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联合内分泌治疗对正常前列腺、前列腺上皮内瘤变和前列腺腺癌的影响。

Effects of combination endocrine treatment on normal prostate, prostatic intraepithelial neoplasia, and prostatic adenocarcinoma.

作者信息

Montironi R, Magi-Galluzzi C, Muzzonigro G, Prete E, Polito M, Fabris G

机构信息

Institute of Morbid Anatomy and Histopathology, School of Medicine, University of Ancona, Nuovo Ospedale Regionale, Italy.

出版信息

J Clin Pathol. 1994 Oct;47(10):906-13. doi: 10.1136/jcp.47.10.906.

DOI:10.1136/jcp.47.10.906
PMID:7525657
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC502174/
Abstract

AIMS

To investigate the effect of combination endocrine treatment (CET) or luteinising hormone releasing hormone agonist and flutamide on non-neoplastic prostate, prostatic intraepithelial neoplasia, and prostatic adenocarcinoma.

METHODS

The morphology, including the mitotic activity, of 12 radical prostatectomies from patients with prostatic adenocarcinoma pretreated for three months with CET was evaluated in haematoxylin and eosin stained sections and compared with an untreated age and stage matched control group.

RESULTS

A differential effect on the non-neoplastic prostate was observed. In fact, the transition zone of the treated prostate showed simplification of the glandular lobules: the ducts and acini were small without undulations of the epithelial border and with a prominent basal cell layer. Within the peripheral zone there was inconspicuous branching of the ducts and acini which looked dilatated and lined by flattened atrophic epithelium. Prostatic intraepithelial neoplasia occurred in scattered ducts and acini in the peripheral zone of 10 of the 12 patients. The epithelial cell lining showed a prominent basal cell layer. A certain degree of secretory cell type stratification was always present. However, crowding was less evident than in the untreated prostate because of cytoplasmic clearing and enlargement as a result of coalescence of vacuoles. The treated adenocarcinomas had neoplastic acini which looked small and shrunken, and areas of individual infiltrating tumour cells separated by abundant interglandular connective tissue. The secretory cells of the nonneoplastic, prostatic intraepithelial neoplasia, and prostatic adenocarcinoma lesions had inconspicuous nucleoli, nuclear shrinkage, chromatin condensation, and cytoplasmic clearing. Apoptotic bodies were easily identifiable in all the cell layers. The lumina were rich in macrophages, sloughed secretory cells with degenerative features, and apoptotic bodies. Mitoses were not observed in any of the treated non-neoplastic prostate, prostatic intraepithelial neoplasia, or prostatic adenocarcinomas, whereas the mitotic frequency increased from non-neoplastic prostate through prostatic intraepithelial neoplasia up to prostatic adenocarcinomas in the untreated specimens.

CONCLUSIONS

CET before radical prostatectomy causes regressive epithelial changes together with enhanced apoptosis and blocked mitotic activity.

摘要

目的

研究联合内分泌治疗(CET)或促黄体生成素释放激素激动剂与氟他胺对非肿瘤性前列腺组织、前列腺上皮内瘤变及前列腺腺癌的影响。

方法

对12例接受了3个月CET预处理的前列腺腺癌患者的根治性前列腺切除术标本进行苏木精-伊红染色,评估其形态学,包括有丝分裂活性,并与未治疗的年龄及分期匹配的对照组进行比较。

结果

观察到对非肿瘤性前列腺组织有不同的影响。实际上,治疗组前列腺的移行区显示腺小叶简化:导管和腺泡较小,上皮边界无起伏,基底细胞层明显。外周区内导管和腺泡分支不明显,看起来扩张,内衬扁平萎缩上皮。12例患者中有10例的外周区散在导管和腺泡出现前列腺上皮内瘤变。上皮细胞内衬显示基底细胞层明显。总是存在一定程度的分泌细胞类型分层。然而,由于空泡融合导致细胞质清亮和增大,拥挤程度比未治疗的前列腺组织中轻。治疗后的腺癌有看起来小而萎缩的肿瘤腺泡,以及由丰富的腺间结缔组织分隔的单个浸润性肿瘤细胞区域。非肿瘤性、前列腺上皮内瘤变及前列腺腺癌病变的分泌细胞核仁不明显、核固缩、染色质凝聚且细胞质清亮。在所有细胞层中均易识别凋亡小体。管腔内富含巨噬细胞、具有退行性特征的脱落分泌细胞及凋亡小体。在任何治疗后的非肿瘤性前列腺组织、前列腺上皮内瘤变或前列腺腺癌中均未观察到有丝分裂,而在未治疗的标本中,有丝分裂频率从非肿瘤性前列腺组织经前列腺上皮内瘤变直至前列腺腺癌逐渐增加。

结论

根治性前列腺切除术前行CET可导致上皮细胞退行性改变,同时增强凋亡并阻断有丝分裂活性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bca/502174/511826de0408/jclinpath00223-0045-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bca/502174/e6cc69ae3ff4/jclinpath00223-0042-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bca/502174/9aa4c86cf1ae/jclinpath00223-0042-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bca/502174/a09e73f2183c/jclinpath00223-0043-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bca/502174/4d6e4510b85b/jclinpath00223-0043-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bca/502174/5320049db987/jclinpath00223-0044-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bca/502174/b3cbfa64d7b7/jclinpath00223-0044-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bca/502174/511826de0408/jclinpath00223-0045-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bca/502174/e6cc69ae3ff4/jclinpath00223-0042-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bca/502174/9aa4c86cf1ae/jclinpath00223-0042-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bca/502174/a09e73f2183c/jclinpath00223-0043-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bca/502174/4d6e4510b85b/jclinpath00223-0043-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bca/502174/5320049db987/jclinpath00223-0044-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bca/502174/b3cbfa64d7b7/jclinpath00223-0044-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bca/502174/511826de0408/jclinpath00223-0045-a.jpg

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