Scott Dehm
University of Minnesota, MN·Medicine & Clinical Research
Prostate cancer cells depend on the androgen receptor (AR), a protein that is switched on by testosterone and then turns on growth genes. Hormone-blocking treatments shut down AR and slow the disease, but tumors eventually become resistant and progress to castration-resistant prostate cancer (CRPC), which is lethal.
- Fields
Medicine & Clinical Research
Genetics
Pharmacology
- Topics
prostate cancer
androgen receptor
androgen deprivation therapy
- Grants
- 2 known grants, through Mar 2028
What they work on
- Determine how AR-blocking therapies induce KLF5, a stem cell transcription factor, and lineage plasticity traits in castration-resistant prostate cancer cells.
- Test whether blocking KLF5 or its downstream target ERBB2, a growth-signaling receptor, can treat, prevent or reverse early steps of lineage plasticity in prostate cancer.
- Build mouse models of CRPC that carry AR gene rearrangements and loss of the PTEN tumor suppressor, and use them to study tumor progression and responses to AR-targeted drugs.
- Map the structure and origin of complex, multi-step AR gene rearrangements using third-generation genome structural variation analysis, and use computational methods to nominate non-AR therapies against these tumors.
More about the research
The work asks how tumors escape these drugs. Some keep AR running through changes in the AR gene itself. Others abandon AR and change into different cell types entirely. Both projects aim to find new ways to target these escape routes.
Why it matters
Most prostate cancer deaths occur when hormone therapies stop controlling the disease. This work could give men with advanced, castration-resistant prostate cancer AR gene rearrangement biomarkers to guide drug choice. It could also yield new drug strategies, such as ERBB2 inhibition, for hard-to-treat lineage-plastic tumors. The team expects successful results could move quickly into clinical trials.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Feng Yang
Baylor College of Medicine, TX·Medicine & Clinical Research
Determine how COP1, an E3 ubiquitin ligase, binds and tags GATA2 for degradation in prostate cancer cells, including castration-resistant and taxane-resistant models.
Susan Logan
New York University, NY·Pharmacology
Test whether macrocycle 13, a synthetic ring-shaped molecule designed to block beta-catenin from binding its DNA partner TCF, suppresses Wnt/beta-catenin signaling in in vivo models of castration-resistant prostate cancer.
Kexin Xu
University of Virginia, VA·Biochemistry
Examine how the m6A-adding enzyme METTL3 binds the nuclear pore protein NUP93 to speed export of m6A-marked mRNAs, using single-molecule microscopy and epitranscriptome-editing tools.
The school
University of Minnesota: 88 labs on PI Pages, $1.4B a year on research, 722 research doctorates a year.
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