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ABSTRACT: Objectives
The intracellular DNA sensor stimulator of interferon genes (STING) has recently been shown to play a vital role in anti-viral and anti-tumor immune responses stimulating cytokine production. While human papillomavirus (HPV) is a causative agent for a subset of head and neck squamous cell carcinoma (HNSCC) with unique etiology and clinical outcome, how the STING pathway is regulated in a virus-induced tumor microenvironment is not well understood. Since STING inactivation likely reflects immunoescape via innate immunity, we hypothesized that its restoration would improve efficacy of the immune modulatory monoclonal antibody (mAb), cetuximab.Materials and methods
We correlated STING protein expression with clinical parameters by immunohistochemistry (n = 106) and
SUBMITTER: Lu S
PROVIDER: S-EPMC5877820 | biostudies-literature | 2018 Mar
REPOSITORIES: biostudies-literature