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There is overwhelming evidence that the human immune system can keep in check the growth of autologous tumors. Yet, this phenomenon is rare and most often tumors survive striking a balance with the host's immune system. The well-documented coexistence of immune cells that can recognize cancer and their targets within the same host is reminiscent of chronic allograft rejection well-controlled by immune suppression or of a lingering tissue-specific autoimmune reaction. In this review, we argue that autologous tumor rejection represents a distinct form of tissue-specific rejection similar to acute allograft rejection or to flares of autoimmunity. Here we discuss similarities within the biology of these phenomena that may converge into a common immunological constant of rejection. The purpose is to simplify the basis of immune rejection to its bare bones critically dissecting the significance of those components proposed by experimental models as harbingers of this final outcome. [ABSTRACT FROM AUTHOR]

Cancer immunotherapy is now established as a powerful way to treat cancer. The recent clinical success of immune checkpoint blockade (antagonists of CTLA-4, PD-1 and PD-L1) highlights both the universal power of treating the immune system across tumour types and the unique features of cancer immunotherapy. Immune-related adverse events, atypical clinical response patterns, durable responses, and clear overall survival benefit distinguish cancer immunotherapy from cytotoxic cancer therapy. Combination immunotherapies that transform non-responders to responders are under rapid development. Current challenges facing the field include incorporating immunotherapy into adjuvant and neoadjuvant cancer therapy, refining dose, schedule and duration of treatment and developing novel surrogate endpoints that accurately capture overall survival benefit early in treatment. As the field rapidly evolves, we must prioritise the development of biomarkers to guide the use of immunotherapies in the most appropriate patients. Immunotherapy is already transforming cancer from a death sentence to a chronic disease for some patients. By making smart, evidence-based decisions in developing next generation immunotherapies, cancer should become an imminently treatable, curable and even preventable disease. [ABSTRACT FROM AUTHOR]

Background: Recent observations suggest that immune-mediated tissue destruction is dependent upon coordinate activation of immune genes expressed by cells of the innate and adaptive immune systems. Methods: Here, we performed a retrospective pilot study to investigate whether the coordinate expression of molecular signature mostly associated with NK cells could be used to segregate breast cancer patients into relapse and relapse-free outcomes. Results: By analyzing primary breast cancer specimens derived from patients who experienced either 58- 116 months (∼5-9 years) relapse-free survival or developed tumor relapse within 9-76 months (∼1-6 years) we found that the expression of molecules involved in activating signaling of NK cells and in NK cells: target interaction is increased in patients with favorable prognosis. Conclusions: The parameters identified in this study, together with the prognostic signature previously reported by our group, highlight the cooperation between the innate and adaptive immune components within the tumor microenvironment. [ABSTRACT FROM AUTHOR]