Why do some tumours spread while others remain localised? The mechanisms governing the metastatic potential of tumour cells remain largely unknown — yet understanding this is crucial for optimising patient care. Using cells from colon cancers, scientists at the University of Geneva (UNIGE) have pinpointed the criteria that influence the risk of metastasis, and identified gene expression signatures that can be used to assess its probability. The team then created an artificial intelligence tool (MangroveGS) capable of transforming these data into predictions for many cancers with unparalleled reliability. These results, published in Cell Reports, pave the way for more precise care and the discovery of new therapeutic targets.

A comprehensive review highlights significant advancements in the microbial biosynthesis of Human Milk Oligosaccharides (HMOs), the vital sugars in breast milk that shape infant gut health and immunity. While key HMOs like 2'-fucosyllactose (2'-FL) are now commercially available, researchers are overcoming technical hurdles to produce more complex HMOs at scale, including 3-fucosyllactose (3-FL) and sialyllactoses (SLs). These developments promise to enhance infant formula and open new doors for functional foods and potential therapeutic applications targeting gut health and immune disorders.

Medical researchers at Flinders University have uncovered an important clue that could help doctors better predict what happens next for people with advanced lung cancer when their first treatment fails.

Rye pollen slows tumor growth in animal models of cancer. Chemists determined the 3D structure of the bioactive molecules in rye pollen. With new blueprint, researchers could develop strategies for cancer treatment.

New study shows that cancer damages its own DNA by pushing key genes to work too hard. Researchers found that the most powerful genetic “on switches” in cancer cells, called super-enhancers, drive unusually intense gene activity. That high gear creates stress on the DNA and can cause dangerous breaks. Cancer cells can often repair this damage, but the process is frequently error-prone, the repeated cycle of breaking and repairing can make these regions more prone to accumulating mutations over time. In short, the same mechanisms that help cancer grow quickly may also make its DNA more fragile, helping explain how tumors continue to evolve and, in some cases, become more aggressive over time.