Pancreatic cancer cachexia is a devastating syndrome marked by unintentional weight loss, skeletal muscle wasting, and metabolic dysfunction that severely impairs patient outcomes. Affecting over 60% of pancreatic cancer patients, cachexia contributes to reduced quality of life, therapy intolerance, and high mortality. In a new comprehensive review published in hLife, researchers from the Peking Union Medical College Hospital and Harvard T.H. Chan School of Public Health highlight how this condition arises not from malnutrition alone, but through complex systemic crosstalk among multiple organs. The review provides a detailed account of the biological drivers of cachexia—including inflammatory cytokines, TGF-β family ligands, catabolic mediators, and tumor-derived extracellular vesicles—and their roles in orchestrating multi-organ deterioration. It also explores cutting-edge animal models and proposes potential therapeutic targets that could disrupt the vicious cycle of body wasting. This work lays a foundation for future clinical strategies to diagnose, monitor, and treat cachexia as a systemic disease.

- Researchers at CiQUS (University of Santiago de Compostela) have developed a strategy to activate an initially inactive molecule through chemical stimuli, enabling it to recognize and bind to a specific DNA structure known as a three-way junction (3WJ).

· These regions, implicated in tumor-related processes, are emerging as promising new targets for precision cancer therapies.

· The study has been featured on the cover of the prestigious journal Journal of the American Chemical Society (JACS).

A first-of-its-kind study, led by LaShae Rolle, a 27 y/o breast cancer researcher, survivor and elite powerlifter, challenges the long-held belief that cancer patients should stick to low- or moderate exercise and suggests that with individualized and symptom-informed exercise planning, even powerlifting can be safe and beneficial.

Specific way genetic material is organized in cells determines its ability to adapt to resist treatment. Scientists modulated this organization with an FDA-approved drug on the market. Strategy prevented cancer cells from adapting, making chemotherapy more effective in lab cultures and animal models of human cancer.