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  1. Article ; Online: Cancer cell-intrinsic mechanisms driving acquired immune tolerance.

    Ghorani, Ehsan / Swanton, Charles / Quezada, Sergio A

    Immunity

    2023  Volume 56, Issue 10, Page(s) 2270–2295

    Abstract: Immune evasion is a hallmark of cancer, enabling tumors to survive contact with the host immune system and evade the cycle of immune recognition and destruction. Here, we review the current understanding of the cancer cell-intrinsic factors driving ... ...

    Abstract Immune evasion is a hallmark of cancer, enabling tumors to survive contact with the host immune system and evade the cycle of immune recognition and destruction. Here, we review the current understanding of the cancer cell-intrinsic factors driving immune evasion. We focus on T cells as key effectors of anti-cancer immunity and argue that cancer cells evade immune destruction by gaining control over pathways that usually serve to maintain physiological tolerance to self. Using this framework, we place recent mechanistic advances in the understanding of cancer immune evasion into broad categories of control over T cell localization, antigen recognition, and acquisition of optimal effector function. We discuss the redundancy in the pathways involved and identify knowledge gaps that must be overcome to better target immune evasion, including the need for better, routinely available tools that incorporate the growing understanding of evasion mechanisms to stratify patients for therapy and trials.
    MeSH term(s) Humans ; Neoplasms ; Immune Tolerance ; T-Lymphocytes ; Immunotherapy ; Immune Evasion
    Language English
    Publishing date 2023-10-11
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 1217235-2
    ISSN 1097-4180 ; 1074-7613
    ISSN (online) 1097-4180
    ISSN 1074-7613
    DOI 10.1016/j.immuni.2023.09.004
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  2. Article ; Online: Deciphering immunoregulatory vulnerabilities in human cancers.

    Gálvez-Cancino, Felipe / Lladser, Alvaro / Quezada, Sergio A

    Nature immunology

    2022  Volume 23, Issue 7, Page(s) 995–996

    MeSH term(s) Humans ; Neoplasms
    Language English
    Publishing date 2022-06-16
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 2016987-5
    ISSN 1529-2916 ; 1529-2908
    ISSN (online) 1529-2916
    ISSN 1529-2908
    DOI 10.1038/s41590-022-01251-w
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  3. Article ; Online: T cell receptor therapeutics: immunological targeting of the intracellular cancer proteome.

    Klebanoff, Christopher A / Chandran, Smita S / Baker, Brian M / Quezada, Sergio A / Ribas, Antoni

    Nature reviews. Drug discovery

    2023  Volume 22, Issue 12, Page(s) 996–1017

    Abstract: The T cell receptor (TCR) complex is a naturally occurring antigen sensor that detects, amplifies and coordinates cellular immune responses to epitopes derived from cell surface and intracellular proteins. Thus, TCRs enable the targeting of proteins ... ...

    Abstract The T cell receptor (TCR) complex is a naturally occurring antigen sensor that detects, amplifies and coordinates cellular immune responses to epitopes derived from cell surface and intracellular proteins. Thus, TCRs enable the targeting of proteins selectively expressed by cancer cells, including neoantigens, cancer germline antigens and viral oncoproteins. As such, TCRs have provided the basis for an emerging class of oncology therapeutics. Herein, we review the current cancer treatment landscape using TCRs and TCR-like molecules. This includes adoptive cell transfer of T cells expressing endogenous or engineered TCRs, TCR bispecific engagers and antibodies specific for human leukocyte antigen (HLA)-bound peptides (TCR mimics). We discuss the unique complexities associated with the clinical development of these therapeutics, such as HLA restriction, TCR retrieval, potency assessment and the potential for cross-reactivity. In addition, we highlight emerging clinical data that establish the antitumour potential of TCR-based therapies, including tumour-infiltrating lymphocytes, for the treatment of diverse human malignancies. Finally, we explore the future of TCR therapeutics, including emerging genome editing methods to safely enhance potency and strategies to streamline patient identification.
    MeSH term(s) Humans ; Proteome/metabolism ; CD8-Positive T-Lymphocytes/metabolism ; Antigens, Neoplasm ; Receptors, Antigen, T-Cell ; Neoplasms/drug therapy
    Chemical Substances Proteome ; Antigens, Neoplasm ; Receptors, Antigen, T-Cell
    Language English
    Publishing date 2023-10-27
    Publishing country England
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2062954-0
    ISSN 1474-1784 ; 1474-1776
    ISSN (online) 1474-1784
    ISSN 1474-1776
    DOI 10.1038/s41573-023-00809-z
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  4. Article ; Online: Induction of islet autoimmunity to defective ribosomal product of the insulin gene as neoantigen after anti-cancer immunotherapy leading to autoimmune diabetes.

