initiation and progression. This has provided the basis for translational research into methylation biomarkers for early detection and prognosis of prostate cancer. Investigations into the causes of these methylation events have yielded little definitive data. Aberrant hypomethylation and how it impacts upon prostate cancer has been less well studied. Herein we discuss the major developments in the fields of prostate cancer and DNA methylation, and how this epigenetic modification can be harnessed to address some of the key issues impeding the successful clinical management of prostate cancer.


RTVP-1, a Tumor Suppressor Inactivated by Methylation in Prostate Cancer

Chengzhen Ren1, Likun Li1, Guang Yang1, Terry L. Timme1,2, Alexei Goltsov1, Chenghui Ren1, Xiaorong Ji1, Josephine Addai1, Hongbin Luo3, Michael M. Ittmann2,3 and Timothy C. Thompson1,2,4,5

1 Scott Department of Urology, Baylor College of Medicine, Houston, Texas; 2 Houston Veterans Affairs Medical Center, Houston, Texas; and Departments of 3 Pathology, 4 Molecular and Cellular Biology, and 5 Radiology, Baylor College of Medicine, Houston, Texas

Cancer Research 64, 969-976, February 1, 2004]
American Association for Cancer Research

We previously identified and characterized a novel p53-regulated gene in mouse prostate cancer cells that was homologous to a human gene that had been identified in brain cancers and termed RTVP-1 or GLIPR. In this report, we document that the human RTVP-1 gene is also regulated by p53 and induces apoptosis in human prostate cancer cell lines. We show that the expression of the human RTVP-1 gene is down-regulated in human prostate cancer specimens compared with normal human prostate tissue at the mRNA and protein levels. We further document epigenetic changes consistent with RTVP-1 being a tumor suppressor in human prostate cancer.


DNA Methylation, Chondrogenesis, and Cartilage Degeneration

Authors: Aigner, Thomas1; Margarethe Gebhard, Pia1; Sesselmann, Stephan1; Soder, Stephan1; Roach, Helmtrud I.1

Source: Current Rheumatology Reviews, Volume 2, Number 3, August 2006, pp. 221-232(12)

Publisher: Bentham Science Publishers


In the last few years there has been an explosion of research into epigenetics and, in particular, the roles of DNA methylation in the normal functioning of the mammalian organism as well as whether changes in methylation status contribute to or cause aberrant gene expression in diseases. While abnormal patterns of DNA methylation in cancer cells have been intensively investigated, little attention has so far been paid to the role of DNA methylation in cartilage and cartilage degeneration. This review summarizes the current knowledge of the mechanism of methylation, its association with transcriptional silencing, possible mechanisms of hyper- and hypomethylation as well as age- and disease related changes in methylation pattern. We discuss the possible involvement of DNA methylation in chondrogenesis as well as its potential importance for cartilage degradation. Overall, epigenetic gene regulation has largely been neglected in cartilage research, but is likely to be an important issue in future. There is increasing evidence that besides cytokines, growth factors and changes in matrix composition, variations in the genetic methylation pattern might also be important determinators of the complex gene expression pattern pathognomically observed in osteoarthritic cartilage tissue.

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