Lake Tahoe, CA, October 11, 2007 Researchers have discovered new small molecules that may prevent prostate cancer cells from turning off normal genes in a process that transforms normal cells into cancer cells. This significant discovery in the field of epigenetics has immediate implications in the development of new diagnostic tests and cancer medications. The findings were presented today at the Prostate Cancer Foundations annual Scientific Retreat. Funding for the research was provided by the Prostate Cancer Foundation, as well as from the National Cancer Institute and the Avon Foundation.
Epigenetics refers to changes to genes other than changes to the DNA sequence itself, such as the addition of molecules to the DNA strand. While the development of cancer can arise from defective or mutated genes, it can also arise from these changes that can actually prevent a cell from acting as it should. Cancer cells exploit this process, putting some genes in cold storage or turned off by modifying the cell DNA in a process known as methylation.
Lead researcher William Nelson, M.D., Ph.D., Professor of Oncology and Urology at the Johns Hopkins Kimmel Cancer Center, explained the findings. One of the proteins in the cell that triggers this process is called a methyl-CpG binding protein, or MBD. We have discovered an antagonist of MBD2 that keeps this protein from binding to methylated genes. If the protein cant bind to the gene, then it cant keep the gene turned off and the gene is turned back on able to act in the way it is supposed to.
Nelson noted that the discovery is particularly exciting because of previous research that shows the importance of being able to alter the methylation process in DNA. When mice were developed without the gene that permits this process, they dont develop cancer. When the gene is removed from cancer cells, they turn on genes again in appropriate ways. The small molecules that weve discovered mimic thi
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