Michigan Researchers Uncover How a 'Frankenstein' Gene Fuels Aggressive Childhood Cancer

By Anastazia Hartman Researchers in the Parolia Lab at the University of Michigan have uncovered how a single genetic event can make Ewing sarcoma—a rare and aggressive bone and soft tissue cancer that primarily affects children and young adults—more dangerous. Their findings reveal that when a gene called STAG2 is lost, the core cancer-driving protein EWS-FLI1 is redirected toward powerful genetic “on switches” that dramatically boost tumor-promoting genes. Ewing sarcomas arise from a genetic accident causing a fusion between two independent genes, EWSR1 and FLI1. When parts of these genes

From Health Lab: Researchers identify new therapeutic target for neuroendocrine tumors in the gastrointestinal tract

By Anastazia Hartman Researchers identify new therapeutic target for neuroendocrine tumors in the gastrointestinal tract Targeting two separate pathways that control lipid synthesis led to longer survival in mouse models By Ananya Sen Neuroendocrine cells are unique in their ability to act both as nerve cells and hormone-making cells. They're scattered throughout the body, including the stomach, intestines, pancreas and lungs. Tumors that arise from these cells are called neuroendocrine tumors and are often rare and slow growing. Around 70% of all neuroendocrine tumors arise in the pancreas or

Vascular STING activation facilitates NK cell anti-tumor immunity in small cell lung cancer

By Anastazia Hartman Small cell lung cancer (SCLC) is an aggressive form of lung cancer, in part because many tumors evade the immune system. SCLC does this by shutting down MHC-I, a molecule that normally acts like a “red flag” to alert T cells to recognize and attack cancer cells. Ironically, this should make SCLC vulnerable to another type of immune cell, natural killer (NK) cells, which are designed to detect and destroy cells that lack MHC-I. NK cells can kill SCLC cells in laboratory settings; however, in SCLC patients, NK cells are largely absent from the tumor environment. Navin R

A New Genome-Wide Tool for Detecting Cancer-Causing Rearrangements in Routine Lymphoma Biopsies

By Anastazia Hartman A collaborative team of researchers from the University of Michigan, New York University, and Arima Genomics has developed a new method that improves the detection of genomic rearrangements in lymphomas and multiple myeloma. The research, published this week in the journal Cell Genomics, was led by Russell Ryan, MD, of the University of Michigan Department of Pathology, and Matija Snuderl, MD, of the New York University Department of Pathology, in collaboration with Anthony Schmitt and colleagues at Arima Genomics, a biotechnology company that developed the assay, called

Targeting a metabolite as a therapy for childhood ependymomas

By Sriram Venneti Ependymomas are the third most common pediatric brain tumor, affecting roughly 250 children in the United States each year. Most cases are diagnosed in children eight years old or younger. Despite decades of research, current treatments extend survival but rarely cure the disease. A new study published in Nature by Dr. Sriram Venneti’s laboratory at the University of Michigan’s Department of Pathology and the Chad Carr Pediatric Brain Tumor Center has identified a surprising driver of ependymoma growth: a molecule called itaconate. The discovery opens the door to new

FDA Approves First-Ever Drug for a Rare and Aggressive Brain Cancer

Department of Pediatrics originally published in 2023 has lead the U.S. Food and Drug Administration (FDA) to accelerate approval of the drug ONC201 now called dordaviprone for the treatment of diffuse midline glioma (DMG) with an H3 K27M mutation. A rare, aggressive brain tumor that primarily affects children and young adults. This marks the first FDA-approved therapy for this form of cancer.

The Path to Discovery

Jennifer Brazil, PhD, Assistant Professor of Pathology at Michigan Medicine began her own research laboratory in 2018. She continued to research the mechanisms by which polymorphonuclear neutrophils (PMN) and epithelial glycans can be targeted to alter neutrophil transepithelial migration and neutrophil function under conditions of intestinal inflammation and repair.