Zitvogel L, Tesniere A, Kroemer GCancer despite immunosurveillance: immunoselection and immunosubversion. Nat Rev Immunol 6(10): 715-727

U805 Institut National de la Santé et de la Recherche Médicale, Faculté de Médecine Paris-Sud-Université Paris XI, Institut Gustave-Roussy, 39 rue Camille-Desmoulins, F-94805 Villejuif, France.
Nature reviews. Immunology (Impact Factor: 34.99). 11/2006; 6(10):715-27. DOI: 10.1038/nri1936
Source: PubMed


Numerous innate and adaptive immune effector cells and molecules participate in the recognition and destruction of cancer cells, a process that is known as cancer immunosurveillance. But cancer cells avoid such immunosurveillance through the outgrowth of poorly immunogenic tumour-cell variants (immunoselection) and through subversion of the immune system (immunosubversion). At the early stages of carcinogenesis, cell-intrinsic barriers to tumour development seem to be associated with stimulation of an active antitumour immune response, whereas overt tumour development seems to correlate with changes in the immunogenic properties of tumour cells. The permanent success of treatments for cancer might depend on using immunogenic chemotherapy to re-establish antitumour immune responses.

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Available from: Antoine Tesniere, Nov 17, 2015
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    • "A link between cancer development and immunosuppression in transplanted patients is well recognized. Over the past decades, a growing body of evidence has emerged demonstrating the dual role of the immune system in cancer, being involved both in tumor development (via chronic inflammation through the innate immune system) and in tumor elimination and control (through the adaptive immune system) [3]. As an example , renal cell carcinoma has been traditionally considered immunogenic, as it does occur at a higher incidence in immunosuppressed patients [4]. "
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    ABSTRACT: Immunodeficiency is associated with higher cancer incidence. However, it is unknown whether there is a link between immunodeficiency and development of multiple primary malignancies. In the present study we analyse this link focusing on kidney-transplanted patients, as they are at higher risk of developing cancer due to the chronic assumption of immunosuppressants. We followed up 1200 patients who underwent kidney transplantation between 1980 and 2012. A total of 77/1200 kidney-transplanted patients developed cancer and 24 of them developed multiple cancers. Most multiple cancers were synchronous with a nonsignificant association between cancer and rejection episodes. In the general cancer population, one-ninth of patients are at higher risk of developing a second tumor over a lifetime; hence it would be reasonable to conclude that, from a merely theoretical and statistical viewpoint, long-term transplanted patients potentially have a higher risk of developing MPMs. However, data did not confirm this assumption, probably because these patients die before a second primary malignancy appears. Despite many observations on the increased incidence of different tumor types in immunodeficient patients and despite immunosuppression certainly being a predisposing factor for the multicancer syndrome, data so far are not robust enough to justify a correlation between immunodeficiency and multiple primary malignancies in transplanted patients.
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    • "It has been predicted that the number of deaths from cancer will continue to grow, with an estimation of 11.5 million deaths in 2030 [1]. Tumor cells share many characteristics, such as enabling replicative immortality, evading cell death, escaping the host immune system, and others [2] [3] [4] [5]. The goal of tumor treatment is to extend the survival of patients by eliminating the tumor and preventing multiple metastases [6] [7]. "
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    • "Moreover, patients who are immunosuppressed also have an impeded response to cancer therapy with a decreased overall and progression-free survival [55,56]. Thus, immune surveillance mechanisms are critical both to the prevention as well the efficacy of conventional treatment of these cancers [57-59] and are a critical component to the therapeutic efficacy of agents for cancer [54,60-62]. "
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    ABSTRACT: The targeted inactivation of a single oncogene can induce dramatic tumor regression, suggesting that cancers are "oncogene addicted." Tumor regression following oncogene inactivation has been thought to be a consequence of restoration of normal physiological programs that induce proliferative arrest, apoptosis, differentiation, and cellular senescence. However, recent observations illustrate that oncogene addiction is highly dependent upon the host immune cells. In particular, CD4(+) helper T cells were shown to be essential to the mechanism by which MYC or BCR-ABL inactivation elicits "oncogene withdrawal." Hence, immune mediators contribute in multiple ways to the pathogenesis, prevention, and treatment of cancer, including mechanisms of tumor initiation, progression, and surveillance, but also oncogene inactivation-mediated tumor regression. Data from both the bench and the bedside illustrates that the inactivation of a driver oncogene can induce activation of the immune system that appears to be essential for sustained tumor regression.
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