Nicholas J. Rossiter

This study identifies a heme-SDH-CoQ axis that helps colorectal cancer cells resist iron-induced oxidative stress and cell death.

The paper identifies fedratinib as a drug that increases endoplasmic reticulum-mitochondria contact sites by inhibiting BRD4, revealing a novel epigenetic pathway linking ERMCS to cellular metabolism.

This study identifies a metabolic vulnerability in colorectal cancer where combining HIF-2 inhibition with cholesterol biosynthesis inhibition using statins enhances ferroptosis, offering a new therapeutic strategy.

This study recharacterizes RSL3 as a broad selenoprotein inhibitor, showing its potential as a therapeutic target for colorectal cancer by inducing ferroptosis.

This study identifies PIKfyve as a targetable vulnerability in pancreatic cancer by showing its role in lipid metabolism and synthetic lethality with KRAS-MAPK inhibitors.