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仓鼠胰腺癌发生的组织发生学：超微结构证据

Histogenesis of pancreatic carcinogenesis in the hamster: ultrastructural evidence.

作者信息

Flaks B

出版信息

Environ Health Perspect. 1984 Jun;56:187-203. doi: 10.1289/ehp.8456187.

DOI:10.1289/ehp.8456187
PMID:6383797
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1568208/
Abstract

Pancreatic carcinogenesis in the Syrian hamster, induced by beta-oxidized derivatives of N-nitroso-di-n-propylamine, constitutes a valuable model of human cancer of the exocrine pancreas. In both species the majority of tumors are adenocarcinomas: superficially, on the basis of their histological appearance, these appear to be ductal in origin. However, sequential analysis, by electron microscopy, of the development of pancreatic neoplasia in the hamster model indicates that acinar cells may participate in the histogenesis of "ductal" adenomas and carcinomas. Acinar cells appear to undergo changes in differentiation, including pseudoductular transformation, giving rise to a new population of cells that resemble ductular or centroacinar types. This new population may then proliferate to form, first, cystic foci and subsequently cystadenomas and adenocarcinomas. Mucous metaplasia appears to develop at late stages of tumor development. Although the participation of ductular and centroacinar cells in pancreatic carcinogenesis cannot be excluded, very few tumors arise from the ductal epithelium. It is possible that some human pancreatic adenocarcinomas may also have their origin from dysplastic acinar cells, by analogy with the hamster model: focal acinar dysplasia being common in human pancreatic cancer patients.

摘要

由N-亚硝基二正丙胺的β-氧化衍生物诱导的叙利亚仓鼠胰腺癌，构成了人类外分泌胰腺癌的一个有价值的模型。在这两个物种中，大多数肿瘤都是腺癌：从表面上看，根据它们的组织学外观，这些肿瘤似乎起源于导管。然而，通过电子显微镜对仓鼠模型中胰腺肿瘤形成过程的连续分析表明，腺泡细胞可能参与了“导管”腺瘤和癌的组织发生。腺泡细胞似乎经历了分化变化，包括假导管化生，产生了一群类似于导管或中央腺泡类型的新细胞。然后这群新细胞可能增殖形成首先是囊性病灶，随后是囊腺瘤和腺癌。黏液化生似乎在肿瘤发展的后期出现。虽然不能排除导管和中央腺泡细胞参与胰腺癌发生，但很少有肿瘤起源于导管上皮。与仓鼠模型类似，一些人类胰腺腺癌也可能起源于发育异常的腺泡细胞：局灶性腺泡发育异常在人类胰腺癌患者中很常见。

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