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      SOCS1 expression in cancer cells: potential roles in promoting antitumor immunity


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          Suppressor of cytokine signaling 1 (SOCS1) is a potent regulator immune cell responses and a proven tumor suppressor. Inhibition of SOCS1 in T cells can boost antitumor immunity, whereas its loss in tumor cells increases tumor aggressivity. Investigations into the tumor suppression mechanisms so far focused on tumor cell-intrinsic functions of SOCS1. However, it is possible that SOCS1 expression in tumor cells also regulate antitumor immune responses in a cell-extrinsic manner via direct and indirect mechanisms. Here, we discuss the evidence supporting the latter, and its implications for antitumor immunity.

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          Oncology meets immunology: the cancer-immunity cycle.

          The genetic and cellular alterations that define cancer provide the immune system with the means to generate T cell responses that recognize and eradicate cancer cells. However, elimination of cancer by T cells is only one step in the Cancer-Immunity Cycle, which manages the delicate balance between the recognition of nonself and the prevention of autoimmunity. Identification of cancer cell T cell inhibitory signals, including PD-L1, has prompted the development of a new class of cancer immunotherapy that specifically hinders immune effector inhibition, reinvigorating and potentially expanding preexisting anticancer immune responses. The presence of suppressive factors in the tumor microenvironment may explain the limited activity observed with previous immune-based therapies and why these therapies may be more effective in combination with agents that target other steps of the cycle. Emerging clinical data suggest that cancer immunotherapy is likely to become a key part of the clinical management of cancer. Copyright © 2013 Elsevier Inc. All rights reserved.
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            Neoantigens in cancer immunotherapy.

            The clinical relevance of T cells in the control of a diverse set of human cancers is now beyond doubt. However, the nature of the antigens that allow the immune system to distinguish cancer cells from noncancer cells has long remained obscure. Recent technological innovations have made it possible to dissect the immune response to patient-specific neoantigens that arise as a consequence of tumor-specific mutations, and emerging data suggest that recognition of such neoantigens is a major factor in the activity of clinical immunotherapies. These observations indicate that neoantigen load may form a biomarker in cancer immunotherapy and provide an incentive for the development of novel therapeutic approaches that selectively enhance T cell reactivity against this class of antigens. Copyright © 2015, American Association for the Advancement of Science.
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              Senescence and tumour clearance is triggered by p53 restoration in murine liver carcinomas.

              Although cancer arises from a combination of mutations in oncogenes and tumour suppressor genes, the extent to which tumour suppressor gene loss is required for maintaining established tumours is poorly understood. p53 is an important tumour suppressor that acts to restrict proliferation in response to DNA damage or deregulation of mitogenic oncogenes, by leading to the induction of various cell cycle checkpoints, apoptosis or cellular senescence. Consequently, p53 mutations increase cell proliferation and survival, and in some settings promote genomic instability and resistance to certain chemotherapies. To determine the consequences of reactivating the p53 pathway in tumours, we used RNA interference (RNAi) to conditionally regulate endogenous p53 expression in a mosaic mouse model of liver carcinoma. We show that even brief reactivation of endogenous p53 in p53-deficient tumours can produce complete tumour regressions. The primary response to p53 was not apoptosis, but instead involved the induction of a cellular senescence program that was associated with differentiation and the upregulation of inflammatory cytokines. This program, although producing only cell cycle arrest in vitro, also triggered an innate immune response that targeted the tumour cells in vivo, thereby contributing to tumour clearance. Our study indicates that p53 loss can be required for the maintenance of aggressive carcinomas, and illustrates how the cellular senescence program can act together with the innate immune system to potently limit tumour growth.

                Author and article information

                URI : https://loop.frontiersin.org/people/418414Role: Role: Role: Role: Role: Role: Role: Role:
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                Front Immunol
                Front Immunol
                Front. Immunol.
                Frontiers in Immunology
                Frontiers Media S.A.
                13 February 2024
                : 15
                : 1362224
                [1] Department of Immunology and Cell Biology, Faculty of Medicine and Health Sciences, Université de Sherbrooke , Sherbrooke, QC, Canada
                Author notes

                Edited by: Howard M. Johnson, University of Florida, United States

                Reviewed by: Zuzanna Urban-Wójciuk, University of Gdansk, Poland

                Chulbul M. Ahmed, University of Florida, United States

                *Correspondence: Subburaj Ilangumaran, Subburaj.Ilangumaran@ 123456Usherbrooke.ca
                Copyright © 2024 Ilangumaran, Gui, Shukla and Ramanathan

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                : 27 December 2023
                : 31 January 2024
                Page count
                Figures: 2, Tables: 0, Equations: 0, References: 150, Pages: 10, Words: 4018
                Funded by: Canadian Institutes of Health Research , doi 10.13039/501100000024;
                The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This study was supported by a Project grant from the Canadian Institutes of Health Research (CIHR) to SI (PJT-153174).
                Custom metadata
                Cancer Immunity and Immunotherapy

                socs1,tumor suppressor,growth control,antigen presentation,tumor immunogenicity,checkpoint inhibition


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