How Cells Avoid Becoming Cancerous

Researchers have described for the first time a web of inter-related responses that cells use to avoid becoming diseased or cancerous after being exposed to a powerful chemical mutagen. The study showed an elaborate system of gene control that is triggered by DNA chemical damage to and provided light on the complexity of DNA repair. The findings could eventually be used to develop drugs to boost DNA repair in response to environmental toxins.

DNA damage is important in coping with environmental toxins and a number of congenital diseases. Scientists have discovered many parts of the DNA-damage-repair machinery, except a 'systems biology' approach that explains how all the parts function together to enable a cell to repair its DNA while under routine assault. Scientists analyzed the effect of exposure of yeast cells to MMS (methyl-methanesulfonate), a chemical known to cause alkylation injury which results in small kinks in the otherwise smoothly curving double helix of DNA. Cells then rapidly identify the damage, stop dividing, excise the damaged DNA, and use several alternate methods to substitute a clean copy of genetic material.

However scientists have been mystified by another group of genes whose expression is sharply affected by DNA damage, but which appear to play no role in repairing the damage itself. They theorized that when a cell's DNA is damaged, the cell may be programmed to also stop dividing and perform a variety of housekeeping chores while it repairs its DNA. This demystifies the long-standing question of why DNA damage influences the expression of hundreds of genes not involved in the actual repair process.