DIETARY TOMATO PRODUCTS AND EXPERIMENTAL PROSTATE CANCER

背景资料。前列腺癌已成为最常被诊断的癌症。 美国男性，特别是非裔美国人的恶性行为 它经历了世界上最高的利率。很可能是一个 影响风险的饮食因素有很多。卫生专业人员 后续研究发现前列腺癌的发病率显著下降 食用西红柿产品的风险。增加了几行 我们小组得出的初步证据支持这一假说 西红柿产品可能会降低风险。生物活跃者 西红柿中可能影响前列腺的物质尚不清楚。 一种可能性是类胡萝卜素番茄红素。更高的血清浓度 番茄红素的含量与降低癌症风险有关 医生健康研究。番茄红素是人体内最常见的类胡萝卜素 对人前列腺细胞具有抗增殖作用。 体外培养。 假设。我们假设饮食中添加西红柿 产品或番茄红素抑制前列腺癌的发生，前列腺癌 肿瘤生长率和特征良好的啮齿动物模型中的转移。 实验方法。日粮中添加番茄的效果 粉末、番茄脂溶性提取物或番茄红素对前列腺癌的作用 将在五个模型中进行评估。(1)。NMU/雄激素诱导的大鼠 前列腺癌的发生。(2)。油井的增长速度 分化、生长缓慢和雄激素敏感的Dunning R3327H 大鼠前列腺癌模型。(3)。MatlyLu的转移性扩散 低分化和雄激素非依赖性前列腺癌 在老鼠身上。(4)。人类低分化的生长速度， 雄激素耐药与P53突变PC-3前列腺癌 SCID小鼠。(5)。人类的生长速度，低分化， 激素依赖性和P53正常的人前列腺LNCaP SCID小鼠的腺癌。 关联性。这些研究将为 了解前列腺癌的病因和预防，以及 一种新的化学预防药物的潜在开发。

Background. Prostate cancer has become the most frequently diagnosed malignancy in American men, particularly the African American population which experiences the highest rates in the world. It is probable that a number of dietary factors modulate risk. The Health Professionals Follow-Up Study has detected a significant reduction in prostate cancer risk with the consumption of tomato products. Several additional lines of preliminary evidence derived by our group support the hypothesis that tomato products may reduce risk. The biologically active substances in tomatoes that may influence the prostate are unknown. One possibility is the carotenoid lycopene. Higher serum concentrations of lycopene are associated with reduced prostrate cancer risk in the Physicians Health Study. Lycopene is the most common carotenoid in the human prostate and has antiproliferative effects on prostate cells in vitro. Hypothesis. We hypothesize that diets supplemented with tomato products or lycopene inhibit de novo prostate carcinogenesis, prostate tumor growth rates, and metastases in well characterized rodent models. Experimental Approach. The effects of diets supplemented with tomato powder, tomato lipophilic extract, or lycopene on prostate carcinogenesis will be evaluated in five models. (1). NMU/androgen-induced rat prostate carcinogenesis. (2). The growth rate of the well differentiated, slow growing and androgen sensitive Dunning R3327H prostate adenocarcinoma in rats. (3). Metastatic spread of the MatLyLu poorly differentiated and androgen independent prostate adenocarcinoma in rats. (4). The growth rate of the human poorly differentiated, androgen resistant, and p53 mutant PC-3 prostate adenocarcinoma in SCID mice. (5). The growth rate of the human, poorly differentiated, hormone dependent, and p53 normal LNCaP human prostate adenocarcinoma in SCID mice. Relevance. These studies will provide critical data for the understanding of prostate cancer etiology and prevention as well as the potential development of a new chemopreventive agent.