Publications
Research articles, reviews, and commentaries listed in reverse chronological order.
Delgado Herrera DDC, Arroyo Roman AA, Campbell RN, et al.
Cancer Letters. 2026;658:218733. doi: 10.1016/j.canlet.2026.218733
We identified a CD133-high, GSTT1-high stem-like population with enhanced tumor-sphere initiation and showed that FGF signaling sustains this state. Patient-derived organoids reproduced this association and revealed increased sensitivity to nintedanib.
Delgado Herrera DDC, Ferrer CM.
Cancer Research. 2026;86(14):3374-3376. doi: 10.1158/0008-5472.CAN-25-1877
We discuss evidence that KRAS/ERK inhibition activates TFEB-dependent lipophagy and fatty acid oxidation, enabling pancreatic cancer cells to survive therapeutic stress. Co-targeting fatty acid oxidation may expose a vulnerability during KRAS-pathway blockade.
Grant G, Ferrer CM.
Trends in Cell Biology. 2026;36(5):377-391. doi: 10.1016/j.tcb.2025.05.006
We examine how macrophages, neutrophils, and T cells can restrain or promote metastasis at distinct stages, from dissemination and circulation to dormancy and reactivation. We also discuss how immune-state heterogeneity affects therapeutic response.
Ferrer CM, Cho HM, Boon R, et al.
Nature Cell Biology. 2024;26(6):975-990. doi: 10.1038/s41556-024-01426-7
We identified GSTT1 as selectively required for pancreatic cancer dissemination and metastatic survival, but dispensable for primary tumor growth. GSTT1 supports slow-cycling metastatic cells by glutathionylating fibronectin and promoting its secretion and deposition.