Deletion of chromosome 1p and loss of expression of alkaline phosphatase indicate progression of meningiomas.
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Meningiomas are cytogenetically characterized by loss of one chromosome 22 as a typical primary aberration and progression-associated secondary chromosome changes, of which monosomy 1p is the most common. The aim of this study was to evaluate the significance of monosomy 1p and enzyme activity loss of tissue nonspecific alkaline phosphatase (ALPL), whose gene maps to chromosome 1p36.1-p34, as parameters for the diagnosis of progression-prone meningiomas. We analyzed smear preparations of 56 meningiomas and additional paraffin sections of 17 of the cases by two-color fluorescence in situ hybridization (FISH) using the D1Z1 and D1Z2 probes and by a metaphase cytogenetic analysis of 30 of these tumors. The results were compared to clinical and morphological parameters and the expression of ALPL. Smear preparations showed deletion of 1p36 in 27% of common-type, 70% of atypical (intermediate-type), and 100% of anaplastic meningiomas. Monosomy 1p, as detected by FISH or the karyotype, was strongly associated with complete loss of ALPL activity. Intermediate-type and anaplastic meningiomas of younger patients displayed an increasing rate of cells with trisomy 1q and relative loss of 1p. The highly significant correlation of FISH results and ALPL histochemistry with clinical parameters gives evidence of their strong prognostic relevance. The complete activity loss of ALPL and the immunologically detected loss of ALPL protein in areas of meningiomas with monosomy 1p indicate a cytogenetically undetectable inactivation of the homologous Alpl allele. The apparently homozygous loss of expression of ALPL supports the notion that Alpl is a candidate tumor suppressor gene in meningiomas. (+info)
Natural history of elderly patients with asymptomatic meningiomas.
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OBJECTIVE: For the treatment of elderly patients with asymptomatic meningiomas, it is important to determine their natural history. Based on results of follow up examinations, the natural history of such patients was clarified and prognostic factors concerning the potential of tumour growth in the aged were identified. METHODS: The clinical records and imaging studies of 40 elderly (over 70 years) patients with asymptomatic meningiomas were analysed. The patients were followed up with repeated imaging studies, and changes in tumour size, clinical signs, and outcomes were evaluated. RESULTS: There were 32 women and eight men with a mean age of 76.1 years. The mean follow up period was 38.4 months, ranging from 6 to 97 months. Six patients died during the follow up period from disorders other than the tumours, and one patient died as a result of the tumour. Twenty six patients (mean follow up period 41.8 months, range 10-97 months) showed no tumour growth. Fourteen patients showed tumour growth (mean follow up period 32.1 months, range 6-88 months). Five (four men and one woman) of these patients became symptomatic. Based on imaging analysis (1) calcification of the tumour was associated with no tumour growth (p=0.036), and (2) the tumour size at the initial diagnosis was related to subsequent tumour growth (p=0.016). Other possible factors related to tumour growth included sex and hyperintensity on MRI T2 weighted images. CONCLUSION: In elderly patients with asymptomatic meningiomas, careful clinical follow up with imaging studies is important. The imaging features mentioned may contribute to prediction of tumour growth. (+info)
Tight association of loss of merlin expression with loss of heterozygosity at chromosome 22q in sporadic meningiomas.
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Mutations of NF2, the gene for neurofibromatosis 2, are detected in 20-30% of sporadic meningiomas, and almost all mutations lead to loss of merlin expression. However, loss of heterozygosity (LOH) at chromosome 22q is found at a much higher frequency, up to 50-70%, and the possibility of another tumor suppressor gene in this region has not been excluded. Furthermore, a recent report proposed that abnormal activation of a protease micro-calpain can be an alternative pathway for merlin loss in meningiomas and schwannomas. To determine the correlation of merlin loss with NF2 genetic alteration or micro-calpain activation, we performed a molecular genetic analysis of 50 sporadic meningiomas and also examined the expression status of merlin and active form micro-calpain. LOH assay of five microsatellite markers franking NF2 revealed LOH in 22 cases, and single-strand conformation polymorphism assay detected six frameshift mutations, two splicing mutations, one nonsense mutation, and one missense mutation, all accompanied by 22q LOH. In addition, a multiplex PCR assay indicated homozygous deletion of NF2 in two cases. Interestingly, a marked decrease of merlin expression was seen exclusively in the 22 cases with 22q LOH. Activated micro-calpain expression was observed in 28 cases at various levels but showed no correlation with merlin status. These data strongly support the notion that NF2 is the sole target of 22q LOH in meningiomas and that loss of merlin expression is always caused by genetic alteration of NF2, following the classic "two hit" theory. (+info)
Midline and far lateral approaches to foramen magnum lesions.
