Guang Peng
University of Texas MD Anderson Cancer Center, TX·Genetics
Ovarian clear-cell carcinoma is the second most common form of ovarian cancer, and survival is poor largely because few treatments work against it. More than half of these tumors carry mutations in ARID1A, a component of SWI/SNF, a protein machine that slides and repositions the spools around which DNA is wound to control which genes can be read.
- Fields
Genetics
Medicine & Clinical Research
Microbiology & Immunology
- Topics
ovarian clear cell carcinoma
chromatin remodeling
DNA damage response
- Grants
- 1 known grant, through Jul 2027
What they work on
- Test whether loss of ARID1A, a subunit of the SWI/SNF chromatin remodeling complex mutated in over half of ovarian clear-cell carcinomas, releases repetitive satellite DNA from transcriptional silencing after ionizing radiation.
- Determine whether ARID1A deficiency acts by impairing DNMT3A-mediated DNA methylation and silencing of heterochromatin satellite sequences, using biochemical and cell biology experiments plus shRNA and CRISPR-Cas9 genetic approaches.
- Establish whether radiation-induced satellite RNA activates the double-stranded RNA sensors RIG-I and MDA5, which normally detect viral RNA, to trigger innate immune signaling in ARID1A-deficient cells.
- Evaluate whether inhibitors of ATM, the kinase that coordinates the response to DNA breaks, enhance radiotherapy and immunotherapy in ARID1A-deficient tumors, using preclinical animal models and ovarian clear-cell carcinoma patient samples.
More about the research
This lab studies how the loss of that machine changes a cell's response to DNA damage, and whether those changes create an opening for radiation therapy combined with immune-based treatment.
Why it matters
Patients with ovarian clear-cell carcinoma currently have few effective options. If loss of ARID1A reliably makes tumors release immune-activating RNA after radiation, that vulnerability could be exploited to design radiation plus immunotherapy regimens matched to a tumor's genetics, potentially extending to the broader group of cancers carrying SWI/SNF mutations.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Vipul Shukla
Northwestern University, IL·Microbiology & Immunology
Define how the Arid1a-dependent cBAF complex, a DNA-packaging remodeler, controls which genes are accessible and active as germinal center B cells mature, testing whether it establishes the germinal center gene program.
Shinya Watanabe
University of Massachusetts Chan Medical School, MA·Biochemistry
Define the roles of brain- and heart-specific DPF1 and DPF3 in the cBAF remodeling complex by rebuilding cBAF with DPF1, DPF2, DPF3 or no DPF protein and comparing nucleosome binding, sliding and ATPase activity.
April M. Weissmiller
Middle Tennessee State University, TN·Biochemistry
Map which genes are bound and regulated by N-MYC and its partner proteins WDR5 and G9a in MYCN-amplified neuroblastoma cells, using genetic, genomic, and chemical-biology approaches to see how combined inhibition reshapes N-MYC-driven transcription.
The school
University of Texas MD Anderson Cancer Center: 23 labs on PI Pages, $1.4B a year on research.
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