Cancer Epigenomics: a review
Epigenetic inactivation of genes that are crucial for the control of normal cell growth is a hallmark of cancer cells. Epigenetic modifications of the DNA do not alter the nucleotide sequence instead they involve the regulation of gene transcription and DNA methylation. Hypermethylation or histone d...
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Veröffentlicht in: | Internet journal of medical update 2011-01, Vol.6 (1), p.51 |
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description | Epigenetic inactivation of genes that are crucial for the control of normal cell growth is a hallmark of cancer cells. Epigenetic modifications of the DNA do not alter the nucleotide sequence instead they involve the regulation of gene transcription and DNA methylation. Hypermethylation or histone deacetylation, which is within the promoter of a tumor suppressor gene, leads to the silencing as well as a deletion or a mutation of that gene. Cancer cells often show aberrant methylation and the frequency of aberrations increases is seen with the progression of disease. Hypermethylation events can occur early in tumorogenesis, involving the disruption of pathways that may predispose cells to malignant transformation. Epigenetic modification such as DNA methylation can be exploited for clinical purposes in cancer patients, first using hypermethylation as a molecular biomarker of cancer cells and second, epigenetic changes which are potentially reversible. KEY WORDS: Cancer; Epigenomics; Methylation |
doi_str_mv | 10.4314/ijmu.v6i1.63977 |
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KEY WORDS: Cancer; Epigenomics; Methylation</description><identifier>ISSN: 1694-0423</identifier><identifier>EISSN: 1694-0423</identifier><identifier>DOI: 10.4314/ijmu.v6i1.63977</identifier><language>eng</language><publisher>Dr. Arun Kumar Agnihotri</publisher><subject>Cancer ; Development and progression ; DNA ; Epigenetic inheritance ; Genetic aspects ; Methylation ; Physiological aspects ; Risk factors</subject><ispartof>Internet journal of medical update, 2011-01, Vol.6 (1), p.51</ispartof><rights>COPYRIGHT 2011 Dr. Arun Kumar Agnihotri</rights><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c269t-b02c0abace684194cd5b103f7eb6fa95e2356cac277de4ad62adb0b28064e86d3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids></links><search><creatorcontrib>Kumar, Robby</creatorcontrib><creatorcontrib>Sharan, Nishant</creatorcontrib><title>Cancer Epigenomics: a review</title><title>Internet journal of medical update</title><description>Epigenetic inactivation of genes that are crucial for the control of normal cell growth is a hallmark of cancer cells. Epigenetic modifications of the DNA do not alter the nucleotide sequence instead they involve the regulation of gene transcription and DNA methylation. Hypermethylation or histone deacetylation, which is within the promoter of a tumor suppressor gene, leads to the silencing as well as a deletion or a mutation of that gene. Cancer cells often show aberrant methylation and the frequency of aberrations increases is seen with the progression of disease. Hypermethylation events can occur early in tumorogenesis, involving the disruption of pathways that may predispose cells to malignant transformation. Epigenetic modification such as DNA methylation can be exploited for clinical purposes in cancer patients, first using hypermethylation as a molecular biomarker of cancer cells and second, epigenetic changes which are potentially reversible. KEY WORDS: Cancer; Epigenomics; Methylation</description><subject>Cancer</subject><subject>Development and progression</subject><subject>DNA</subject><subject>Epigenetic inheritance</subject><subject>Genetic aspects</subject><subject>Methylation</subject><subject>Physiological aspects</subject><subject>Risk factors</subject><issn>1694-0423</issn><issn>1694-0423</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><recordid>eNptkMtLw0AQhxdRsFbPXjwEBG9J95VN4q2E-oCCFz0vk82k3ZJH2U0r_vdNrIcWZA4zDN9vGD5C7hmNpGByZjfNLtoryyIlsiS5IBOmMhlSycXlyXxNbrzfUKoYl3xCHnJoDbpgsbUrbLvGGv8cQOBwb_H7llxVUHu8--tT8vWy-MzfwuXH63s-X4aGq6wPC8oNhQIMqlSyTJoyLhgVVYKFqiCLkYtYGTA8SUqUUCoOZUELnlIlMVWlmJLH490V1KhtW3W9A9NYb_Scy1TSWNJsoKJ_qKFKHN7uWqzssD8LPJ0E1gh1v_Zdvett1_pzcHYEjeu8d1jprbMNuB_NqB7l6lGuHuXqX7niAOaua1c</recordid><startdate>20110101</startdate><enddate>20110101</enddate><creator>Kumar, Robby</creator><creator>Sharan, Nishant</creator><general>Dr. Arun Kumar Agnihotri</general><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>20110101</creationdate><title>Cancer Epigenomics: a review</title><author>Kumar, Robby ; Sharan, Nishant</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c269t-b02c0abace684194cd5b103f7eb6fa95e2356cac277de4ad62adb0b28064e86d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Cancer</topic><topic>Development and progression</topic><topic>DNA</topic><topic>Epigenetic inheritance</topic><topic>Genetic aspects</topic><topic>Methylation</topic><topic>Physiological aspects</topic><topic>Risk factors</topic><toplevel>online_resources</toplevel><creatorcontrib>Kumar, Robby</creatorcontrib><creatorcontrib>Sharan, Nishant</creatorcontrib><collection>CrossRef</collection><jtitle>Internet journal of medical update</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kumar, Robby</au><au>Sharan, Nishant</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cancer Epigenomics: a review</atitle><jtitle>Internet journal of medical update</jtitle><date>2011-01-01</date><risdate>2011</risdate><volume>6</volume><issue>1</issue><spage>51</spage><pages>51-</pages><issn>1694-0423</issn><eissn>1694-0423</eissn><abstract>Epigenetic inactivation of genes that are crucial for the control of normal cell growth is a hallmark of cancer cells. Epigenetic modifications of the DNA do not alter the nucleotide sequence instead they involve the regulation of gene transcription and DNA methylation. Hypermethylation or histone deacetylation, which is within the promoter of a tumor suppressor gene, leads to the silencing as well as a deletion or a mutation of that gene. Cancer cells often show aberrant methylation and the frequency of aberrations increases is seen with the progression of disease. Hypermethylation events can occur early in tumorogenesis, involving the disruption of pathways that may predispose cells to malignant transformation. Epigenetic modification such as DNA methylation can be exploited for clinical purposes in cancer patients, first using hypermethylation as a molecular biomarker of cancer cells and second, epigenetic changes which are potentially reversible. KEY WORDS: Cancer; Epigenomics; Methylation</abstract><pub>Dr. Arun Kumar Agnihotri</pub><doi>10.4314/ijmu.v6i1.63977</doi></addata></record> |
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source | African Journals Online (Open Access); EZB-FREE-00999 freely available EZB journals |
subjects | Cancer Development and progression DNA Epigenetic inheritance Genetic aspects Methylation Physiological aspects Risk factors |
title | Cancer Epigenomics: a review |
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