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      Current Approaches for Combination Therapy of Cancer: The Role of Immunogenic Cell Death

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          Abstract

          Cell death resistance is a key feature of tumor cells. One of the main anticancer therapies is increasing the susceptibility of cells to death. Cancer cells have developed a capability of tumor immune escape. Hence, restoring the immunogenicity of cancer cells can be suggested as an effective approach against cancer. Accumulating evidence proposes that several anticancer agents provoke the release of danger-associated molecular patterns (DAMPs) that are determinants of immunogenicity and stimulate immunogenic cell death (ICD). It has been suggested that ICD inducers are two different types according to their various activities. Here, we review the well-characterized DAMPs and focus on the different types of ICD inducers and recent combination therapies that can augment the immunogenicity of cancer cells.

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          Mechanisms of resistance to immune checkpoint inhibitors

          Russell Jenkins, David Barbie, Keith Flaherty (2018)
          Immune checkpoint inhibitors (ICI) targeting CTLA-4 and the PD-1/PD-L1 axis have shown unprecedented clinical activity in several types of cancer and are rapidly transforming the practice of medical oncology. Whereas cytotoxic chemotherapy and small molecule inhibitors (‘targeted therapies’) largely act on cancer cells directly, immune checkpoint inhibitors reinvigorate anti-tumour immune responses by disrupting co-inhibitory T-cell signalling. While resistance routinely develops in patients treated with conventional cancer therapies and targeted therapies, durable responses suggestive of long-lasting immunologic memory are commonly seen in large subsets of patients treated with ICI. However, initial response appears to be a binary event, with most non-responders to single-agent ICI therapy progressing at a rate consistent with the natural history of disease. In addition, late relapses are now emerging with longer follow-up of clinical trial populations, suggesting the emergence of acquired resistance. As robust biomarkers to predict clinical response and/or resistance remain elusive, the mechanisms underlying innate (primary) and acquired (secondary) resistance are largely inferred from pre-clinical studies and correlative clinical data. Improved understanding of molecular and immunologic mechanisms of ICI response (and resistance) may not only identify novel predictive and/or prognostic biomarkers, but also ultimately guide optimal combination/sequencing of ICI therapy in the clinic. Here we review the emerging clinical and pre-clinical data identifying novel mechanisms of innate and acquired resistance to immune checkpoint inhibition.
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            Cell-surface calreticulin initiates clearance of viable or apoptotic cells through trans-activation of LRP on the phagocyte.

            Shyra Gardai, Kathleen McPhillips, S. Frasch … (2005)
            Apoptotic-cell removal is critical for development, tissue homeostasis, and resolution of inflammation. Although many candidate systems exist, only phosphatidylserine has been identified as a general recognition ligand on apoptotic cells. We demonstrate here that calreticulin acts as a second general recognition ligand by binding and activating LDL-receptor-related protein (LRP) on the engulfing cell. Since surface calreticulin is also found on viable cells, a mechanism preventing inadvertent uptake was sought. Disruption of interactions between CD47 (integrin-associated protein) on the target cell and SIRPalpha (SHPS-1), a heavily glycosylated transmembrane protein on the engulfing cell, permitted uptake of viable cells in a calreticulin/LRP-dependent manner. On apoptotic cells, CD47 was altered and/or lost and no longer activated SIRPalpha. These changes on the apoptotic cell create an environment where "don't eat me" signals are rendered inactive and "eat me" signals, including calreticulin and phosphatidylserine, congregate together and signal for removal.
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              Immunogenic Chemotherapy Sensitizes Tumors to Checkpoint Blockade Therapy.

              Christina Pfirschke, Camilla Engblom, Steffen Rickelt … (2016)
              Checkpoint blockade immunotherapies can be extraordinarily effective, but might benefit only the minority of patients whose tumors are pre-infiltrated by T cells. Here, using lung adenocarcinoma mouse models, including genetic models, we show that autochthonous tumors that lacked T cell infiltration and resisted current treatment options could be successfully sensitized to host antitumor T cell immunity when appropriately selected immunogenic drugs (e.g., oxaliplatin combined with cyclophosphamide for treatment against tumors expressing oncogenic Kras and lacking Trp53) were used. The antitumor response was triggered by direct drug actions on tumor cells, relied on innate immune sensing through toll-like receptor 4 signaling, and ultimately depended on CD8(+) T cell antitumor immunity. Furthermore, instigating tumor infiltration by T cells sensitized tumors to checkpoint inhibition and controlled cancer durably. These findings indicate that the proportion of cancers responding to checkpoint therapy can be feasibly and substantially expanded by combining checkpoint blockade with immunogenic drugs.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Cancers (Basel)
                Journal ID (iso-abbrev): Cancers (Basel)
                Journal ID (publisher-id): cancers
                Title: Cancers
                Publisher: MDPI
                ISSN (Electronic): 2072-6694
                Publication date (Electronic): 23 April 2020
                Publication date Collection: April 2020
                Volume: 12
                Issue: 4
                Electronic Location Identifier: 1047
                Affiliations
                [1 ]Immunology Research Center, Tabriz University of Medical Sciences, Tabriz 5165665811, Iran; zahraasadzadeh2834@ 123456gmail.com (Z.A.); shar.safaee@ 123456gmail.com (S.S.); hajiasgharzadeh@ 123456yahoo.com (K.H.); afshin.derakhshani94@ 123456gmail.com (A.D.)
                [2 ]Department of Immunology and Microbiology, Faculty of Medicine, Ardabil University of Medical Sciences, Ardabil 5618985991, Iran; safarzadehelham@ 123456yahoo.com
                [3 ]Research & Development Lab, BSD Robotics, 4500 Brisbane, Australia; ali_baradaran79@ 123456hotmail.com
                [4 ]Department of Cancer and Inflammation Research, Institute for Molecular Medicine, University of Southern Denmark, 5230 Odense, Denmark; ali_mohammadi6868@ 123456yahoo.com
                [5 ]IRCCS Istituto Tumori “Giovanni Paolo II” of Bari, 70124 Bari, Italy; argentieroantonella@ 123456gmail.com
                [6 ]Department of Biomedical Sciences and Human Oncology, University of Bari “Aldo Moro”, 70124 Bari, Italy
                [7 ]Department of Immunology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz 5166614766, Iran
                Author notes
                [* ]Correspondence: n.silvestris@ 123456oncologico.bari.it (N.S.); baradaranb@ 123456tbzmed.ac.ir (B.B.); Tel.: +98-413-337-1440 (B.B.)
                [†]

                The first two authors contributed equally to this work.

                Author information
                https://orcid.org/0000-0003-4593-4803
                https://orcid.org/0000-0002-3243-233X
                https://orcid.org/0000-0001-7814-7318
                https://orcid.org/0000-0002-8642-6795
                Article
                Publisher ID: cancers-12-01047
                DOI: 10.3390/cancers12041047
                PMC ID: 7226590
                PubMed ID: 32340275
                SO-VID: 7c5c22c4-4eef-49da-8d1a-cfdf56bb5eda
                Copyright © © 2020 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 12 March 2020
                Date accepted : 17 April 2020
                Categories
                Subject: Review

                Keywords: immunogenic cell death,damps,combination therapy
                Data availability:
                Keywords: immunogenic cell death, damps, combination therapy

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