    van Tienhoven, Rene / Jansen, Diahann T S L / Park, Miso / Williams, John C / Larkin, James / Quezada, Sergio A / Roep, Bart O

    Frontiers in immunology

    2024  Volume 15, Page(s) 1384406

    Abstract: Introduction: The autoimmune response in type 1 diabetes (T1D), in which the beta cells expressing aberrant or modified proteins are killed, resembles an effective antitumor response. Defective ribosomal protein products in tumors are targets of the ... ...

    Abstract Introduction: The autoimmune response in type 1 diabetes (T1D), in which the beta cells expressing aberrant or modified proteins are killed, resembles an effective antitumor response. Defective ribosomal protein products in tumors are targets of the anti-tumor immune response that is unleashed by immune checkpoint inhibitor (ICI) treatment in cancer patients. We recently described a defective ribosomal product of the insulin gene (INS-DRiP) that is expressed in stressed beta cells and targeted by diabetogenic T cells. T1D patient-derived INS-DRiP specific T cells can kill beta cells and are present in the insulitic lesion. T cells reactive to INS-DRiP epitopes are part of the normal T cell repertoire and are believed to be kept in check by immune regulation without causing autoimmunity.
    Method: T cell autoreactivity was tested using a combinatorial HLA multimer technology measuring a range of epitopes of islet autoantigens and neoantigen INS-DRiP. INS-DRiP expression in human pancreas and insulinoma sections was tested by immunohistochemistry.
    Results: Here we report the induction of islet autoimmunity to INS-DRiP and diabetes after ICI treatment and successful tumor remission. Following ICI treatment, T cells of the cancer patient were primed against INS-DRiP among other diabetogenic antigens, while there was no sign of autoimmunity to this neoantigen before ICI treatment. Next, we demonstrated the expression of INS-DRiP as neoantigen in both pancreatic islets and insulinoma by staining with a monoclonal antibody to INS-DRiP.
    Discussion: These results bridge cancer and T1D as two sides of the same coin and point to neoantigen expression in normal islets and insulinoma that may serve as target of both islet autoimmunity and tumor-related autoimmunity.
    MeSH term(s) Humans ; Diabetes Mellitus, Type 1/genetics ; Diabetes Mellitus, Type 1/therapy ; Autoimmunity/genetics ; Insulinoma/genetics ; Insulinoma/therapy ; Insulinoma/complications ; Autoantigens ; Insulin ; Epitopes ; Immunotherapy/methods ; Pancreatic Neoplasms
    Chemical Substances Autoantigens ; Insulin ; Epitopes
    Language English
    Publishing date 2024-03-26
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2024.1384406
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  5. Article ; Online: Lost in Translation: Deciphering the Mechanism of Action of Anti-human CTLA-4.

    Quezada, Sergio A / Peggs, Karl S

    Clinical cancer research : an official journal of the American Association for Cancer Research

    2018  Volume 25, Issue 4, Page(s) 1130–1132

    Abstract: Despite a number of preclinical studies demonstrating that the activity of anti-CTLA-4 antibodies in murine models of cancer relies on effector T-cell activation and regulatory T cell depletion, the activity of the clinical antibodies remains ... ...

    Abstract Despite a number of preclinical studies demonstrating that the activity of anti-CTLA-4 antibodies in murine models of cancer relies on effector T-cell activation and regulatory T cell depletion, the activity of the clinical antibodies remains controversial. To decipher such mechanisms is critical to the development of novel and more potent immunotherapies.See related article by Sharma et al., p. 1233.
    MeSH term(s) Animals ; CTLA-4 Antigen ; Forkhead Transcription Factors ; Humans ; Immunotherapy ; Mice ; Neoplasms ; T-Lymphocytes, Regulatory
    Chemical Substances CTLA-4 Antigen ; FOXP3 protein, human ; Forkhead Transcription Factors ; Foxp3 protein, mouse
    Language English
    Publishing date 2018-10-05
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 1225457-5
    ISSN 1557-3265 ; 1078-0432
    ISSN (online) 1557-3265
    ISSN 1078-0432
    DOI 10.1158/1078-0432.CCR-18-2509
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    Zs.A 4223: Show issues Location:
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  6. Article ; Online: Chromatin regulation and immune escape.

