The Beatty Laboratory incorporates both basic science research and clinical investigation to define strategies for leveraging the immune system for the treatment of cancer. Our mission is to define mechanisms of resistance and response to immunotherapy in an effort to design effective strategies to condition tumors and patients for enhanced therapeutic responsiveness.
In 2019, an estimated 56,770 people will be diagnosed with pancreatic cancer in the United States and 45,750 will die from their disease in the same year. The 5-year survival remains <10% emphasizing the continued need for further advancements aimed at improving clinical outcomes.
The lab’s main focus is pancreatic cancer, a malignancy that has demonstrated remarkable resistance to all forms of therapy. We believe that understanding the biology underlying this therapeutic resistance will have implications not only for pancreatic cancer but also many other malignancies.
Recent work has implicated the role of the immune system in regulating therapeutic resistance to both cytotoxic therapies (e.g. chemotherapy and radiation therapy) as well as immunotherapy. Pancreatic cancer is heavily infiltrated by immune cells and in the setting of an insult (e.g. inflammation or cytotoxic therapy), malignant cells respond by increasing the recruitment of immune cells capable of supporting tumor survival, growth and spread. We have shown that either inhibiting this immune reaction or redirecting it with anti-tumor potential can enhance the efficacy of cytotoxic therapies. We have also discovered that subsets of immune cells residing outside of tumors have a critical role in defining the immune reaction within a tumor. Together, these findings provide promise that pancreatic cancer may be “conditioned” with enhanced therapeutic responsiveness.
A major goal within the laboratory is to understand the “connectome” of immune cells within tumors and to identify mechanisms that define the biology of immune cell communities within tumors. To do so, we are using sophisticated mouse models of pancreatic cancer to discover novel treatment algorithms, collaborating within clinical investigators to understand human immune cell biology within metastatic and primary tumors and contributing to novel clinical efforts to revolutionize our approach to advancing therapeutics in the clinic.
Collectively, we hope that our investigations will help to dissect treatment pathways that can be combined and sequenced to impact the natural history of cancer and improve patient outcomes.This