OCT 03, 2018 09:00 AM PDT

Mechanisms of Myeloid Immunosuppression: Functional Characterization of the Tumor Microenvironment Using Single and Multiplex IHC

SPONSORED BY: Cell Signaling Technology
C.E. CREDITS: P.A.C.E. CE | Florida CE
Speakers
  • IHC Specialist, Cell Signaling Technology
    Biography
      Chris has close to ten years of experience working with a variety of immunohistochemical techniques and technologies. His main focus over this time has been development and validation of IHC grade antibodies in a number of research areas. This has required a deep understanding of not only the IHC assay itself but also expression profiles of the human proteome in normal and diseased tissues. The main area of focus has been immuno-oncology, where Chris has developed automated IHC assays for novel I/O targets and provided support for multiple pre-clinical programs. His experience also includes design and development of multiplex immunofluorescent IHC assay panels and implementation of IHC digital quantitation software.

    Abstract:
    DATE: October 3, 2018
    TIME:  9:00am PDT, 12:00pm EDT
     
    Infiltrating myeloid cells constitute a significant component of the suppressive tumor microenvironment (TME) and possibly contribute to therapeutic failures. An understanding of the immune regulatory context of the TME is required to harness the power of the antitumor immune response. Here, we present solutions to better understand the TME in a context-dependent manner. Using highly validated antibodies, immunohistochemical techniques are employed in a seven-color TSA-based multiplex panel along with single and dual-plex chromogenic stains to visualize biomarker expression in an array of tumor types. Newly validated Arginase1 and IDO1 monoclonal antibodies add a functional readout of the immunosuppressive TME to phenotypic marker analysis.
     
    Learning Objectives:
    • Understand the importance of the immune regulatory context of the TME
    • Learn about solutions to better understand the TME in a context-dependent manner

    Show Resources
    Show Resources
    Connect with us