ADT with SBRT versus SBRT alone for hormone-sensitive oligorecurrent prostate cancer (RADIOSA): a randomised, open-label, phase 2 clinical trial.

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Abstract

[Indexed for MEDLINE] Conflict of interest statement: Declaration of interests The Division of Radiation Oncology of the European Institute of Oncology IRCCS received research funding from the Italian Association for Cancer Research, Fondazione Istituto Europeo di Oncologia-Centro Cardiologico Monzino, Accuray, and Ion Beam applications. NF has received honoraria for consulting, an advisory role, speaker bureau, travel, or research grants from Merck Sharp & Dohme, Merck, Novartis, AstraZeneca, Roche, Menarini, Daiichi Sankyo, GSK, Gilead, Sysmex, Veracyte, Sakura, Leica Biosystems, Lilly, and Pfizer. These companies had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results. BAJ-F received speakers fees from Bayer, Accuray, Astellas, IBA, Ipsen, AstraZeneca, Tecnologie avanzate, Recordati, and Novartis. BAJ-F participated in the advisory boards of Accuray, Bayer, and Seagen, all outside the current project. CT received travel support and honorarium from Boston Scientific, Diffusion Pharmaceuticals, and Vision RT. CT participated in advisory boards for Bayer, Telix, Lantheus, and Molli Surgical and receives royalties from Wolter Kluwer, all outside the current project. All other authors declare no competing interests. 10. Cancer Cell. 2023 Jan 9;41(1):106-123.e10. doi: 10.1016/j.ccell.2022.11.014. Epub 2022 Dec 15. IL-5-producing CD4(+) T cells and eosinophils cooperate to enhance response to immune checkpoint blockade in breast cancer. Blomberg OS(1), Spagnuolo L(2), Garner H(2), Voorwerk L(3), Isaeva OI(4), van Dyk E(5), Bakker N(2), Chalabi M(6), Klaver C(3), Duijst M(3), Kersten K(3), Brüggemann M(3), Pastoors D(2), Hau CS(2), Vrijland K(2), Raeven EAM(2), Kaldenbach D(2), Kos K(1), Afonina IS(7), Kaptein P(8), Hoes L(9), Theelen WSME(10), Baas P(10), Voest EE(9), Beyaert R(7), Thommen DS(8), Wessels LFA(11), de Visser KE(12), Kok M(13). Author information: (1)Division of Tumor Biology & Immunology, The Netherlands Cancer Institute, Amsterdam, the Netherlands; Oncode Institute, Utrecht, the Netherlands; Department of Immunology, Leiden University Medical Centre, Leiden, the Netherlands. (2)Division of Tumor Biology & Immunology, The Netherlands Cancer Institute, Amsterdam, the Netherlands; Oncode Institute, Utrecht, the Netherlands. (3)Division of Tumor Biology & Immunology, The Netherlands Cancer Institute, Amsterdam, the Netherlands. (4)Division of Tumor Biology & Immunology, The Netherlands Cancer Institute, Amsterdam, the Netherlands; Division of Molecular Carcinogenesis, The Netherlands Cancer Institute, Amsterdam, the Netherlands. (5)Division of Tumor Biology & Immunology, The Netherlands Cancer Institute, Amsterdam, the Netherlands; Oncode Institute, Utrecht, the Netherlands; Division of Molecular Carcinogenesis, The Netherlands Cancer Institute, Amsterdam, the Netherlands. (6)Division of Molecular Oncology & Immunology, The Netherlands Cancer Institute, Amsterdam, the Netherlands; Department of Gastrointestinal Oncology, The Netherlands Cancer Institute, Amsterdam, the Netherlands; Department of Medical Oncology, The Netherlands Cancer Institute, Amsterdam, the Netherlands. (7)VIB-UGent Center for Inflammation Research, Ghent University, Ghent, Belgium; Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium. (8)Division of Molecular Oncology & Immunology, The Netherlands Cancer Institute, Amsterdam, the Netherlands. (9)Oncode Institute, Utrecht, the Netherlands; Division of Molecular Oncology & Immunology, The Netherlands Cancer Institute, Amsterdam, the Netherlands; Department of Medical Oncology, The Netherlands Cancer Institute, Amsterdam, the Netherlands. (10)Department of Thoracic Oncology, The Netherlands Cancer Institute, Amsterdam, the Netherlands. (11)Oncode Institute, Utrecht, the Netherlands; Division of Molecular Carcinogenesis, The Netherlands Cancer Institute, Amsterdam, the Netherlands. (12)Division of Tumor Biology & Immunology, The Netherlands Cancer Institute, Amsterdam, the Netherlands; Oncode Institute, Utrecht, the Netherlands; Department of Immunology, Leiden University Medical Centre, Leiden, the Netherlands. Electronic address: k.d.visser@nki.nl. (13)Division of Tumor Biology & Immunology, The Netherlands Cancer Institute, Amsterdam, the Netherlands; Department of Medical Oncology, The Netherlands Cancer Institute, Amsterdam, the Netherlands. Electronic address: m.kok@nki.nl. Comment in Cancer Cell. 2023 Jan 9;41(1):9-11. doi: 10.1016/j.ccell.2022.11.008. Nat Rev Immunol. 2023 Feb;23(2):72. doi: 10.1038/s41577-022-00832-y. Mol Oncol. 2023 Apr;17(4):545-547. doi: 10.1002/1878-0261.13413. Immune checkpoint blockade (ICB) has heralded a new era in cancer therapy. Research into the mechanisms underlying response to ICB has predominantly focused on T cells; however, effective immune responses require tightly regulated crosstalk between innate and adaptive immune cells. Here, we combine unbiased analysis of blood and tumors from metastatic breast cancer patients treated with ICB with mechanistic studies in mouse models of breast cancer. We observe an increase in systemic and intratumoral eosinophils in patients and mice responding to ICB treatment. Mechanistically, ICB increased IL-5 production by CD4+ T cells, stimulating elevated eosinophil production from the bone marrow, leading to systemic eosinophil expansion. Additional induction of IL-33 by ICB-cisplatin combination or recombinant IL-33 promotes intratumoral eosinophil infiltration and eosinophil-dependent CD8+ T cell activation to enhance ICB response. This work demonstrates the critical role of eosinophils in ICB response and provides proof-of-principle for eosinophil engagement to enhance ICB efficacy. Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved. DOI: 10.1016/j.ccell.2022.11.014