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Twenty patients with foramen magnum lesions were operated upon in the last 5 years at Postgraduate Institute of Medical Education and Research, Chandigarh. The common presenting features were quadriparesis, quadriplegia, diminished sensations, neck pain and respiratory insufficiency. The lesions encountered were meningiomas, neurofibromas, posterior inferior cerebellar artery aneurysms, neurenteric cyst and chordoma. Patients with posterior or posterolaterally placed lesions were operated by the midline posterior approach while those with anterior or anterolateral lesions were managed by the far lateral approach. All mass lesions were excised completely and the aneurysms were clipped. Seventeen patients made good neurological recovery while three died. The latter three patients presented very late. The merits of various surgical approaches to the foramen magnum are discussed. (+info)
Unusual mode of spread and presentation of meningioma: a case report.
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Although rare, extracranial extension of a meningioma has been well documented. An interesting natural history of neglected meningioma with skull vault hyperostosis and predominantly extracranial extension is described. Following surgical resection of the highly vascular meningioma, the patient developed fatal coagulopathy. (+info)
The effects of exogenous growth factors on matrix metalloproteinase secretion by human brain tumour cells.
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Matrix metalloproteinases (MMPs) are a growing family of zinc-dependent endopeptidases that are capable of degrading various components of the extracellular matrix. These enzymes have been implicated in a variety of physiological and pathological conditions including embryogenesis and tumour invasion. The synthesis of many MMPs is thought to be regulated by growth factors, cytokines and hormones. In this study, we investigated the effects of five exogenous growth factors known to be expressed by gliomas [epidermal growth factor (EGF), basic growth factor (bFGF), transforming growth factor beta (TGF-beta1,2) and vascular endothelial growth factor (VEGF)].on MMP-2 and MMP-9 expression in an ependymoma, two grade III astrocytomas, a grade III oligoastrocytoma and a benign meningioma. Zymogram analysis revealed that the effects of the growth factors depended upon the cell lines used in the study. Growth factors generally up-regulated MMP-2 and MMP-9 expression in the gliomas but were least effective in the meningioma; the effect being most prominent with TGF-beta1 and TGF-beta2 in all the cell lines. It is hypothesized that paracrine growth factor interplay may be crucial in the regulation of MMP expression by glioma invasion of the normal brain. (+info)
MR imaging features of clear-cell meningioma with diffuse leptomeningeal seeding.
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Clear-cell meningioma is a rare disease entity showing a more aggressive nature, clinically, than those of other subtypes of meningioma. It occurs in younger persons and commonly in the spinal canal. The recurrence rate has been reported to be as high as 60%. We present a case of clear-cell meningioma in a 17-year-old man in whom initial MR imaging showed localized leptomeningeal enhancement that had progressed into the entire subarachnoid space after surgical resection of the primary tumor. (+info)
An iatrogenic epidemic of benign meningioma.
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Head irradiation, the acceptable mode of treatment for tinea capitis in the past, is recognized today as a causative factor for meningioma. This treatment was applied en mass to immigrants coming to Israel from North Africa and the Middle East during the 1950s. In order to estimate the effect of the differential radiation treatment on the rates of meningioma in the total population, the authors assessed time trends of this disease in Israel over the past 40 years by main ethnic origin. Cohort analysis shows a marked incidence rise in the North African-born cohorts born in 1940-1954 starting from the 1980s. A similar pattern is seen in the Middle Eastern born, although the increase is not as sharp. In consequence, there is a crossover of the interethnic incidence curves in the 1940-1949 cohort. Comparison of the relative risk between 1940-1954 cohorts that comprised most of the irradiated with 1930-1939 cohorts, who were largely free of the radiation, shows that the North African born have the largest relative risk of 4.62, followed by the Middle Eastern born, with a relative risk of 1.95, while the European-American born have a relative risk close to 1. The differences between the three areas of birth are statistically significant. The data illustrate the potential risk of administering highly potent therapy for an essentially benign disease that led, in turn, to a drastic change in the national meningioma pattern. (+info)