A team of researchers from the University of California at Los Angeles (UCLA) Jonsson Comprehensive Cancer Center has been awarded two research grants totaling $6 million from the National Institutes of Health (NIH) to identify new ways to treat pancreatic cancer.
Caius Radu, MD
Timothy Donahue, MD
“Pancreatic cancer is one of the most challenging cancers to treat,” said Caius Radu, MD, Professor of Molecular and Medical Pharmacology at the David Geffen School of Medicine at UCLA. “The lack of effective treatments suggests there is an inadequate understanding of the biologic complexity of the disease and the mechanisms behind its resistance to therapies that work in treating other types of cancers.”
The two grant-supported projects, which aim to untangle those complexities and identify potential new immunotherapeutic approaches, will be co-led by Dr. Radu and Timothy Donahue, MD, Professor of Surgery and Chief of Surgical Oncology at the Geffen School of Medicine and Surgical Director of the UCLA Agi Hirshberg Center for Pancreatic Diseases.
Two Projects
The first grant project will focus on mutations to the KRAS gene, which are implicated in nearly all pancreatic cancer cases. Working with Zev Wainberg, MD, Associate Professor of Medicine at the Geffen School of Medicine and Co-Director of UCLA Health’s gastrointestinal oncology program, the team will specifically target these KRAS oncogenes. In addition, they will investigate the mechanisms behind pancreatic cancer cells’ overproduction of adenosine, a metabolite that can suppress the body’s cancer-killing T cells.
Zev Wainberg, MD
The second project will focus on interferon signaling in pancreatic cancer. The team will seek to identify vulnerabilities in tumor cells’ interferon signaling process that can be leveraged for effective therapeutic strategies. The researchers have already found that interferon signaling is upregulated in a subset of human pancreatic cancer cells and functions to deplete nucleotides. They will continue to examine the mechanisms in place to counterbalance the nucleotide-depleting and potentially deleterious effects of interferon signaling.
