Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2017 Apr;96(16):e6111.
doi: 10.1097/MD.0000000000006111.

Association between ALDH2 Glu487Lys polymorphism and the risk of esophageal cancer

Affiliations
Review

Association between ALDH2 Glu487Lys polymorphism and the risk of esophageal cancer

Kang Liu et al. Medicine (Baltimore). 2017 Apr.

Abstract

Objective: A meta-analysis was carried out to further evaluate the relationship between ALDH2 Glu487Lys polymorphism and esophageal cancer risk.

Methods: A total number of 15 studies that included 3812 cases and 7376 controls were identified for our meta-analysis.

Results: Our findings indicated that individuals with the combination of Glu/Lys and Lys/Lys genotype had an increased risk of getting esophageal cancer (GA + AA vs. GG: odds ratio [OR] 1.36, 95% confidence interval [CI] 0.93-2.00, P = 0.113) with a shift pattern. Although Lys/Lys genotype carriers showed areduced esophageal cancer risk (AA vs. GA + GG: OR 0.41, 95% CI 0.23-0.72, P = 0.002). Similarly, a negative association was observed under homozygote comparison (AA vs. GG: OR 0.49, 95% CI 0.29-0.85, P = 0.011). In the China subgroup analysis, the similar results were found.

Conclusions: This meta-analysis concluded that there was a strong association between ALDH2 Glu487Lys polymorphism and the risk of esophageal cancer. It further confirmed that ALDH2 Glu487Lys polymorphism was a high-risk factor for esophageal cancer.

PubMed Disclaimer

Conflict of interest statement

The authors report no conflicts of interest.

Figures

Figure 1
Figure 1
Flow chart of selection of studies and specific reasons for exclusion from our meta-analysis.
Figure 2
Figure 2
Forest plots (A, C, and E) and Begg funnel plot (B, D, and F) for all studies under dominant model (A and B), recessive model (C and D), and homozygote model (E and F).
Figure 3
Figure 3
Forest plots (A, C, and E) and Begg funnel plot (B, D, and F) for China subgroup under dominant model (A and B), recessive model (C and D), and homozygote model (E and F).

Similar articles

Cited by

References

    1. Rice TW, Rusch VW, Apperson-Hansen C, et al. Worldwide esophageal cancer collaboration. Dis Esophagus 2009;22:1–8. - PubMed
    1. Su M, Liu M, Tian D-P, et al. Temporal trends of esophageal cancer during1995-2004inNanao Island, an extremely high-risk area in China. Eur J Epidemiol 2007;22:43–8. - PubMed
    1. Uemura N, Kondo T. Current advances in esophageal cancer proteomics. Biochim Biophys Acta 2015;1854:687–95. - PubMed
    1. Hanaoka T, Tsugane S, Ando N, et al. Alcohol consumption and risk of esophageal cancer in japan: a case-control study in seven hospitals. Jpn J Clin Oncol 1994;24:241–6. - PubMed
    1. Crabb DW, Edenberg HJ, Bosron WF, Li TK. Genotypes for aldehyde dehydrogenase deficiency and alcohol sensitivity. The inactive ALDH2(2) allele is dominant. J Clin Invest 1989;83:314–6. - PMC - PubMed

MeSH terms

Substances