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Epigenetic Epidemiology of Cancer

The epigenome has been proposed as a biosensor of past or cumulative exposures and could also be a disease mediator. Human cancers exhibit a wide range of epigenetic alterations characterized by progressive acquisition during tumorigenesis and potential reversibility. Epigenetic changes may occur ea...

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Main Authors:	Herceg, Zdenko, Ghantous, Akram, Chung, Felicia Fei Lei *
Other Authors:	Michels, Karin B.
Format:	Book Section
Published:	Springer Cham 2022
Subjects:	QH Natural history RC Internal medicine
Online Access:	http://eprints.sunway.edu.my/3008/ https://link.springer.com/chapter/10.1007/978-3-030-94475-9_13
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id	my.sunway.eprints.3008
record_format	eprints
spelling	my.sunway.eprints.30082024-08-06T03:26:42Z http://eprints.sunway.edu.my/3008/ Epigenetic Epidemiology of Cancer Herceg, Zdenko Ghantous, Akram Chung, Felicia Fei Lei * QH Natural history RC Internal medicine The epigenome has been proposed as a biosensor of past or cumulative exposures and could also be a disease mediator. Human cancers exhibit a wide range of epigenetic alterations characterized by progressive acquisition during tumorigenesis and potential reversibility. Epigenetic changes may occur early in cancer development, supporting the notion that disrupted epigenetic mechanisms precede and promote malignant transformation. Recent exciting advances in epigenomics that allow the analysis of the epigenome with unprecedented resolution have galvanized investigations in epigenetic epidemiology of cancer. Epigenome states are regulated by three basic mechanisms: DNA methylation, posttranslational histone modifications, and non-coding RNAs (ncRNAs). DNA methylation is the best characterized epigenetic modification, and it is the most extensively studied in epigenetic epidemiology. Whereas it has long been established that DNA methylation (and other epigenetic) changes are ubiquitous in tumour tissue, many recent studies provided evidence that cancer risk- and exposure-associated epigenetic changes can be detected in non-malignant adjacent tissues or surrogate tissues (such as peripheral blood), providing attractive targets for discovering novel biomarkers of exposure and risk stratification. In this chapter, we review evidence from retrospective and prospective studies supporting the utility of epigenetic markers as predictors of predisposition to cancer and risk stratification. We also discuss changes in the “epigenetic clock” associated with cancer susceptibility as well as the potential of identifying epigenetic markers from negative surgical margins as predictors of cancer recurrence risk. Springer Cham Michels, Karin B. 2022-04-14 Book Section PeerReviewed Herceg, Zdenko and Ghantous, Akram and Chung, Felicia Fei Lei * (2022) Epigenetic Epidemiology of Cancer. In: Epigenetic Epidemiology. Springer Cham, Berlin, pp. 325-342. ISBN 9783030944759 https://link.springer.com/chapter/10.1007/978-3-030-94475-9_13 10.1007/978-3-030-94475-9_13
institution	Sunway University
building	Sunway Campus Library
collection	Institutional Repository
continent	Asia
country	Malaysia
content_provider	Sunway University
content_source	Sunway Institutional Repository
url_provider	http://eprints.sunway.edu.my/
topic	QH Natural history RC Internal medicine
spellingShingle	QH Natural history RC Internal medicine Herceg, Zdenko Ghantous, Akram Chung, Felicia Fei Lei * Epigenetic Epidemiology of Cancer
description	The epigenome has been proposed as a biosensor of past or cumulative exposures and could also be a disease mediator. Human cancers exhibit a wide range of epigenetic alterations characterized by progressive acquisition during tumorigenesis and potential reversibility. Epigenetic changes may occur early in cancer development, supporting the notion that disrupted epigenetic mechanisms precede and promote malignant transformation. Recent exciting advances in epigenomics that allow the analysis of the epigenome with unprecedented resolution have galvanized investigations in epigenetic epidemiology of cancer. Epigenome states are regulated by three basic mechanisms: DNA methylation, posttranslational histone modifications, and non-coding RNAs (ncRNAs). DNA methylation is the best characterized epigenetic modification, and it is the most extensively studied in epigenetic epidemiology. Whereas it has long been established that DNA methylation (and other epigenetic) changes are ubiquitous in tumour tissue, many recent studies provided evidence that cancer risk- and exposure-associated epigenetic changes can be detected in non-malignant adjacent tissues or surrogate tissues (such as peripheral blood), providing attractive targets for discovering novel biomarkers of exposure and risk stratification. In this chapter, we review evidence from retrospective and prospective studies supporting the utility of epigenetic markers as predictors of predisposition to cancer and risk stratification. We also discuss changes in the “epigenetic clock” associated with cancer susceptibility as well as the potential of identifying epigenetic markers from negative surgical margins as predictors of cancer recurrence risk.
author2	Michels, Karin B.
author_facet	Michels, Karin B. Herceg, Zdenko Ghantous, Akram Chung, Felicia Fei Lei *
format	Book Section
author	Herceg, Zdenko Ghantous, Akram Chung, Felicia Fei Lei *
author_sort	Herceg, Zdenko
title	Epigenetic Epidemiology of Cancer
title_short	Epigenetic Epidemiology of Cancer
title_full	Epigenetic Epidemiology of Cancer
title_fullStr	Epigenetic Epidemiology of Cancer
title_full_unstemmed	Epigenetic Epidemiology of Cancer
title_sort	epigenetic epidemiology of cancer
publisher	Springer Cham
publishDate	2022
url	http://eprints.sunway.edu.my/3008/ https://link.springer.com/chapter/10.1007/978-3-030-94475-9_13
_version_	1806692471912005632
score	13.211869

Epigenetic Epidemiology of Cancer

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