International Research Chemistry Awards

  As antibiotic-resistant infections rise and are projected to cause up to 10 million deaths per year by 2050, scientists are looking to bacteriophages, viruses that infect bacteria, as an alternative. A new study shows how these phages use a tiny RNA molecule, called PreS, to hijack bacterial cells and boost their own replication. By acting as a hidden genetic "switch" that rewires key bacterial genes, PreS helps the virus copy its DNA more efficiently, offering important insights that could guide the design of smarter phage-based therapies. A new study from the Hebrew University of Jerusalem reveals how viruses that infect bacteria, called bacteriophages or "phages," use a tiny piece of genetic material to hijack bacterial cells and make more copies of themselves. The research shows that a very small RNA molecule, called PreS, acts like a hidden "switch" inside the bacterial cell. By flipping this switch, the virus can change how the bacterial cell works...

  Researchers at The University of Texas MD Anderson Cancer Center have identified a targetable driver of brain metastases in patients with aggressive inflammatory breast cancer. The study uncovers a novel role for soluble E-cadherin (sEcad) in promoting tumor invasion while resisting cancer cell death and triggering brain inflammation via the CXCR2 signaling pathway. The results suggest that targeting sEcad or the CXCR2 pathway could treat or prevent brain metastasis. The study, published in Neuro-Oncology, was led by Xiaoding Hu, M.D., Ph.D., instructor of Breast Medical Oncology , and Bisrat Debeb, D.V.M., Ph.D., associate professor of Breast Medical Oncology. What prompted the researchers' interest in E-cadherin in brain metastasis? Brain metastasis is a common complication of advanced breast cancer, with a particularly high risk in inflammatory breast cancer. However, there are no effective therapies because the underlying mechanisms remain poorly understood. Previous work by ...

  UCLA scientists have developed advanced miniature 3D tumor organoid models that make it possible to study glioblastoma tumors in a setting that closely mirrors the human brain, shedding light on how the aggressive cancer interacts with surrounding brain cells and the immune system to become more invasive and resistant to therapy. The organoid models, described in two complementary studies published in Cell Reports, are built from human stem cells and recreate the complex mix of cell types found in the human brain. This approach allows researchers to directly observe how patient-derived tumors communicate with healthy brain tissue, revealing vulnerabilities that could be targeted with more personalized therapies. Model helps identify hidden regulator of tumor aggressiveness The first model, called the Human Organoid Tumor Transplantation (HOTT) system, reveals how glioblastoma communicates with surrounding brain cells to change its identity, invade tissue and resist treatment. Usi...

  Scientists at the Icahn School of Medicine at Mount Sinai have developed an experimental immunotherapy that takes an unconventional approach to metastatic cancer: instead of going after cancer cells directly, it targets the cells that protect them. The study, published in the January 22 online issue of Cancer Cell, a Cell Press Journal [DOI 10.1016/j.ccell.2025.12.021], was conducted in aggressive preclinical models of metastatic ovarian and lung cancer. It points to a new strategy for treating advanced-stage solid tumors. In a strategy modeled after the famed Trojan horse, the treatment enters the tumors by targeting cells called macrophages that guard the cancer cells, disarms these protectors, and opens up the tumor's gates for the immune system to enter and wipe out the cancer cells. Metastatic cancers cause the vast majority of cancer-related deaths, and solid tumors such as lung and ovarian cancer have proven especially difficult to treat with current immunotherapies. One m...

  The cancer gene MYC camouflages tumors by suppressing alarm signals that normally activate the immune system. This finding from a new study offers a promising way to improve existing cancer therapies as well as develop new ones. Could this mark a shift in how we think about cancer therapy? At least in the laboratory, evidence suggests it may be. An international research team has succeeded in deciphering a key mechanism that controls the growth of pancreatic cancers. The scientists identified a potential central mechanism by which cancer cells protect themselves from attack by the body's own immune system. Blocking this mechanism resulted in a dramatic reduction in tumors in laboratory animals. A look at the central driver of cell division The results of the study have now been published in Cell. The research was primarily carried out by Leonie Uhl, Amel Aziba and Sinah Löbbert, along with other collaborators from the University of Würzburg (JMU), Massachusetts Institute of Techn...

  A chain of immune reactions in the gut—driven by a key signaling protein and a surge of white blood cells from the bone marrow—may help explain why people with inflammatory bowel disease (IBD) have a higher risk of colorectal cancer, according to a preclinical study by Weill Cornell Medicine investigators. The findings point to new possibilities for diagnosis, monitoring and treatment of IBD. The study began with a focus on TL1A, an inflammatory immune signaling protein known to be associated with IBD and colorectal cancer. Experimental drugs that block TL1A activity have shown great promise against IBD in clinical trials, but how the signaling protein promotes the disease and associated tumors has been unclear. The study, published Jan. 22 in Immunity, demonstrates that in an animal model TL1A has much of its impact through immune cells in the gut called ILC3s. When these cells are activated by TL1A, they summon a surge of white blood cells called neutrophils from the bone marro...