The skin is the largest organ of the body and has many different functions. The epidermis as the most superficial layer of the skin forms the first barrier of protection from invasion of foreign substances into the body. The skin is an essential part of the immune system. Immune cells of the epidermis and dermis participate in the defence against pathogens, in particular through T lymphocytes in transit, tissue macrophages and a network of cutaneous dendritic cells (DCs), which are key for perception of danger and initiating both innate and adaptive protective responses (I). DCs are antigen-presenting cells derived from the hematopoietic stem cell (2). LCs are the DCs of the epidermis (3). Skin resident LCs are well characterized and regarded as typical immature DCs. The identification of antigen, and the subsequent activation and migration of LCs towards the draining lymph nodes are well-studied processes (4). It is quite remarkable that, as early as 1868. Paul Langerhans discovered the stellate-shaped epidermal cells that now bear his name (5). However, 100 years were subsequently needed to establish the fact that LCs are potent antigen-presenting cells appertaining to the leukocyte system (6). In parallel, the pioneering work of Steinman and Cohn leading to the identification of splenic DCs (7) formed the basis for connecting LCs to the emerging DCs system. One common feature of DCs is their amazing faculty to present protein-derived peptide antigens to naive T lymphocytes (8). LC constituents of the skin immune system, are a network of dendritic major histocompatibility complex (MHC) class II antigen-presenting cells involved in initiation of cutaneous immune responses (9). LCs are important for presentation tumour-associated antigens. Probably they are integral in host resistance against malignant neoplasms that emerge in the epidermis. Local or distant progression of a malignant tumour is critically important for further destiny of patients. It is influenced by many factors dependent on the biological behaviour of tumour cells. The question of failure of the immune defence, where antigen presentation is a key component, must also be assessed. Whether LCs in tumour act the same way as LCs in normal tissues or whether the tumours injure LCs phenotype and function remains unknown (10). LCs have been studied in a variety of cancers ( 11-16). However, despite the significant amount of investigation in the past few years, a function of LCs in skin tumours is only partially known.Squamous cell carcinoma (SCC) is relatively common skin tumour which if untreated, generally has a progressive clinical course with development of metastatic disease and often lethal outcome (17). With invasive SCC, masses of malignant kératinocytes extend through the basement membrane demonstrating different levels of atypia ranging from well differentiated to anaplastic. Having crossed over into the dermis they can metastasize.Actinic keratosis (AK). also known as solar or senile keratosis is by far the most common precancerous dermatos...

Human mitochondrial ribosomal protein MRPS18-2 (S18-2) is encoded by a cellular gene that is located on the human chromosome 6p21.3. We discovered that overexpression of the S18-2 protein led to immortalization and de-differentiation of primary rat embryonic fibroblasts. Cells showed anchorage-independent growth pattern. Moreover, pathways characteristic for rapidly proliferating cells were upregulated then. It is possible that the S18-2 overexpression induced disturbance in cell cycle regulation. We found that overexpression of S18-2 protein in human cancer cell lines led to an appearance of multinucleated cells in the selected clones.

Malignant diseases, such as proliferative skin lesions are characterized by inappropriate cell increase. Activation of proto-oncogenes and inactivation of tumour suppressor genes are the harmful genetic events that are responsible for malignant transformation (1). Carcinogenesis in the skin is a complicated process characterized by the appearance of cells which have escaped from the normal growth control mechanisms, following in an increase of proliferative activity in the cells (2). The prevalent risk factors for skin cancer are exposure to ultraviolet (UV) radiation and fair skin that is receptive to sunburn. Increasing frequency of exposure, immune status, age, male gender and DNA repair disorders such as xeroderma pigmentosum also assist to increased risk (3). The association between UV exposure and cancer is powerful for SCC but less well-defined for BCC, as nearly one third of all BCC originates in anatomical sites receiving minimal UV exposure. Skin temperature may also be a risk factor. Cultured immortalized human kératinocytes have been shown to spontaneously transform to a tumorigenic phenotype when incubated at elevated temperature (4). Some investigations indicate that human papilloma virus infection may be a risk factor for skin cancer, though the relationship is not clear (5). Solid-organ transplant recipients are at extremely high risk for SCC (6). The long-term immunosuppressive therapy is probably the cause of the increased frequency of SCC in these patients, particularly in persons with chronic actinic damage (7).The mechanism of UV-induced photo carcinogenesis appears to implicate the inactivation of the p53 tumour suppressor gene (8). Several studies have reported that p53 distortions play a critical role in the development and progression of various human malignancies. The p53 gene is involved in the regulation of cell cycle control and apoptosis'. Mutations in this gene could presumably cancel p53 function, allowing accumulation of mutant cells due to loss of the UV-induced apoptosis of DNA-damaged cells (9). This leads to clonal expansion of p53-mutated kératinocytes, which could eventually acquire the second mutation that leads to the progression to multiple mutations. They can be accumulated. Therefore, this clonal expansion is regarded as a key initiating step in epidermal carcinogenesis (10). Precancerous dermatoses occur prior to development of epidermal malignancies (6). Because skin lesions are visible and easily accessible, skin cancer provides us with an excellent model for studying the development and growth of cancer in humans. Furthermore, the carcinogenic agents to the skin are well known. This is of special interest so far as UV radiation is the most important carcinogen and puts a specific signature on the DNA (10).Actinic keratosis (AK), also known as senile or solar keratosis is the most common precancerous dermatosis and is attributable to UV radiation (11). This UV-induced lesion is usually seen as multiple lesions in sun-exposed skin in elderly persons. This sunrelated d...