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Harnessing Androgen-Driven Immune Modulation to Enhance Immunotherapy for Endocrine Cancers

Award Number: K99CA307604
ORGANIZATION: NATIONAL CANCER INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: TRAINING/TRAINEESHIP
PERIOD OF PERFORMANCE START DATE: 05/01/2026
PERIOD OF PERFORMANCE END DATE: 04/30/2028

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Harnessing Androgen-Driven Immune Modulation to Enhance Immunotherapy for Endocrine Cancers - PROJECT SUMMARY Immunotherapy has transformed cancer treatment, yet patients with endocrine tumors, including adrenal and ovarian cancers, rarely benefit due to poor immune infiltration and activation in steroid-rich environments. Androgens, traditionally viewed as cancer-promoting, may enhance anti-tumor immunity. High androgen receptor expression correlates with improved outcomes in adrenal, ovarian, and select breast cancers; however, the mechanisms underlying these effects remain poorly understood. Using a mouse model of adrenal cancer, my work revealed a sex bias in tumor incidence, with males exhibiting lower tumor burden, which was associated with androgen-driven immune activation. Androgen-secreting adrenal tumors in the clinic show better prognosis and greater immune infiltration, while androgen deprivation in our mouse model reduces intratumoral myeloid and lymphoid cells. Androgen supplementation increases circulating inflammatory monocytes, suggesting a tumor-protective role via immune activation. Similar androgen-driven immune responses occur in the ovary, paralleling clinical data linking androgens to reduced ovarian cancer risk. These findings support a translational potential for androgen-mediated immunity across endocrine malignancies. In the K99 phase, I will investigate how androgens enhance myeloid and lymphoid immune responses to improve ICB efficacy in ACC. Aim 1 will assess how androgens modulate myeloid cell function and recruit the adaptive immune response to promote anti-tumor immunity. I will use a syngeneic ACC mouse model with immune cell depletion and ICB, real-time ultrasound tumor tracking, and Xenium transcriptomics to dissect androgen-driven immune mechanisms. Findings will be validated in androgen-secreting ACC patient tumors. In the R00 phase, I will extend this work to ovarian cancer, a leading cause of gynecologic cancer mortality. Aim 2 will examine how androgen signaling enhances immune infiltration in the ovary and whether this can improve ICB efficacy in ovarian cancer. I will use AR-deficient myeloid mouse models, syngeneic ovarian tumor injections, and Xenium transcriptomics to define androgen-mediated immune effects. This will establish a potential rationale for androgen-based immunotherapeutics in ovarian cancer. My career development plan includes training in tumor immunology, Xenium transcriptomics, and ovarian cancer biology, supported by mentorship from leaders in the field. The research environment at Huntsman Cancer Institute offers state-of-the-art resources and collaborative opportunities to achieve these goals. The K99/R00 award will enable me to establish my independent research lab, where I aim to advance our understanding of how hormones impact the tumor immune environment and ultimately use this to improve therapeutic strategies.


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 = $126,933 )
2026	2026	UNIVERSITY OF UTAH	201 PRESIDENTS CIR	SALT LAKE CITY	UT	84112	SALT LAKE	USA	Cancer Research Manpower	000	1	4/29/2026	NEW	$126,933
														Subtotal = $126,933

Grand Total All Awards = $126,933

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Harnessing Androgen-Driven Immune Modulation to Enhance Immunotherapy for Endocrine Cancers

Award Number: K99CA307604

ORGANIZATION: NATIONAL CANCER INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: TRAINING/TRAINEESHIP

PERIOD OF PERFORMANCE START DATE: 05/01/2026

PERIOD OF PERFORMANCE END DATE: 04/30/2028

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