# Activating p53 for colorectal cancer prevention

> **NIH NIH R01** · UNIVERSITY OF TX MD ANDERSON CAN CTR · 2020 · $424,809

## Abstract

PROJECT SUMMARY:
p53 is a crucial tumor suppressor that stops tumor development in most species and is the most frequently
inactivated gene in human cancers. Although about 50% of cancer patients harbor mutant p53, many tumors at
early stages of tumor development retain wild type p53. The presence of wild-type p53 in cancer precursor
lesions presents an excellent opportunity for chemoprevention by activating p53 to suppress tumor
progression. The MDM2 protein is a key negative regulator of p53 and plays a primary role in antagonizing p53
through direct interaction. Small molecule MDM2 inhibitors that block the MDM2–p53 protein–protein
interaction would liberate p53 from MDM2, thereby restoring the tumor suppressor function of wild-type p53.
We hypothesize that enhancement of wild-type p53 functions by blocking MDM2-p53 interaction in
precursor lesions using MDM2 inhibitor is an effective approach for cancer prevention. We propose to
test this hypothesis in ApcMin/+ mice, a model for familial adenomatous polyposis. If succeed, our study will pave
a new way for cancer chemoprevention.

## Key facts

- **NIH application ID:** 9923443
- **Project number:** 5R01CA214954-03
- **Recipient organization:** UNIVERSITY OF TX MD ANDERSON CAN CTR
- **Principal Investigator:** Xiangwei Wu
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $424,809
- **Award type:** 5
- **Project period:** 2018-06-12 → 2023-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9923443

## Citation

> US National Institutes of Health, RePORTER application 9923443, Activating p53 for colorectal cancer prevention (5R01CA214954-03). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/9923443. Licensed CC0.

---

*[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*