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Cancer Epidemiology and Prevention$
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Michael Thun, Martha S. Linet, James R. Cerhan, Christopher A. Haiman, and David Schottenfeld

Print publication date: 2017

Print ISBN-13: 9780190238667

Published to Oxford Scholarship Online: December 2017

DOI: 10.1093/oso/9780190238667.001.0001

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PRINTED FROM OXFORD SCHOLARSHIP ONLINE (www.oxfordscholarship.com). (c) Copyright Oxford University Press, 2019. All Rights Reserved. An individual user may print out a PDF of a single chapter of a monograph in OSO for personal use. date: 12 November 2019

Biology of Neoplasia

Biology of Neoplasia

Chapter:
(p.9) 2 Biology of Neoplasia
Source:
Cancer Epidemiology and Prevention
Author(s):

Michael Dean

Karobi Moitra

Publisher:
Oxford University Press
DOI:10.1093/oso/9780190238667.003.0002

The term “cancer” encompasses a large heterogeneous group of diseases that involve uncontrolled cell growth, division, and survival, culminating in local invasion and/or distant metastases. Cancer is fundamentally a genetic disease at the cellular level. Tumors occur because clones of abnormal cells acquire multiple lesions in DNA, nearly always involving mutations, chromosomal rearrangements, and extensive alteration of the epigenome. Up to 10% of cancers also involve inherited germline mutations that are moderately to highly penetrant. Cancers begin as localized growths or premalignant lesions that may regress or disappear spontaneously, or progress to a malignant primary tumor. The somatic changes that drive abnormal growth involve activating mutations of specific oncogenes, inactivation of tumor suppressor genes, and/or disruption of epigenetic controls. The latter can result from methylation or the modification of histones and other proteins that affect the remodeling of chromosomes. Numerous non-inherited factors can cause cancer by accelerating these events.

Keywords:   oncogene, tumor suppressor gene, inflammation, cancer, mutation, epigenome

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