International Research Chemistry Awards

  A groundbreaking study from Brown University Health researchers has identified a crucial factor that may help improve treatment for glioblastoma , one of the most aggressive and common forms of adult brain cancer. The findings, published November 10 in Cell Reports, reveal how differences among cells within a single tumor influence the cancer's response to chemotherapy, and introduce a promising new therapy designed to tip the odds in the patients' favor. Glioblastoma is notoriously difficult to treat. One of the key reasons is that no two cells within the tumor behave exactly alike. Even inside one tumor, some cells may respond to treatment while others resist it, allowing the cancer to persist and grow. For decades, scientists have known that tumors are composed of diverse cells, but the biological forces driving these differences, and their impact on treatment, have remained elusive. Chen's team discovered that a small molecule called miR-181d acts like a master switch...

  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...