When molecular disaster strikes, causing structural damage to DNA, players in two important pathways talk to each other to help contain the wreckage, scientists at The University of Texas M. D. Anderson Cancer Center report in the August edition of Cell.

A new UC Davis study that explains the actions of a gene mutation that causes early onset cancer provides a fundamental insight into the mechanism of DNA-break repair.

Ionizing radiation, toxic chemicals, and other agents continually damage the body's DNA, threatening life and health: unrepaired DNA can lead to mutations, which in turn can lead to diseases like cancer. Intricate DNA repair mechanisms in the cells' nuclei are constantly working to fix what's broken, but whether the repair work happens "on the road" — right where the damage occurs — or "in the shop" — at specific regions of the nucleus — is an unanswered question.

When a strand of DNA breaks in the body's cells, it normally does not take long until it has been repaired. Now researchers at the Swedish medical university Karolinska Institutet have discovered a new mechanism that helps to explain how the cell performs these repairs. The results are presented in Science.

A protein long known to be involved in protecting cells from genetic damage has been found to play an even more important role in protecting the cell's offspring.

Scientists from the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Cancer Institute (NCI), and Integrative Bioinformatics Inc. have made an important discovery about the role of an enzyme called ataxia telangiectasia mutated protein (ATM) in the body’s ability to repair damaged DNA. NIAMS and NCI are part of the National Institutes of Health (NIH).

Scientists probing the details of viral infection have discovered an intriguing surprise: in mice, herpes viruses hijack their host cells' tools for fixing DNA damage and use those tools to enhance their own reproduction.

Chronic active hepatitis C (HCV) remains the strongest connection to the development of hepatocellular carcinoma (HCC, liver cancer). Unfortunately, the mechanism behind hepatitis-associated cancer remains puzzling. Such effects as oxidative stress and DNA damage are known to occur in hepatitis, through which the role of the liver in nucleic acid metabolism may be impacted.