# A20 and Tumor Immune Responses

> **NIH NIH R01** · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · 2024 · $552,874

## Abstract

Abstract
Immunosuppressive and homeostatic mechanisms prevent immune cells and tissues from eliminating solid
tumors, limiting the efficacy of anti-tumor immunity. Precise dissection of these homeostatic mechanisms can
lead to better understanding of how tumors persist and grow within tissues. Our prior studies demonstrate that
the A20 protein is a potent regulator of immune homeostasis, regulating both pro-inflammatory and cell death
signals. Our recent preliminary data reveal that A20 is highly expressed in tumor microenvironments and that
one specific biochemical motif of this protein restrains both acute and anamnestic antitumor immunity. This
proposal will dissect the cellular and molecular pathways by which A20 regulates anti-tumor immunity.

## Key facts

- **NIH application ID:** 10990973
- **Project number:** 1R01CA288237-01A1
- **Recipient organization:** UNIVERSITY OF CALIFORNIA, SAN FRANCISCO
- **Principal Investigator:** AVERIL I MA
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $552,874
- **Award type:** 1
- **Project period:** 2024-08-01 → 2029-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10990973

## Citation

> US National Institutes of Health, RePORTER application 10990973, A20 and Tumor Immune Responses (1R01CA288237-01A1). Retrieved via AI Analytics 2026-06-16 from https://api.ai-analytics.org/grant/nih/10990973. Licensed CC0.

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