Erzeugung von Magen- und Pankreas-Krebs beim Meerschweinchen durch Methylnitroso-harnstoff und-urethan

Druckrey, H.; Ivanković, S.; J, Bücheler; Preußmann, R.; Thomas, C.

doi:10.1007/bf00524349

Cited by 58 publications

(8 citation statements)

References 29 publications

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“…In 1968 Driickery et al [37] showed that the prolonged administration of methylnitrosourethan or methylnitrosourea (MNU) in drinking water to random bred guinea pigs produced adenocarcinomas of the pancreas in 25% of the animals in between 740 to 800 days. This model was improved by Reddy and associates [38,39], who gave freshly dissolved MNU once a week to inbred NIH strain 13 guinea pigs.…”

Section: Guinea Pigmentioning

confidence: 99%

Animal models of exocrine pancreatic carcinogenesis

Rao

1987

Cancer Metast Rev

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In order to understand the evolution, histogenesis, and biological behaviour of exocrine pancreatic carcinoma, some reproducible experimental models have been developed in certain rodent species. To date, more than 16 chemicals, many of them structurally unrelated, have been shown to induce pancreatic tumors. Although some of these chemicals appear species specific in their effect on the pancreas, others have been shown to be capable of inducing pancreatic tumors in more than one species. In hamsters, the administration of diisopropylnitrosamine or its oxidized metabolites leads to the development of ductal adenocarcinomas that histologically resemble human pancreatic carcinomas. The histogenesis of the ductal type of adenocarcinoma in hamsters is complex, and appears to involve both the duct cells and dedifferentiated acinar cells. All pancreatic tumors in rats develop from acinar cells showing variable degrees of differentiation, regardless of the type of carcinogen used. The type of pancreatic lesions that develop in mice are also of acinar cell origin. In guinea pigs the tumors are adenocarcinomas of the ductal type and are shown to be derived from dedifferentiated acinar cells that have undergone duct-like transformation. Irrespective of the type of tumor that develops in these experimental animals, all of these models can be successfully used to evaluate the various modifying (risk) factors and biological behaviour of these neoplasms.

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Section: Guinea Pigmentioning

confidence: 99%

Animal models of exocrine pancreatic carcinogenesis

Rao

1987

Cancer Metast Rev

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“…In the guinea pig, pancreatic adenocarcinomas can be induced by N-methyl-N-nitrosourea (MNU) or N-methyl-N-nitrosourethane (55)(56)(57), albeit at the cost of a high initial mortality and relatively low incidence. The histological appearance of these tumors suggests a ductal histogenesis, but Reddy and Rao (57,58) have observed that MNU causes acinar cells to proliferate and undergo dedifferentiation, giving rise to pseudoductular structures.…”

Section: Guinea Pigmentioning

confidence: 99%

Histogenesis of pancreatic carcinogenesis in the hamster: ultrastructural evidence.

Flaks¹

1984

Environ Health Perspect

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Pancreatic carcinogenesis in the Syrian hamster, induced by 3-oxidized derivatives of N-nitroso-di-npropylamine, 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.

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“…The major obstacles to the development of such models are the unusual anatomic and functional relationships of the pancreas, with its multiple vascular and lymphatic connections, and its well-known vulnerability to manipulation (auto-digestion and pancreatitis). Previous workers have attempted to circumvent these difficulties by utilizing solid, implanted pellets for carcinogen delivery but have found that this approach generally either results in extensive tissue damage or has had no effect upon the pancreas (Lowenhaupt, 1949).At the present time there are no known chemical agents that will selectively induce pancreatic carcinoma in animal species other than the guinea-pig (Druckrey et al, 1968;Reddy et al, 1974). Therefore, this investigation was undertaken in order to evaluate a spectrum of proven carcinogens having possible pancreatic activity, employing a unique delivery system so that maximal carcinogenic effect would be localized to the pancreas.…”

mentioning

confidence: 92%

Preneoplastic changes in rabbit pancreatic duct cells produced by dimethylhydrazine

Elkort

Handler

Mozden

1975

Intl Journal of Cancer

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Permeation catheters containing 40% dimethylhydrazine (DMH) were implanted into the main pancreatic duct of New Zealand white rabbits. The catheters were constructed of silicone polycarbonate with a 4- to 10-day carcinogen release rate. Rabbits implanted with catheters containing DMH showed pancreatic ductal cell hyperplasia, metaplasia and dysplasia with periductal cell infiltration, adenosis and adenoma formation. These changes began approximately 9 to 12 weeks after implantation and persisted for 75 to 80 weeks. Specificity of the delivery system appeared to be excellent in that pathologic effects were observed only in the pancreatic and peripancreatic tissues. Moreover, these effects were probably directly related to the implanted carcinogen since similar maintained effects were not observed in control animals.

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Erzeugung von Magen- und Pankreas-Krebs beim Meerschweinchen durch Methylnitroso-harnstoff und-urethan

Cited by 58 publications

References 29 publications

Animal models of exocrine pancreatic carcinogenesis

Animal models of exocrine pancreatic carcinogenesis

Histogenesis of pancreatic carcinogenesis in the hamster: ultrastructural evidence.

Preneoplastic changes in rabbit pancreatic duct cells produced by dimethylhydrazine

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