OCT 10, 2018 10:30 AM PDT

Metabolic Networks in the Tumor Microenvironment

Sponsored by: Agilent
Speaker
  • Assistant Professor, Department of Molecular and Integrative Physiology, Department of Internal Medicine, Division of Gastroenterology and Hepatology, Rogel Cancer Center, University of Mich
    Biography
      Costas A. Lyssiotis obtained his bachelor's degree in Chemistry and Biochemistry from the University of Michigan in 2004, his PhD in Chemical Biology from The Scripps Research Institute in 2010, and then completed postdoctoral training in the laboratory of Lewis C. Cantley at Harvard and Cornell. In 2015, Dr. Lyssiotis joined the faculty at the University of Michigan with appointments in the Departments of Physiology and Medicine. His lab studies the biochemical pathways and metabolic requirements that enable tumor survival and growth. This work spans the areas of cancer metabolism, the tumor microenvironment and immunometabolism using and developing protocols in mass spectrometry-based metabolomics. Ultimately, his group aims to transition new information about these processes into targeted therapies for cancer and other diseases. He is the recipient of several junior scholar awards including being named a Lefkofsky Scholar, a Kimmel Scholar, an AACR NextGen young investigator, a Dale F. Frey Breakthrough Scientist, and a V Foundation Fellow.

    Abstract

    Pancreatic tumors are dynamic pseudo-organs that contain numerous cell types interacting to create unique physiology. A typical pancreatic tumor is made up largely of stromal fibroblasts and immune cell populations, rather than cancer cells. These non-malignant cells act collaboratively to create a dense fibrotic matrix that blocks cancer cells from accessing nutrients and oxygen by inhibiting vascularization. The cancer cells are thus in a state of near-starvation and must employ unorthodox methods to obtain nutrients to support their bioenergetic and biosynthetic needs. Our group has provided foundational work describing the cell autonomous reprogramming of metabolic processes in the cancer cells to facilitate survival and growth under these challenging circumstances. Beyond cell intrinsic metabolic alterations, pancreatic cancer cells also work cooperatively with the non-cancer cells in the tumor microenvironment through the exchange of growth factors, signaling molecules and metabolites. In this seminar, I will describe new work illuminating pathways of metabolic crosstalk among pancreatic cancer-associated fibroblasts, tumor associated macrophages, and malignant pancreatic cancer cells in maintenance of tumor growth, survival and therapeutic resistance. 

    For Research Use Only. Not for use in diagnostic procedures.

    Learning Objectives: 

    1. Pancreatic cancer is the most deadly major cancer, and this owes in large part to the lack of effective therapies
    2. Pancreatic tumors are nutrient and oxygen limited and are composed of numerous cell types that interact to promote growth and survival
    3. Metabolic networks exist among the cells in pancreatic tumors that facilitate growth, survival, and promote therapeutic resistance


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