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Investigating immunomodulation of p53 mutant ovarian cancer

Award Number: F30CA306004
ORGANIZATION: NATIONAL CANCER INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 08/06/2026
PERIOD OF PERFORMANCE END DATE: 08/05/2029

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Investigating immunomodulation of p53 mutant ovarian cancer - PROJECT SUMMARY Ovarian cancer is the deadliest gynecologic malignancy. High grade serous ovarian cancer (HGSOC) is the most common and lethal subtype of ovarian cancer and has a 5-year overall survival of approximately 30%. Treatment of HGSOC remains challenging because most patients are diagnosed when the cancer is at an advanced stage, and relapse after standard-of-care therapy is common. Although immune-targeting strategies such as immune- checkpoint blockade have shown minimal efficacy in treating HGSOC, increased infiltration of T cells in HGSOC tumors has been shown to significantly improve overall survival in HGSOC. HGSOC tumors are characterized by mutations in the p53 tumor suppressor at diagnosis. Recently, we determined that p53-deleted murine cancers and p53-mutant human breast cancer depend on MDM2 for their survival. This finding challenges a long-held view that only cancers with functional p53 are vulnerable to loss of MDM2. We have developed a proteolysis- targeting chimera (PROTAC) to target MDM2 for degradation and demonstrated its efficacy and specificity in p53-mutant triple negative breast cancer. Our preliminary data indicate that this MDM2-PROTAC not only induces apoptosis in p53-mutant HGSOC, but also activates pathways that can modulate the tumor microenvironment of HGSOC and facilitate anti-tumor immunity. Taken together, our MDM2-PROTAC has significant translational potential for HGSOC because it can both eliminate cancer cells and potentially enhance anti-tumor immunity. Aim 1 of this project will define the molecular mechanisms by which MDM2 degradation triggers immune signaling pathways in HGSOC cells, and Aim 2 will investigate the effects on the immune microenvironment in HGSOC. To achieve these goals, I will learn multiple experimental approaches and interface with clinicians and basic scientists to foster my training in translational research. Completion of this proposed study will elucidate the relationship between MDM2 loss and immune signaling in HGSOC and reveal a novel potential approach to enhancing anti-tumor immunity in HGSOC. This proposal will support my training and career development to prepare me for a career as an independent physician-scientist in translational cancer research that improves patient outcomes.


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 = $51,477 )
2026	2026	THOMAS JEFFERSON UNIVERSITY	1020 WALNUT ST STE 1	PHILADELPHIA	PA	19107	PHILADELPHIA	USA	Cancer Research Manpower	000	1	8/6/2026	NEW	$51,477
2026	2026	THOMAS JEFFERSON UNIVERSITY	1020 WALNUT ST STE 1	PHILADELPHIA	PA	19107	PHILADELPHIA	USA	Cancer Research Manpower	001	1	8/6/2026	NEW	$0
														Subtotal = $51,477

Grand Total All Awards = $51,477

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Investigating immunomodulation of p53 mutant ovarian cancer

Award Number: F30CA306004

ORGANIZATION: NATIONAL CANCER INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 08/06/2026

PERIOD OF PERFORMANCE END DATE: 08/05/2029

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