Ferguson is also a co-author of a related study of Mre11 published online this week in Nature. The two new studies together reveal that the same protein that assures normal B-cell function also plays a role in a type of gene damage associated with both cancer and aging.

The Nature Structural and Molecular Biology study shows that the body needs Mre11 action to properly repair double strand breaks in B cells, allowing the immune system to function correctly. But the Nature study reveals that Mre11's repair action at the ends of chromosomes, called telomeres, can facilitate catastrophic chromosome fusing. Fused chromosomes are implicated in cancer and aging.

What's next

In further research in mice, Ferguson and his team are now searching for specific evidence that double strand breaks get "misrepaired" in ways that lead to B-cell lymphoma. The research may eventually lead to human trials of new strategies in cancer diagnosis and treatment.

Additional authors: Maria Dinkelmann and Elizabeth Spehalski, co-first authors, U-M Department of Pathology; Trina Stoneham, Jeffrey Buis and Yipin Wu, U-M Department of Pathology; JoAnn M. Sekiguchi, U-M Departments of Internal Medicine and Human Genetics.

Funding: National Institutes of Health, Sidney Kimmel Cancer Research Foundation, University of Michigan Cancer Center. Ferguson recently was awarded funding for five years as a Leukemia & Lymphoma Society Scholar.

Citations: Nature Structural and Molecular Biology, doi: 10.1038/nsmb.1639; Nature, doi:10.1038/nature08196

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