Anti-immune defences involving down-regulation of MHC-I or beta-catenin activation do not explain immune coldness of pancreatic or ileal neuroendocrine tumors

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Introduction: Our previous study demonstrated pancreatic (PNET) and ileal neuroendocrine tumors (INETs) are immunologically cold, containing very few tumor infiltrating lymphocytes (TILs) compared to non-small cell lung cancers. This raises the questions of whether there is in fact, a weak anti-tumor immune response taking place or whether the tumors are deploying effective anti-immune defences such as down-regulation of MHC class I or activation of β-catenin signalling.

Aim(s): To assess whether down regulation of MHC class I and activation of β-catenin pathway could explain the immune cold tumor microenvironment seen in PNET and INETs.

Materials and methods: Multiplex immunohistochemistry was performed on 10 PNETs and 10 INETs (5 CD8+ high and 5 CD8+ low) using anti-synaptophysin and anti-HLA class 1 antibodies. Anti-β-catenin antibody was used to assess for nuclear expression of β-catenin indicating activated pathway in both primary tumors and their liver metastases.

Conference: 18th Annual ENETS Concerence (2021)

Presenting Author: Tanno L

Authors: Tanno L, Naheed S, Lopez M, Taylor J, Machado M,

Keywords: pancreatic neuroendocrine tumor, ileal neuroendocrine tumor, beta-catenin pathway, tumor immune microenvironment, major histocompatibility complex 1,