Immune cells are capable of detecting infections just like a sniffer dog, using special sensors known as Toll-like receptors, or TLRs for short. But what signals activate TLRs, and what is the relationship between the scale and nature of this activation and the substance being detected? In a recent study, researchers from the University of Bonn and the University Hospital Bonn (UKB) used an innovative method to answer these questions. The approach that they took might help to speed up the search for drugs to combat infectious diseases, cancer, diabetes or dementia.

Researchers at Uppsala University and KTH Royal Institute of Technology have developed a new form of precision medicine, an antibody, with the potential to treat several types of cancer. Researchers have managed to combine three different functions in the antibody, which together strongly amplify the effect of T cells on the cancer tumour. The study has been published in Nature Communications.

Researchers have developed a unique type of antibody that both targets and delivers a drug package via the antibody itself, while simultaneously activating the immune system ("3-in-1 design") for personalised immunotherapy treatments.

Even treated with the most advanced therapies, patients with glioblastoma - an aggressive brain cancer - typically survive less than two years after diagnosis. Efforts to treat this cancer with the latest immunotherapies have been unsuccessful, likely because glioblastoma cells have few, if any, natural targets for the immune system to attack.

In a cell-based study, scientists at Washington University School of Medicine in St. Louis have forced glioblastoma cells to display immune system targets, potentially making them visible to immune cells and newly vulnerable to immunotherapies.

Scientists have uncovered how certain E. coli bacteria in the gut promote colon cancer by binding to intestinal cells and releasing a DNA-damaging toxin. The study, published in Nature, sheds light on a new approach to potentially reduce cancer risk. The study was performed by the teams of Prof. Lars Vereecke (VIB-UGent Center for Inflammation Research) and Prof. Han Remaut (VIB-VUB Center for Structural Biology).

As the hunt for effective cancer therapies intensifies, some scientists are turning back to look at old drugs in a new light. The anti-malarial hydroxychloroquine is one such drug that has been "repurposed" to fight cancer. Despite its effectiveness at blocking the resupply of needed resources to cancer cells, clinical trial results have been disappointing, in part because cancer cells eventually become resistant to the drug.

"As tumors grow very quickly, consume a lot of oxygen and their vascular growth can't necessarily keep pace, they often contain areas that are poorly supplied with oxygen," explains Johannes Karges. These areas, often in the center of the tumor, frequently survive treatment with conventional drugs, so that the tumor initially shrinks but doesn't disappear completely. This is because the therapeutic agents require oxygen to be effective.

A technological breakthrough by medical researchers at Tel Aviv University enabled the discovery of a cancer mechanism that prevents the immune system from attacking tumors. The researchers were surprised to find that reversing this mechanism stimulates the immune system to fight the cancer cells, even in types of cancer considered resistant to prevailing forms of immunotherapy. The breakthrough was led by Prof. Carmit Levy, Prof. Yaron Carmi, and PhD student Avishai Maliah from TAU's Faculty of Medical & Health Sciences. The paper was published in the leading journal Nature Communications.