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Dr. Thomas Boyer awarded NIH grants to study uterine fibroids

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Author: Joe Feist | Category: In The News | Cell Biology, Genetics & Molecular Medicine (CGM) | Cell Biology, Genetics and Molecular Medicine | March 06, 2018

Thomas G. Boyer, Ph.D., professor of molecular medicine at UT Health San Antonio, has received two related NIH R01 grants to study uterine leiomyomas, also called uterine fibroids.

The first grant was for $1.56 million; the most recent, a five-year award for $3.8 million, was a multi-PI grant to Dr. Boyer and Ayman Al-Hendy, M.D., Ph.D., a professor of obstetrics and gynecology at the University of Illinois at Chicago.

“Both awards have been made possible by a productive, ongoing collaboration with Dr. Robert Schenken and his team in the Department of OB/GYN here at UT Health San Antonio,” said Dr. Boyer.

“Uterine fibroids represent the most common gynecological tumors in women worldwide, with annual health care costs estimated in the hundreds of billions of dollars,” Dr. Boyer said. “Although benign, these tumors nonetheless account for significant gynecological and reproductive dysfunction, ranging from profuse menstrual bleeding and pelvic pain to infertility, recurrent miscarriage, and preterm labor. No long-term non-surgical treatment option currently exists for UFs, and deeper insight into underlying tumor etiology is key to the development of new therapies.”

Dr. Boyer added that his research is based on the discovery that mutations in a gene called MED12 are responsible for 50 percent to 80 percent of uterine fibroids in women of diverse racial and ethnic backgrounds, including Hispanic women of South Texas.

Uterine fibroids also disproportionately affect women of color, particularly African American women. While the basis for this risk disparity is not fully understood, recent studies implicate vitamin D deficiency as a major contributor. The funded studies seek to explore the relationship between vitamin D deficiency and genomic instability as a driving force in uterine fibroids carrying MED12 mutations.

This article was originally published in The Newsroom

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