Cytochrome P450 1A1 gene polymorphisms and digestive tract cancer susceptibility: a meta‐analysis. Issue 9 (6th April 2016)

• Record Type: Journal Article
• Authors: Ren, Anjing; Qin, Tingting; Wang, Qianqian; Du, Haina; Zhong, Donghua; Hua, Yibing; Zhu, Lingjun
• Is Part Of: Journal of cellular and molecular medicine. Volume 20:Issue 9(2016)
• Page Start: 1620
• Page End: 1631
• Publication Date: 2016-04-06
• Subjects: CYP1A1 -- digestive tract cancer -- polymorphism -- meta‐analysis; Cytology; Medicine; Molecular Biology; Cytologie -- Périodiques; Médecine -- Périodiques; Biologie moléculaire -- Périodiques; Cytology -- Periodicals; Medicine -- Periodicals; Molecular biology -- Periodicals; 611.01805
• DOI: 10.1111/jcmm.12853
• Languages: English
• ISSNs: 1582-1838

Abstract

Abstract: Cytochrome P450 1A1 (CYP1A1) is a phase I enzyme that regulates the metabolism of environmental carcinogens and alter the susceptibility to various cancers. Many studies have investigated the association between the CYP1A1 MspI and Ile462Val polymorphisms and digestive tract cancer (DTC) risk in different groups of populations, but their results were inconsistent. The PubMed and Embase Database were searched for case–control studies published up to 30th September, 2015. Data were extracted and pooled odds ratios (ORs) with 95% confidence intervals (CIs) were calculated to assess the relationship. Totally, 39 case–control studies (9094 cases and 12, 487 controls) were included. The G allele in Ile/Val polymorphism was significantly associated with elevated DTC risk with per‐allele OR of 1.24 (95% CI = 1.09–1.41, P = 0.001). Similar results were also detected under the other genetic models. Evidence was only found to support an association between MspI polymorphism and DTC in the subgroups of caucasian and mixed individuals, but not in the whole population (the dominant model: OR = 1.19, 95% CI = 0.94–1.91, P = 0.146). In conclusion, our results suggest that the CYP1A1 polymorphisms are potential risk factors for DTC. And large sample size and well‐designed studies with detailed clinical information are needed to more precisely evaluate our founding.