James V. Alvarez

This study examines how breast cancer cell lines adapt to serum-free defined medium, revealing differences in proliferation, adhesion, and lipid metabolism across cell lines.

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.

This study identifies Pik3c3 as a vulnerability in dormancy-prone breast cancer cells, showing its inhibition reduces metastasis in preclinical models.

This study shows APOBEC3 activity supports drug-tolerant persister cells in EGFR inhibitor-resistant lung cancer by promoting transdifferentiation and mutation acquisition.

This study identifies mitochondrial oxidative phosphorylation as a metabolic vulnerability in endocrine-tolerant persister ER+ breast cancer cells, suggesting therapeutic targeting of mitochondrial function could prevent recurrence.

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.