Telomerase expression in intracranial tumours: prognostic potential for malignant gliomas and meningiomas.
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AIM: To evaluate the diagnostic value of telomerase expression in intracranial tumours. METHODS: 98 surgical specimens from different neoplasms were analysed by the telomeric repeat amplification protocol (TRAP) and the presence of telomerase compared with the histological diagnosis and the proliferation index. RESULTS: A high degree of positivity for telomerase activity was found in glioblastomas and atypical/anaplastic meningiomas. Telomerase activity was poorly detected in anaplastic astrocytomas. CONCLUSIONS: The TRAP assay seems to be a valuable index for identifying meningeal tumours with aggressive behaviour. (+info)
Clinical value of 24-hour delayed imaging in somatostatin receptor scintigraphy for meningioma.
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Somatostatin receptor scintigraphy (SRS) using 111In-octreotide has proven useful in patients suspected of having meningiomas. Delayed imaging is regularly performed up to 24 h postinjection. However, this procedure is time consuming and expensive. Therefore, we investigated whether 24-h imaging may be omitted in these patients. METHODS: After clinical examination and standard MRI, 71 patients were suspected of having 92 meningioma lesions. Before surgery, all patients underwent SRS after intravenous injection of 200 MBq (5.4 mCi) 111In-octreotide. Planar whole-body images were obtained at 10 min and 1, 4 and 24 h, and SPECT was performed at 4 and 24 h. Results of SRS in all lesions were evaluated with respect to histology and time of image acquisition. RESULTS: SRS yielded 58 true-positive, 20 true-negative and 14 false-negative results, with the false-negatives all less than 5 mL (2.3+/-2.1 mL) in volume. In 52 of 58 true-positive lesions (89.7%), diagnosis could be established by 4-h imaging without further information by 24-h imaging. In 10 of the 52 lesions, SPECT was necessary to confirm planar findings. Imaging at 24 h was necessary in only 6 of 58 true-positive lesions (10.3%): 3 patients who had intracranial relapse of meningioma (volume < 5 mL) and 3 who had spinal meningioma. Thus, a diagnosis of intracranial meningioma could be established in 52 of 55 lesions (95%) using a 4-h imaging protocol. CONCLUSION: With a 4-h acquisition protocol that includes SPECT imaging, SRS yields sufficient information in patients suspected of having intracranial meningiomas. Delayed imaging at 24 h is recommended only for patients who have small meningiomas (volume < 5 mL), spinal localizations or negative SRS at 4 h. (+info)
Tentorial meningioma encroaching the transverse sinuses and sigmoid sinus junction area associated with dural arteriovenous fistulous malformation: a case report.
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A 62-year-old woman was evaluated for tinnitis and headache. Magnetic resonance imaging and angiography revealed the coexistence of a tentorial tumor encroaching the junction of the right transverse-sigmoid sinuses, and dural arteriovenous fistulous malformation (AVFM) of the right transverse sinus. AVFM was not manipulated at all during the surgery. The pathology was fibroblastic meningioma. Postoperatively, the dural AVFM completely disappeared on follow-up angiography. The fistulas were occluded also after surgery, even though there was no manipulation of the AVFM. It is suggested that the right dominant transverse-sigmoid sinuses are partially occluded by tentorial meningioma, developing the dural arteriovenous fistula of the right transverse sinus. An acquired origin of the dural AVFM was suggested in this case. (+info)
Long-term magnetic resonance imaging follow-up of asymptomatic sellar tumors. -- their natural history and surgical indications.
