Search PubMed⌕ Search

Biomedical subjects

E Kunze

Publications and source records attributed to E Kunze.

At least 91 records · Page 5Linked to original sources
PubMed1979

Relation of adenomatous hyperplasia of the gastric mucosa to carcinogenesis.

Experimental studies of stomach carcinogenesis were carried out in two series of Wistar rats (66 and 174 animals). In both series submucosal foci of adenomatous hyperplasia were observed either without atypia, or with atypia at different, gradually increasing degrees. The number of these focal lesions in the submucosa (87 in the first series) was smaller than that of focal dysplastic changes with varying grades of atypia within the mucosa. On the basis of different degrees of atypia observed in these adenomatous hyperplasias, we have to assume that a phase shifting occurs in those areas that show lower grades or absence of atypia. In the framework of carcinogenesis this kind of adenomatous hyperplasia is interpreted as an incomplete or incompletely persisting carcinogenesis. In analogy to our experimental findings we found identical lesions in three human cases where different grades of atypia were observed distant from the primary stomach cancer. These results are discussed with reference to the animal experiments and to the literature.

Adenoma↗
PubMed1976

Stages of transformation in the development of N-butyl-N-(4-hydroxybutyl)-nitrosamine-induced transitional cell carcinomas in the urinary bladder of rats.

The histogenesis of papillary and nonpapillary transitional cell carcinomas were studied morphologically and autoradiographically in 177 female Wistar rats after oral application of N-butyl-N-(4-hydroxybutyl)-nitrosamine with varying exposure and induction times. By far the largest proportion of carcinomas developed by a malignant transformation of preexisting papillomas or their precursors, the papillary hyperplasias. The transition into a focally malignant growth did not take place abruptly, but occurred stepwise through different successive stages of transformation, each having its own distinct morphological character. The first stage consisted of a focal, sharpely defined cellular atypia. In a further stage carcinomata in situ developed out of the atypical foci and progressed finally in a last stage of transformation into a circumscript infiltrative growth. The successive development of each stage occurred independent of any further carcinogen application after transformation was initiated at the molecular level. The number of papillomas with transformation stages increased with a lengthening of the exposure and induction time. 74.4% of all the registered papillomas had been transformed. Consequently papillomas must be considered potentially highly malignant. The 3H-TdR index was 4.2 times higher in atypical urothelial areas (7.6%) and 7.5 times higher in carcinomata in situ (14.3%) than in the surrounding papillomatous structures which appeared light microscopically benign. The latter demonstrated a rather constant 3H-TdR index, whether they bordered on atypical foci (1.8%) or carcinomata in situ (1.9%). The length of exposure and induction time exercised no significant influence on the degree of proliferative activity. The development of transitional cell carcinomas from a primary carcinoma in situ (intraurothelial carcinoma) played a much less significant role.

Animals↗
PubMed1975

Focal loss of alkaline phosphatase and increase of proliferation in preneoplastic areas of the rat urothelium after administration of n-butyl-n-(4-hydroxybutyl)-nitrosamine and n-[4-(5-nitro-2-furyl)-2-thiazolyl] formamide.

Development of tumours of the urinarY bladder was studied in 59 Male and female Sprague-Dawley and Wistar rats with combined enzyme-histochemical and autoradiographic methods after oral application of n-butyl-n-(4-hydroxybutyl)-nitrosamine (BBN) and n-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT). as the first carcinogenic lesion detectable by light-microscopy a focal, sharply defined irreversible loss of alkaline phosphatase activity was consistently demonstrated in the urothelium, which appeared normal histologically and cytologically. In about 2/3 of the cases, NADH-diaphorase activity was markedly reduced in identical regions. The enzyme-deficient areas are to be considered as preneoplastic, because papillomas and carcinomas developed from them through different stages of hyperplasia. As a rule, these also were characterized by total loss of alkaline phosphatase activity and attenuation of the NADH-diaphorase in all parts or circumscribed areas. Autoradiographically 3H-thymidine-labelling index revealed a 43.2-fold (BBN) and 22.6-fold (FANFT) increase, respectively, in the enzyme-deficient areas, as compared with the surrounding emzyme-containing urothelium. After 54 hrs of continous labelling, there was a mean 3H-thymidine-labelling index of 54.9% in the enzyme-negative regions. The physiological mode of regeneration was no longer maintained in the areas of enzyme deficiency as there was an increased proliferation of suprabasal cells. Areas of papillomas that showed a marked attention of NADH-diaphorase had a 3H-thymidine-labelling index 4.5 (BBN) and 3.1 (FANFT) greater than the surrounding areas with preserved enzyme activity. Since loss of alkaline phosphatase activity occurs regulary and consistently after application of carcinogens with chemically different structures it appears to indicate the initial phase of tumor development in the urinary bladder of the rat.

Administration, Oral↗