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Role of ATAD2 in Prostate Cancer Progression and Metastasis

Award Number: R37CA299197
ORGANIZATION: NATIONAL CANCER INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 05/01/2026
PERIOD OF PERFORMANCE END DATE: 04/30/2031

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Role of ATAD2 in Prostate Cancer Progression and Metastasis - Prostate cancer remains the second-leading cause of cancer-related deaths in US men, mainly due to metastatic disease. Metastasis occurs most frequently in bones, thus entailing significant patient morbidity including pain, propensity to fractures and potential spinal cord compression. Moreover, the bone is a favored reservoir for undetectable disseminated tumor cells that maintain minimal residual disease and can thus critically define future patient outcomes. Despite this pressing clinical need, the mechanisms of progression to bone metastasis remain incompletely understood. Our overall goal is thus to understand the functional determinants of progression to lethal metastatic prostate cancer in order to develop more efficient therapies. Given that tumor progression and metastasis occur through multiple steps involving interactions with different benign cells and tissues, experimental models in which prostate cancer progression may be studied in a whole immunocompetent organism may help identify hitherto unappreciated mechanisms of progression. Our preliminary studies using novel mouse and human prostate cancer models show that ATAD2, an epigenetic and transcriptional regulator, is a critical mediator of metastasis (including bone) and of antitumoral immune responses. ATAD2 is progressively overexpressed during prostate cancer progression and may be an important therapeutic target because of its restricted expression in normal adult tissues as well as the presence of a potentially druggable and specific bromodomain. Furthermore, despite its widely reported association to worse survival in multiple cancer types, remarkably little is known about its functional role in metastasis. In this proposal we will determine the functional significance of ATAD2 expression for prostate cancer progression and metastasis. We will focus on its ability to modulate bone colonization and antitumoral immune responses, two critically relevant steps in the development of metastasis, and uncover the chromatin and transcriptional mechanisms through which it acts. Using state-of-the art syngeneic mouse models, ex-vivo epigenetic editing, human organoids and advanced tissue engineering technologies, our expert multidisciplinary team is uniquely poised to have a positive impact on our understanding of how tumor cells progress to lethal metastatic disease. Our studies will uncover novel mechanisms linking metastasis and immune escape, paving the way for future biomarker driven targeted therapies that may lead to durable and systemic therapeutic responses in currently incurable metastatic disease.


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 = $682,886 )
2026	2026	ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI	1 GUSTAVE L LEVY PL	NEW YORK	NY	10029	NEW YORK	USA	Cancer Biology Research	000	1	4/21/2026	NEW	$682,886
														Subtotal = $682,886

Grand Total All Awards = $682,886

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Role of ATAD2 in Prostate Cancer Progression and Metastasis

Award Number: R37CA299197

ORGANIZATION: NATIONAL CANCER INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 05/01/2026

PERIOD OF PERFORMANCE END DATE: 04/30/2031

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