# Defining the functions and translational potential of ferroptosis

> **NIH NIH R35** · COLUMBIA UNIV NEW YORK MORNINGSIDE · 2020 · $955,184

## Abstract

Ferroptosis in a new form of regulated, non-apoptotic cell death that we discovered; we
have determined the major mechanisms regulating activation of ferroptosis and several
contexts where it can be induced in sensitized tumors. We found that ferroptosis is
ultimately characterized by excessive lipid peroxidation upon loss of activity of the lipid
repair enzyme glutathione peroxidase 4 (Gpx4). We propose here the hypothesis that
lipid peroxidation serves as a signal to detect a scarcity of nutrients needed tor repair of
oxidative damage, and that ferroptosis serves as an innate tumor suppression
mechanism to eliminate nascent tumors experiencing such oxidative stress. We further
propose to elucidate mechanisms driving ferroptosis in specific cancer contexts, and
whether it is feasible to create precision small molecule activators of ferroptosis that
eliminate tumors that have become addicted to this repair pathway.

## Key facts

- **NIH application ID:** 9978733
- **Project number:** 5R35CA209896-05
- **Recipient organization:** COLUMBIA UNIV NEW YORK MORNINGSIDE
- **Principal Investigator:** Brent R. Stockwell
- **Activity code:** R35 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $955,184
- **Award type:** 5
- **Project period:** 2016-09-02 → 2023-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9978733

## Citation

> US National Institutes of Health, RePORTER application 9978733, Defining the functions and translational potential of ferroptosis (5R35CA209896-05). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/9978733. Licensed CC0.

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