Langerhans cells (LCs) are bone marrow-derived dendritic cells (DCs) that represent 2-3% of the entire cell population of the human skin, known to have an ability to present antigens to T lymphocytes. Moreover, there is evidence that LCs are probably capable of inducing the local cytotoxic type T-cell-mediated response against the tumour-associated antigens. In the past two decades, a dramatic increase has been noted in the incidence of basal cell carcinoma (BCC) and squamous cell carcinoma (SCC). The purpose of this study was to critically assess the results of available studies quantitatively assessing the LCs in nonmelanoma skin cancers and try to establish a conclusion of its possible impact on their future treatment. The PubMed, EMBASE, and the Web of Science databases were searched, which returned 948 citations. After a thorough analysis of full article texts, 30 studies have been chosen, including 11 of the BCC, 12 of the SCC specimens, and 7 analysing both tumour types. There was an overall trend towards slightly higher numbers of LCs in BCC than in SCC; however, these tendencies were discrepant between the studies. We presume that such differences could be caused by various staining techniques with a broad spectrum of specificity, including anti-S100, anti-CD1a, and ATPase activity staining used for LCs identification. We hypothesise that as there is a high inconsistency between the results of the studies, as far as the densities of LCs observed in the specimens are concerned, it seems that the mechanism of the influence of LCs on the antitumoural immune response is complicated. Finally, as at present, there is a paucity of available risk scores for the recurrence or progression of BCC or SCC, the creation of classification stratifying that risk including the density of LCs could bring additional information both for the physician and the patient.

Basal cell carcinoma (BCC) and squamous cell carcinoma (SCC) are the most frequently diagnosed cancers, generating significant medical and financial problems. Cutaneous carcinogenesis is a very complex process characterized by genetic and molecular alterations, and mediated by various proteins and pathways. Cell adhesion molecules (CAMs) are transmembrane proteins responsible for cell-to-cell and cell-to-extracellular matrix adhesion, engaged in all steps of tumor progression. Based on their structures they are divided into five major groups: cadherins, integrins, selectins, immunoglobulins and CD44 family. Cadherins, integrins and CD44 are the most studied in the context of non-melanoma skin cancers. The differences in expression of adhesion molecules may be related to the invasiveness of these tumors, through the loss of tissue integrity, neovascularization and alterations in intercellular signaling processes. In this article, each group of CAMs is briefly described and the present knowledge on their role in the development of non-melanoma skin cancers is summarized.Non-melanoma skin cancers (NMSC) are the most frequently diagnosed malignancies and their prevalence has increased dramatically over the last 30 years. Basal cell carcinoma (BCC) and squamous cell carcinoma (SCC) represent 99% of all NMSC. BCC, which constitutes 70% of NMSC develops from basal epithelial cells of hair follicles or pluripotent epidermal basal cells and has a metastatic rate of only 0.0028-0.05% (1). Depending on the different features of tumor cells, there are many histological types of BCC, with different, but still low metastatic potential (2). SCC develops from the proliferating squamous layer of the epidermis, shows a metastatic rate of 0,1-9,9% and contributes to approximately 75% of deaths due to NMSC (3, 4). Although both skin cancers generally have a good prognosis, due to their high prevalence, they generate significant medical and financial problems worldwide. The most important risk factor of NMSC is exposure to the ultraviolet radiation, and both ultraviolet (UV) B and UVA play crucial roles in skin carcinogenesis affecting every stage, including direct cellular damage, production of reactive oxygen species, DNA alterations, and impairment of cell-mediated immune response (5).A wide variety of risk factors of NMSC is known, such as Fitzpatrick I and II skin phototypes, age over 50 years, family history of skin cancers, chronic immunosuppression, long-lasting ulceration, and scars. In addition, exposure to carcinogenic substances, like arsenic and tobacco, HPV viruses, actinic keratosis, and chronic dermatoses, including lichen sclerosus, lupus erythematosus, and lichen planus, are associated with a higher risk of SCC (6).Carcinogenesis is a very complex process; it is mediated by various proteins and pathways and characterized by genetic and molecular alterations. Changes in the expression or function of cell adhesion molecules (CAM) are involved in all steps of the progression of the malignancy, starting from the detachm...

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