外分泌胰腺癌和内分泌胰腺之间的联系。

P M Pour, B Schmied
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引用次数: 47

摘要

结论:我们实验室20年来的实验和人体研究表明胰岛在导管型腺癌发展中的重要性。我们认为,在导管内发展的胰腺癌,但更常见的是在胰岛内,源于分布在导管树和胰岛内的胰腺干细胞。背景:胰腺癌的组织发生仍有争议。导管细胞、导管细胞和腺泡细胞都被认为是肿瘤的祖细胞。我们的长期人体和实验研究表明,胰腺导管腺癌发生在导管细胞和胰岛。本文提供了支持性研究。方法:本文采用近20年来对叙利亚仓鼠进行的多项人体研究和实验研究。建立仓鼠和人胰岛,电镜、免疫组织化学、细胞遗传学和分子生物学观察其生长和形态变化。结果:使用仓鼠胰腺癌模型的研究表明,大多数胰腺腺癌在胰岛内发展,最有可能来自干细胞,干细胞也被认为是在导管内发展的肿瘤的祖细胞。对新建立的人类和仓鼠胰岛的研究证实了胰岛细胞分化和恶性肿瘤的巨大潜力。胰岛细胞的高恶性易感性可能与其高药物代谢酶和高增殖率有关。饮食研究表明,高脂肪饮食对胰腺癌发生的促进作用与能量摄入无关,而与其对胰岛细胞复制的影响有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The link between exocrine pancreatic cancer and the endocrine pancreas.

Conclusion: Experimental and human studies during 20 years of research in our laboratories point to the importance of pancreatic islets in the development of ductal-type adenocarcinomas. We believe that pancreatic cancer that develops within ducts, but more frequently within islets, derives from pancreatic stem cells that are distributed within the ductal trees and within the islets.

Background: The histogenesis of pancreatic cancer is still debatable. Ductal, ductular, and acinar cells all have been declared the tumor progenitor cells. Our long-term human and experimental studies indicate that pancreatic ductal adenocarcinomas arise within ductal cells and islets. Supporting studies are presented in this article.

Methods: Several human studies and experimental studies on Syrian hamsters conducted within the last 20 years were used in this article. Hamster and human islets were established, and their growth and morphologic changes were examined electron microscopically, immunohistochemically, cytogenetically, and molecular biologically.

Results: Studies using the hamster pancreatic cancer model showed that most pancreatic adenocarcinomas develop within islets, most probably from stem cells, which are also believed to be the progenitor cells for tumors that develop within ducts. Studies in newly established human and hamster islets culture validated the immense potential of islet cells to differentiate and become malignant. The higher susceptibility of islet cells to become malignant could be related to their high drug-metabolizing enzymes and their high proliferation rate. Dietary studies indicate that the promoting effect of a high-fat diet on pancreatic carcinogenesis is unrelated to the energy intake, but rather is related to its effect on islet cell replication.

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