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Meta-Analysis
. 2013;8(1):e53308.
doi: 10.1371/journal.pone.0053308. Epub 2013 Jan 22.

Association of +331G/A PgR polymorphism with susceptibility to female reproductive cancer: evidence from a meta-analysis

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Meta-Analysis

Association of +331G/A PgR polymorphism with susceptibility to female reproductive cancer: evidence from a meta-analysis

Sanjib Chaudhary et al. PLoS One. 2013.

Abstract

The progesterone receptor (PgR), a sex steroid hormone receptor that binds progesterone is critical for normal breast development. The PgR (+331G/A, rs10895068) promoter polymorphism is associated with cancer risk possibly by altering the expression of progesterone receptor B isoform. Previous studies have provided inconsistent results. To validate the association between the PgR +331G/A polymorphism and female reproductive cancer risk (breast, endometrial and ovarian cancer), we performed a meta-analysis of 19 studies (19,978 cases and 24,525 controls) by using the CMA Version 2 software. Odds ratios (ORs) and 95% confidence intervals (CIs) were used to assess the strength of the associations. The overall results indicated that the variant allele and genotypes were associated with a mild increase in overall female reproductive cancer risk (A vs. G: OR = 1.063, 95% CI = 1.001-1.129; AA+AG vs. GG: OR = 1.067, 95% CI = 1.002-1.136). The results suggest that the PgR +331G/A polymorphism might be associated with an increased female reproductive cancer risk.

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Conflict of interest statement

Competing Interests: The authors declare that they have no conflict of interest.

Figures

Figure 1
Figure 1. Forest plot of overall cancer risk associated with +331G/A PgR polymorphism.
The squares and horizontal lines correspond to the study-specific OR and 95% CI. The area of the squares reflects the weight of the respective study. The diamond represents the pooled OR and 95% CI. Forest plots evaluating the association of overall allele (I), and dominant (II) genetic model with cancer risk are presented. Breast cancer, endometrial cancer and ovarian cancer denoted as a, b, and c respectively.

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Grants and funding

SC, AKP and DRM were supported by Department of Biotechnology, Council of Scientific and Industrial Research and Indian Council of Medical Research respectively. This work was supported by intramural grant of Institute of Life Sciences, Department of Biotechnology, Government of India. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.