Genetically Engineered Mice shows Clues to blow away Cancer

Deleting two genes in mice responsible for repairing DNA strands damaged by oxidation leads to several types of tumors, providing additional evidence that such stress contributes to the development of cancer. That’s the conclusion of a recent study in DNA Repair by researchers at the National Institute of Standards and Technology (NIST), Oregon Health and Science University (OHSU) and the New York University School of Medicine (NYUSM).

Although all cells need oxygen to survive, the element also can be stressful to cells and their components—particularly DNA—as part of “reactive species” in the environment, such as free radicals and peroxides. The damage levied on DNA by these compounds can include lesions, breaks, cross-links and deletions—errors in our normal genetic codes that, if left unchecked, may accelerate the aging process and increase susceptibility to several disease states. In humans, DNA repair genes produce enzymes called DNA glycosylases that excise sections of DNA strands already modified by oxidative stress, and thus protect the genetic material.

One of these repair genes, neil1, was identified and characterized in 2002 by Sankar Mitra and his team at the University of Texas Medical Branch in collaboration with NIST researchers Miral Dizdaroglu and Pawel Jaruga. The gene produces a DNA repair protein, NEIL1 that is nearly identical in humans and mice. Therefore, a mouse serves a perfect model for studying the biological function of the neil1 gene in both species. The researchers state that their results emphasize the role of DNA repair in preventing carcinogenesis. The work may lead to the development of new measurement methods and reference materials for accurate and reproducible assessments of DNA damage and repair and contribute to understanding the role of oxidatively induced DNA damage and its repair in carcinogenesis. Future studies will focus on the role of NEIL1 in disease processes.