Abstract
This review discusses the microenvironment of evolving and established conventional oral squamous cell carcinoma, by far the most common oral cancer. The focus of this paper is mainly on the more recent data that describe the role of microorganisms, host-microbial interactions, and in particular, the contributions of cell-surface toll-like receptors on immune system cells and on normal and malignant epithelial cells to their functions that support carcinogenesis. Because carcinomas arising at various host surfaces share much in common, additional information available from studies of other carcinomas is included in the discussion. Accumulating evidence reveals the complex toll-like receptor-mediated tumor-supporting input into many aspects of carcinogenesis via malignant cells, stromal immune cells and non-immune cells, complicating the search for effective treatments.
Highlights
The vast majority of oral cancer cases are represented by squamous cell carcinoma (SCC) arising at the mucosal surface of the oral cavity
Another area of study that has the potential to significantly impact upon the approach to patient treatment is the complex host-microbiome interaction network operating throughout the natural history of carcinogenesis in the oral mucosa
A key point of interest for further discussion is that, while the environment of oral epithelial dysplasia and oral SCC (OSCC) exhibits shifts in microbial abundance, diversity, and metabolic activities, current understanding is that the colonizers are a mix of commensals and some opportunistic pathogens, all expressing microbe-associated molecular patterns (MAMP) that are common to commensals and pathogens
Summary
The vast majority of oral cancer cases are represented by squamous cell carcinoma (SCC) arising at the mucosal surface of the oral cavity. While newer modalities show promise, when used in combination, the improvements in prognosis so far are small, which necessitates further consideration of other mechanisms Another area of study that has the potential to significantly impact upon the approach to patient treatment is the complex host-microbiome interaction network operating throughout the natural history of carcinogenesis in the oral mucosa. No specific microorganism is known to initiate oral carcinogenesis, but evidence does support a role for host-microbial interactions in cancer progression, which is the focus of this review. These interactions will be discussed in the context of normal and transformed surface epithelium. Structures deep to the lamina propria differ from one subsite to another
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