Cytogenetic studies of human brain tumors and their clinical significance. II. Meningioma

Saadi, A. Al; Latimer, F R; Madercic, M.; Robbins, Thomas O.

doi:10.1016/0165-4608(87)90140-3

Cited by 94 publications

(32 citation statements)

References 22 publications

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“…Bloomfield et al 1987;A1-Saadi et al 1987). Chromosome 1 aberrations are involved in many solid tumors (Atkin 1986) and in neuroectodermal neoplasms (Brodeur et al 1981;Bigner et al 1986) Thus the aberrations of chromosome 1 detected in this study are not surprising.…”

Section: Discussionmentioning

confidence: 53%

Detection of chromosome aberrations in metaphase and interphase tumor cells by in situ hybridization using chromosome-specific library probes

et al. 1988

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Summary. Chromosome aberrations in two glioma cell lines were analyzed using biotinylated DNA library probes that specifically decorate chromosomes 1, 4, 7, 18 and 22 from pter to qter. Numerical changes, deletions and rearrangements of these chromosomes were readily visualized in metaphase spreads, as well as in early prophase and interphase nuclei. Complete chromosomes, deleted chromosomes and segments of translocated chromosomes were rapidly delineated in very complex karyotypes. Simultaneous hybridizations with additional subregional probes were used to fllrther define aberrant chromosomes. Digital image analysis was used to quantitate the total complement of specific chromosomal DNAs in individual metaphase and interphase cells of each cell line. In spite of the fact that both glioma lines have been passaged in vitro for many years, an under-representation of chromosome 22 and an over-representation of chromosome 7 (specifically 7p) were observed. These observations agree with previous studies on gliomas. In addition, sequences of chromosome 4 were also found to be under-represented, especially in TC 593. These analyses indicate the power of these methods for pinpointing chromosome segments that are altered in specific types of tumors.

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Section: Discussionmentioning

confidence: 53%

Detection of chromosome aberrations in metaphase and interphase tumor cells by in situ hybridization using chromosome-specific library probes

et al. 1988

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“…It has been suggested that 14q24.3-q32.33 may also represent a critical chromosome region that is lost not only in meningioma tumors (3,41), but also in Ewing's sarcoma (42) and in leiomyosarcoma (43). In this sense, specific deletions of 14q22-24 and 14q32, where the AKT (44), ELK-2 (45; a member of the ETS family of oncogenes), and TC1-1 (46; another oncogene) genes are located, appear to be of particular relevance.…”

Section: Discussionmentioning

confidence: 99%

Incidence of numerical chromosome aberrations in meningioma tumors as revealed by fluorescence in situ hybridization using 10 chromosome‐specific probes

et al. 2002

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Objective: Although information on the cytogenetic characteristics of meningioma tumors has accumulated progressively over the past few decades, information on the genetic heterogeneity of meningiomas is still scanty. The aim of the present study was to analyze by interphase fluorescence in situ hybridization (FISH) the incidence of numerical abnormalities for chromosomes 1, 9, 10, 11, 14, 15, 17, 22, X, and Y in a group of 70 consecutive meningioma tumors. Another goal was to establish the potential associations among the altered chromosomes, as a way to assess both intertumoral and intratumoral heterogeneity. Methods: For the purpose of the study, 70 patients diagnosed with meningioma were analyzed. Interphase FISH for the detection of numerical abnormalities for chromosomes 1, 9, 10, 11, 14, 15, 17, 22, X, and Y was applied to fresh tumor samples from each of the patients studied. Results: The overall incidence of numerical abnormalities was 76%. Chromosome Y in males and chromosome 22 in the whole series were the most common abnormalities (46% and 61%, respectively). Despite the finding that monosomy of chromosome 22/22q -deletions are the most frequent individual abnormality (53%), we have observed that chromosome gains are significantly more common than chromosome losses (60% versus 40%). Chromosome gains corresponded to abnormalities of chromosomes 1 (27%), 9 (25%), 10 (23%), 11 (22%), 14 (33%), 15 (22%), 17 (23%), and X in females (35%) and males (23%) whereas chromosome losses apart from chromosome 22 frequently involved chromosomes 14 (19%), X in males (23%), and Y in males (32%). Although an association was found among most gained chromosomes on one side and chromosome losses on the other side, different association patterns were observed. Furthermore, in the latter group, monosomy 22/22q -was associated with monosomy X in females and monosomy 14/14q -was associated with nulisomy Y in males. In addition, chromosome losses usually involved a large proportion of the tumor cells whereas chromosome gains were restricted to small tumor cell clones, including tetraploid cells. Conclusions: Our results show that meningiomas are genetically heterogeneous tumors that display different patterns of numerical chromosome changes, as assessed by interphase FISH. Cytometry (Clin. Cytometry) 50:153-159, 2002.

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“…Loss of chromosome 14 has been described in meningioma (Katsuyama et al, 1986;Al Saadi et al, 1987), neuroblastoma (Suzuki et al, 1989), Ewing's Sarcoma (Turc-Carel et al, 1988) and Leiomyosarcoma (Boghosian et al, 1989). Furthermore, the description of chromosomal translocations that involve the same cytogenetic band on chromosome 14 suggest that a common genetic locus might be involved in the pathway towards tumorigenesis (Katsuyama et al, 1986;Al Saadi et al, 1987;Seizinger et al, 1987) as well as in other solid tumors such as neuroblastoma (Suzuki et al, 1989;Srivatsan et al, 1991), breast tumors (Gebhart et al, 1986;Bello and Rey, 1989), ovarian tumors (Atkin et al, 1990), astrocytoma (Bigner et al, 1986), retinoblastoma (Chaum et al, 1984) and malignant melanoma (Pedersen and Wang, 1989). One malignant meningioma was identi®ed which showed loss of heterozygosity for the markers D14S13 (pCMM101) and D14S16 (THH37) but retention of heterozygosity for the proximal¯anking marker D14S23 or the distal anking marker D14S23.…”

Section: Discussionmentioning

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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Cytogenetic studies of human brain tumors and their clinical significance. II. Meningioma

Cited by 94 publications

References 22 publications

Detection of chromosome aberrations in metaphase and interphase tumor cells by in situ hybridization using chromosome-specific library probes

Detection of chromosome aberrations in metaphase and interphase tumor cells by in situ hybridization using chromosome-specific library probes

Incidence of numerical chromosome aberrations in meningioma tumors as revealed by fluorescence in situ hybridization using 10 chromosome‐specific probes

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

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