Priyamvada Rai
University of Miami, FL·Biology
How do tumors start, how do they grow and stop responding to chemotherapy, and what weak points do cancer cells have that new treatments could exploit? These questions drive a basic-science cancer research program that Priyamvada Rai co-leads with Scott Welford at the Sylvester Comprehensive Cancer Center.
- Fields
Biology
Medicine & Clinical Research
Biochemistry
- Topics
tumor biology
cancer biology
tumor initiation
- Grants
- 1 known grant, through Jun 2029
What they work on
- Uncover the mechanisms that start tumors, including how stress-response and redox signaling pathways in cancer cells and their surrounding tissue switch on gene networks that drive cancer.
- Investigate how tumors progress and become resistant to chemotherapy, studying both cancer cells and the tumor microenvironment, including immune regulation and inflammation.
- Identify and characterize molecular weak points in cancer, such as the receptor AVPR1A in castration-resistant prostate cancer and chemerin signaling in kidney cancer, as possible treatment targets.
More about the research
The grant supports this program as a whole rather than a single lab project.
Why it matters
Patients with cancers common in South Florida could eventually benefit as the program identifies new drug targets and explains why tumors stop responding to chemotherapy. Examples include a receptor target in castration-resistant prostate cancer and a fat-tissue signal involved in obesity-related kidney cancer. Findings are shared with clinical colleagues to help shape future 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.
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.
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.
The school
University of Miami: 30 labs on PI Pages, $559M a year on research, 297 research doctorates a year.
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