# Role of ATAD2 in Prostate Cancer Progression and Metastasis

> **NIH CA R01** · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · 2026 · $682,886

## Abstract

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 

## Key facts

- **NIH application ID:** 11298124
- **Project number:** 1R01CA299197-01A1
- **Recipient organization:** ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI
- **Principal Investigator:** Juan Martin Arriaga
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** CA
- **Fiscal year:** 2026
- **Award amount:** $682,886
- **Award type:** 1
- **Project period:** 2026-05-01T00:00:00 → 2031-04-30T00:00:00

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/11298124

## Citation

> US National Institutes of Health, RePORTER application 11298124, Role of ATAD2 in Prostate Cancer Progression and Metastasis (1R01CA299197-01A1). Retrieved via AI Analytics 2026-05-18 from https://api.ai-analytics.org/grant/nih/11298124. Licensed CC0.

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