美国罗切斯特医学中心的研究人员发现，男性体内特有的一种激素，可能是男性罹患膀胱癌机率高于女性的原因之一。
根据这篇发表于Journal of the National Cancer Institute的研究，研究人员表示，他们在动物实验中发现，造成雄性实验小鼠患膀胱癌机率较高的原因，可能与体内的一种睾丸刺激激素有关。
研究报告指出，人类男性体内也有起类似作用的激素，这种激素会使男性体内的膀胱癌细胞更加活跃。研究人员指出，这种激素只是可能导致膀胱癌的原因之一。
根据美国癌症协会统计，美国目前有5万名男性膀胱癌患者和1.7万名女性膀胱癌患者，前者人数是后者的近3倍。
参与这项研究的美国罗切斯特医学中心的泌尿学系主任Edward Messing表示，研究人员过去曾认为，吸烟和工业化学污染是男性患膀胱癌机率高于女性的原因。但近年来，吸烟的女性和接触工业化学污染的女性越来越多，然而她们罹患膀胱癌的机率仍低于男性，因此有理由相信，男性特有的这种激素，是导致男性患膀胱癌机率高于女性的重要原因之一。
（编译/姜欣慧） (资料来源 : Bio.com)
原始出处:
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: chang@urmc.rochester.edu ).
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.
