A Korea University research team has discovered that pitavastatin, a widely used lipid-lowering drug, can directly inhibit the Mcl-1 protein—an essential survival factor for therapy-resistant triple-negative breast cancer (TNBC). By blocking Mcl-1–dependent mitochondrial protection, pitavastatin eliminates cancer stem-like cells, suppresses metastasis, and restores paclitaxel sensitivity in preclinical models. This repurposed drug may offer a safer, faster-to-deploy therapeutic strategy for patients with aggressive or chemotherapy-refractory TNBC.

Cells have a remarkable housekeeping system: proteins that are no longer needed, defective, or potentially harmful are labeled with a molecular “tag” and dismantled in the cellular recycling machinery. This process, known as the ubiquitin-proteasome system, is crucial for health and survival. Now, an international team of scientists led by CeMM, AITHYRA and the Max Planck Institute of Molecular Physiology in Dortmund has identified a new class of small molecules that harness this natural system to accelerate the removal of an immune-modulating enzyme called IDO1. The findings, published in Nature Chemistry (DOI: 10.1038/s41557-025-02021-5), introduce a new concept in drug discovery that could transform how we target difficult proteins in cancer and beyond.

Researchers at Duke University combined Dynamic Optical Contrast Imaging (DOCI) with AI to improve thyroid cancer detection and surgical planning. DOCI captures the natural autofluorescence of tissue without dyes, and machine-learning models use this data to classify cancer subtypes and generate precise tumor maps. This approach shows promise for providing real-time, label-free guidance during surgery, potentially reducing unnecessary procedures and improving patient outcomes.