Oral cavity cancers occur predominantly at sites of potential dental and denture trauma, especially in nonsmokers without other risk factors. Recognizing teeth irritation as a potential carcinogen would have an impact on prevention and treatment strategies.

Actinic Keratosis (AK), Intraepidermal Carcinoma (IEC), and Squamous Cell Carcinoma (SCC) are generally considered to be advancing stages of the same disease spectrum. However, while AK often regress spontaneously, and IEC often regress in response to immune-activating treatments, SCC typically do not regress. Therefore, it is vital to define whether fundamental immunological changes occur during progression to SCC. Here we show that proinflammatory cytokine expression, chemokine expression, and immune cell infiltration density change during progression to SCC. Our findings suggest a switch from predominantly proinflammatory cytokine production to chemokine production is a key feature of progression from precancer to cancer. Together, these observations propose a model that can underpin current research and open new avenues of exploration into the clinical significance of these profiles with respect to immunotherapeutic or other treatment outcomes.

Chemokines play a significant role in attracting immune cells to extravasate to areas of peak expression in response to various stimuli. IL-8, MIP-1α and MIP-1β are known to be highly expressed in multiple cancers, as well as benign skin conditions. Their role in cutaneous Squamous Cell Carcinoma has yet to be established. 67 lesions suspicious for keratinocytic malignancy were sampled from 37 patients and tested for chemokine expression via Flow Cytometry. Each lesion was measured for thickness, histopathological grading, and immune cell infiltration score. Expression of the chemokines IL-8 and MIP-1α