A novel mRNA drug, 3’UTRMYC1-18 (UTRxM1-18), has demonstrated notable efficacy in preclinical models of aggressive pancreatic cancer, addressing a disease that is often resistant to conventional treatments.

Two back-to-back papers published in Nature on Sept. 10, 2025, shed new light on the unexpected role of neurons in shaping the evolution of small-cell lung cancer (SCLC). It’s already known that, in gliomas, cerebral cancer cells actively damage axons, contributing to tumor progression through direct neural disruption. Comparable nerve-tumor interactions have been reported in peripheral cancers, where tumor-induced nerve disruption promotes inflammation and an immunosuppressive microenvironment linked to immunotherapy resistance.

Patients with relapsed/refractory multiple myeloma (r/r MM) treated with Carsgen Therapeutics Holdings Ltd.’s CAR T therapy, zevorcabtagene autoleucel (zevor-cel, CT-053), have shown durable responses lasting nearly five years.

N6-methyladenosine (m6A) modification, mainly controlled by the m6A methyltransferase METTL3, is crucial for RNA regulation and the development of leukemia. However, how METTL3 stability and function are regulated after translation is not fully understood. Since O-GlcNAcylation commonly modifies nuclear and cytosolic proteins, researchers have hypothesized that METTL3 may be O-GlcNAcylated, affecting its stability and oncogenic activity in myeloid malignancies.

Glioblastoma multiforme (GBM) is the most aggressive and common type of brain cancer in adults, with a dismal prognosis despite current treatments. Previous work found that neurodevelopmental pathways drive glioma tumor initiation, maintenance and progression through fetal oncogenes, which are active in development and cancer but largely absent in adult tissues, offering precise therapeutic targets with minimal off-target effects.