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The clinical response to cancer therapies involves the complex interplay between the systemic, tumoral, and stromal immune response as well as the direct impact of treatments on cancer cells. Each individual's immunological and cancer histories are different, and their carcinogen exposures may differ. This means that even though two patients with oral tumors may carry an identical mutation in TP53, they are likely to have different pre-existing immune responses to their tumors. These differences may arise due to their distinct accessory mutations, genetic backgrounds, and may relate to clinical factors including previous chemotherapy exposure and concurrent medical comorbidities. In isolation, their cancer cells may respond similarly to cancer therapy, but due to their baseline variability in pre-existing immune responses, patients can have different responses to identical therapies. In this review we discuss how the immune environment of tumors develops, the critical immune cell populations in advanced cancers, and how immune interventions can manipulate the immune environment of patients with pre-malignancies or advanced cancers to improve therapeutic outcomes.

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Oral squamous cell carcinoma is an extremely malignant tumour: in order to reduce mortality and morbidity, early diagnosis and treatment is the clinician's best weapon.

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Oral cancer (OC) is an uncommon malignancy in Western countries, being one of the most common cancers in some high-risk areas of the world. It is a largely preventable cancer, since most of the different risk factors identified, such as tobacco use, alcohol consumption, and betel nut chewing, are behaviors that increase the likelihood of the disease. Given its high mortality, early diagnosis is of utmost importance. Prevention and the anticipation of diagnosis begin with identification of potentially malignant lesions of the oral mucosa and with local conditions promoting chronic inflammation. Therefore, every lesion must be recognized promptly and treated adequately. The clinical recognition and evaluation of oral mucosal lesions can detect up to 99% of oral cancers/premalignancies. As stated by the World Health Organization, any suspicious lesion that does not subside within two weeks from detection and removal of local causes of irritation must be biopsied. Surgical biopsy remains the gold standard for diagnosis of oral cancer. Adjunctive tools have been developed and studied to help clinicians in the diagnostic pathway, such as toluidine blue vital staining and autofluorescence imaging. In the near future other methods, i.e., identification of salivary markers of progression may help in reducing mortality due to oral cancer.

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BACKGROUND: Skin cancer incidence is rising, placing a burden on healthcare systems worldwide. This problem may even be more extensive than expected, since registration of (pre)malignancies of the skin is poor. OBJECTIVE: To provide insight into the numbers of (pre)malignancies in patients with actinic keratosis (AK) or basal cell carcinoma (BCC) in 2 university and 2 general hospitals. METHODS: The types and numbers of previous tumours and of tumours during a two-year follow-up were collected from 574 patients. RESULTS: Mean time between the first diagnosed (pre)malignancy and time of inclusion was 6.6 years. Overall, 60% had multiple types of (pre)malignancies. In BCC patients, 61% had multiple BCCs, in patients with squamous cell carcinoma (SCC), 40% had multiple SCCs. The combination 'BCC and SCC' occurred in 10%, 'BCC and AK' in 47%, 'SCC and AK' in 14%. CONCLUSION: High numbers of patients with multiple (pre)malignancies were found in this patient population in university and general hospitals, which may well reflect the Dutch hospital population. We conclude that skin cancer patients are more extensively affected than was expected up till now. Consequently, the management of skin cancer may be in need of adaptation in near future and the question arises whether dermatologists have the capacity for providing care for all these patients.

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