Douglas B. Fox

This study identifies de novo pyrimidine synthesis as a metabolic vulnerability in recurrent breast cancer cells that suppresses ferroptosis, with DHODH inhibition selectively targeting these cells.

The paper identifies HECTD4 as a tumor and metastasis suppressor that targets COX-2 for degradation, with COX-2 stabilization driving pro-tumorigenic effects in breast cancer.

This study identifies CDKN1B as a regulator of drug-tolerant persister CTCs by preventing polyploidy after mitotic inhibitor treatment in breast cancer.

This study identifies NRF2-driven metabolic reprogramming as essential for breast cancer recurrence after oncogene inhibition and shows it can be targeted with glutaminase inhibitors.