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This Week in BMC Cancer: Oct 17, 2011

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In BMC Cancer this week, researchers in Sweden present a meta-analysis on the risk of liver cancer after alcohol cessation. It is well-established that drinking alcohol raises a person's risk of liver cancer, but the effect of stopping drinking is not as well known. For this study, the authors conducted a review of available literature, and found that cessation of drinking decreases the risk of liver cancer by about 6 percent to 7 percent a year. "As an illustration it is estimated that a time period of 23 years is required after drinking cessation, with a correspondingly large 95 percent confidence interval of 14 to 70 years, for the risk of liver cancer to be equal to that of never drinkers," the authors write. However, as there have been so few studies done on this topic, it's not possible to extrapolate the findings of this study to the general population, the team says, adding that more work is required.

Also in BMC Cancer this week, researchers in Germany explore the association between variants in DNA repair genes and the risk of various cancers and pre-cancerous lesions like chronic atrophic gastritis. The researchers analyzed data from a cohort of 533 gastritis cases and 1,054 controls, both with polymorphisms in 11 DNA repair genes, but found no association for any of the polymorphisms they studied. "On the basis of a large number of CAG cases, they do not support associations of DNA repair pathway SNPs with CAG risk, but suggest the need of larger studies to disclose or exclude potential weak associations, or of studies with full coverage of candidate genes," the team adds.

Finally in BMC Cancer this week, a team of researchers in Canada report that the Nck2 adaptor protein promotes human melanoma cell proliferation, migration, and invasion in vitro, and primary tumor growth in vivo. The team analyzed Nck2 expression in various cancer cell lines at different stages of progression, and assessed the tumor growth rate of Nck2-over-expressing human melanoma cells in mice. They found that Nck2 expression is consistently increased in various metastatic cancer cell lines, and that Nck2 over-expression is implicated in increased growth and migration of melanoma cells. "Collectively, our data indicate that Nck2 effectively influences human melanoma phenotype progression," the authors write. "This study provides new insights regarding cancer progression that could impact on the therapeutic strategies targeting cancer."

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