Rachel J. House

This study identifies a non-canonical metabolic pathway in cancer cells that uses β-hydroxybutyrate for fatty acid synthesis, supporting tumor growth under lipid-limited conditions.

The paper shows lipid-starved cancer cells are more sensitive to ferroptosis due to increased PUFA trafficking into phospholipids, challenging the assumption that PUFA levels directly determine ferroptosis susceptibility.

The paper shows that metabolite extracts contain active enzymes and demonstrates a new workflow to remove proteins for improved metabolomics.

This study investigates how NF1 deficiency affects metabolic reprogramming in ER+ breast cancer and identifies potential therapeutic synergies between metabolic and targeted inhibitors.