The H. L. Snyder Medical Foundation has arranged for Dr. William Hahn, from Dana Farber Cancer Institute at Harvard Medical School, to give 2 presentations about his research on Prostate Cancer and how our genome can guide clinical decision making.  Dr. Hahn’s objective is finding more effective ways to treat Prostate Cancer and the emphasis of the lab is to understand the clinical and functional consequences of DNA sequence variation.

The presentation will be on:

Title:                Genetics / Prostate Cancer
Date:               Thursday, September 15, 2016

Place & Time:  Southwestern College, Mossman Hall, Room 101 at 3:15 pm to 4:30 pm and is free to the public.

Place & Time:  Winfield Country Club; Social: at 6:00 pm to 6:30 pm, Dinner served at 6:30 pm and Dr. Hahn’s presentation approximately starting at 7:15 pm.
RSVP’s and your check are necessary by September 8, 2016.  Cost is $21.00 a person.  Please send RSVP and check to HLSMF, 1407 Wheat Road, Winfield, KS  67156.

Novel gene may present new target for prostate cancer drugs

More than a decade ago, Dr. Hahn created mouse models with tumors that require androgen to grow, meaning that they cannot grow in female or castrated mice, and whose tissue closely mimics that found in normal, healthy mice. With funding from the H. L. Snyder Medical Foundation, Dr. Hahn and his team used these models to study castrate-resistant prostate cancer (CRPC) and identify the kinase proteins that allow androgen-dependent cells to form tumors in castrate animals.

Through genetic screening, Dr. Hahn and his colleagues identified NEK6 as a kinase—an enzyme that causes other molecules in a cell to become either active or inactive—that helps to turn off the p53 tumor suppressor gene and is required for the survival of CRPC tumors. They also discovered that NEK6 drives tumor growth when androgens are absent, suggesting that targeting this enzyme with small-molecule drugs may be an effective CRPC treatment. Dr. Hahn and his colleagues are currently preparing a manuscript for publication to highlight these findings.

Gene fusion affects chromatin formation to drive prostate tumor development

It remains unknown why the TMPRSS2/ERG gene fusion causes many of the genes associated with cancer cell growth and survival to become abnormally activated by testosterone in prostate cancer. This gene fusion, which is observed in more than 50 percent of prostate cancers, often indicates the presence of a highly aggressive form of the disease.

With support from the Snyder Medical Foundation, Dr. Hahn and his colleagues have shown that this gene fusion affects the formation of chromatin—a condensed mass of DNA and proteins that forms chromosomes in a cell—and consequently drives prostate tumor development. Genes that remodel chromatin are often altered in cancer. As there are no existing treatments that specifically target the TMPRSS2/ERG fusion, Dr. Hahn’s preliminary findings provide an opportunity to develop therapeutics that effectively target TMPRSS2/ERG in prostate cancer.