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Prostate Cancer

Advances in Immunotherapy

  • Therapy Review
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Abstract

The absence of curative therapies for advanced or recurrent forms of prostate cancer has prompted a vigorous search for novel treatment strategies. Immunotherapy encompasses one particularly promising systemic approach to the treatment of prostate cancer. Immune-based strategies for treating prostate cancer have recently been facilitated by the identification of a number of prostate tissue/tumour antigens that can be targeted, either by antibody or T cells, to promote prostate tumour cell injury or death. These same prostate antigens can also be used for the construction of vaccines to induce prostate-specific T cell-mediated immunity. Greater insight into specific mechanisms that govern antigen-specific T cell activation has brought with it a number of innovative methods to induce and enhance T cell-mediated responses against prostate tumours. For instance, auto-logous dendritic cells loaded with prostate antigens have proved useful to induce prostate-specific T cell activation. Similarly, in vivo manipulations of T cell costimulatory pathway receptors can greatly facilitate tumour-specific T cell activation and potentiate T cell-mediated responses against a number of malignancies, including prostate cancer. For example, blocking T cell cytotoxic lymphocyte-associated antigen 4 (CTLA-4) receptor binding to its ligand prevents the down-regulation of T cell responses and can even potentiate T cell antitumoural immunity in mouse models of prostate cancer. Androgen ablation (AA) may induce prostate tumour/tissue-specific T cell mediated inflammation and, as such, a phase II trial is currently in progress to ascertain whether CTLA-4 blockade can enhance AA-induced treatment responses in patients with advanced prostate cancer. Nevertheless, further basic and clinical investigation is still required to establish immunotherapy as a true prostate cancer treatment option.

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Acknowledgments

This review has been supported, in part, by funding provided by National Institutes of Health/National Cancer Institiute Grant CA 82185 (E.D.K.), Department of Defense Grants PC991568 (E.D.K.) and CaPCURE (E.D.K., J.P.A., A.A.H.). E.D.K. is a past American Foundation for Urologic Disease Scholar and American Cancer Society Clinical Oncology Fellow.

The authors have no conflicts of interest directly relevant to the contents of this manuscript.

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Authors and Affiliations

  1. Departments of Microbiology, Immunology and Urology, SUNY Upstate Medical University, Syracuse, New York, New York, USA

    Arthur A. Hurwitz

  2. Department of Urology, Loyola University of Chicago, Maywood, Chicago, Illinois, USA

    Paul Yanover

  3. Cancer Immunology Program of the Cardinal Bernardin Cancer Center, Loyola University of Chicago, Maywood, Chicago, Illinois, USA

    Mary Markowitz

  4. Department of Molecular and Cell Biology, Cancer Research Laboratory, Howard Hughes Medical Institute, University of California at Berkeley, Berkeley, California, USA

    James P. Allison

  5. Departments of Urology and Immunology and the Comprehensive Cancer Center, Mayo Clinic, 200 First Street SW, Rochester, 55905, USA

    Eugene D. Kwon

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  1. Arthur A. Hurwitz
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Correspondence to Eugene D. Kwon.

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Hurwitz, A.A., Yanover, P., Markowitz, M. et al. Prostate Cancer. BioDrugs 17, 131–138 (2003). https://doi.org/10.2165/00063030-200317020-00005

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