AACR Highlights: Monday, September 9
Cancer cells divide uncontrollably resulting in a flood of new tumor cells and this uncontrolled metabolic wave requires energy. But metabolism is altered in pancreatic cancer and scientists are trying to understand the molecular underpinnings of the nutrients of choice for various cell types. These new insights into cancer metabolism kicked off the third and final day of plenary sessions at the AACR special conference on pancreatic cancer, bringing together the best minds in pancreatic cancer research. Also on the docket: new model systems, animals and beyond. Scientists are using genetically engineered mouse models that closely recapitulate human pancreatic cancer as well as organoids, small three-dimensional tumors that are grown right from the cells of patients’ tumors. Organoids in particular are potentially bringing us one step closer to personalized medicine for pancreatic cancer patients.
The Nutritional Needs of Cancer Cells
In his presentation on cancer metabolism, Matthew Vander Heiden, M.D., Ph.D., of Koch Institute for Integrative Cancer Research at Massachusetts Institute of Technology (MIT), Cambridge, Massachusetts, explained how cancer cells rely on different nutrients than normal cells. Vander Heiden’s team researches the nutrients required by pancreatic tumors and, more broadly, how metabolism is regulated to influence different stages of tumor biology. The hope is that by gaining a better understanding of what nutrients cancer cells use and the drivers that determine how those nutrients are used, new therapies can be developed. Already, researchers have determined the nutrients a particular tumor uses is based upon its lineage, tissue environment and genetic mutation. Other work by this research group is identifying ways the availability of certain nutrients affects a tumor’s sensitivity to the chemotherapeutic agent gemcitabine.
Mouse Models Aid Research
The research of Tyler Jacks, Ph.D., also of the Koch Institute, focuses on a series of mouse strains engineered to carry mutations in genes known to be involved in human cancer. He presented information on how obesity accelerates pancreatic cancer progression in mice. But early weight loss intercepts this progression. This link is regulated by cholecystokinin, technically called pancreozymin, a gastrointestinal peptide hormone that stimulates the digestion of fats and proteins. Jacks also spoke about why the immune system does not recognize pancreatic tumors, which is a major challenge to effective immunotherapy. Significant effort has focused on learning how tumors evade the immune response. Through the use of elegant mouse modeling, Jacks showed that pancreatic tumors evade immune clearance. While T cells can infiltrate the tumors and recognize targets present on the tumor, they do not kill the tumor. Future work will decipher ways to encourage these T cells to find the tumor and then destroy it.
“The conference covered a broad array of important scientific research being conducted in the hopes of bringing better treatments to patients. The topics presented during the three days of plenary sessions provided extraordinary insights into the current state of pancreatic cancer research,” says meeting cochair Elizabeth M. Jaffee, M.D., of Johns Hopkins Sidney Kimmel Comprehensive Cancer Center, Baltimore, Maryland; she is also the chief medical advisor for the Lustgarten Foundation. The pancreatic cancer research community is already looking forward to next year’s event.