Funded Investigators
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| Scott Hiebert, Ph.D. |
| Vanderbilt University |
HDAC3 as a Therapeutic Target in BCL6-dependent Lymphoma
Twenty years of research has revealed to researchers that a cancer known as B-cell lymphoma starts with the malfunction of BCL6, a gene important in controlling cell growth and death. As a result, this breakdown causes abnormal function of HDAC3, another epigenetic control element leading to abnormal gene programs, and ultimately cancer. Scientists believe that by eliminating BCL6, they can turn the genes back on and kill the cancer cells.
Dr. Hiebert and his colleagues have obtained drugs that inhibit HDAC3 and want to test it as a new cancer therapy. If the researchers can inhibit HDAC3, which is critical in the development of B-cell lymphoma, they hope to knock out the disease completely. This work should complement the exciting work the Melnick group, which has already identified a BCL6 inhibitor as part of a SWCRF collaborative program.
Hiebert's research will be part of the top 1 percent of grants funded by the NationalInstitutes of Health this year. His research is an example of the high caliber work that is funded in part by the NIH and the SWCRF.
