Abstract

This article is protected by copyright. All rights reserved. Oral squamous cell carcinoma (OSCC) is a major subcategory of head and neck squamous cell carcinomas (HNSCC) and is currently the 6th highest cause of cancer mortality world-wide (Bray et al., 2018; Siegel, Miller, & Jemal, 2019). Despite current treatments such as surgery with adjunctive radiation and chemotherapy, the 5-year survival has remained at 50% for decades (Kumar, Nanavati, Modi, & Dobariya, 2016; Rivera, 2015). Most human solid cancers are believed to be driven by chronic inflammation that instigates nascent tumour proliferation (dysplasia), transformation and metastasis while conversely suppressing anti-tumour immune responses (Taniguchi & Karin, 2018). Inflammation promoted by dysregulated NF-κB (nuclear factor of kappa B) is also a hallmark of early OSCC (Cancer Genome Atlas, 2015; Tang et al., 2015). Lack of knowledge of this molecular driver is a key feature limiting curative outcomes.

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