Los Angeles, CA – August 14, 2025 – The Terasaki Institute for Biomedical Innovation announces a significant advancement in addressing the fight against cancer-associated cachexia (CAC), a life-threatening syndrome responsible for over one-third of cancer-related deaths. Published in Cell, the study led by Dr. Aliesha O’Raw, Principal Investigator at the Institute, demonstrates that modulating the vagus nerve can effectively halt the progression of cachexia, enhance chemotherapy outcomes, and improve survival in preclinical models.

Despite significant advancements in medicine, cancer remains a major health challenge and the leading cause of mortality worldwide, highlighting the urgent need for continued research to identify robust biomarkers for the early detection, prognosis, and treatment across multiple cancer types.

Glioblastoma multiforme (GBM), the most aggressive tumor of the central nervous system, is highly malignant, resistant to existing drug therapies and associated with high mortality rates. Overexpression of B-cell lymphoma 6 (BCL6) has been frequently observed in GBM patients, highlighting the urgent need for potent BCL6 inhibitors as a novel treatment strategy.

Oral squamous cell carcinoma (OSCC) is one of the most common malignant tumors of the head and neck. Oral submucous fibrosis (OSF), which develops into OSCC, has become a relatively common pathway in oral mucosal carcinogenesis, with a transformation rate ranging from 3% to 19%. Hence, it is critical to elucidate the key molecular events of OSF tumorigenesis for the prevention and early diagnosis of OSCC.

An international team of scientists published findings August 7, 2025, in Cancer Discovery helping to explain why a common form of pediatric cancer called neuroblastoma is often treated successfully with chemotherapy but prone to relapse in several years.

Cancer cells with many copies of the MYCN oncogene on circular extra-chromosomal DNA elements (ecDNA) grow quickly but are more easily destroyed by chemotherapy. Tumor cells with fewer copies of the oncogene located on ecDNA enter a zombie-like state known as senescence where they persist but no longer divide to make new cells. These zombie cells are unaffected by chemotherapy and can be reactivated a year or two later, triggering the cancer to relapse.