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INVITED SPEAKERS ABSTRACTS

Immunity and melanoma

Frangia-Tsivou, K.

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doi: 10.1097/01.cmr.0000382775.21311.0c
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Melanoma's development is a multiple step procedure, influenced by factors related to the melanoma cell itself as well as to the local microenvironment and the extrinsic environment (UV radiation, chemical carcinogens). Progression of the neoplastic procedure is correlated to the ability of melanoma cells to downregulate or evade the immunological mechanisms against carcinogenesis. The immune system plays an essential monitoring role with respect to developing primary and metastatic tumors, through both antibody-mediated and T-cell-mediated pathways. Initially, neoplastic cells are destroyed, but later on mutated neoplastic cells survive and progression of the neoplastic procedure is noted. Cytokines that inhibit dendritic cell maturation and migration to lymph nodes, growth factors and adhesion molecules have been shown to have an impact on melanoma cell growth and angiogenesis. T-cells specifically recognize and destroy tumor cells, while dendritic cells, macrophages and B cells activate a secondary immune response.

Immunological clonal heterogeneity of melanoma cells in the primary lesion has been correlated to the extension of the tumour into the secondary sites. Regression phenomenon in both primary or metastatic melanomas is considered to be also immunologically mediated, with lymph node metastatic deposits being possibly responsible for the production of clonal T-cells capable of destruction of melanoma cells.

Immunophenotype and cytogenetic abnormalities of secondary melanoma deposits differ from those of the primary tumor. Therefore, modern therapeutic schemes in order to be effective should be individualized not only per patient, but also per stage of progression of the disease. Future progress in melanoma treatment should include biologic agents that target specific melanoma or T cell antibodies.

© 2010 Lippincott Williams & Wilkins, Inc.