Peter Lewis
University of Wisconsin-Madison, WI·Biochemistry
Every cell carries the same DNA, so cells must switch genes on and off to become the right cell type. Much of that switching happens through chemical marks placed on histones, the spool-like proteins that DNA wraps around.
- Fields
Biochemistry
Genetics
Medicine & Clinical Research
- Topics
chromatin
epigenetics
histone modification
- Grants
- 1 known grant, through Dec 2026
What they work on
- 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.
- Determine how PRC2 is targeted to CpG islands, the cytosine- and guanine-rich DNA stretches near gene promoters, in gliomas where overall H3K27 methylation is depleted.
- Define the biochemical mechanism by which EZHIP inhibits PRC2 catalysis of the repressive histone mark H3K27me3.
- Map how loss of H3K27 methylation by K27M or EZHIP changes expression of tumor suppressor genes, cellular differentiation and proliferation in glioma models.
More about the research
In some childhood brain tumors, a single mutation in a histone scrambles this marking system, which is thought to help drive the cancer. Understanding how that happens is the goal here.
Why it matters
Pediatric gliomas carrying the H3 K27M mutation or high EZHIP levels have poor prognoses and lack effective therapies. Pinpointing how these factors misdirect the gene-silencing machinery, and why the remaining activity appears to support tumor growth, could reveal targets for drugs aimed specifically at these tumors.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Matija Snuderl
New York University, NY·Medicine & Clinical Research
Compare epigenetic machinery and gene expression in mature versus primitive regions of human medulloblastoma tissue, using high-resolution genomic and epigenetic profiling.
Laura Banaszynski
University of Texas Southwestern Medical Center, TX·Genetics
Determine how phosphorylation of the histone variant H3.3 at its unique serine stimulates p300, an enzyme that acetylates histones, to produce the enhancer mark H3K27ac in mouse embryonic stem cells.
Stefanie Galban
University of Michigan, MI·Medicine & Clinical Research
Determine how ALDH1A3 and ALDH2, enzymes marking cancer stem cells, are controlled by the H3 K27M histone mutation and by IL1β from microglia, using isogenic DIPG models in vitro and in vivo.
The school
University of Wisconsin-Madison: 91 labs on PI Pages, $1.9B a year on research, 854 research doctorates a year.
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