"These findings help demonstrate that regardless what different environmental factors in Russia may be at play, the genetic variations still seem to be influencing risk in that population," said Jaako Lappalainen, M.D., assistant professor of psychiatry in the Center for the Translational Neuroscience of Alcoholism at Yale, and first author of the study.

The variations are in a subtype of gamma-amino butyric acid (GABA) receptor, which is the most abundant inhibitory neurotransmitter in the brain. Two large genetic studies in the U.S. last year identified an association between genetic variations in the GABRA2 receptor subtype and risk for alcohol dependence, Lappalainen said.

"There are braking neurotransmitters and accelerating neurotransmitters," he said. "GABA is one of the braking neurotransmitters. It puts the brakes on neurons so that they don't get out of control. Activating the function of GABA receptors usually decreases activity in brain neurons and can decrease activity of the entire brain and body, as occurs in general anesthesia. Some of alcohol's effects appear to be mediated through GABRA2."

This gene is often found in persons who do not become alcoholic, but its presence causes a small increase in risk that appears to be consistent across U.S. and Russian populations, Lappalainen said. It is not known how the mechanism increases the risk.

For this study, researchers recruited and drew blood samples from 113 Russian alcohol-dependent men at a St. Petersburg treatment center and100 local military personnel as controls. Each sample was genotyped for seven GABRA2 single nucleotide polymorphisms (SNPs), which are variations between individuals in the genetic code. Lappalainen and his colleagues found significant associations between two SNPs and alcohol dependence. The structure and frequencies of the variations were similar in both U.S. and Russian populations.

Lappalainen stressed that other genes have been implicated in alcoholism and that the risk of alcohol dependence is also dependent on environment and behavior.

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As part of their research to develop the new technology, the team, based at the University of Liverpool Cancer Research Centre, analysed the methylation profile of 47 genes in lung specimens from 48 patients with a history of smoking. The genes that were selected were known to be involved in cancer development and in this study they were able to accurately determine the relationship between gene methylation in normal and tumour tissue, which in the long term will be of enormous value in identifying high risk individuals.

Professor John Field, Director of the Roy Castle Lung Cancer Research Programme, said: "Early detection of lung cancer is the prime objective of our research programme. This depends on the identification of early biomarkers in patients who are at risk of developing the disease prior to clinical symptoms.

"The partnership between the University and Sequenom has provided a breakthrough in our goal to detect early genetic changes in individuals who are at the highest risk.

The research is being presented this week at the 96th annual meeting of the American Association for Cancer Research (AACR) in Anaheim, California.

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