Many treatments fall under the umbrella of Complementary and Alternative Medicine or CAM. Some of the most commonly used CAM therapies include: Acupuncture Chiropractic Food counseling Herbalism Massa...
Ana Sandoiu published an article that was fact checked by Jasmin Collier looking at the new predisposition mechanism for colon cancer that has been found by scientists. This new novel mechanism interferes with our DNA’s ability to repair itself and genetically predisposing some people to colon cancer.
The journal Nature Chemistry published the new study. The first author of the study is Kevin J. McDonnell from the Norris Comprehensive Cancer Center who is based at the University of Southern California in Los Angeles.
Jacqueline Barton, is the study co-author, a John G. Kirkwood and Arthur A. Noyes Professor of Chemistry at the California Institute of Technology in Pasadena, and the first researcher who identified a DNA process called DNA charge transport over 2 decades ago.
The process of DNA charge transport refers to the process in which electrons move through our DNA’s double helix, that sends signals to so-called DNA repair proteins and tells them to start fixing damage found along the way. Researchers show how a genetic variant commonly found in colon cancer disrupts this DNA charge transport process. This may have important implications for colon cancer prevention.
The team focused on a mutation in a gene called MUTYH that normally provides instructions for creating a DNA repair protein. However, genetic mutations in MUTYH affect the DNA’s ability to repair its own errors. The mutations have also been associated with polyposis, or the formation of polyps in the colon that may lead to cancer later. The MUTYH mutation focused on was called C306W that affects MUTYH’s ability to retain and keep a tiny cluster of iron and sulfur atoms together inside the protein.
Several experiments revealed the C306W mutation makes the iron-sulfur cluster degrade when coming into contact with oxygen. Iron-sulfur clusters are key for DNA repair, so the degradation prevents the MUTYH protein from doing its DNA fixing job.
McDonnell and colleagues conclude they have documented and provided an explanation for the novel mechanism of colonic polyposis and cancer predisposition linked to electrochemical compromise of the MUTYH cluster.
This may pave the way for novel prevention strategies against colon cancer. The work provides a strategy for thinking about how to possibly stabilize these repair proteins and restore their ability to carry out long-range signaling through DNA, so the repair proteins can find and fix the mutations in DNA before they lead to cancer.
Dr Fredda Branyon