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Association between P16(INK4a) Promoter Methylation and Ovarian Cancer: A Meta-Analysis of 12 Published Studies

BACKGROUND: Ovarian cancer is the primary cause of death in women diagnosed with gynecological malignancies worldwide. Absence of early symptoms prevents prompt diagnosis or successful therapeutic intervention. P16(INK4a) is a well-known tumor suppressor gene (TSG). Aberrant methylation of TSG promo...

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Autores principales: Xiao, Xiyue, Cai, Fucheng, Niu, Xun, Shi, Hao, Zhong, Yi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5029926/
https://www.ncbi.nlm.nih.gov/pubmed/27648827
http://dx.doi.org/10.1371/journal.pone.0163257
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author Xiao, Xiyue
Cai, Fucheng
Niu, Xun
Shi, Hao
Zhong, Yi
author_facet Xiao, Xiyue
Cai, Fucheng
Niu, Xun
Shi, Hao
Zhong, Yi
author_sort Xiao, Xiyue
collection PubMed
description BACKGROUND: Ovarian cancer is the primary cause of death in women diagnosed with gynecological malignancies worldwide. Absence of early symptoms prevents prompt diagnosis or successful therapeutic intervention. P16(INK4a) is a well-known tumor suppressor gene (TSG). Aberrant methylation of TSG promoter is an important epigenetic silencing mechanism leading to ovarian cancer progression. Studies have reported differences in methylation frequencies of the p16(INK4a) promoter between ovarian cancer and the corresponding control group. However, the association between p16(INK4a) promoter methylation and ovarian cancer remains unclear and controversial. Therefore, a meta-analysis was conducted to clarify the relationship between p16(INK4a) promoter methylation and ovarian cancer. METHODS: PubMed, Web of Science, EMBASE and CNKI were searched to identify eligible studies for the evaluation of the association between p16(INK4a) promoter methylation and ovarian cancer. Odds ratio (ORs) and 95% confidence intervals (95%CI) were calculated to determine the strength of association between p16(INK4a) promoter methylation and ovarian cancer. RESULTS: A total of 612 ovarian cancer patients and 289 controls from 12 eligible studies were included in the meta-analysis. Overall, a significant association was observed between p16(INK4a) methylation status and ovarian cancer risk using a fixed-effects model (OR = 2.02, 95% CI = 1.39–2.94). CONCLUSION: The results of our meta-analysis show that aberrant methylation of p16(INK4a) promoter was significantly associated with ovarian cancer. It may represent a promising molecular marker to monitor the disease and provides new insights into the treatment of human ovarian cancer.
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spelling pubmed-50299262016-10-10 Association between P16(INK4a) Promoter Methylation and Ovarian Cancer: A Meta-Analysis of 12 Published Studies Xiao, Xiyue Cai, Fucheng Niu, Xun Shi, Hao Zhong, Yi PLoS One Research Article BACKGROUND: Ovarian cancer is the primary cause of death in women diagnosed with gynecological malignancies worldwide. Absence of early symptoms prevents prompt diagnosis or successful therapeutic intervention. P16(INK4a) is a well-known tumor suppressor gene (TSG). Aberrant methylation of TSG promoter is an important epigenetic silencing mechanism leading to ovarian cancer progression. Studies have reported differences in methylation frequencies of the p16(INK4a) promoter between ovarian cancer and the corresponding control group. However, the association between p16(INK4a) promoter methylation and ovarian cancer remains unclear and controversial. Therefore, a meta-analysis was conducted to clarify the relationship between p16(INK4a) promoter methylation and ovarian cancer. METHODS: PubMed, Web of Science, EMBASE and CNKI were searched to identify eligible studies for the evaluation of the association between p16(INK4a) promoter methylation and ovarian cancer. Odds ratio (ORs) and 95% confidence intervals (95%CI) were calculated to determine the strength of association between p16(INK4a) promoter methylation and ovarian cancer. RESULTS: A total of 612 ovarian cancer patients and 289 controls from 12 eligible studies were included in the meta-analysis. Overall, a significant association was observed between p16(INK4a) methylation status and ovarian cancer risk using a fixed-effects model (OR = 2.02, 95% CI = 1.39–2.94). CONCLUSION: The results of our meta-analysis show that aberrant methylation of p16(INK4a) promoter was significantly associated with ovarian cancer. It may represent a promising molecular marker to monitor the disease and provides new insights into the treatment of human ovarian cancer. Public Library of Science 2016-09-20 /pmc/articles/PMC5029926/ /pubmed/27648827 http://dx.doi.org/10.1371/journal.pone.0163257 Text en © 2016 Xiao et al http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Article
Xiao, Xiyue
Cai, Fucheng
Niu, Xun
Shi, Hao
Zhong, Yi
Association between P16(INK4a) Promoter Methylation and Ovarian Cancer: A Meta-Analysis of 12 Published Studies
title Association between P16(INK4a) Promoter Methylation and Ovarian Cancer: A Meta-Analysis of 12 Published Studies
title_full Association between P16(INK4a) Promoter Methylation and Ovarian Cancer: A Meta-Analysis of 12 Published Studies
title_fullStr Association between P16(INK4a) Promoter Methylation and Ovarian Cancer: A Meta-Analysis of 12 Published Studies
title_full_unstemmed Association between P16(INK4a) Promoter Methylation and Ovarian Cancer: A Meta-Analysis of 12 Published Studies
title_short Association between P16(INK4a) Promoter Methylation and Ovarian Cancer: A Meta-Analysis of 12 Published Studies
title_sort association between p16(ink4a) promoter methylation and ovarian cancer: a meta-analysis of 12 published studies
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5029926/
https://www.ncbi.nlm.nih.gov/pubmed/27648827
http://dx.doi.org/10.1371/journal.pone.0163257
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