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Cancer Cells Rely on Healthy Genes for Survival

Cancer cells incorporate a number of mutated genes to wreak havoc on our healthy human bodies. However, findings from a recent study now indicate that cancer cells also rely heavily on the presence of non-mutated genes for survival. Researchers at Harvard Medical School and Brigham and Women’s Hospital carried out the study.

The researchers made their discovery through a technique known as RNA interference (RNAi). Through this process, the production of thousands of proteins are blocked, and then cells are monitored to see which proteins are the most necessary for survival.

As it turns out, many normal proteins are vital to the life of cancer cells. When some of these proteins were dropped sufficiently, the cancer cells died. Interestingly, normal cells did not appear to be as dependent on these proteins, often surviving under conditions where the cancer cells did not.

Researchers believe this dependence on non-mutated genes serves as a type of stress reduction for the cancer cells. Abnormal tumor cells are subject to higher levels of DNA replication and protein production. Researcher Ji Luo states that normal genes “probably help them deal with the problems that develop as a result of the inappropriate presence of growth and survival signaling in tumor cells.”

Through the research, the team identified 50 proteins that kill cancer cells (but not normal cells) when normal production is blocked. These proteins now serve as new potential avenues for cancer treatment.

The hope is that drugs may be produced that effectively augment the levels of these proteins so that cancer cells are killed and normal cells survive.

Funding for the project came from several different sources, including the AACR Prevent Cancer Foundation AstraZeneca Fellowship in Translational Lung Cancer Research, the Damon Runyon Cancer Research Foundation, the National Institutes of Health, the Department of Defense and the Susan G. Komen for the Cure Foundation

Resource: http://web.med.harvard.edu/sites/RELEASES/html/052809_elledge.html