Bonkhoff H, Remberger K
Institut für Pathologie, Abteilung Allgemeine und Spezielle Pathologie, Universität des Saarlandes, Homburg.
Pathologe. 1998 Jan;19(1):12-20. doi: 10.1007/s002920050250.
Enlargement of the prostate is an age-related, physiological process that is unique in human tissue. The prostate gland is the most common site of neoplastic disorders in men. Despite the growing impact of the various prostate diseases in terms of morbidity and mortality, the pathogenesis of benign prostate hyperplasia (BPH) and prostate cancer remains poorly understood. This reflects the complex composition of the gland with different anatomic, cellular and functional compartments that are differentially involved in benign and malignant disease processes. The present review summarizes new concepts on the morphogenesis of normal and abnormal growth in the human prostate. There is increasing evidence that prostatic stem cells are located in the basal cell layer that is basically involved in normal growth and the development of glandular hyperplasia and prostate cancer. High-grade prostatic intraepithelial neoplasia is considered the most likely precursor of clinically important cancer of the peripheral zone. Severe differentiation and proliferation abnormalities occur during malignant transformation of the prostatic epithelium. These premalignant changes are associated with abnormal expression of growth factor receptors, oncogene and suppressor gene products and genetic instability. During the process of stromal invasion the transformed cells lose their basal cell phenotype and produce basement membrane-like matrices. Common prostate cancer is mainly composed of exocrine cell types that remain androgen-responsive even in hormone-independent disease. The frequent occurrence of neuroendocrine differentiation in common prostate cancer reflects the differentiation potency of its stem cells. The endocrine phenotype derives from exocrine tumor cells via intermediate (amphicrine) cell types. Neuroendocrine tumor cells consistently lack the nuclear androgen receptor and represent an androgen-insensitive cell population in prostate cancer.
前列腺增生是一种与年龄相关的生理过程，在人体组织中独具特色。前列腺是男性肿瘤性疾病最常见的发病部位。尽管各种前列腺疾病在发病率和死亡率方面的影响日益增大，但良性前列腺增生（BPH）和前列腺癌的发病机制仍知之甚少。这反映了前列腺复杂的组成结构，其不同的解剖、细胞和功能区室在良性和恶性疾病过程中发挥着不同的作用。本综述总结了关于人类前列腺正常和异常生长形态发生的新概念。越来越多的证据表明，前列腺干细胞位于基底细胞层，该层基本参与正常生长以及腺体增生和前列腺癌的发展。高级别前列腺上皮内瘤变被认为是外周区具有临床重要意义癌症最可能的前驱病变。前列腺上皮恶性转化过程中会出现严重的分化和增殖异常。这些癌前变化与生长因子受体、癌基因和抑癌基因产物的异常表达以及基因不稳定有关。在间质浸润过程中，转化细胞失去其基底细胞表型并产生类似基底膜的基质。常见的前列腺癌主要由外分泌细胞类型组成，即使在激素非依赖性疾病中，这些细胞仍对雄激素有反应。常见前列腺癌中神经内分泌分化的频繁出现反映了其干细胞的分化潜能。内分泌表型通过中间（双分泌）细胞类型源自外分泌肿瘤细胞。神经内分泌肿瘤细胞始终缺乏核雄激素受体，代表前列腺癌中对雄激素不敏感的细胞群体。
