美國羅切斯特醫(yī)學中心的研究人員發(fā)現(xiàn),，男性體內特有的一種激素,，可能是男性罹患膀胱癌機率高于女性的原因之一,。
根據(jù)這篇發(fā)表于Journal of the National Cancer Institute的研究,，研究人員表示，他們在動物實驗中發(fā)現(xiàn),，造成雄性實驗小鼠患膀胱癌機率較高的原因,，可能與體內的一種睪丸刺激激素有關。
研究報告指出,，人類男性體內也有起類似作用的激素,，這種激素會使男性體內的膀胱癌細胞更加活躍,。研究人員指出，這種激素只是可能導致膀胱癌的原因之一,。
根據(jù)美國癌癥協(xié)會統(tǒng)計,，美國目前有5萬名男性膀胱癌患者和1.7萬名女性膀胱癌患者，前者人數(shù)是后者的近3倍,。
參與這項研究的美國羅切斯特醫(yī)學中心的泌尿學系主任Edward Messing表示,，研究人員過去曾認為，吸煙和工業(yè)化學污染是男性患膀胱癌機率高于女性的原因,。但近年來,，吸煙的女性和接觸工業(yè)化學污染的女性越來越多，然而她們罹患膀胱癌的機率仍低于男性,，因此有理由相信,，男性特有的這種激素，是導致男性患膀胱癌機率高于女性的重要原因之一,。
（編譯/姜欣慧） (資料來源 : Bio.com)
原始出處:
JNCI Journal of the National Cancer Institute 2007 99(7):558-568; doi:10.1093/jnci/djk113
Promotion of Bladder Cancer Development and Progression by Androgen Receptor Signals
Hiroshi Miyamoto, Zhiming Yang, Yei-Tsung Chen, Hitoshi Ishiguro, Hiroji Uemura, Yoshinobu Kubota, Yoji Nagashima, Yu-Jia Chang, Yueh-Chiang Hu, Meng-Yin Tsai, Shuyuan Yeh, Edward M. Messing, Chawnshang Chang
Affiliations of authors: Departments of Pathology and Urology, University of Rochester Medical Center, Rochester, NY (HM, ZY, YTC, YJC, YCH, SY, EMM, CC); Departments of Urology (HI, HU, YK) and Molecular Pathology (YN), Yokohama City University Graduate School of Medicine, Yokohama, Japan; Reproductive Medicine Institute, Chang Gung University Memorial Hospital, Kaohsiung, Taiwan (MYT)
Correspondence to: Chawnshang Chang, PhD, Departments of Pathology and Urology, University of Rochester Medical Center, 601 Elmwood Ave, Box 626, Rochester, NY 14642 (e-mail: [email protected] ).
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.
