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Chapter category: Oncology

Gene Profiling for the Prediction of Tumor Response to Treatment: The Case of Immunotherapy

Chapter authors:
Vladia Monsurrò and Francesco M. Marincola

Although anticancer immune responses can occur, the biological mechanisms responsible for them remain largely unexplained. Immunologists have extensively studied specific interactions between immune and cancer cells and have identified cofactors that may modulate the effectiveness of such interactions. In particular, as a result of the increasing molecular understanding of the basis for tumor/host interactions, their complexity has become manifest, leading to the conclusion that no single mechanism can model in humans the phenomenon of tumor rejection. It is likely that, due to human and disease heterogeneity, distinct trails lead to a final common pathway responsible for immune-mediated tumor regression. The synergy of the innate and adaptive immune response is likely to be required for successful tumor rejection. These two systems may act by enhancing and remodeling each of the functions by being recruited and activated at the tumor site by molecules with immune modulatory properties produced in the tumor micro-environment by cancer or tumor-associated normal cells. Such complexity could only be recently appreciated in its extent by high-throughput tools capable of providing a global view of biological processes as they occur. In this chapter, we will present selected examples of high-throughput gene expression profiling that may contribute to the understanding of anticancer immune responses. By following the simplified model of tumor-specific immunization, it has become apparent that factors other than direct T-cell/tumor cell interactions need to be considered when studying the mechanisms leading to immune rejection of cancer. The genetic background of individual patients may affect the immune response. It is becoming increasingly recognized that polymorphism in humans is not limited to genes associated with antigen presentation.1 In addition, the biological make up of individual tumors may affect T-cell function through pathways independent of HLA/epitope T-cell receptor engagement.2,3 To obtain a global view of this complexity encompassing human and tumor heterogeneity, a broader approach to the study of tumor immunology is needed. Tools that allow a comprehensive view of tumor/host interactions will be necessary to identify the biological requirements for tumor rejection.4

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