Oncogene, Published online: 02 October 2026; doi:10.1038/s41388-026-03990-8

Colorectal cancer is often treated with oxaliplatin, but many tumors become less responsive over time, making treatment harder. This study aimed to understand one way cancer cells escape oxaliplatin and to identify a possible way to restore drug response. The researchers studied colorectal cancer cells, drug-resistant cells, mouse tumor models, and tumor-like structures grown from patient samples. They found that oxaliplatin stress lowers a mitochondrial protein called TFAM. This allows mitochondrial DNA to leak into the cell fluid and switch on a survival signal involving TBK1. This signal helps cancer cells clear damaged cell parts and survive treatment. Blocking TBK1 reduced this protective response and made resistant tumors more sensitive to oxaliplatin. These findings suggest that combining oxaliplatin with a TBK1-blocking treatment may help overcome drug resistance in colorectal cancer in the future.

Synergizing with senescence-inducing therapies, uPAR CAR T cells eradicate primary and metastatic solid tumors with minimal myelodepletion by targeting both tumor cells and the stroma in preclinical models.

β-hydroxybutyrate (BHB), the ketone body associated with a ketogenic diet, metabolically reprograms and fuels CAR T cells to achieve proliferation, cytokine production, and superior tumor control. These findings suggest that BHB supplementation may be a practical way to boost adoptive cancer immunotherapy.

Histidine scanning represents a broadly applicable technique for the identification of critical interaction sites within TCRs and other mechanosensory receptors to enhance receptor signaling strength and augment therapeutic efficacy via the catch bond mechanism.

Nature Biotechnology, Published online: 13 March 2026; doi:10.1038/s41587-026-03057-9

A trispecific macrophage engager amplifies the antitumor response of macrophages in solid tumors.

Oncogene, Published online: 07 March 2026; doi:10.1038/s41388-026-03712-0

Arginine methylation-dependent stabilization of SUV39H1 promotes breast cancer growth