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Conventional cancer treatments mediate their effects via the direct elimination of tumor cells. Nonetheless, recent evidence indicates that radiotherapy and some chemotherapeutic agents can also induce specific immune responses that contribute to therapeutic outcomes. Two major tumor-intrinsic changes that determine the immune response against tumors have been identified: the translocation of calreticulin to the plasma membrane and the release of high-mobility group box 1 protein. Together, these changes improve engulfment and processing of apoptotic bodies by dendritic cells, which are involved in the cross-priming of antitumor T lymphocytes in vivo. We review these two molecular mechanisms that dictate the radio/chemotherapy-elicited antitumor immune response and discuss how this knowledge can be clinically exploited to predict and also ameliorate the success of chemo/radiotherapy. [ABSTRACT FROM AUTHOR]

The concept of immunogenic chemotherapy that has recently emerged relies upon the capacity of a cytotoxic compound to trigger a cell-death modality. This modality elicits cross-priming by dendritic cells of tumor antigen-specific T cells that will contribute to the tumoricidal activity of the compound and protect the host against relapse. In contrast, most anticancer drugs elicit nonimmunogenic apoptosis that is not accompanied with an immunizing property. This review will discuss some molecular and metabolic changes required at the level of the tumor that must engage key pathways at the level of the host for the induction of Tc1 polarized-protective T cell responses during chemotherapy. We will summarize the immune adjuvants that can boost the immunogenicity of cell death to augment the efficacy of chemotherapy. [ABSTRACT FROM AUTHOR]