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Unusual Tumor-Suppressor Gene Switches Off in Lung Cancer

by Medindia Content Team on Jan 19 2006 6:04 PM

Researchers at Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute, have found a tumor suppressor gene that could be of vital significance in the development of head and neck cancers as well as lung cancer. Their study shows that activating this particular gene could slow up the development of the aforementioned cancers.

The gene, called TCF21 is switched off in tumor cells through a process called DNA methylation. This particular process is reversible and by targeting drugs at this the development of lung cancer can be halted. Tumor-suppressor genes are basically those that prevent the cells from growing without control. When one of these genes is switched off, it could trigger the growth of cancer. In the current study, which appeared online in the January 13 early edition of the Proceedings of the National Academy of Sciences, it was found that TCF21 is pretty unusual since it can alter normal epithelial cells turning them into mesenchymal cells. This particular cell has the ability to migrate to other parts of the body. Therefore, researchers suggest that silencing the TCF21 gene can help in the cancer spreading to other parts of the body. β€œThe fact that this gene is silenced in many cancer types strongly suggests that it plays an important role in cancer development,” said lead investigator Christoph Plass, a professor of molecular virology, immunology and medical genetics and a researcher in the OSU Human Cancer Genetics Program. First author Laura T. Smith added, "Because this gene is silenced by DNA methylation, it might be possible to reactivate it using drugs that reverse the methylation process. This could provide a new strategy for treating these cancers.” Plass' team is now looking at the role of TCF21 in the spread of cancer.

Funding from the National Cancer Institute and the National Institute of Dental and Craniofacial Research supported this research. Contact: Darrell E. Ward, Medical Center Communications, 614-293-3737, or [email protected]


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