Persistence of gamma-glutamyl transpeptidase-positive foci during hamster buccal pouch carcinogenesis.

This study describes the kinetics of induction and growth as well as the property of persistence of gamma-glutamyl transpeptidase (GGT)-stained cell populations (GGT-positive foci) induced in hamster buccal pouch epithelium by a 5-week regimen of biweekly topical applications of 7, 12-dimethylbenz(a)anthracene (DMBA). During such treatment, and at various times thereafter, GGT-positive foci were detected and quantitated in whole mounts of pouch epithelium stained histochemically for GGT activity. A comparison of GGT-positive foci at the completion of the DMBA regimen and at 10 weeks thereafter revealed no significant decrease in either the number or the size of the foci. During the same 10-week posttreatment period, several dysplastic and occasional neoplastic lesions, some of which displayed patchy GGT activity, developed in the pouch epithelium of DMBA-treated animals. Twenty-two hamsters were sacrificed between the 15th and 34th weeks of the experiment for histological and histochemical study. Fifteen of these animals had grossly visible epithelial neoplasms, and the 11 which could be evaluated using the whole-mount technique had a few residual GGT-positive foci. None of the 33 control animals evaluated at various times during the experiment developed any gross, microscopic, or GGT-positive lesions. These data indicate that, following a 5-week regimen of DMBA applications, an appreciable number of GGT-positive foci persist throughout the latent period, during which dysplastic and neoplastic buccal pouch lesions develop. The expression of GGT activity in early hyperplastic and dysplastic lesions and its persistence in several animals provide additional support for the hypothesis that GGT-positive foci may represent sites of subsequent neoplastic development.

Nodular regenerative hyperplasia of the liver associated with macroglobulinemia. A clue to the pathogenesis.

Nodular regenerative hyperplasia of the liver is an infrequent condition characterized by transformation of the hepatic parenchyma into nodules with only mild fibrosis. Little is known about the etiology except that there is usually an underlying chronic disease, such as Felty's syndrome, which antedates the development of clinical liver disease. It is poorly understood how the associated diseases contribute to the pathogenesis of nodular regenerative hyperplasia. Presented are four cases of nodular regenerative hyperplasia in which macroglobulinemia was also present. This new association suggests to us a hypothesis for the pathogenesis of nodular regenerative hyperplasia. Histologic examination of the livers in these and other cases of nodular regenerative hyperplasia reveals widespread obliteration of the small portal veins. Postmortem angiography of one liver in the present series demonstrated that the nodules were well perfused and that the atrophic areas were poorly perfused with portal blood. This supports the view that atrophy of lobules results from a lack of portal blood supply and that nodules develop from lobules well supplied with portal blood. In each of the clinical conditions associated with nodular regenerative hyperplasia, including macroglobulinemia, inflammatory or thrombotic vascular lesions are found in many organs. Therefore, nodular regenerative hyperplasia may be the hepatic expression of a more widespread vascular disease.

Interhemispheric cyst of neuroepithelial origin in association with partial agenesis of the corpus callosum. Case report and review of the literature.

The authors report an adult patient with a symptomatic interhemispheric cyst demonstrated by computerized tomography (CT), angiography, and at surgery. Choroid plexus epithelium was identified arising from the inner aspect of the cyst wall. Partial agenesis of the corpus callosum is postulated on the basis of the CT findings and the presence of choroid plexus in the interhemispheric cyst.

Thorotrast-induced meningioma. Case report.

The authors report an adult patient with a symptomatic intracranial meningioma that was demonstrated by computerized tomography, angiography, and at surgery. The meningioma had occurred at a site where 19 years previously thorium dioxide had been injected into an abscess cavity. Pathological examination revealed the presence of thorium granules within the meningioma.