ArticleNature2018
IL-23 secreted by myeloid cells drives castration-resistant prostate cancer.
Article in Nature, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 260 papers, 4 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
260 citing papers in PubMed, 4 syntheses or guidelines pooled it, 377 citations in OpenAlex.
- Circulating myeloid-derived suppressor cells and survival in prostate cancer patients: systematic review and meta-analysis.Prostate cancer and prostatic diseases · 2023Pooled it
- What Do We Have to Know about PD-L1 Expression in Prostate Cancer? A Systematic Literature Review. Part 5: Epigenetic Regulation of PD-L1.International journal of molecular sciences · 2021Pooled it
- What Do We Have to Know about PD-L1 Expression in Prostate Cancer? A Systematic Literature Review. Part 3: PD-L1, Intracellular Signaling Pathways and Tumor Microenvironment.International journal of molecular sciences · 2021Pooled it
- What Do We Have to Know about PD-L1 Expression in Prostate Cancer? A Systematic Literature Review. Part 4: Experimental Treatments in Pre-Clinical Studies (Cell Lines and Mouse Models).International journal of molecular sciences · 2021Pooled it
- Immune biomarkers of response and resistance to ipilimumab and nivolumab in metastatic castration-resistant prostate cancer.Science advances · 2026Trial
- Clonal Hematopoiesis and Clinical Outcomes in Metastatic Castration-Resistant Prostate Cancer Patients Given Androgen Receptor Pathway Inhibitors (Alliance A031201).Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Trial
- A Modular Trial of Androgen Signaling Inhibitor Combinations Testing a Risk-Adapted Strategy in Patients with Metastatic Castration-Resistant Prostate Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Trial
- CXCR2 antagonist navarixin in combination with pembrolizumab in select advanced solid tumors: a phase 2 randomized trial.Investigational new drugs · 2024Trial
- Clinical and immunologic impact of short-course enzalutamide alone and with immunotherapy in non-metastatic castration sensitive prostate cancer.Journal for immunotherapy of cancer · 2021Trial
- Neuromedin U 'innervation' reprograms myeloid immunosuppression in neuroendocrine prostate cancer.Oncogene · 2026Article
- Ineffectiveness of immune checkpoint inhibitors in prostate cancer: is it just a question of '-mabs'?The Journal of pathology · 2026Review
- KMT9 drives T cell exclusion and dysfunction by promoting PMN-MDSCs infiltration and ARG1 expression in prostate cancer.Molecular cancer · 2026Article
- Human Group IIA Secreted Phospholipase AInternational journal of molecular sciences · 2026Review
- Review
- A Phase I trial of the anti-IL23 monoclonal antibody tildrakizumab, in combination with abiraterone acetate, for the treatment of metastatic castration-resistant prostate cancer.Investigational new drugs · 2026Article
- RelB/ILF2-GM-CSF loop sustains tumor-MDSC communication in prostate cancer immunosuppression.Cell death & disease · 2026Article
- Multidimensional explanations and future perspectives on the limited efficacy of immunotherapy in prostate cancer.Asian journal of andrology · 2026Review
- ANXA2-mediated Phagocytosis Generates ARAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Inflammatory and Epigenetic Biomarkers in Prostate Disease: Current Evidence, Clinical Limitations, and Future Multimarker Strategies.Diagnostics (Basel, Switzerland) · 2026Review
- An Implantable Scaffold Sequentially Releasing STING Agonist and B7-H3 Antibody for Bone Metastasis Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
200 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Commented on by
- Commented on by
Authors and funding
27 authors at 8 institutions in 3 countries.
Funding
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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.