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Abstract Title:

IL-23 secreted by myeloid cells drives castration-resistant prostate cancer.

Abstract Source:

Nature. 2018 Jun 27. Epub 2018 Jun 27. PMID: 29950727

Abstract Author(s):

Arianna Calcinotto, Clarissa Spataro, Elena Zagato, Diletta Di Mitri, Veronica Gil, Mateus Crespo, Gaston De Bernardis, Marco Losa, Michela Mirenda, Emiliano Pasquini, Andrea Rinaldi, Semini Sumanasuriya, Maryou B Lambros, Antje Neeb, Roberta Lucianò, Carlo A Bravi, Daniel Nava-Rodrigues, David Dolling, Tommaso Prayer-Galetti, Ana Ferreira, Alberto Briganti, Antonio Esposito, Simon Barry, Wei Yuan, Adam Sharp, Johann de Bono, Andrea Alimonti

Article Affiliation:

Arianna Calcinotto

Abstract:

Patients with prostate cancer frequently show resistance to androgen-deprivation therapy, a condition known as castration-resistant prostate cancer (CRPC). Acquiring a better understanding of the mechanisms that control the development of CRPC remains an unmet clinical need. The well-established dependency of cancer cells on the tumour microenvironment indicates that the microenvironment might control the emergence of CRPC. Here we identify IL-23 produced by myeloid-derived suppressor cells (MDSCs) as a driver of CRPC in mice and patients with CRPC. Mechanistically, IL-23 secreted by MDSCs can activate the androgen receptor pathway in prostate tumour cells, promoting cell survival and proliferation in androgen-deprived conditions. Intra-tumour MDSC infiltration and IL-23 concentration are increased in blood and tumour samples from patients with CRPC. Antibody-mediated inactivation of IL-23 restored sensitivity to androgen-deprivation therapy in mice. Taken together, these results reveal that MDSCs promote CRPC by acting in a non-cell autonomous manner. Treatments that block IL-23 can oppose MDSC-mediated resistance to castration in prostate cancer and synergize with standard therapies.

Study Type : In Vitro Study

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Sayer Ji
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