DAPK1 Promoter Methylation and Cervical Cancer Risk: A Systematic Review and a Meta-Analysis
The Death-Associated Protein Kinase 1 (DAPK1) gene has been frequently investigated in cervical cancer (CC). The aim of the present study was to carry out a systematic review and a meta-analysis in order to evaluate DAPK1 promoter methylation as an epigenetic marker for CC risk. A systematic literat...
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description | The Death-Associated Protein Kinase 1 (DAPK1) gene has been frequently investigated in cervical cancer (CC). The aim of the present study was to carry out a systematic review and a meta-analysis in order to evaluate DAPK1 promoter methylation as an epigenetic marker for CC risk.
A systematic literature search was carried out. The Cochrane software package Review Manager 5.2 was used. The fixed-effects or random-effects models, according to heterogeneity across studies, were used to calculate odds ratios (ORs) and 95% Confidence Intervals (CIs). Furthermore, subgroup analyses were conducted by histological type, assays used to evaluate DAPK1 promoter methylation, and control sample source.
A total of 20 papers, published between 2001 and 2014, on 1929 samples, were included in the meta-analysis. DAPK1 promoter methylation was associated with an increased CC risk based on the random effects model (OR: 21.20; 95%CI = 11.14-40.35). Omitting the most heterogeneous study, the between study heterogeneity decreased and the association increased (OR: 24.13; 95% CI = 15.83-36.78). The association was also confirmed in all the subgroups analyses.
A significant strong association between DAPK1 promoter methylation and CC was shown and confirmed independently by histological tumor type, method used to evaluate methylation and source of control samples. Methylation markers may have value in early detection of CC precursor lesions, provide added reassurances of safety for women who are candidates for less frequent screens, and predict outcomes of women infected with human papilloma virus. |
doi_str_mv | 10.1371/journal.pone.0135078 |
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A systematic literature search was carried out. The Cochrane software package Review Manager 5.2 was used. The fixed-effects or random-effects models, according to heterogeneity across studies, were used to calculate odds ratios (ORs) and 95% Confidence Intervals (CIs). Furthermore, subgroup analyses were conducted by histological type, assays used to evaluate DAPK1 promoter methylation, and control sample source.
A total of 20 papers, published between 2001 and 2014, on 1929 samples, were included in the meta-analysis. DAPK1 promoter methylation was associated with an increased CC risk based on the random effects model (OR: 21.20; 95%CI = 11.14-40.35). Omitting the most heterogeneous study, the between study heterogeneity decreased and the association increased (OR: 24.13; 95% CI = 15.83-36.78). The association was also confirmed in all the subgroups analyses.
A significant strong association between DAPK1 promoter methylation and CC was shown and confirmed independently by histological tumor type, method used to evaluate methylation and source of control samples. Methylation markers may have value in early detection of CC precursor lesions, provide added reassurances of safety for women who are candidates for less frequent screens, and predict outcomes of women infected with human papilloma virus.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0135078</identifier><identifier>PMID: 26267895</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Cancer ; Cervical cancer ; Cervix ; Confidence intervals ; Death-associated protein kinase ; Death-Associated Protein Kinases - genetics ; DNA Methylation ; Female ; Health risks ; Heterogeneity ; Human papillomavirus ; Humans ; Kinases ; Lesions ; Meta-analysis ; Odds Ratio ; Promoter Regions, Genetic ; Proteins ; Reviews ; Risk ; Screens ; Squamous cell carcinoma ; Stem cells ; Subgroups ; Systematic review ; Uterine Cervical Neoplasms - epidemiology ; Uterine Cervical Neoplasms - genetics ; Uterine Cervical Neoplasms - pathology ; Viruses</subject><ispartof>PloS one, 2015-08, Vol.10 (8), p.e0135078-e0135078</ispartof><rights>2015 Agodi et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2015 Agodi et al 2015 Agodi et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c475t-45582a66008232bc787a87cd907e46ffd50f81791deca230054c0fb1b52255253</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4534406/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4534406/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,886,2103,2929,23871,27929,27930,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26267895$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Calogero, Raffaele A</contributor><creatorcontrib>Agodi, Antonella</creatorcontrib><creatorcontrib>Barchitta, Martina</creatorcontrib><creatorcontrib>Quattrocchi, Annalisa</creatorcontrib><creatorcontrib>Maugeri, Andrea</creatorcontrib><creatorcontrib>Vinciguerra, Manlio</creatorcontrib><title>DAPK1 Promoter Methylation and Cervical Cancer Risk: A Systematic Review and a Meta-Analysis</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>The Death-Associated Protein Kinase 1 (DAPK1) gene has been frequently investigated in cervical cancer (CC). The aim of the present study was to carry out a systematic review and a meta-analysis in order to evaluate DAPK1 promoter methylation as an epigenetic marker for CC risk.
A systematic literature search was carried out. The Cochrane software package Review Manager 5.2 was used. The fixed-effects or random-effects models, according to heterogeneity across studies, were used to calculate odds ratios (ORs) and 95% Confidence Intervals (CIs). Furthermore, subgroup analyses were conducted by histological type, assays used to evaluate DAPK1 promoter methylation, and control sample source.
