Glial tumors are the most common tumors of the nervous system, affecting individuals at any age. Since understanding of the molecular pathologies underlying human gliomas is still very poor, the treatment and therefore prognosis of this malignancy could not yet be improved. In order to determine whether different glioblastoma-associated genomic aberrations may serve as prognostic markers in combination with histopathological findings, 20 primary glioblastoma multiforme tumors were screened by comparative genomic hybridization, and the results were compared with histopathological and clinical features. All tumors showed genomic copy aberrations detected by comparative genomic hybridization. Regional and numerical increases in chromosome 7 copy number were the most frequently seen abnormality (10/20 tumors), followed by loss of chromosome 10 (8/20). Both of these aberrations were associated with shorter surveillance time. Chromosome 12q amplification was detected in seven tumors. Loss of 17p, 1p, and 19q in combination was seen in three cases. One of them was a giant cell GBM, whereas the remaining two cases were still alive. Combination of chromosome 1p and 19q deletions was also seen in a case with long surveillance. According to the preliminary findings of this study, in addition to the EGFR gene, amplification of other genes on chromosome 7 and the deletion of PTEN gene and other cancer-related genes on chromosome 10 appeared important to the development of glioblastoma multiforme and were associated with poor prognosis, whereas the combination of chromosome 1p and 19q deletions seems to be an informative molecular marker for better prognosis. The clinical features and genetic alterations of primary and secondary glioblastoma multiforme should be compared in large series to clarify the effective prognostic markers; and further molecular analyses focused on chromosomes 7 and 10 will be very helpful for understanding the molecular mechanisms underlying the progression of glioblastoma.

HISTORY AND PRESENTATION. A case of a 3-year-old child with a right upper pulsatile eyelid swelling following a falling injury 3 months before is described. Computerized tomography (CT) and magnetic resonance imaging (MRI) revealed a fracture of the orbital roof, a basofrontal dural tear and a direct communication of the cystic cavity with the subarachnoid space. TREATMENT AND OUTCOME. The patient underwent dural repair for cerebrospinal fluid (CSF) leakage and was discharged in good health.

Object: In the present study, we compared ventricular pressures (VP) and the progression of ventricular enlargement in a new experimental neonatal hydrocephalus model, to gain an understanding of how communicating hydrocephalus progresses. Methods: Kaolin was injected into the subarachnoid space at the cranial convexity of neonatal rats. Gross examination was performed on the 3rd, 5th and 7th days, and ultrasonographic examination on the 15th day, and at the end of the 1st and 2nd months following the kaolin application. Ventricular size indexes (VSI) were calculated in the case of a large ventricular dilatation. VPs were assessed on the 15th day, and at the end of the 1st and 2nd months, with a computerized data acquisition system. Conclusions: In the 1st and 2nd months VSIs were significantly higher than in control rats on the 15th day after kaolin administration. VP on the 15th day was significantly increased compared with that in control rats. VP in the 1st month was still high, but had subsided. In the 2nd month VP was not increased over control. In the late stages, the progression of infantile communicating hydrocephalus is not related to VP levels.

This is a report of a 3-year-old boy with intracranial penetration of a nasogastric tube causing brain damage in the left frontal lobe. A computed tomography (CT) showed passage of the nasogastric tube via a fracture of the cribriform plate into the intracranial cavity. The tube was manually removed under antibiotic prophylaxis. The patient then underwent dural repair for rinorrhoea and was discharged in good health.

The 21-aminosteroids (lazaroids) are a new family of steroid compounds that inhibit lipid peroxidation reactions. They are novel antioxidant agents, which have been shown to have antiproliferative properties on cancer cells and also are thought to prevent free radical-mediated blood-brain barrier damage. In order to understand the effect of lazaroids on glioma, we tested U-83836E and U-74389G at doses ranging between 0.1–100 μM on primary cultures of gliobiastoma multiforme from three patients, rat C6 glioma cell line, and 5th subculture established from one of the patients. The effects of both compounds on cell proliferation were determined using 3-(4,5-dimethyl thiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) colorimetric assay U-83836E in the primary cultures was found to have 50% inhibitory concentrations (IC50) of 6.30, 6.75 and 6.50 μM, respectively. The IC50 value of U-74389G was calculated as 91 μM in only one of the patients. On C6 glioma cells, while the IC50 of U-83836E was 45 μM, U-74389G showed no cytotoxic effect. On the 5th subculture, U-83836E had an IC50 of 37.5 μM, but the cytotoxic effects of U-74389G was less than in that of the primary culture. In conclusion, these compounds were found to be more cytotoxic in primary culture than the cell lines and there were also differences between their members in the inhibition of cell survival.

In Fischer 344 rats, 9L tumors were implanted in the left cerebral hemisphere. Compared with control animals not operated on, rats treated with an LD10 dose of BCNU 1 hour before or 1 or 12 hours after surgery on Day 16 postimplant had an increased life span of over 200% (greater than a 6 log cell kill). Minimal effect on survival was found when BCNU was administered during surgery. On the other hand, BCNU administered 12 hours before or 24 or 72 hours after surgery did not show any additive effect of surgery on BCNU treatment. These results suggest that in a clinical setting, a bolus of BCNU administered to tumor patients within 12 hours of surgery might increase substantially the total tumor cell kill compared with surgical resection alone.

A rat brain tumor model was prepared by stereotactically implanting 4×104 cultured 9L tumor cells in the cerebral hemisphere. The tumor bearing rats exhibited weight loss after two weeks, developed neurological symptoms several days later and died 19-20 days post-implant. Tumor take was 100% and the lethal tumor weighed 279 mg. The tumors had a doubling time of 39.5 hours. Cell kinetic parameters determined by PLM curve analysis 14-16 days post-implant were: TC-19.3 hrs.; TG1-8.6 hrs.; TS-7.6 hrs.; TG2-2.9 hrs.; and TM-0.2 hrs. The growth fraction was 0.55 and the cell loss factor was 0.24. The effectiveness of combined modality therapy on this model was analyzed in terms of survival, tumor size and colony forming efficiency. BCNU administered on day 16 post-implant produced an ILS of 122% while treatment on day 10 produced an ILS of only 60%, which corresponded to a 3-3.5 log cell kill and 2-2.5 log cell kill, respectively. Microsurgical removal of tumors on days 13 and 16 post-implant produced an ILS of 28% (1 log cell kill) and 56% (2 log cell kill). Surgery performed more than 3 days before or after BCNU therapy was less effective than BCNU alone on day 16. An ILS of over 200% (< 7 log kill) was achieved when BCNU was given 1 hr. before or 1 hr. and 12 hrs. after surgery performed on day 16. BCNU was not effective when administered during the surgical procedure. Cell kinetic parameters of both perturbed and unperturbed tumor cell populations can be used to design even more effective combined modality therapy.