Tumor necrosis factor receptor type 1 (TNFR1) and c-Myc are important in signal transduction in tumor necrosis factor-a (TNF-a)-induced cytotoxicity, whereas activation of nuclear factor-kB (NF-kB) protects against TNF-a-induced apoptosis. This study investigated the expression of NF-kB, TNFR1, and c-Myc in human astrocytoma tissues by reverse transcriptase-polymerase chain reaction (PCR) and immunohistochemical analysis. TNFR1 messenger ribonucleic acid (mRNA) and c-Myc mRNA were frequently expressed in malignant astrocytomas, especially in glioblastomas, compared with low-grade astrocytomas by PCR analysis. TNFR1 and c-Myc mRNAs were barely detectable in normal brain tissues. NF-kB p50 and p65 subunit mRNAs were detected in various grades of astrocytomas, with frequent expression in malignant astrocytomas. The presence of activated NF-kB was confirmed by nuclear localization in neoplastic astrocytes as determined by immunohistochemistry. Both p50 and p65 subunits were inhomogeneously expressed in neoplastic astrocytes of glioblastoma, but only in a few scattered tumor cells in low-grade astrocytoma, and almost undetectable in normal brain tissues. These results indicate that TNFR1 and c-Myc are overexpressed in malignant astrocytomas, and this may increase the cellular sensitivity to the cytotoxic action of TNF-a. NF-kB p50 and p65 were simultaneously induced and activated in malignant astrocytomas. Our results suggest that the constitutive activation of NF-kB subunits in malignant astrocytoma, especially in glioblastoma, could be associated with the resistance to TNF-a immunotherapy, and indicates new therapeutic strategies for malignant astrocytomas.

Neuroendoscopic procedures can provide histological diagnosis, define the tumor-midbrain interrelationship, and be highly effective in treating obstructive hydrocephalus and in removing tectal tumors. This procedure may receive clinical application as a new management strategy for tectal glioma.

These results indicate that the expression of heparanase was downregulated in GBM in vivo, which rarely metastasizes to distant organs outside the central nervous system. Heparanase is not implicated in the invasiveness of GBM to surrounding healthy brain tissue in vivo.

A 13-year-old girl presented with an exceedingly rare case of primary yolk sac tumor located within the lateral ventricle, manifesting as headache, nausea, and diplopia. Magnetic resonance imaging revealed a 4-cm-diameter solid enhanced mass within the left inferior horn of the lateral ventricle. The tumor was removed subtotally via left middle temporal corticotomy. The histological and immunohistochemical diagnosis was pure yolk sac tumor. The serum alpha-fetoprotein (AFP) level was elevated at 1957.2 ng/ml and the serum beta-human chorionic gonadotropin level was 4 mIU/ml after surgery. The patient underwent radiotherapy (whole brain, 30 Gy; tumor bed, 21 Gy; whole spinal axis, 30 Gy) and chemotherapy (ifosfamide, cisplatin, etoposide). After three treatment cycles, the serum AFP level had decreased to 4.5 ng/ml. However, the tumor recurred with cerebrospinal fluid dissemination after nine cycles of chemotherapy. She died 18 months after surgery. The possibility of germ cell tumor should be considered in pediatric patients with brain tumors occurring outside the pineal or suprasellar region.

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