Noshuyo byori = Brain tumor pathology最新文献

Using PCR-SSCP and immunohistochemical analyses, mutations of the p53 tumor suppressor gene were examined in 5 cases of primary malignant lymphoma of the brain (diffuse large cell type). By PCR-SSCP and nucleotide analyses, p53 gene mutations were seen in 2 of the 5 cases. The mutation in one case was a missense G: C-T:A transversion at codon 176 (TGC-TTC; Cys-Phe) which was located in the highly conserved domains and adjoined a previously proposed hot spot codon (codon 175) in various tumors. p53 immunoreactivity was also shown in this case. The mutation in another case was a nonsense G:C-A:T transition at codon 52 (TGG-TGA; Trp-stop codon) leading to a truncated p53 peptide. Thus, these mutations may have actually given rise to serious structural and functional alterations of the p53 protein. These findings suggested that the p53 gene mutation was related with oncogenesis in the primary malignant lymphoma of the brain.

It has recently been shown that the bcl-2 gene is involved in the growth and development of certain tumors by suppressing apoptosis. To explore the possible involvement of the Bcl-2 protein in gliomas, three human glioma cell lines (T98G, A172, and U251) were examined for the presence of this protein. It could be documented by confocal laser microscopy that the Bcl-2 protein was localized mainly in mitochondria and nuclear membrane of T98G cells. Flow cytometric analysis revealed that 71-87% of the cultured glioma cells expressed the Bcl-2 protein. Treatment of U251 cells with ACNU for 24 h induced increased Bcl-2 protein expression; induction was dose dependent. Exposure of T98G and A172 cells to ACNU did not affect their Bcl-2 protein levels. Southern blot analysis revealed no chromosomal translocation in the cells studied. These findings suggest that Bcl-2 protein overexpression in glioma cells may partly contribute to tumor growth and tolerance to chemotherapeutic agents.

This report is to demonstrate that specimen pretreated with tannic acid before osmification permits the ultrastructural identification of multilamellar phospholipids in 23 of the 30 meningiomas. The phospholipids very often had a fingerprint-like appearance, and were found within the cytoplasm of meningioma cells, among the plasma membranes and in the extracellular matrices. A preferential ultrastructural localization of multilamellar phospholipids to the glycogen-rich area within the cytoplasm was seen in 5 cases. They were intermingled with glycogen granules, or the latter were precipitated on the phospholipids. It is suggested that glycogen may serve as a source of energy for precursors of phospholipid synthesis in meningioma cells.

Camptothecin-11 (CPT-11) is a new derivation of camptothecin, a plant alkaloid antitumor agent. Previous studies indicated that antitumor activity of CPT-11 was mediated through interaction of the drugs with its target enzyme, DNA topoisomerase I (topo I). In this study, we studied the relation between sensitivity to CPT-11 and topo I activity of glioma cells. Furthermore, we established CPT-11 resistant cell lines in order to elucidate potential mechanisms of drug resistance. A clear correlation between the sensitivities to CPT-11 and topo I activities in surgical glioma specimens was demonstrated. Activities of topo I in CPT-11 sensitive group (IC50 values for CPT-11; < 50 micrograms/ml) tended to be higher than those in CPT-11 resistant group (IC50 values; > or = 50). Topo I activity may serve as a novel marker to predict the sensitivity of gliomas to topo inhibitors. CPT-11 resistance cell lines (T98G/CPT-11 and C6) respectively exhibit a 5.4- and 7.3-fold increase in resistance to CPT-11. No differences in topo I activity and intracellular accumulation of CPT-11 were observed between parent and CPT-11 resistant lines. On the other hand, topo I from T98G/CPT-11 and C6/CPT-11 cells were at least 4- and 2-fold resistant to the inhibitory effect of the CPT-11 on the relaxation activity of topo I in comparison with their parent lines. This enzymological difference may be responsible for the resistance to CPT-11.