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Serial magnetic resonance (MR) images and clinical symptoms were analyzed in 23 patients with sellar lesions, who were followed up without initial therapy for mass reduction to evaluate their natural history and surgical indication for these lesions. The patients were aged 17 to 78 years (mean 47.3 years) and the follow-up period was 1.5 to 11.6 years (mean 5.1 years). Lesions were divided into two types based on the MR imaging findings, regardless of their histological types. Type C was cystic with or without enhancement of the smooth and thin wall. Type S had enhanced solid components. Ten patients had Type C tumors. Three patients presented with sudden onset of headache. The tumor size spontaneously decreased with intensity change, indicating pituitary apoplexy as the trigger of the onset and intensity change. Four patients presented with the visual disturbance which improved with the reduction of tumor size, but three patients deteriorated and required surgery. The operation revealed Rathke's cleft cyst. The remaining three patients were found incidentally and have been asymptomatic without MR imaging changes. Thirteen patients had Type S tumors. Six patients of nine with 14 mm or larger tumors developed symptomatic tumor enlargement over the follow-up period of 1.2 to 8.6 years (mean 4.9 years) and required treatment. The remainder showed no change. Type C tumors frequently shrink or even disappear spontaneously. We can justify conservative follow-up of Type C tumors in patients with no or only transient symptoms. Type S tumors, larger than 14 mm in size, need closer observation or treatment because they often enlarge and become symptomatic. (+info)
Regional treatment of epidermal growth factor receptor vIII-expressing neoplastic meningitis with a single-chain immunotoxin, MR-1.
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The incidence of neoplastic meningitis is on the rise. Neoplastic meningitis can result from a direct seeding of the neuraxis by primary brain tumors or by hematogeneous spread of systemic solid tumors. A frequent genetic alteration in primary brain tumors such as gliomas is an in-frame deletion in the epidermal growth factor receptor (EGFR) gene EGFRvIII, which brings together what were normally distant polypeptide sequences in the intact receptor. A novel glycine is formed at the fusion junction, resulting in a unique and tumor-specific target. By using phage display, we have isolated a single-chain antibody specific for the EGFRvIII mutation and expressed it with a modified form of the Pseudomonas exotoxin to form the immunotoxin MR1scFvPE38KDEL (MR-1). The multiple dose toxicity and therapeutic efficacy of MR-1 immunotoxin were tested in an athymic rat model of neoplastic meningitis. The maximally tolerated doses in non-tumor-bearing rats were three doses of 3 microg each. For therapeutic studies, the target was a neoplastic meningitis induced by intrathecal inoculation of the EGFRvIII-expressing human glioma U87MG.deltaEGFR. A dose escalation study compared the survival of three equal doses of 1, 2, and 3 microg of MR-1 immunotoxin with saline or 3 microg of the control immunotoxin specific for the interleukin 2 receptor, anti-Tac. All animals treated with three doses of saline or 3 microg of anti-Tac died, with median survival of 7 and 10 days, respectively. There were 75% (six of eight) long-term survivors in the group treated with three doses of 1 microg and 57% (four of seven) long-term survivors in the groups treated with three doses of either 2 or 3 microg of MR-1 immunotoxin. None of the MR-1 immunotoxin-treated groups reached median survival by the termination of the study at 53 days. Therefore, median survival was estimated to be >53 days, resulting in an estimated increase in median survival of >657% compared with saline and 430% versus anti-Tac. Compartmental therapy with three doses of 2 microg of MR-1 immunotoxin is effective in the treatment of EGFRvIII-expressing neoplastic meningitis. This dose was found to have no clinical or histopathological effects on non-tumor-bearing animals. MR-1 immunotoxin is, therefore, considered specific and safe within its therapeutic window. Phase I clinical trials for tumors invading the intrathecal space that express the EGFRvIII target should be initiated. (+info)
Comparison of CSF cytology and spinal magnetic resonance imaging in the detection of leptomeningeal disease in pediatric medulloblastoma or primitive neuroectodermal tumor.
