Vaginal fluid 6-phosphogluconic dehydrogenase activity in relation to uterine malignancy.
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Adult↗
Biomedical subjects
D S Longnecker
Publications and source records attributed to D S Longnecker.
Effects of sex steroid hormones on pancreatic cancer in the rat.
The incidence of spontaneous and induced neoplasms of the exocrine pancreas in rats is higher in males than in females. Castration, ovariectomy, and hormone replacement with estradiol and testosterone have been shown to influence the growth of carcinogen-induced preneoplastic foci in the azaserine-rat model of pancreatic carcinogenesis. Similar hormonal treatments have also influenced the growth of an azaserine-induced poorly differentiated acinar cell carcinoma that can be transplanted syngeneically in Lewis rats. The effect on growth of preneoplastic lesions and carcinomas is similar. The preneoplastic lesions and transplanted tumors grow faster in intact male rats than in castrated rats, and the growth of the lesions and tumors is inhibited by estrogen treatment. It appears that testosterone supports the growth of preneoplastic foci and carcinomas, whereas estrogen inhibits such growth. The mechanism is unknown and may be direct, or an indirect effect may be mediated through a peptide hormone. Tamoxifen treatment did not significantly influence the growth of the transplanted carcinomas in the rat model.
Animals↗
Binding of [14C] azaserine to DNA and protein in the rat and hamster.
The binding of [14C] azaserine or its metabolites to DNA and protein in the organs of rats and hamsters was determined at various time after treatment with [14C] azaserine. The specific activity of 14C labelling of DNA and protein was determined. Rat liver DNA and protein were most extensively labelled at 90 min post-injection, but by 24 h the specific activity decreased to the levels found in pancreas and kidney. Thymus contained negligible amounts of radioactivity at all time-points. DNA and protein from hamster pancreas contained more label than did DNA and protein from rat pancreas. The results suggest that factors other than DNA binding play a role in determining the species and organ specificity of azaserine.
Animals↗
Recent results in animal models of pancreatic carcinoma: histogenesis of tumors.
Animal models of carcinoma of the pancreas provide new information regarding the pathways for histogenesis of the tumors. Four models, induced by chemical carcinogens or transgenic methods, are reviewed briefly from this perspective. Recent reports indicate that carcinomas with a ductal phenotype can arise from transformed acinar cells in rodents. A transgenic mouse model provides evidence that anaplastic carcinomas and islet cell tumors may arise from primitive cells that express the elastase gene, yet retain the potential to differentiate as islet cells. In a nitrosamine-induced hamster model, ductal carcinomas appear to arise directly from ductal cells. Carcinomas in this model contained mutations in the c-K-ras oncogene that are similar to those reported in about 75 percent of human pancreatic carcinomas, whereas acinar cell carcinomas of rats lacked this mutation. The histologic type of a carcinoma may reflect the cell of origin, but this statement is not always true. Therefore, classification of tumors on the basis of phenotype rather than on the presumed cell of origin is recommended. Among the animal models, the carcinomas in hamster pancreas rank as most similar to human pancreatic ductal adenocarcinomas in regard to the phenotype of the tumors and the prevalence of the c-K-ras mutation.
Animals↗
Trial of a simplified vaginal fluid 6-phosphogluconic dehydrogenase assay method in screening for cancer.
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Body Fluids↗
Oxidative and conjugative metabolism of xenobiotics by isolated rat and hamster acinar cells.
Isolated rat and hamster acinar cell suspensions possess the ability to carry out the cytochrome P-450-dependent O-deethylation of 7-ethoxycoumarin, 2-,3-, and 4-hydroxylation of biphenyl and 3-hydroxylation of benzo(a)pyrene. Rat and hamster acinar cells isolated from 5,6-benzoflavone-pretreated animals oxidize all three substrates at measurable rates. These rates are considerably lower (16-210-fold in the rat and 290-2670-fold in the hamster) than those in incubations using hepatocytes isolated from 5,6-benzoflavone-pretreated animals. Hydroxylation of biphenyl at the 2-, 3-, and 4-positions proceeds at similar rates in rat acinar cells. The rate of 3-hydroxybiphenyl formation is barely detectable in hamster acinar cells where the rates of 2- and 4-hydroxybiphenyl formation are slower than in the rat. No detectable oxidation products of 7-ethoxycoumarin, biphenyl, or benzo(a)pyrene are found with acinar cells of either species isolated from untreated and phenobarbital-pretreated animals. The O-deethylation of 7-ethoxycoumarin in rat and hamster acinar cells is decreased in the presence of inhibitors of the cytochrome P-450-dependent monooxygenase system, 7,8-benzoflavone being much more effective than metyrapone. The deethylation product of 7-ethoxycoumarin, 7-hydroxycoumarin, is conjugated with sulfate and glucuronic acid moieties at appreciable rates by acinar cells isolated from both rat and hamster. Pretreatment of rats and hamsters with either 5,6-benzoflavone or phenobarbital has little effect on the rates of conjugation in isolated acinar cell preparations.
Animals↗
Observations on the etiology and pathogenesis of intraductal papillary-mucinous neoplasms of the pancreas.
During the last two decades, intraductal papillary-mucinous neoplasms have been recognised as a group that should be distinguished from ductal adenocarcinomas. The literature for these tumors is confusing with the use of many different terms such as mucinous duct ectasia and, sometimes, there is a failure to distinguish them from mucinous cystic tumors. The recognition and apparently increasing incidence of these neoplasms is perhaps entirely attributable to improved diagnostic and imaging methods such as endoscopic retrograde pancreatography and computerized tomography. Experimental, molecular, and epidemiologic data suggest that the etiology of IPMN overlaps that of solid ductal adenocarcinomas.
Adenocarcinoma, Mucinous↗