Thomas G Boyer
University of Texas Health Science Center at San Antonio, TX·Biochemistry
Uterine fibroids (UFs) are noncancerous tumors of the uterine muscle wall, called the myometrium. They are the most important benign tumor threat to women's health worldwide, and beyond surgery there is no long-term, non-invasive treatment.
- Fields
Biochemistry
Genetics
Medicine & Clinical Research
- Topics
uterine fibroids
leiomyoma
myometrium
- Grants
- 2 known grants, through May 2027
What they work on
- Determine how fibroid-causing MED12 mutations destabilize the T-loop of the CDK8 enzyme and reduce its substrate binding and activity, using structural biology and biochemistry.
- Test whether loss of Mediator kinase activity reprograms myometrial stem cells into fibroid-forming cells by changing genome-wide enhancers and gene output, including tumor formation in mice.
- Test whether stalled RNA polymerase II causes R-loops and replication stress that break chromosomes in MED12-mutant fibroids, and evaluate ATR-axis inhibitors in a preclinical mouse model.
- Map the m6A RNA modification on mRNAs and chromosome-associated regulatory RNAs in paired fibroid and normal myometrium, and test how METTL3 and RBM15 cooperate in reshaping it.
- Ask whether overactive METTL3 RNA methylation transforms myometrial stem cells and drives fibroid growth, and test bromodomain (BRD) inhibitors for efficacy and safety in a fibroid mouse model.
More about the research
Each fibroid starts when a single myometrial stem cell is transformed and grows into a tumor. Two projects ask what drives that change at the molecular level, and whether the faulty steps can be targeted with drugs. One focuses on the most common fibroid mutation. The other focuses on chemical tags on RNA.
Why it matters
Most women with uterine fibroids have few options besides surgery. By pinpointing how MED12 mutations and abnormal RNA methylation drive fibroid growth, this work could lead to non-hormonal, non-surgical drug treatments. ATR-axis inhibitors and BRD inhibitors are already being tested as drug candidates, and the projects will evaluate them in mouse models of human fibroids, especially the common MED12-mutant subtype.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Mazhar Adli
Northwestern University, IL·Genetics
Create human cell models of uterine fibroids by using CRISPR to engineer specific MED12 mutations, and determine how these mutations drive tumor formation.
Yunsun Nam
University of Texas Southwestern Medical Center, TX·Biochemistry
Determine how heavy metals alter the efficiency and specificity of METTL3-METTL14, the enzyme that adds m6A marks to mRNA, and how metal-driven m6A changes link to chromatin and DNA methylation.
Lili Wang
Columbia University, NY·Medicine & Clinical Research
Determine how the MGA/MYC/NME1 pathway, a growth program switched on when the gene Mga is silenced, changes tumor-cell properties during the CLL-to-Richter's transformation, using the lab's mouse RT model.
The school
University of Texas Health Science Center at San Antonio: 15 labs on PI Pages, $313M a year on research, 149 research doctorates a year.
More about University of Texas Health Science Center at San Antonio
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