Siddhartha Mitra, PhD

​Specialty

Immune microenvironment regulation and immune evasion in brain tumors

Location

University of Colorado Anschutz Medical Campus, Dept of Pediatrics, Aurora

Program Objective

To determine the molecular mechanisms whereby brain tumors evade immune-surveillance by myeloid cells.

Program Description

Some current areas of focus include:

The Mitra lab is part of the Morgan Adams Pediatric Brain Tumor Research Program within the Department of Pediatrics Hematology/Oncology/Bone Marrow Transplantation section of the University Of Colorado School Of Medicine based in Denver, Colorado, USA. The Mitra lab brings together three distinct fields of research: Immuno-Oncology, neurodevelopment, and brain tumor oncology. The lab focuses on the mechanisms of immune-surveillance in brain tumors by cells of the the innate immune system. As one of the earliest immunologic defense mechanisms developed in the body, is independent of mutational load and provides a unique effector mechanisms of macrophages and brain resident microglia that are often present in high numbers within the brain tumor microenvironment. While most studies have demonstrated tumor-associated macrophages to promote tumor growth, we have recently shown that inhibiting the myeloid checkpoint pathway (the CD47-SIRPα signaling axis) suppresses the “don’t eat me” signal and allows for efficient macrophage-mediated phagocytosis of different types of brain tumors (Science Translation Medicine, 15 Mar 2017) and are now continuing our investigations on understanding the immune microenvironment and immune-evasion pathways in brain tumors. A major interest of the laboratory focuses on translational immune-Oncology to understand and leverage the mechanisms of efferocytosis and immunogenic cell death to develop better immune modulating drugs against adult and pediatric brain tumors. The members of the lab will be part of a unique brain tumor research program which encompasses seven labs whose expertise ranges from single cell RNA sequencing, autophagy and oncogenic signaling pathway.

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