Hyperplastic nodules

Matsui, O., Kadoya, M., Kameyama, T., Yoshikawa, X, Aral, K., Gabata, T., Kakashima, T., Nakanuma, Y., Terada, T., Ida. M. Adenomatosis hyperplastic nodules in the cirrhotic liver differentiation from hepatocellular carcinoma with MR imaging. Radiology 1989 173 123-126... 

The immunoaffinity purification method, followed by LC/MS analysis, has also been used in other toxicological studies. When aged mice (32 weeks) were orally administered microcystin-LR at 500 pg/kg, 62% of the aged mice showed hepatic injury, whereas such changes in the liver were not found in young mice (5 weeks).Upon uptake of orally administered microcystin-LR at 500 pg/ kg, the toxin into the liver was confirmed by Frit-FAB LC/MS after the immunoaffinity purification. When microcystin-LR was intraperitoneally injected 100 times at 20 pg/kg into male ICR mice (5 weeks old, Charles River Japan, Atsugi, Japan) for 28 weeks, multiple hyperplastic nodules up to 5 mm in diameter were observed in every liver. Microcystin-LR and its cysteine conjugate were identified from the isolated mouse livers. 

Pancreas Foci of acinar cell alteration Hyperplastic nodules Atypical acinar cell nodules... 

Enomoto, K., and Farber, E. (1982). Kinetics of phenotypic maturation of remodehng of hyperplastic nodules during liver carcinogenesis. Cancer Res 42(6), 2330-2335. 

Maximal response of hyperplastic nodules of liver in female rats. (Ref. 30)... 

There is sufficient evidence for the carcinogenicity of ETU in experimental animals. When administrated in the diet, ETU induced increased incidences of thyroid follicular cell carcinomas and papillary carcinomas with some metastases and liver hyperplastic nodules in rats of both sexes. There is inadequate evidence fw the carcinogenicity of ETU in humans [42]. ETU is used primarily as an accelerator for vulcanizing polychloropene and polyacrylate rubbers. The primary routes of potential human exposure to ETU are inhalation, ingestion and dermal contact. Potential occupational exposure also occurs during the manufacture of Cumulation and rqrplication of fungicides and insecticides prepmed from ETU. Residues of the compound have been found in 28 different commercial ethylenebisdithiocarbamates products [59]. 

In the hepatic two-stage carcinogenesis test, in which DEN and 0.09% PB were used as an initiator and as a promoter, respectively, none of the mice in group I to III had hyperplastic nodules of liver, and all of mice in the positive control group (IV) had hyperplastic nodules, a total of 47... 

Groups Treatment Total No. of hyperplastic nodule No. of hyperplastic nodule per mouse % of mice with hyperplastic nodule... 

Yamamoto H, Yamashita Y, Takahashi M (1996) Development of hepatomas in hyperplastic nodules induced in the rat liver detection with superparamagnetic iron oxide-enhanced magnetic resonance imaging. Acad Radiol 3 330-335... 

It was reported that DEN-initiated enzyme-altered foci develop to form hepatocellular carcinomas [16]. However, it was reported that the vast majority of foci and hyperplastic nodules disappear after removal of the animals from the carcinogenic diet [17]. In the present series of experiment, we administered PB as a promoter continu-... 

The mechanism of action of drug induced hepatocellular tumors is quite similar to epidermal carcinogenesis. There are a series of biochemical changes such as enzyme induction that are parallel in liver and skin. Hyperplastic nodules result from promoter treatment and these nodules regress if the promoting stimulus is removed up to a critical point, after which the nodule is committed to develop into a hepatoma. The preneoplasic nodules contain enzyme altered foci for y-glutamyltranspeptidase, canalicular ATPase, glu-cose-6-phosphatase and iron deficient foci (Pitot et al., 1982). It is not clear whether or not all of the enzyme alTered foci result in hepatomas but they are certainly direct evidence of enhanced clonal growth or cell section and proliferation of presumably initiated cells. The promotional model can be modified by hormonal and dietary factors and this model has potential use for extrapolation to the human population. 

Promotion in the urinary bladder is similar to other models since the lesions go through the stages of hyperplasia, hyperplastic nodules and later form carcinomas. Cell proliferation in the urinary bladder is an essential part of the promotion process (Hicks and Chowaniec, 1977). Focal hyperplasia, dysplasia and a high number of mitotic figures in transitional cells and urothelium are common in animals fed dietary saccharin (Chowaniec and Hicks, 1979). Male and female rats administered saccharin in the drinking water consumed less water and voluntarily less diet than if saccharin was mixed in the diet, and they did not develop bladder tumors (Chowaniec and Hicks, 1979). While increased cell proliferation is an essential component of the promotional process, hyperplasia may not be a sufficient stimulus for promotion. Isoproterenol given to rats caused urothelia hyperplasia but did not enhance MNU initiated bladder tumors (Hicks, 1980). Clearly, other biochemical properties of saccharin have to be investigated since hyperplasia... 

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