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Cancer cells must continuously adapt to metabolic stresses imposed by rapid growth, the tumor microenvironment, and cancer therapies. Our research seeks to understand how cancer cells survive or die under metabolic stress and how metabolic liabilities can be exploited to induce cancer cell death and overcome therapy resistance.

A major focus of our laboratory is metabolically regulated cell death. Our work spans three interconnected forms of cell death:

• ferroptosis, an iron-dependent form of cell death driven by lipid peroxidation
• disulfidptosis, a form of cell death caused by disulfide stress
• cuproptosis, a copper-dependent form of cell death

By investigating how nutrient availability, metabolic pathways, redox homeostasis and metal metabolism regulate these cell-death processes, we aim to uncover fundamental principles governing cancer cell fitness and vulnerability.

Ultimately, our goal is to translate these discoveries into therapeutic interventions that exploit cancer-specific metabolic vulnerabilities and overcome resistance to cancer therapies, including radiotherapy and other treatment modalities.