Gilbert Rahme
Stony Brook University, NY·Genetics·Early-career
Diffuse gliomas are brain tumors that remain incurable despite aggressive therapy. Knowing how they start is a key step toward better treatments.
- Fields
Genetics
Biology
Neuroscience
- Topics
glioma
brain tumor
IDH1 mutation
- Grants
- 1 known grant, last ended Aug 2026
What they work on
- Model glioma-associated epigenetic changes in oligodendrocyte progenitor cells by disrupting the CTCF insulator near the PDGFRA growth gene and silencing the CDKN2A tumor suppressor.
- Test in living animals whether disrupting the PDGFRA insulator together with losing CDKN2A is sufficient to turn oligodendrocyte progenitor cells into diffuse gliomas.
- Test whether methylation changes at the PDGFRA insulator and CDKN2A promoter are passed on through cell division as tumor drivers, including the role of DNMT1, the enzyme that maintains DNA methylation.
More about the research
Most diffuse gliomas carry mutations in IDH1 (isocitrate dehydrogenase 1), a metabolic enzyme. The mutant enzyme causes widespread DNA hypermethylation, meaning extra chemical tags on DNA that change how genes are used. This epigenetic change could drive tumors by silencing genes that suppress cancer. It could also activate cancer-promoting genes by disrupting CTCF insulator sites, boundaries that divide the genome into 3D neighborhoods called topologically associated domains (TADs). Gene switches called enhancers normally only reach genes within their own TAD.
Why it matters
Patients with diffuse gliomas, especially IDH1-mutant tumors, have no cure. By showing whether inherited epigenetic changes alone can start these tumors, this work could reveal new targets for therapy. The findings may also apply to other incurable cancers marked by widespread epigenetic reprogramming.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Todd Waldman
Georgetown University, DC·Genetics
Determine how STAG2-regulated chromatin loops, especially those anchored by CTCF and H3K27me3, control nearby gene expression in glioblastoma cells and tumors, using Hi-C, RNA-seq and the HiCorr/DeepLoop loop-detection pipelines.
Peter Lewis
University of Wisconsin-Madison, WI·Biochemistry
Define how residual PRC2 activity, the leftover gene-silencing capacity remaining after inhibition, promotes growth of pediatric glioma cells carrying the H3 K27M oncohistone or the EZHIP protein, using genetic and genomic approaches.
Lanlan Shen
Baylor College of Medicine, TX·Genetics
Use inducible dCas9-SunTagTET1 mice, which carry a DNA-targeting CRISPR tool linked to a methylation-removing enzyme, to remove DNA methylation precisely at chosen genes in living animals.
The school
Stony Brook University: 32 labs on PI Pages, $319M a year on research, 289 research doctorates a year.
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