An attractive, yet hitherto unproven concept predicts that the promotion of tumor regression should elicit the host's immune response against residual tumor cells to achieve an optimal therapeutic effect. In a way, chemo- or radiotherapy must trigger "danger signals" emitted from immunogenic cell death and hence elicit "danger associated molecular patterns" to stimulate powerful anticancer immune responses. Here, based on the recent experimental and clinical evidence, we will discuss the molecular identity of the multiple checkpoints that dictate the success of "immunogenic chemotherapy" at the levels of the drug, of the tumor cell and of the host immune system.
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