The Impact Of Genetic Variation And Cancer Heterogeneity On Immune Responsiveness

It is obvious that prediction of immune responsiveness is very beneficial because it can spare the pain and unnecessary therapy to a patient with an expectedly short life span. In addition, it may add the conceptual value of approaching the understanding of the biological process responsible for immune response which in turn may lead to more focused therapies.

As we previously discussed, genetic background may influence immune responsiveness. However, the genetic background of patients has not been extensively scrutinized as a predictor of immune responsiveness (16). Obvious genetic markers that may affect immune responsiveness are the HLA complex that codes for molecules responsible for antigen presentation to T cells (51). However, correlates between HLA phenotype and treatment outcome or survival failed to provide conclusive evidence that individual variability in antigen presentation may determine immune responsiveness in the context of anti-cancer immune therapy (18;52;53). Others have pointed to other polymorphisms as harbingers of immune responsiveness. For instance polymorphisms of the IL-10 gene appears to be responsible for differential levels of expression of this cytokine in various conditions. Interestingly, individuals with a phenotype associated with low IL-2 production appear to bear an increased incidence of melanoma and prostate cancer suggesting a surprisingly protective role of this cytokine against cancer growth (23;54). More generally, this finding suggests that a genetic predisposition may modulate cancer growth through the action of immune regulatory molecules. However, there is no information about the relevance of various genetic factors associated with immune function and response to therapy. Indeed, awareness to this aspect of immune polymorphism only recently has been appreciated as a significant factor that may significantly modulate immune pathology (16;54) and only recently techniques suitable for the screening at a genome wide level of polymorphism(s) in clinical settings have been described (16;55).

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