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ADH2 And ALDH2 Are Associated With Esophageal Cancer, Study Shows

Date:
October 31, 2007
Source:
World Journal of Gastroenterology
Summary:
Esophageal cancer is a global health problem. A new study found that alcohol dehydrogenase 2 (ADH2) and aldehyde dehydrogenase 2 (ALDH2) genotypes are associated with esophageal cancer risk in Chinese. Furthermore, individuals with ADH2*1 allele and ALDH2*2 allele showed an elevated risk of developing esophageal cancer, especially among alcohol drinkers.

Esophageal cancer is a global health problem. A study led by Dr. Chun-Xia Yang recruited 191 esophageal cancer patients and 198 healthy controls from Yanting County. The research found that alcohol dehydrogenase 2 (ADH2) and aldehyde dehydrogenase 2 (ALDH2) genotypes are associated with esophageal cancer risk in Chinese. Furthermore, individuals with ADH2*1 allele and ALDH2*2 allele showed an elevated risk of developing esophageal cancer, especially among alcohol drinkers.

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As the seventh leading cause of cancer death worldwide, the occurrence of esophageal cancer varies by geographic area, ethnic group and gender. Esophageal cancer is thought to be triggered by a variety of environmental factors which interact with the host genome. Researchers have long been seeking the etiology of esophageal cancer. Many studies have been conducted on gene-environment interaction and gene polymorphisms for esophageal cancer.

One research article was published on November 21 in the World Journal of Gastroenterology to clarify the impact of alcohol dehydrogenase 2 (ADH2) and aldehyde dehydrogenase 2 (ALDH2) polymorphisms on esophageal cancer risk. This research team led by Dr. Chun-Xia Yang collected a cohort of 191 patients and 198 controls in Yanting, a rural county of Sichuan Province in China. Each participant completed a questionnaire and provided 1 mL of blood, which gave the team enough information about environmental and genetic factors on esophageal cancer.

This research reported that the ALDH2*1/*2 and ADH2*1 allele potentiate the carcinogenic effects of alcohol on the esophagus, and the two genotypes could modulate individual differences in alcohol-oxidizing capacity and drinking behavior. The acetaldehyde concentrations in the blood of individuals with inactive ALDH2*1/*2 is much higher than in those with active ALDH2 after drinking. ADH2*1 allele carriers tend to have experienced binge-drinking and withdrawal symptoms earlier in life. Accordingly, alcohol drinkers carrying ALDH2*1/*2 or ADH2*1 allele had a higher risk of developing esophageal cancer.

Furthermore, both the ADH2* 1 and ALDH2* 2 allele indicate a longer exposure to alcohol and highly-concentrated acetaldehyde, thus greatly increasing the individual‘―s susceptibility to esophageal cancer.

The ALDH2*2 allele genotype studied by Dr. Chun-Xia Yang is prevalent in Asians. The results of this study suggest the need for further exploration on the relationship between genetics and esophageal cancer and will certainly be helpful in creating prevention strategies against esophageal cancer in China.

Reference: Yang SJ, Wang HY, Li XQ, Du HZ, Zheng CJ, Chen HG, MuXY, Yang CX. Genetic polymorphisms of ADH2 and ALDH2association with esophageal cancer risk in southwest China. World J Gastroenterol 2007; 13(43): 5760-5764


Story Source:

The above story is based on materials provided by World Journal of Gastroenterology. Note: Materials may be edited for content and length.


Cite This Page:

World Journal of Gastroenterology. "ADH2 And ALDH2 Are Associated With Esophageal Cancer, Study Shows." ScienceDaily. ScienceDaily, 31 October 2007. <www.sciencedaily.com/releases/2007/10/071031090823.htm>.
World Journal of Gastroenterology. (2007, October 31). ADH2 And ALDH2 Are Associated With Esophageal Cancer, Study Shows. ScienceDaily. Retrieved December 21, 2014 from www.sciencedaily.com/releases/2007/10/071031090823.htm
World Journal of Gastroenterology. "ADH2 And ALDH2 Are Associated With Esophageal Cancer, Study Shows." ScienceDaily. www.sciencedaily.com/releases/2007/10/071031090823.htm (accessed December 21, 2014).

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