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PURPOSE: Leptomeningeal disease (LMD) significantly affects the prognosis and treatment of pediatric patients with medulloblastoma or primitive neuroectodermal tumor (PNET). Examination of CSF for malignant cells, detection of LMD on spinal magnetic resonance imaging (MRI), or both are the methods routinely used to diagnose LMD. A recent study suggested 100% correlation between CSF and MRI findings in children with medulloblastoma. To determine the validity of this hypothesis, we compared the rate of detection of LMD between concurrent lumbar CSF cytology and spinal MRI performed at diagnosis in patients with medulloblastoma or PNET. PATIENTS AND METHODS: As a part of diagnostic staging, 106 consecutive patients newly diagnosed with medulloblastoma or PNET were evaluated with concurrent lumbar CSF cytology and spinal MRI. CSF cytology was examined for the presence of malignant cells and spinal MRI was reviewed independently for the presence of LMD. RESULTS: Thirty-four patients (32%) were diagnosed with LMD based on CSF cytology, spinal MRI, or both. There were 21 discordant results. Nine patients (8.5%) with positive MRI had negative CSF cytology. Twelve patients (11.3%) with positive CSF cytology had negative MRIs. The exact 95% upper bounds on the proportion of patients with LMD whose disease would have gone undetected using either CSF cytology or MRI as the only diagnostic modality were calculated at 14.4% and 17.7%, respectively. CONCLUSION: With the use of either CSF cytology or spinal MRI alone, LMD would be missed in up to 14% to 18% of patients with medulloblastoma or PNET. Thus, both CSF cytology and spinal MRI should routinely be used to diagnose LMD in patients with medulloblastoma or PNET. (+info)
Retinoic acid stimulates meningioma cell adhesion to the extracellular matrix and inhibits invasion.
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Meningiomas are tumours derived from the arachnoid and pia mater. During embryogenesis, these membranes develop from the migrating craniofacial neural crest. We have previously demonstrated that meningiomas have characteristic features of embryonic meninges. Craniofacial neural crest derivatives are affected during normal development and migration by retinoic acid. We speculated, therefore, that meningioma cell migration and invasion would be affected in a similar way. In this study we investigated the mechanisms of invasion and migration in meningiomas and the effects of retinoic acid (RA). We found that low doses of RA inhibit in vitro invasion in meningioma cells, without affecting cell proliferation or viability. The matrix metalloproteinases MMP-2 (72 kDa gelatinase) and MMP-9 (92 kDa gelatinase), which play a key role in invasion in other tumours, are not affected by RA. RA inhibits cell migration on collagen I and fibronectin. A possible mechanism for these effects is provided by the fact that RA strongly stimulates adhesion of meningioma cells to extracellular matrix substrates. As in vitro invasion, migration and decreased adhesion to the extracellular matrix correlate with the clinical manifestation of tumour invasion, we conclude that RA induces a non-invasive phenotype in meningioma cells. (+info)
Preoperative embolization of intracranial meningiomas with a fibrin glue preparation.
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BACKGROUND AND PURPOSE: Preoperative embolization expands the spectrum of meningioma that can be operated on safely. Our goal was to achieve the distalmost loading of the vascular bed and confluent tumor necrosis with a fibrin glue preparation in the preoperative embolization of meningiomas. METHODS: Between 1992 and 1997, 80 patients with a meningioma had diagnostic angiography with a standard transfemoral Seldinger technique, performed with a 6F guiding catheter and digital subtraction angiography. Preoperative embolization was carried out in the same session with an additional microcatheter system. Fibrin glue was the only component used. In all cases, CT was performed immediately after embolization; in nine patients, MR imaging was also performed. RESULTS: Angiography verified the elimination of tumor blush in all patients. The high-density areas seen on postembolization CT scans, caused by the fibrin glue dispersed in the embolized supply area, were found to be necrotic at surgery and were easily removed by suction. Two (2.5%) of the 80 patients had complications associated with embolization that resulted in neurologic deficits. CONCLUSION: The most effective preoperative embolization of tumors requires a distalmost loading of the vascular bed. Fibrin glue, which is easy to use and safe to handle, causes confluent tumor necrosis within the injected vascular territory. (+info)