    Ghorani, Ehsan / Quezada, Sergio A

    Science (New York, N.Y.)

    2018  Volume 359, Issue 6377, Page(s) 745–746

    MeSH term(s) Chromatin ; Humans ; Tumor Escape/immunology
    Chemical Substances Chromatin
    Language English
    Publishing date 2018-02-15
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 128410-1
    ISSN 1095-9203 ; 0036-8075
    ISSN (online) 1095-9203
    ISSN 0036-8075
    DOI 10.1126/science.aat0383
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  7. Article ; Online: Urokinase-type plasminogen activator (uPA) regulates invasion and matrix remodelling in colorectal cancer.

    Micalet, Auxtine / Tappouni, Luke J / Peszko, Katarzyna / Karagianni, Despoina / Lam, Ashley / Counsell, John R / Quezada, Sergio A / Moeendarbary, Emad / Cheema, Umber

    Matrix biology plus

    2023  Volume 19-20, Page(s) 100137

    Abstract: Background: Cancer cells remodel their local physical environment through processes of matrix reorganisation, deposition, stiffening and degradation. Urokinase-type plasminogen activator (uPA), which is encoded by the : Methods: To this aim, we used ... ...

    Abstract Background: Cancer cells remodel their local physical environment through processes of matrix reorganisation, deposition, stiffening and degradation. Urokinase-type plasminogen activator (uPA), which is encoded by the
    Methods: To this aim, we used an engineered 3D
    Results: We showed that uPA is highly expressed in invasive breast and colorectal cancers, and these invasive cancer cells locally degrade their TME.
    Conclusion: This work supports the role of uPA in matrix degradation. It demonstrates that the invasion of cancer cells was significantly reduced when enzymatic breakdown of the TME matrix was prevented. Collectively, this provides strong evidence of the effectiveness of targeting uPA as a mechano-based cancer therapy.
    Language English
    Publishing date 2023-11-15
    Publishing country Netherlands
    Document type Journal Article
    ISSN 2590-0285
    ISSN (online) 2590-0285
    DOI 10.1016/j.mbplus.2023.100137
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  8. Article ; Online: Fcγ receptors and immunomodulatory antibodies in cancer.

    Galvez-Cancino, Felipe / Simpson, Alexander P / Costoya, Cristobal / Matos, Ignacio / Qian, Danwen / Peggs, Karl S / Litchfield, Kevin / Quezada, Sergio A

    Nature reviews. Cancer

    2023  Volume 24, Issue 1, Page(s) 51–71

    Abstract: The discovery of both cytotoxic T lymphocyte-associated antigen 4 (CTLA4) and programmed cell death protein 1 (PD1) as negative regulators of antitumour immunity led to the development of numerous immunomodulatory antibodies as cancer treatments. ... ...

    Abstract The discovery of both cytotoxic T lymphocyte-associated antigen 4 (CTLA4) and programmed cell death protein 1 (PD1) as negative regulators of antitumour immunity led to the development of numerous immunomodulatory antibodies as cancer treatments. Preclinical studies have demonstrated that the efficacy of immunoglobulin G (IgG)-based therapies depends not only on their ability to block or engage their targets but also on the antibody's constant region (Fc) and its interactions with Fcγ receptors (FcγRs). Fc-FcγR interactions are essential for the activity of tumour-targeting antibodies, such as rituximab, trastuzumab and cetuximab, where the killing of tumour cells occurs at least in part due to these mechanisms. However, our understanding of these interactions in the context of immunomodulatory antibodies designed to boost antitumour immunity remains less explored. In this Review, we discuss our current understanding of the contribution of FcγRs to the in vivo activity of immunomodulatory antibodies and the challenges of translating results from preclinical models into the clinic. In addition, we review the impact of genetic variability of human FcγRs on the activity of therapeutic antibodies and how antibody engineering is being utilized to develop the next generation of cancer immunotherapies.
    MeSH term(s) Humans ; Receptors, IgG/genetics ; Receptors, IgG/metabolism ; Immunoglobulin G/metabolism ; Immunomodulation ; Immunotherapy ; Neoplasms/therapy
    Chemical Substances Receptors, IgG ; Immunoglobulin G
    Language English
    Publishing date 2023-12-07
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2062767-1
    ISSN 1474-1768 ; 1474-175X
    ISSN (online) 1474-1768
    ISSN 1474-175X
    DOI 10.1038/s41568-023-00637-8
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  9. Article ; Online: The tumour ecology of quiescence: Niches across scales of complexity.

