Spinal cord herniation: report of two cases and review of the literature.

Idiopathic herniation of the spinal cord is an extremely rare disorder which may cause progressive myelopathy. Two cases of this entity reported herein were both examined using MRI and CT myelography. The typical appearance of this disease with or without a dorsal intradural arachnoid cyst is focal ventral displacement of the mid-thoracic spinal cord, mimicking an isolated intradural spinal arachnoid cyst on MRI. CT myelography using thin slice sections is useful in the diagnosis of this disease.

Partial degradation of T-cell signal transduction molecules by contaminating granulocytes during protein extraction of splenic T cells from tumor-bearing mice.

Flavone-8-acetic acid plus recombinant human interleukin 2 is a successful antitumor therapy in mice bearing the Renca murine renal cell carcinoma. This report demonstrates that T cells, particularly CD8+ T cells, are critical for the generation of this response. Initial experiments examining T-cell signal transduction proteins demonstrated that T cells from Renca-bearing mice had undetectable levels of p56lck and zeta-chain of the T-cell receptor and that flavone-8-acetic acid and recombinant human interleukin 2 therapy could be used as a model for reversal of these alterations. However, further experimentation showed that the majority of the reduction in zeta-chain and part of the reduction in p56lck was due to degradation of these molecules during protein extraction caused by mature granulocytes contaminating the enriched T-cell population. This was not the case for nuclear c-Rel or NF kappa B p65, which remained at undetectable/reduced levels in the absence of granulocytes, confirming our previous data that transcription factor alterations exist in tumor-bearing mice. Thus, most of the reduction in zeta-chain in T cells from Renca-bearing mice is due to granulocyte contamination and emphasizes the need to use pure T-cell populations and/or sufficient amounts and types of protease inhibitors when quantitating proteins in T cells from tumor-bearing mice.

Suppression of anchorage-independent growth of human glioblastoma cell by major histocompatibility complex class I gene-transfection.

The host's immune system discriminates tumor cells from normal cells by recognizing the major histocompatibility complex (MHC) class I antigen expressed on the tumor cell membrane. However, the role of MHC class I antigen in tumor cells has not yet been clarified. In this study, the influence of MHC class I antigen expression on the tumorigenicity of a human glioblastoma cell line (KMG4) is examined. Barely detectable levels of MHC class I messenger ribonucleic acid were found to express in KMG4 cells by Northern blot analysis using mouse MHC class I (H-2Ld) and human leukocyte antigen (HLA)-B7 genes as probes. The H-2Ld gene connected at the downstream end of murine mammary tumor virus (MMTV)-promoter was cotransfected with the neomycine-resistant gene pSV2-neo into KMG4 cells, and the drug-resistant cells were selected. The KMG4 cells (KMG4-MMTV-Ld), which acquired the MHC class I gene were detected by Northern blot analysis with H-2Ld as the probe, and by immunohistochemistry using the H-2Ld-specific monoclonal antibody. Tumorigenicity, as determined by colony-forming ability in soft agar, was then compared between MHC class I-expressing KMG4-MMTV-Ld and nonexpressing control cells. The MHC class I-expressing cells were found to be deprived of colony-forming ability, indicating that MHC class I antigen could negatively influence the anchorage-independent cell growth of the human glioblastoma cell line KMG4.

Cystic pineocytoma--case report.

Pineocytoma and pineoblastoma, originating from pineal parenchyma, are rare and usually solid. An unusual case of totally cystic pineocytoma in a 37-year-old female is reported. The tumor showed neuronal differentiation and had a good outcome. Prominent calcification associated with pineocytoma and pineoblastoma is an useful finding to differentiate these from benign pineal cysts.

Nucleolar organizer regions in various human brain tumors.

Nucleolar organizer regions (NOR's) are loops of deoxyribonucleic acid (DNA) which transcribe to ribosomal ribonucleic acid (RNA) by RNA polymerase I. They possess vital significance in the ultimate synthesis of cellular proteins. A silver colloid staining technique for demonstration of NOR-associated proteins (Ag-NOR's) was applied to paraffin-embedded sections from 128 varied brain tumors and to chromosomal preparations from cultured brain-tumor cells. There was a statistically significant difference in the mean number of Ag-NOR's per nucleus between low-grade tumors (1.98/nucleus) and high-grade tumors (2.95/nucleus). It is suggested that the mean number of Ag-NOR's may represent the proliferative potential of brain tumors. Furthermore, high-grade tumors usually showed relatively large Ag-NOR's in a scattered distribution. In chromosomal preparations, the cultured cells displayed five to 12 Ag-NOR's on acrocentric chromosomes. Five of eight cell lines examined demonstrated ectopic Ag-NOR's. This simple staining technique can be easily applied to routinely processed paraffin-embedded sections and will become a useful tool for quick estimation of the proliferative potential of human brain tumors.

V-src genes in two cell lines of so-called RSV-transformed human cells are defective and inactive.

Trial of Rous sarcoma virus (RSV) induction by cell fusion with chick embryo cells (CEC) and wing web test from so-called RSV-transformed human cells, KC and RSb cells, was unsuccessful. The loss of RSV inducibility was also confirmed by DNA transfection method. Southern blot and northern blot hybridization of DNA and RNA from those cells with the v-src probe revealed that the v-src genes in those cells were defective and not expressed. On the other hand, the v-src gene in RSV-transformed mouse and rat cells was complete and transforming virus was inducible from them.

Suppression of murine leukemia virus-mediated 3Y1 cell fusion by expression of mouse MHC class I.

Rat 3Y1 fibroblasts transformed by adenovirus type 12 or its E1A gene formed syncytia by cocultivation with Friend murine leukemia virus (MuLV)-producing cells. On the other hand, parental 3Y1 cells and those derivatives induced by other tumor viruses or chemical carcinogen showed no MuLV-mediated syncytium formation [N. Momozaki et al. (1990) Arch. Virol. 115: 123-126]. The expression of major histocompatibility complex (MHC) class I mRNA and antigens was significantly reduced in these Ad12- and E1A-transformed 3Y1 cells. In contrast, other tumor virus-and chemical carcinogen-transformed 3Y1 cells expressed MHC class I almost in normal levels as did parental 3Y1 cells. Furthermore, Ad12-transformed 3Y1 cells which started to express the transfected exogenous MHC class I gene, H-2Ld, showed no more MuLV-mediated 3Y1 cell fusion. These results indicate that the expression of MHC class I on the cell membrane is closely related to the inhibition of 3Y1 cell fusion by MuLV.

Selective syncytium formation by murine leukemia virus in rat 3Y1 fibroblasts transformed by adenovirus type 12 or its E1A gene.

3Y1 rat fibroblasts transformed by adenovirus type 12 or by its E1A gene formed syncytia when cocultivated with the Friend as well as other ecotropic murine leukemia-virus-producing cells. In contrast, the parental 3Y1 cells and those transformed by other tumor viruses or by a chemical carcinogen exhibited no syncytium formation.