Intracranial endodermal sinus tumors associated with growth hormone replacement therapy in a girl.

The primary intracranial endodermal sinus tumor (EST) is regarded as a rare histological subtype that is often associated with components of other germ cell tumors, and there are no reports on the onset of intracranial ESTs after growth hormone (GH) replacement therapy. The authors report an extremely rare case of pure primary EST associated with GH replacement therapy. A 15-year-old girl with GH deficiency experienced headache, nausea, and vomiting after GH replacement therapy for a 17-month period. Magnetic resonance imaging showed 2 tumor masses located in the pineal region and frontal horn of the right lateral ventricle, respectively. Before surgery, the authors administered 1 cycle of neoadjuvant chemotherapy, which shrank the tumor and facilitated surgical intervention. The larger mass located in the pineal region was removed via a right occipital transtentorial approach, and postoperative histopathological analysis revealed a pure EST. While there is a clear association between the initiation of GH replacement therapy and the development of the EST in this case, the causal effect cannot be specified. Nevertheless, this case demonstrates that GH replacement therapy must be used cautiously.

Intracranial metastases of induced lung carcinomas in rats.

Through 25 weekly subcutaneous injections of dipentylnitrosamine (DPNA), metastasizing lung carcinomas were induced in 56 Hann: Wistar rats. Among them nine animals had intracranial metastases. Four metastases were localized in the pituitary, three in the choroid plexus of the IIIrd ventricle, one in the choroid plexus of the IVth ventricle, and one in the brain-stem. Thus, the preferential sites of intracranial metastasis were the choroid plexus of the ventricles and the pituitary. No metastatic spread was found in the cerebral hemisphere. Five of the metastatic tumours resembled the primary pulmonary adenocarcinoma. In the other four, the primary was an adenosquamous carcinoma but only adenocarcinomatous components were present in the metastasis.

The effect of hyperosmotic blood-brain barrier disruption on blood-to-tissue transport in ENU-induced gliomas.

Hyperosmotic blood-brain barrier disruption transiently increases the rate of blood-to-tissue transport of water-soluble compounds to normal brain and has been used in brain tumor patients to increase the delivery of chemotherapeutic drugs. This method remains controversial; debate concerns the extent to which it increases drug delivery to brain tumors. Ethylnitrosourea (ENU)-induced gliomas in rats have the lowest rate of blood-to-tissue transfer of the water-soluble compound alpha-aminoisobutyric acid of all experimental brain tumors studied to date. To gain further understanding about the effects of hyperosmotic blood-brain barrier disruption in brain tumors, we measured the unidirectional blood-to-tissue transfer constant of alpha-aminoisobutyric acid in ENU-induced brain tumors in rats after hyperosmotic disruption. Hyperosmotic blood-brain barrier disruption with 1.6 osmolar mannitol resulted in an averaged whole-tumor transfer constant of 0.013 +/- 0.003 (standard error) mL/(g/min), compared to a transfer constant of 0.007 +/- 0.002 mL/(g/min) for ENU-induced gliomas in the contralateral undisrupted hemisphere, a difference that was not significant. In contrast, hyperosmotic blood-brain barrier disruption produced a large and significant increase in the transfer constant of alpha-aminoisobutyric acid in tumor-free cortex (from 0.002 +/- 0.001 to 0.05 +/- 0.011 mL/[g/min]) and in tumor-free corpus callosum (from 0.001 +/- 0.003 to 0.017 +/- 0.005 mL/[g/min]). Hyperosmotic blood-brain barrier disruption does not appear to be an efficient method with which to increase the rate of delivery of water-soluble drugs to brain tumors but does result in a significant increase in the delivery rate of these drugs to normal brain tissue.

[Experimental brain tumors produced transplacentally by ethylnitrosourea (IV): ultrastructure studied by using transmission and scanning electron microscope (author's transl)].

The fine structure of rat gliomas induced transplacentally with a single i.p. dose of 50 mg/kg of Ethylnitrosourea has been studied by using transmission and scanning electron microscope. The subependymal matrix layers of the fetus which was affected by ENU have showed irregular and rough arrangements with expanded extracellular spaces as compared with that of control rats. The cells of subependymal layer seemed to form the microtumor. A so-called "microtumor", which was found in a 8 week old, has been composed of small round cells. The fine structures of these cells have showed the characteristics in primitive oligodendroglioma. The characteristics of the fine structure of astrocytoma cells was identified by both TEM and SEM. The fine structure of subependymal glioma cells was often pleomorphic. These gliomas contained a mixture of primitive oligodendrocytes and ependymal cells together with anaplastic glial cells. With increasing size, the glioma has become more pleomorphic with a mixture of neoplastic oligodendrocytes, astrocytes and ependymal cells, and ependymoma like cells have showed neither cilia nor junctional complex. Abnormal vascular structure in the tumor has been reconfirmed by injection replica scanning electron microscope method. The fine structure of the separated single tumor cell surface was also studied by scanning electron microscope. The differences of the cells surface between that of astrocytoma cell and oligodendroglioma cells were clearly noticed.