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Acral melanoma is one of the most aggressive and fast-growing forms of cutaneous melanoma and is characterized by a predominant location on the palms and feet. Primary tumors, metastases, and normal tissue samples from five acral melanoma patients were examined by massive parallel sequencing, focusing on the coding regions of 4100 genes involved in the origin and progression of hereditary and oncology diseases. Somatic mutations were found in genes related to cell division, proliferation, and apoptosis (BRAF, NRAS, VAV1, GATA1, and GCM2); cell adhesion (CTNND2 and ITGB4); angiogenesis (VEGFA); and the regulation of energy metabolism (BCS1L). Comparisons of target DNA sequences between morphologically normal and primary tumor tissues and between normal and metastatic tissues identified the candidate genes responsible for rapid metastasis in acral melanoma.

The oncolytic potential of the attenuated mumps virus (MV) vaccine strain Leningrad-3 (L-3) was evaluated in a panel of four human metastatic melanoma cell lines. The lines were shown to be susceptible and permissive to MV infection. Efficient MV replication led to death of melanoma cells, but the effect differed among the cell lines. Possible mechanisms mediating the selectivity of MV L-3 towards the cell lines were explored. Replicative and oncolytic activity of MV was found to depend on the expression pattern of type I interferon genes. None of the melanoma cell lines showed induction of expression of the total spectrum of genes required to inhibit virus replication. Based on the results, MV L-3 was assumed to be a promising oncolytic agent for human melanoma cells.

Autophagy is an evolutionarily established process of maintaining the cell integrity by lysosomal recycling of their own cytosolic proteins, macromolecules, organelles, and protein aggregates. Autophagy is regulated by a group of autophagy-related genes (ATG) and is detected at the basal level in almost all cells of the body. Alterations in the autophagy-associated signaling pathways often occur in various pathologies, including malignant neoplasms. Numerous experimental and clinical trials demonstrated the important role of autophagy in mechanisms of chemoresistance or chemosensitivity to a wide range of antitumor agents. This review describes the molecular mechanisms of autophagy and its interaction with apoptosis. The possibilities of modulating the autophagy level in tumor cells to increase the efficacy of anticancer therapy are estimated.