Mapping of chromosomal gains and losses in primitive neuroectodermal tumors by comparative genomic hybridization

Schütz, Barbara R.; Scheurlen, Wolfram; Krauß, Jürgen; Manoir, Stanislas du; Joos, Stefan; Bentz, Martin; Lichter, Peter

doi:10.1002/(sici)1098-2264(199607)16:3<196::aid-gcc7>3.0.co;2-u

Cited by 71 publications

(17 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Only 3/31 (10%) of the medulloblastomas in our study showed gene amplification, consistent with previous studies of primary tumours (Bigner and Vogelstein, 1990;Heim and Mitelman, 1993;Batra et al, 1994;Schütz et al, 1996;Reardon et al, 1997) and none of our cases had amplifications at previously reported loci. This gives added weight to the suggestion that the high proportion of cell lines with MYC amplification may be due to a selective advantage for in vitro growth conferred by this abnormality (Bigner and Vogelstein, 1990;Batra et al, 1994).…”

Section: Discussionsupporting

confidence: 93%

“…The findings of gain of 17q with reciprocal loss of 17p in 26% of our cases of medulloblastoma are consistent with cytogenetic reports (Biegel et al, 1989;Bigner et al, 1997), with two smaller series of cases studied using CGH (Schütz et al, 1996;Reardon et al, 1997), and with findings of LOH on 17p (Cogen et al, 1990;Blaeker et al, 1996). The relative importance of 17p loss and 17q gain remains unclear.…”

Section: Discussionsupporting

confidence: 90%

“…Loss of all or part of 9q, including 9q22, has been found in a proportion of PNETs in each of the published CGH series (Schütz et al, 1996;Reardon et al, 1997). Although all of our cases show loss of a region large enough to be seen clearly in a conventional cytogenetic preparation, interstitial losses of 9q have not been reported in cytogenetic studies of PNET.…”

Section: Discussionmentioning

confidence: 98%

“…Two previous studies (Schütz et al, 1996;Reardon et al, 1997) found widely different numbers of abnormalities in medulloblastomas using CGH. The aims of this study were to screen a series of CNS PNETs, mostly medulloblastomas, for chromosomal imbalance as revealed by CGH, to test the hypothesis that histological and immunophenotypical differences among variants of PNET are associated with specific genetic abnormalities, and to assess the prognostic value of any commonly observed genetic abnormalities.…”

mentioning

confidence: 92%

See 3 more Smart Citations

Comparative genomic hybridization and histological variation in primitive neuroectodermal tumours

et al. 1999

View full text Add to dashboard Cite

SummaryThe objective of this study was to test the hypothesis that chromosomal imbalances in central nervous system primitive neuroectodermal tumours (PNETs) reflect site and histology. We used comparative genomic hybridization to study 37 cases of PNET, of which four were cerebral and 31 were medulloblastomas classified histologically as classic (n = 17) or nodular/desmoplastic (n = 14). Tumour immunophenotype was characterized with antibodies to neuroglial, mesenchymal and epithelial markers. Chromosomal imbalances were detected in 28 medulloblastomas (90%), and significant associations between tumour variants and genetic abnormalities were demonstrated. Aberrations suggesting isochromosome 17q were present in eight (26%) medulloblastomas, of which seven were classic variants. None of these cases, or a further six with gain of 17q, showed immunoreactivity for glial fibrillary acidic protein. Loss on 9q was found in six cases (19%), five of them nodular/desmoplastic. Loss of 22 occurred in four (13%), all classic medulloblastomas in young patients with a poor outcome and immunoreactivity for more than one epithelial or mesenchymal marker. Different patterns of imbalance were found in the cerebral PNETs. There were no abnormalities of chromosome 17, but all three cases with imbalance showed losses of 3p12.3-p14.

show abstract

Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 98%

mentioning

confidence: 92%

See 2 more Smart Citations

Comparative genomic hybridization and histological variation in primitive neuroectodermal tumours

et al. 1999

View full text Add to dashboard Cite

show abstract

“…Double minutes are observed that result from ampli®cation and/or fragmentation of chromosome 13. Interestingly gains in chromosomes 2, 4 and 13 have been reported in PNET and medulloblastoma (Schutz et al, 1996) or in medulloblastoma cell lines previously (Pietsch et al, 1994;Bigner et al, 1988).…”

Section: Discussionmentioning

confidence: 71%

Human primitive neuroectodermal tumour cells behave as multipotent neural precursors in response to FGF2

Dufay

Rudkin

et al. 1998

Oncogene

View full text Add to dashboard Cite

Primitive neuroectodermal tumours (PNET) are thought to derive from the malignant transformation of pluripotent CNS precursors although this hypothesis has yet to be tested in vitro. Here we show that cells of a human PNET cell line`Dev' express functional ®broblast growth factor (FGF) receptors (FGFR) and respond to FGF2 as multipotent CNS precursors. FGF2 induces tyrosine phosphorylation of FGFR-1 and FGFR-2 and many cellular substrates including MAP kinases and stimulates proliferation. Cells detach from plastic substrates and proliferate to form large clusters of undi erentiated cells. After adhesion to polylysine, cells migrate out from the clusters and di erentiate. The majority of di erentiated cells express neuronal phenotypes but distinct subpopulations express oligodendrocytic and astrocytic markers. Mature neural di erentiation markers are not otherwise detected in Dev cells in de®ned medium. Identical results were obtained with 12 monoclonal subclones as well as the parent cell line, con®rming that Dev cells are multipotent. This extends evidence that multipotent CNS precursors are the cellular substrate from which certain PNET develop and shows that FGF2 is a potent proliferation and di erentiation inducer for PNET cells in vitro, suggesting that FGF2 may also modulate the evolution of PNET in vivo. Finally our results suggest that PNET cell lines may provide models to elucidate the biology of human multipotent CNS precursors.

show abstract

Comparative genomic hybridization as a tool in tumour cytogenetics

James

1999

J. Pathol.

View full text Add to dashboard Cite

The quality of cytogenetic analysis of solid tumours has greatly improved in the past decade, but a number of technical difficulties remain which limit the characterization of solid tumour chromosomes by conventional cytogenetics alone. The identification of regions of chromosomal abnormality has been aided by the introduction of molecular cytogenetic techniques such as fluorescence in situ hybridization (FISH). Of these, a recently developed approach, comparative genomic hybridization (CGH), has had a particular impact on the cytogenetic analysis of solid tumours. It incorporates the sensitivity of in situ techniques and overcomes many of the drawbacks of conventional cytogenetic analysis. This review first outlines the CGH method, giving details for the preparation of DNA probes and target human metaphase chromosomes together with information on the in situ technique and data handling criteria used in our laboratory. It then presents an overview of some of the current applications of CGH, together with a discussion of future directions in the field. Copyright © 1999 John Wiley & Sons, Ltd.

show abstract

Mapping of chromosomal gains and losses in primitive neuroectodermal tumors by comparative genomic hybridization

Cited by 71 publications

References 28 publications

Comparative genomic hybridization and histological variation in primitive neuroectodermal tumours

Comparative genomic hybridization and histological variation in primitive neuroectodermal tumours

Human primitive neuroectodermal tumour cells behave as multipotent neural precursors in response to FGF2

Comparative genomic hybridization as a tool in tumour cytogenetics

Contact Info

Product

Resources

About