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Cited by 401

The DOI matches its Crossref record; 23 of the 23 references it cites were found in a registry or an index.

Promotion of Bladder Cancer Development and Progression by Androgen Receptor Signals

Open access
Miyamoto, H., Yang, Z., Chen, Y.-T., Ishiguro, H., Uemura, H., Kubota, Y., Nagashima, Y., Chang, Y.-J., Hu, Y.-C., Tsai, M.-Y., Yeh, S., Messing, E. M., Chang, C.·2007·JNCI Journal of the National Cancer Institute

Abstract

BACKGROUND: Males have a higher incidence of bladder cancer than females, but the reason remains unknown. Unlike prostate cancer, human bladder cancer is not generally considered to be dependent on hormone activity. We investigated the possible involvement of androgens and the androgen receptor (AR) in bladder cancer. METHODS: We used N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) to induce bladder cancer in wild-type male and female mice, with and without castration in males, and in AR knockout (ARKO) male and female mice, with and without dihydrotestosterone (DHT) supplementation in males. We also treated human bladder cancer cell lines, including TCC-SUP and UMUC3, and mouse xenograft models established from these same lines with androgen deprivation therapy (antiandrogen treatment or castration), AR-small-interfering RNA (AR-siRNA), or the anti-AR molecule ASC-J9, which causes selective degradation of the AR. RESULTS: More than 92% of wild-type male and 42% of wild-type female mice treated with BBN eventually developed bladder cancer, whereas none of the male or female ARKO mice did. Treatment with BBN induced bladder cancer in 25% of ARKO mice supplemented with DHT and in 50% of castrated wild-type male mice. Androgen deprivation of AR-positive human bladder cancer cells by androgen depletion in vitro or castration in mice and/or by treatment with the antiandrogen flutamide in vitro or in vivo, as well as AR knockdown by AR-siRNA or by ASC-J9, suppressed cell proliferation in vitro and xenograft tumor growth in vivo. CONCLUSIONS: Our findings implicate the involvement of both androgens and the AR in bladder cancer. Targeting AR and androgens may provide novel chemopreventive and therapeutic approaches for bladder cancer.

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Crossref · 10.1093/jnci/djk113

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Metadata

Authors
Miyamoto, H., Yang, Z., Chen, Y.-T., Ishiguro, H., Uemura, H., Kubota, Y., Nagashima, Y., Chang, Y.-J., Hu, Y.-C., Tsai, M.-Y., Yeh, S., Messing, E. M., & Chang, C.
Venue
JNCI Journal of the National Cancer Institute
Published
2007-04-03
Volume
99
Issue
7
Pages
558-568
ISSN
  • 0027-8874 (ISSN-L)
  • 1460-2105
OpenAlex
W2134555283
Cited by
401
References
23
FWCI
8.56
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Promotion of Bladder Cancer Development and Progression by Androgen Receptor Signals. https://app.cochat.ai/papers/10.1093/jnci/djk113
The paper
Miyamoto, H., Yang, Z., Chen, Y.-T., Ishiguro, H., Uemura, H., Kubota, Y., Nagashima, Y., Chang, Y.-J., Hu, Y.-C., Tsai, M.-Y., Yeh, S., Messing, E. M., & Chang, C. (2007). Promotion of Bladder Cancer Development and Progression by Androgen Receptor Signals. JNCI Journal of the National Cancer Institute. https://doi.org/10.1093/jnci/djk113

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.