Susan Logan
New York University, NY·Pharmacology
Prostate cancer is the most common cancer among men and the third most common cause of cancer death in men. Men whose disease stays in the prostate usually do well, but once it spreads, only about 30% survive five years.
- Fields
Pharmacology
Medicine & Clinical Research
Chemistry
- Topics
prostate cancer
Wnt signaling
beta-catenin
- Grants
- 1 known grant, through May 2029
What they work on
- 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.
- Determine whether inhibiting beta-catenin with macrocycle 13 slows growth of prostate tumors that have become resistant to androgen-receptor-targeting drugs such as enzalutamide.
- Determine how blocking beta-catenin signaling affects immune cells in prostate cancer models.
More about the research
Most treatments block the androgen receptor (AR), a protein that responds to male hormones and drives tumor growth. Tumors eventually become resistant to these drugs, including the newer ones, enzalutamide and abiraterone, and progress to castration-resistant prostate cancer (CRPC). New strategies are needed to get around this resistance.
Why it matters
Men with metastatic, castration-resistant prostate cancer often stop responding to androgen-blocking drugs such as enzalutamide and abiraterone. A molecule that shuts down beta-catenin-driven gene activity could offer a new way to treat these resistant tumors or to delay resistance. Work on immune effects could also show how such a drug interacts with the body's defenses against the tumor.
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.
Scott Dehm
University of Minnesota, MN·Medicine & Clinical Research
Determine how AR-blocking therapies induce KLF5, a stem cell transcription factor, and lineage plasticity traits in castration-resistant prostate cancer cells.
Shaomeng Wang
University of Michigan, MI·Pharmacology
Optimize orally active small-molecule degraders that destroy both CBP and p300, paired histone acetyltransferases that switch on gene programs, and test them as a therapy for advanced, castration-resistant prostate cancer in mouse models.
The school
New York University: 72 labs on PI Pages, $1.5B a year on research, 540 research doctorates a year.
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