    Castillo, Simon P / Galvez-Cancino, Felipe / Liu, Jiali / Pollard, Steven M / Quezada, Sergio A / Yuan, Yinyin

    Seminars in cancer biology

    2023  Volume 92, Page(s) 139–149

    Abstract: Quiescence is a state of cell cycle arrest, allowing cancer cells to evade anti-proliferative cancer therapies. Quiescent cancer stem cells are thought to be responsible for treatment resistance in glioblastoma, an aggressive brain cancer with poor ... ...

    Abstract Quiescence is a state of cell cycle arrest, allowing cancer cells to evade anti-proliferative cancer therapies. Quiescent cancer stem cells are thought to be responsible for treatment resistance in glioblastoma, an aggressive brain cancer with poor patient outcomes. However, the regulation of quiescence in glioblastoma cells involves a myriad of intrinsic and extrinsic mechanisms that are not fully understood. In this review, we synthesise the literature on quiescence regulatory mechanisms in the context of glioblastoma and propose an ecological perspective to stemness-like phenotypes anchored to the contemporary concepts of niche theory. From this perspective, the cell cycle regulation is multiscale and multidimensional, where the niche dimensions extend to extrinsic variables in the tumour microenvironment that shape cell fate. Within this conceptual framework and powered by ecological niche modelling, the discovery of microenvironmental variables related to hypoxia and mechanosignalling that modulate proliferative plasticity and intratumor immune activity may open new avenues for therapeutic targeting of emerging biological vulnerabilities in glioblastoma.
    MeSH term(s) Humans ; Glioblastoma/pathology ; Brain Neoplasms/pathology ; Brain/metabolism ; Neoplastic Stem Cells/metabolism ; Cell Differentiation ; Tumor Microenvironment
    Language English
    Publishing date 2023-04-08
    Publishing country England
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1033980-2
    ISSN 1096-3650 ; 1044-579X
    ISSN (online) 1096-3650
    ISSN 1044-579X
    DOI 10.1016/j.semcancer.2023.04.004
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  10. Article ; Online: Regulatory T cells in cancer: where are we now?

    Gallimore, Awen / Quezada, Sergio A / Roychoudhuri, Rahul

    Immunology

    2019  Volume 157, Issue 3, Page(s) 187–189

    Abstract: There have been substantial strides forward in our understanding of the contribution of regulatory T (Treg) cells to cancer immunosuppression. In this issue, we present a series of papers highlighting emerging themes on this topic relevant not only to ... ...

    Abstract There have been substantial strides forward in our understanding of the contribution of regulatory T (Treg) cells to cancer immunosuppression. In this issue, we present a series of papers highlighting emerging themes on this topic relevant not only to our understanding of the fundamental biology of tumour immunosuppression but also to the design of new immunotherapeutic approaches. The substantially shared biology of CD4
    MeSH term(s) Animals ; Humans ; Immunotherapy/adverse effects ; Lymphocytes, Tumor-Infiltrating/immunology ; Lymphocytes, Tumor-Infiltrating/pathology ; Neoplasms/immunology ; Neoplasms/pathology ; Neoplasms/therapy ; Phenotype ; Signal Transduction ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/pathology ; Tumor Escape
    Language English
    Publishing date 2019-06-21
    Publishing country England
    Document type Editorial ; Introductory Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80124-0
    ISSN 1365-2567 ; 0019-2805 ; 0953-4954
    ISSN (online) 1365-2567
    ISSN 0019-2805 ; 0953-4954
    DOI 10.1111/imm.13088
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