A total of 20 papers, published between 2001 and 2014, on 1929 samples, were included in the meta-analysis. DAPK1 promoter methylation was associated with an increased CC risk based on the random effects model (OR: 21.20; 95%CI = 11.14-40.35). Omitting the most heterogeneous study, the between study heterogeneity decreased and the association increased (OR: 24.13; 95% CI = 15.83-36.78). The association was also confirmed in all the subgroups analyses.
A significant strong association between DAPK1 promoter methylation and CC was shown and confirmed independently by histological tumor type, method used to evaluate methylation and source of control samples. Methylation markers may have value in early detection of CC precursor lesions, provide added reassurances of safety for women who are candidates for less frequent screens, and predict outcomes of women infected with human papilloma virus.</description><subject>Cancer</subject><subject>Cervical cancer</subject><subject>Cervix</subject><subject>Confidence intervals</subject><subject>Death-associated protein kinase</subject><subject>Death-Associated Protein Kinases - genetics</subject><subject>DNA Methylation</subject><subject>Female</subject><subject>Health risks</subject><subject>Heterogeneity</subject><subject>Human papillomavirus</subject><subject>Humans</subject><subject>Kinases</subject><subject>Lesions</subject><subject>Meta-analysis</subject><subject>Odds Ratio</subject><subject>Promoter Regions, Genetic</subject><subject>Proteins</subject><subject>Reviews</subject><subject>Risk</subject><subject>Screens</subject><subject>Squamous cell carcinoma</subject><subject>Stem cells</subject><subject>Subgroups</subject><subject>Systematic review</subject><subject>Uterine Cervical Neoplasms - 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genetics</topic><topic>DNA Methylation</topic><topic>Female</topic><topic>Health risks</topic><topic>Heterogeneity</topic><topic>Human papillomavirus</topic><topic>Humans</topic><topic>Kinases</topic><topic>Lesions</topic><topic>Meta-analysis</topic><topic>Odds Ratio</topic><topic>Promoter Regions, Genetic</topic><topic>Proteins</topic><topic>Reviews</topic><topic>Risk</topic><topic>Screens</topic><topic>Squamous cell carcinoma</topic><topic>Stem cells</topic><topic>Subgroups</topic><topic>Systematic review</topic><topic>Uterine Cervical Neoplasms - epidemiology</topic><topic>Uterine Cervical Neoplasms - genetics</topic><topic>Uterine Cervical Neoplasms - pathology</topic><topic>Viruses</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Agodi, Antonella</creatorcontrib><creatorcontrib>Barchitta, Martina</creatorcontrib><creatorcontrib>Quattrocchi, Annalisa</creatorcontrib><creatorcontrib>Maugeri, Andrea</creatorcontrib><creatorcontrib>Vinciguerra, Manlio</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Agodi, Antonella</au><au>Barchitta, Martina</au><au>Quattrocchi, Annalisa</au><au>Maugeri, Andrea</au><au>Vinciguerra, Manlio</au><au>Calogero, Raffaele A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>DAPK1 Promoter Methylation and Cervical Cancer Risk: A Systematic Review and a Meta-Analysis</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2015-08-12</date><risdate>2015</risdate><volume>10</volume><issue>8</issue><spage>e0135078</spage><epage>e0135078</epage><pages>e0135078-e0135078</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>The Death-Associated Protein Kinase 1 (DAPK1) gene has been frequently investigated in cervical cancer (CC). The aim of the present study was to carry out a systematic review and a meta-analysis in order to evaluate DAPK1 promoter methylation as an epigenetic marker for CC risk.
A systematic literature search was carried out. The Cochrane software package Review Manager 5.2 was used. The fixed-effects or random-effects models, according to heterogeneity across studies, were used to calculate odds ratios (ORs) and 95% Confidence Intervals (CIs). Furthermore, subgroup analyses were conducted by histological type, assays used to evaluate DAPK1 promoter methylation, and control sample source.
A total of 20 papers, published between 2001 and 2014, on 1929 samples, were included in the meta-analysis. DAPK1 promoter methylation was associated with an increased CC risk based on the random effects model (OR: 21.20; 95%CI = 11.14-40.35). Omitting the most heterogeneous study, the between study heterogeneity decreased and the association increased (OR: 24.13; 95% CI = 15.83-36.78). The association was also confirmed in all the subgroups analyses.
A significant strong association between DAPK1 promoter methylation and CC was shown and confirmed independently by histological tumor type, method used to evaluate methylation and source of control samples. Methylation markers may have value in early detection of CC precursor lesions, provide added reassurances of safety for women who are candidates for less frequent screens, and predict outcomes of women infected with human papilloma virus.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>26267895</pmid><doi>10.1371/journal.pone.0135078</doi><oa>free_for_read</oa></addata></record> |
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subjects | Cancer Cervical cancer Cervix Confidence intervals Death-associated protein kinase Death-Associated Protein Kinases - genetics DNA Methylation Female Health risks Heterogeneity Human papillomavirus Humans Kinases Lesions Meta-analysis Odds Ratio Promoter Regions, Genetic Proteins Reviews Risk Screens Squamous cell carcinoma Stem cells Subgroups Systematic review Uterine Cervical Neoplasms - epidemiology Uterine Cervical Neoplasms - genetics Uterine Cervical Neoplasms - pathology Viruses |
title | DAPK1 Promoter Methylation and Cervical Cancer Risk: A Systematic Review and a Meta-Analysis |
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