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Examining the mechanisms of response to anti-androgen therapies in aggressive genitourinary cancers

Award Number: K22CA282361
ORGANIZATION: NATIONAL CANCER INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: TRAINING/TRAINEESHIP
PERIOD OF PERFORMANCE START DATE: 07/01/2026
PERIOD OF PERFORMANCE END DATE: 06/30/2029

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Examining the mechanisms of response to anti-androgen therapies in aggressive genitourinary cancers - Project Summary Patients with aggressive prostate cancer initially exhibit strong responses to androgen deprivation therapy (ADT) to block androgen-mediated cell proliferation. However, despite this strong response to ADT, these patients will ultimately develop resistance and progress into castration-resistant prostate cancer (CRPC). The mechanisms underlying this response or resistance to ADT in early-stage cancers remain largely unknown. The foundation for this proposal derives from our work examining primary prostate cancer specimens from a Phase II clinical trial examining intense neoadjuvant ADT (inADT) in patients with locally advanced prostate cancer who would otherwise be ineligible for surgery. By examining the genomic and transcriptomic features of these tumors at an early stage, we are able to identify new drivers of early-stage prostate cancer progression. We identified residual cancer burden (RCB) after treatment, which serves as a surrogate for overall progression-free survival, and then stratified patients into those who exhibited either exceptional response (ER) or incomplete/non-response (INR). This allows us to examine the genomic and transcriptomic differences between the classes, which led to our central hypothesis that a subset of genetic alterations driving tumorigenesis predispose tumor sensitivity or resistance to ADT. Our preliminary data highlight the EGFR family, and specifically HER2, is overexpressed in poorly responding tumors with low Androgen Receptor (AR) signaling, while the tumor suppressor phosphatase, INPP4B, as significantly overexpressed in ER samples compared to INR To identify mechanisms predisposing prostate tumors to intrinsic response or resistance to inADT, we will determine 1) the mechanism underlying HER2-mediated proliferation in an AR-low environment; and 2) how INPP4B phosphatase activity drives response to ADT. In Aim 1, we will examine HER2-mediated signaling to drive prostate cancer proliferation in an AR-low environment. In Aim 2, we will determine how INPP4B mediates prostate cancer cell sensitivity ot ADT, both in PTEN-intact and PTEN-null tumors. This work will advance our understanding of the mechanisms underlying early stage prostate cancer cell response to ADT, which will provide new insights into potential mechanisms to phenocopy these results to improve overall survival of aggressive prostate cancer.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2026 ( Subtotal = $194,929 )
2026	2026	CLARK ATLANTA UNIVERSITY, INC.	223 JAMES P BRAWLEY DR SW	ATLANTA	GA	30314	FULTON	USA	Cancer Research Manpower	000	1	6/30/2026	NEW	$194,929
														Subtotal = $194,929

Grand Total All Awards = $194,929

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Examining the mechanisms of response to anti-androgen therapies in aggressive genitourinary cancers

Award Number: K22CA282361

ORGANIZATION: NATIONAL CANCER INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: TRAINING/TRAINEESHIP

PERIOD OF PERFORMANCE START DATE: 07/01/2026

PERIOD OF PERFORMANCE END DATE: 06/30/2029

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