氯喹诺(锌离子)和卡麦角林(催乳素多巴胺激动剂)治疗终末雄激素非依赖性前列腺癌的有效治疗方法。为什么?怎么做?

Leslie C Costello, Renty B Franklin
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引用次数: 0

摘要

与正常和良性前列腺的高锌水平相比,所有前列腺癌病例都表现出恶性前列腺中锌含量显著降低的特征。目前还没有报道证实的前列腺癌病例,恶性肿瘤表现出存在于正常前列腺腺泡上皮中的高锌水平。锌的减少是通过下调ZIP1锌转运蛋白来实现的,这阻止了细胞毒性锌水平的吸收和积累。因此,前列腺癌是一种“zip1缺陷”的恶性肿瘤。睾酮和催乳素是调节外周区(恶性肿瘤发生和发展的部位)腺泡上皮细胞生长、增殖、代谢和功能活动的主要激素。睾酮调节为晚期前列腺癌雄激素消融术治疗提供了基础,导致晚期雄激素不依赖型恶性肿瘤的发展。雄激素非依赖型恶性肿瘤在催乳素的影响下进展。这些关系为晚期前列腺癌的预防和治疗提供了依据。氯喹诺(锌离子载体;5-氯-7-碘喹啉-8-醇)在zip1缺陷的恶性细胞中促进锌的运输和积累,并诱导细胞毒性作用。卡麦角林(多巴胺激动剂)用于减少催乳素的产生及其在雄激素非依赖性恶性肿瘤进展中的作用。我们提出一个氯喹诺/卡麦角林治疗方案,将有效流产晚期前列腺癌。FDA政策允许对这些患者采用这种治疗方案。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

A Proposed Efficacious Treatment with Clioquinol (Zinc Ionophore) and Cabergoline (Prolactin Dopamine Agonist) for the Treatment of Terminal Androgen-independent Prostate Cancer. Why and How?

A Proposed Efficacious Treatment with Clioquinol (Zinc Ionophore) and Cabergoline (Prolactin Dopamine Agonist) for the Treatment of Terminal Androgen-independent Prostate Cancer. Why and How?

A Proposed Efficacious Treatment with Clioquinol (Zinc Ionophore) and Cabergoline (Prolactin Dopamine Agonist) for the Treatment of Terminal Androgen-independent Prostate Cancer. Why and How?

A Proposed Efficacious Treatment with Clioquinol (Zinc Ionophore) and Cabergoline (Prolactin Dopamine Agonist) for the Treatment of Terminal Androgen-independent Prostate Cancer. Why and How?

All cases of prostate cancer exhibit the hallmark condition of marked decrease in zinc in malignancy compared to the high zinc levels in the normal and benign prostate. There exists no reported corroborated case of prostate cancer in which malignancy exhibits the high zinc levels that exist in the normal prostate acinar epithelium. The decrease in zinc is achieved by the downregulation of ZIP1 zinc transporter, which prevents the uptake and accumulation of cytotoxic zinc levels. Thus, prostate cancer is a "ZIP1-deficient" malignancy. Testosterone and prolactin are the major hormones that similarly regulate the growth, proliferation, metabolism, and functional activities of the acinar epithelial cells in the peripheral zone (the site of development and progression of malignancy). Testosterone regulation provides the basis for androgen ablation treatment of advanced prostate cancer, which leads to the development of terminal androgen-independent malignancy. Androgen-independent malignancy progresses under the influence of prolactin. These relationships provide the basis for the prevention and treatment of advanced prostate cancer. Clioquinol (zinc ionophore; 5-chloro-7-iodoquinolin-8-ol) is employed to facilitate zinc transport and accumulation in the ZIP1-deficient malignant cells and induce cytotoxic effects. Cabergoline (dopamine agonist) is employed to decrease prolactin production and its role in the progression of androgen-independent malignancy. We propose a clioquinol/cabergoline treatment regimen that will be efficacious for aborting terminal advanced prostate cancer. FDA policies permit this treatment regimen to be employed for these patients.

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