Correlation between cytogenetic and histopathological findings in 65 human meningiomas

Casalone, Rosario; Simi, Paolo; Granata, Paola; Minelli, E.; Giudici, A.; Butti, G.; Solero, C. L.

doi:10.1016/0165-4608(90)90088-r

Cited by 57 publications

(21 citation statements)

References 12 publications

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“…Cytogenetic analysis of meningiomas previously provided evidences of the nonrandom involvement of chromosome 22 in about 60% of tumors, suggesting that inactivation of tumor suppressor loci (the NF2 gene is now identi®ed as one of them) located in this chromosome might represent an early step in meningioma tumorigenesis (Zang, 1982;Al Saadi et al, 1987;Maltby et al, 1988;Rey et al, 1988;Casalone et al, 1990). Non-random loss of chromosome 14 and structural rearrangements of chromosome 1, generally leading to the loss of short arm regions, were also identi®ed as characteristic cytogenetic features of meningiomas; to a lesser degree, abnormalities of chromosomes 7,8,10,18,19 and 20 have also been found (Rey et al, 1988;Casalone et al, 1990;Casartelli et al, 1989;Poulsgard et al, 1993;Vagner-Capodano et al, 1993;LekanneDeprez et al, 1995;Lopez Gines et al, 1995;Schneider et al, 1995;Perry et al, 1996). The accumulation of chromosomal abnormalities secondary to chromosome 22 loss, frequently in parallel to the genesis of grade II and III tumors, allowed the proposal that meningiomas might display clonal progression through a pattern, implying the accumulation of several genetic anomalies in which monosomy of chromosome 22 would represent an early step (Rey et al, 1988;Poulsgard et al, 1993).…”

Section: Introductionmentioning

confidence: 99%

NF2 gene mutations and allelic status of 1p, 14q and 22q in sporadic meningiomas

Mj²,

et al. 1999

Oncogene

144

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Section: Introductionmentioning

confidence: 99%

NF2 gene mutations and allelic status of 1p, 14q and 22q in sporadic meningiomas

Mj²,

et al. 1999

Oncogene

144

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“…The ®rst clues to ®nding genetic loci possibly involved in tumor initiation or progression in meningiomas and schwannomas were provided by cytogenetic studies that demonstrated loss of chromosome 22 as the most common chromosomal abnormality in these tumors (Zankl and Zang, 1972;Casalone et al, 1990). Other investigators examined loci on chromosome 22 with polymorphic DNA markers and established that LOH on this chromosome was a common pathogenic mechanism for tumor formation in meningiomas as well as acoustic neuromas (Seizinger et al, 1986(Seizinger et al, , 1987Dumanski et al, 1987).…”

Section: Introductionmentioning

confidence: 99%

Frequent loss of chromosome 14 in atypical and malignant meningioma: identification of a putative `tumor progression' locus

et al. 1997

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Formation of meningiomas has been associated with the loss of genetic material on chromosome 22. To approach the additional chromosomal events that underlie progression of these tumors to malignancy, we have examined several other chromosomal regions for loss of heterozygosity (LOH) in these tumors. Fifty-eight tumors, comprising 43 benign meningiomas, 11 atypical meningiomas and four malignant meningiomas, were examined. While the loss of chromosome 22 was seen in approximately half of all these tumors, regardless of their malignancy, the most frequent chromosomal losses observed in the malignant and atypical tumors were on the long arm of chromosome 14. Thirty-nine tumors were informative for at least one of the three markers on chromosome 14 that we tested. Of these, 7/14 malignant and atypical tumors showed LOH in contrast to only 1/ 25 benign tumors. Other loci that showed LOH in malignant tumors, although at a much lower frequency, were on chromosomes 17p and 1p. The high frequency of LOH for loci on chromosome 14q in atypical and malignant tumors suggests the presence of a tumor progression gene at this locus. In one of the malignant meningiomas heterozygosity was lost at D14S13 and D14S16 but retained at the proximal marker D14S43 as well as the more distal marker D14S23. This suggests that an interstitial deletion occurred in this tumor which should be useful for further re®ning the position of the putative tumor progression locus.

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“…Loss of chromosome 22 is the most common aberration and has been detected in 40% to 70% of cases. 4,16,25,30,31) Recent studies have demonstrated that the neurofibromatosis type 2 (NF2) gene, a tumor suppressor gene, is located at the 22q12 locus 21,27) and is the gene involved in the etiology of meningiomas, since most cases have mutations in this region. 9,22) The presence of mutations and/or loss of NF2 gene in meningiomas of all malignancy grades indicates that inactivation of this tumor suppressor gene represents an early genetic event in the pathogenesis of meningiomas.…”

Section: Introductionmentioning

confidence: 99%

Detection of Chromosomal Imbalances in Spinal Meningiomas by Comparative Genomic Hybridization.

Arslantaş

Artan

Öner

et al. 2003

Neurol. Med. Chir.(Tokyo)

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Little is known about genetic mutations during the malignant progression of spinal meningiomas. This study investigated genomic changes across the entire genome in spinal meningioma samples to determine possible mechanism(s) of tumorigenesis. Paraffin-embedded tissue sections of 16 spinal meningiomas were analyzed by the comparative genomic hybridization (CGH) technique. Lymphocytes of the patients were evaluated as controls. Genomic change was detected in 11 samples. Complete or partial loss of chromosome 22 was the most commonly seen abnormality in eight cases. Chromosome losses on 1p, 9p, and 10q and gains on 5p and 17q were the other abnormalities. These changes are all frequently seen in meningiomas, but are mostly specific to atypical and anaplastic meningiomas. However, in the present study, copy number changes on chromosomes 9p (3 samples), 17q (2 samples), and 1p (2 samples) were seen even in the benign tumors. Our results suggest that in addition to the neurofibromatosis type 2 tumor suppressor gene, other cancer-related genes located on 1p, 9p, 10q, and 17q might be involved in the etiology of spinal meningiomas.

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Correlation between cytogenetic and histopathological findings in 65 human meningiomas

Cited by 57 publications

References 12 publications

NF2 gene mutations and allelic status of 1p, 14q and 22q in sporadic meningiomas

NF2 gene mutations and allelic status of 1p, 14q and 22q in sporadic meningiomas

Frequent loss of chromosome 14 in atypical and malignant meningioma: identification of a putative `tumor progression' locus

Detection of Chromosomal Imbalances in Spinal Meningiomas by Comparative Genomic Hybridization.

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