Genetic Polymorphisms And Cancer Heterogeneity

Genetic polymorphism is the genesis of the diversity of human beings. Polymorphisms are particularly frequent in genes associated with immune function possibly resulting from an evolutionary adaptation of the organism facing an ever changing environment (16). Although, several genes associated with immune function may bear relevance to tumor/host interaction(s) (17), most studies attempting to link human polymorphism to immune responsiveness have been focused on the associations between the Human Leukocyte Antigen (HLA) complex and disease occurrence or response to therapy. However, an extensive analysis of patients with metastatic melanoma treated with systemic interleukin-2 administration failed to convincingly identify a correlation between HLA phenotype, immune responsiveness and toxicity (18). Extended studies based on polymorphism of lymphokines, chemokines and their receptors have demonstrated an association in individual susceptibility to immune pathology, survival of transplanted organs or predisposition to cancer (19;20) (21-23) (16). The vast majority of polymorphism found in cytokine genes and their receptors are located in the promoter, intronic and 3' untranslated regions. The sequence variances occurring in untranslated regions of the gene can, however, still affect gene expression and function. In addition, promoter polymorphism may disrupt or abolish binding of regulatory elements such as NF-AB, Jak, STAT and other molecules involved in signal transduction pathways. Furthermore, some of this molecules central to cytokine expression levels are polymorphic themselves. Finally, intronic variation may affect enhancer/silencer sequences and certain polymorphisms may alter the structure of transcription factor binding elements (24). Thus, in the future more focus should be put in the understanding of genetic traits that may affect the ability of individuals to mount effective immune responses against their cancers.

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