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At least 343 records · Page 19Linked to original sources
PubMed1983

Growth enhancement of prolactin-sensitive mammary tumor by periaqueductal gray stimulation.

The weight of prolactin-insensitive and prolactin-sensitive tumors implanted in female rats was measured upon their sacrifice. The group that received periaqueductal gray (PAG) stimulation subsequent to prolactin-sensitive tumor implantation had statistically higher incidence of enhanced tumor growth than non-PAG stimulated control group (P less than .001). There was no statistically significant difference seen in the tumor growth in rats implanted with prolactin insensitive tumor, whether or not they had PAG stimulation. These results suggest that enhanced tumor growth with PAG stimulation may be related to prolactin release, previously reported to occur with beta-endorphin and opiate administration.

Animals↗
PubMed1983

Thyroid modifications in male and female rats treated with the hepatocarcinogen beta-blocker ZAMI 1305.

The morphology of the thyroid gland from Wistar rats treated for 6 months with the beta-blocker DL-1-(2-nitro-5-methyl-phenoxy)-3-tert-butyl-amino-propan-2-ol (ZAMI 1305), a potent sex-dependent hepatocarcinogen, was studied. A significant high incidence of cases with thyroid hyperplasia is found among female rats, the only sex susceptible to the carcinogenic effect of ZAMI 1305. Thyroid hyperplasia is instead much less evident in male rats. In female rats the increase in the relative thyroid weight is directly related to the gravity of the predominant liver lesion (clear cell foci, neoplastic nodules, hepatocellular carcinomas). The results suggest an influence of the preneoplastic and neoplastic liver on thyroid gland.

Adrenergic beta-Antagonists↗
PubMed1978

Expression of RNA of an endogenous replication-defective retrovirus in rat mammary adenocarcinomas induced by 7,12-dimethylbenz[a]anthracene.

An investigation into the possible relationship between chemical carcinogen induction of rat mammary tumors and the expression of an endogenous retroviral genome was initiated. Mammary tumors were induced in female SD rats with 7,12-dimethylbenz[a]anthracene (DMBA). Tumors, identified histologically as mammary adenocarcinomas, were analyzed for RNA of a replication-defective endogenous retrovirus or RNA of a helper-independent endogenous type C virus. Expression of RNA of the replication-defective virus was detected in mammary tumors weighing 0.2--2.0 g. Larger tumors, for which histologic examination revealed proportionally more fibroblastic tissue than epithelial cells, did not contain comparable concentrations of this viral RNA. RNA homologous to a helper-independent rat type C retrovirus was not detected in tumors of any size. A cell line was established from a primary DMBA-induced mammary adenocarcinoma and appeared similar to the small mammary tumors with respect to endogenous type C viral RNA expression. We discuss possible implications of the expression of endogenous replication-defective viruses for use as markers for the effects of chemical carcinogens.

9,10-Dimethyl-1,2-benzanthracene↗