Publication Date:
2012-04-25
Description:
The p 73 gene (1p36–33) is involved in cancer development through cell growth inhibition by inducing apoptosis in a p 53-like manner. The p 73 G4C14-to-A4T14 dinucleotide polymorphism, consisting of two single-nucleotide polymorphisms in the non-coding region of exon 2 that are in complete linkage disequilibrium, has been extensively studied in association with cancer risk. We performed a meta-analysis of published studies that examined the association between this p 73 G4C14-to-A4T14 polymorphism and cancer by searching for relevant studies on Medline and Embase up to February 28, 2010. Pooling data from 19 case–control studies that included 6510 cancer cases and 5711 controls, we found that carriers of the p 73 G4C14-to-A4T14 homozygous variant genotype (AT/AT) had an increased global risk of cancer [odds ratio (OR) = 1.30, 95% confidence interval (CI), 1.03–1.65]. There was no evidence of an effect modification of p 73 AT/AT by age, gender, ethnicity or smoking status in subgroup analyses; however, a 1.35-fold statistically significant increased risk was found among individuals 〈55 years old. In case-only analysis, the homozygous p 73 G4C14-to-A4T14 variant of p 73 genotype was associated with the presence of the p 53 exon 4 Arg72Pro allele (OR = 1.30, 95% CI, 1.02–1.64), which is suggestive of a biological interaction between the two genes in carcinogenesis. In conclusion, the p 73 G4C14-to-A4T14 homozygous variant genotype might be a risk factor for cancer, especially in combination with the p 53 exon 4 Arg72Pro polymorphism. Further studies looking at p 73 G4C14-to-A4T14 and p 53 exon 4 Arg72Pro interaction are required to support our findings.
Print ISSN:
0267-8357
Electronic ISSN:
1464-3804
Topics:
Biology
,
Medicine
