Chromosomal evolution in malignant human gliomas starts with specific and usually numerical deviations

Bigner, Sandra H.; Mark, Joachim; Bullard, Dennis E.; Mahaley, M. S.; Bigner, Darell D.

doi:10.1016/0165-4608(86)90172-x

Cited by 123 publications

(47 citation statements)

References 27 publications

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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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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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“…As indicated by the term 'multiforme', the tumour is characterised by a pleomorphic cellular population. Chromosome banding techniques (Bigner et al, 1984(Bigner et al, , 1986 …”

Section: Discussionmentioning

confidence: 99%

Selective in vitro replication of herpes simplex virus type 1 (HSV-1) ICP34.5 null mutants in primary human CNS tumours - evaluation of a potentially effective clinical therapy

McKie

Maclean²,

Lewis³

et al. 1996

Br J Cancer

107

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“…However, several groups have noted that adequate chromosome analyses of both primary cultures and of solid glioma samples are problematic [ 1,21. These difficulties are generally encountered in all cytogenetic analyses of solid tumors; many tumor preparations do not contain sufficient numbers of well-spread and banded metaphase cells, and a large number of mitotic cells within solid tumors are inaccessible for analysis.…”

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confidence: 99%

Rapid interphase and metaphase assessment of specific chromosomal changes in neuroectodermal tumor cells by in situ hybridization with chemically modified DNA probes

Cremer

Tesin

Hopman

et al. 1988

Experimental Cell Research

152

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Repeated DNAs from the constitutive heterochromatin of human chromosomes 1 and 18 were used as probes in nonradioactive in situ hybridization experiments to define specific numerical and structural chromosome aberrations in three human glioma cell lines and one neuroblastoma cell line. The number of spots detected in interphase nuclei of these tumor cell lines and in normal diploid nuclei correlated well with metaphase counts of chromosomes specifically labeled by in situ hybridization. Rapid and reliable assessments of aneuploid chromosome numbers in tumor lines in double hybridization experiments were achieved, and rare cells with bizarre phenotype and chromosome constitution could be evaluated in a given tumor cell population. Even with suboptimal or rare chromosome spreads specific chromosome aberrations were delineated. As more extensive probe sets become available this approach will become increasingly powerful for uncovering various genetic alterations and their progression in tumor cells. 0 1988 Academic Press. Inc.Specific chromosome aberrations are thought to be important in the development of malignant human gliomas. However, several groups have noted that adequate chromosome analyses of both primary cultures and of solid glioma samples are problematic [ 1, 21. These difficulties are generally encountered in all cytogenetic analyses of solid tumors; many tumor preparations do not contain sufficient numbers of well-spread and banded metaphase cells, and a large number of mitotic cells within solid tumors are inaccessible for analysis. With such small samples of mitotic cells it is difficult to determine if a chromosomal pattern is representative of the whole tumor cell population. Thus specific numerical and structural aberrations in a given tumor type are difficult to confirm on a broad scale, and rare aberrant cells with special malignant propensities may also be overlooked. Furthermore the analysis of complex chromosome changes in very aneuploid cells requires the detailed attention of highly skilled observers. Even when these time consuming analyses are performed by experienced cytogeneticists, it is difficult to pinpoint chromosomal breakpoints and segments involved in duplication, deletion, or translocation [l].We are attempting to develop procedures and DNA probe sets for visualization of specific numerical and structural aberrations in tumor cells. The detection of chromosome abnormalities in interphase nuclei, an approach termed "interphase cytogenetics"[3], appears to be a useful addition to the classical metaphase analysis. The examination of numerical aberrations in interphase nuclei can yield ' TO whom reprint requests should be addressed 199

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Chromosomal evolution in malignant human gliomas starts with specific and usually numerical deviations

Cited by 123 publications

References 27 publications

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

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

Selective in vitro replication of herpes simplex virus type 1 (HSV-1) ICP34.5 null mutants in primary human CNS tumours - evaluation of a potentially effective clinical therapy

Rapid interphase and metaphase assessment of specific chromosomal changes in neuroectodermal tumor cells by in situ hybridization with chemically modified DNA probes

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