Thirty-three children harboring brain stem glioma were treated at Nagoya University, Department of Neurosurgery during in the 16-year period from 1976 to 1991. Infantile brain stem glioma is so rare and we have only two cases (6.1%) of all 33 cases. This paper reported clinico-pathological investigation of infantile brain stem glioma. Case 1: Patient 1 was born after 38 weeks gestation, and he showed no mental nor physical retardation. His parents noticed his torticollis at 4 months of age. MRI showed exophytic abnormal enhanced mass behind the medulla oblongata. The mass was partially removed by craniectomy, and its pathological study revealed astrocytoma grade II. Since 3 months after the operation, torticollis had been gradually improved and disappeared completely 6 months later. Case 2: Patient 2 born after 41 weeks gestation, two cafe-au-lait spots were seen on the abdominal skin and hemangiomas were seen on the left shoulder and femoral area. For the initial symptoms, left oculomotor palsy was recognized at 2 months old. CT showed intrinsic enhanced abnormal mass in the mid brain up to the pons and then it invaded into right frontal lobe soon. Open biopsy was performed and the pathological examination revealed astrocytoma grade III. After IAR therapy (Interferon-beta 140 x 10(4), ACNU 20 mg x 2. Radiation; whole brain 40.8 Gy, focal 9 Gy), although left oculomotor palsy was improved temporarily, the tumor enlarged invasively and the patient died at 11 months old.

Monoclonal antibody (MCA) G-22 reacts selectively with human glioblastoma. Whole immunoglobulin G (IgG) and the F(ab')2 fragment of G-22 were labeled with indium-111, and injected into athymic nude mice bearing xenografts of a human glioblastoma cell line (U-251-MG). Radiolabeled G-22 retained its antigen-binding activity allowing clear visualization of transplanted tumors. Although the 111In-labeled F(ab')2 fragment had a higher tumor-to-tissue ratio than whole IgG, tumor concentration of 111In-labeled G-22 MCA was higher in the latter and it provided much better images for a longer time when visualized by gamma-scintigraphy. These results suggest that 111In-labeled G-22 may be a useful agent for brain tumor imaging.

A case of solitary leptomeningeal extracerebral glioma is reported. A 75-year-old man was admitted to our hospital because of headache and right hemiparesis. CT scan and carotid angiography revealed a tumor in the left convexity. At operation, the tumor was located between the dura mater and the arachnoid membrane and adhered to the brain surface only in a limited area. Histological study including immunostain and electron microscopy showed the tumor as anaplastic oligo-astrocytoma. We speculate that our case may originate from a heterotopic glial nest in the dural border cell layer of dura mater. This explanation seems likely because the tumor was located mostly in the subdural space.

The authors present four autopsy cases of primary CNS lymphoma. In each case death was due to different causes. Case 1 was a typical cerebral herniation. Case 2 was brain stem lymphoma diffusely spread after leukemoid reaction. Patient 3 died because of cerebral and brain stem degeneration without evidence of lymphoma cells. Case 4 was unique and the cause of death was not even established by autopsy (definite unknown death case). Taking together these facts, the authors consider the patho-physiology of CNS lymphoma and indicate that herniation is not frequent after various therapeutic treatments.

This report deals with the operative and histopathological findings in 14 meningiomas of 13 patients who were subjected to preoperative embolization. This procedure facilitated the removal of 11 of the 14 tumors and minimized blood loss. In the majority of cases the following histopathological findings were documented: 1) Presence of emboli and thrombi within the tumor and/or dural vessels; 2) associated vascular thrombosis; 3) ischemic changes of the tumor cells; 4) pathologic evidence of infarction with or without inflammatory response, and 5) diffuse or nodular necrosis and surviving tumor cell clusters with an island-like appearance. In two tumors in which the histological diagnosis of typical meningioma was difficult, large necrotic areas comprising over two-thirds of the whole specimens were seen with the naked eye.

This report presents seven cases of intravascular malignant lymphomatosis (IML). The patients exhibited clinical signs and symptoms of multiple cerebral infarctions and polyradiculopathy, but in each case the diagnosis of IML was only established by postmortem examination. The autopsies revealed that almost every organ was involved and that there were atypical cells which had proliferated intravascularly. This was especially remarkable in the central nervous system. Extravascular extension of the tumor cells was rarely observed. It was documented by immunohistochemical studies that the abnormal cells were B cell lymphoma cells with a high proliferative capacity. Factor VIII, an endothelial cell-related antigen, was detected in the cytoplasm of the tumor cells of two cases (28%), but this finding was considered to represent a non-specific absorption of factor VIII from the thrombi.