- Split View
-
Views
-
Cite
Cite
Naji Aldosari, Rodney N. Wiltshire, Amalia Dutra, Evelin Schrock, Roger E. McLendon, Henry S. Friedman, Darell D. Bigner, Sandra H. Bigner, Comprehensive molecular cytogenetic investigation of chromosomal abnormalities in human medulloblastoma cell lines and xenograft, Neuro-Oncology, Volume 4, Issue 2, April 2002, Pages 75–85, https://doi.org/10.1093/neuonc/4.2.75
- Share Icon Share
Abstract
Cell lines and xenografts derived from medulloblastomas are useful tools to investigate the chromosomal changes in these tumors. Here we used G-banding, fluorescence in situ hybridization (FISH), spectral karyotyping (SKY), and comparative genomic hybridization to study 4 medulloblastoma cell lines and 1 xenograft. Cell line D-425 Med had a relatively simple karyotype, with a terminal deletion of 10q and amplification of MYC in double-minutes (dmins). FISH demonstrated that an apparent isochromosome (17q) by routine karyotyping was actually an unbalanced translocation between 2 copies of chromosome 17. Cell line D-556 Med also had a simple near-diploid stemline with an unbalanced 1;13 translocation resulting in a gain of 1q, an isochromosome (17q), and dmins. These findings were initially described using routine G-banded preparations, and FISH showed that the dmins were an amplification of MYC and the i(17q) was an isodicentric 17q chromosome. The other finding was confirmed by FISH, SKY, and comparative genomic hybridization. Cell lines D-721 Med and D-581 Med had complex karyotypic patterns that could be completely characterized only when FISH and SKY were used. Xenograft D-690 Med also had a complex pattern that FISH and SKY were helpful in completely elucidating. Interestingly, balanced reciprocal translocations were seen as well as complicated unbalanced translocations and marker chromosomes. Comparative genomic hybridization demonstrated only a deletion of 10q22-10q24, supporting the idea that despite the complexity of the chromosomal rearrangements, minimal alterations in the overall chromosomal content had occurred. This study demonstrates that routine cytogenetic preparations are adequate to describe chromosomal abnormalities in occasional medulloblastoma samples, but a broader spectrum of molecular cytogenetic methods is required to completely analyze most of these tumor samples.
References
Adinolfi, M., and Davies, A.F. (
Aldosari, N., Rasheed, B.K.A., McLendon, R.E., Friedman, H.S., Bigner, D.D., and Bigner, S.H. (
Bigner, S.H., and Schrock, E. (
Bigner, S.H., and Vogelstein, B. (
Bigner, S.H., Mark, J., Friedman, H.S., Biegel, J.A., and Bigner, D.D. (
Bigner, S.H., Friedman, H.S., Vogelstein, B., Oakes, W.J., and Bigner, D.D. (
Bigner, S.H., McLendon, R.E., Fuchs, H., McKeever, P.E., and Friedman, H.S. (
Friedman, H.S., Bigner, S.H., McComb, R.D., Schold, S.C., Jr., Pasternak, J.F., Groothuis, D.R., and Bigner, D.D. (
Giangaspero, F., Bigner, S.H., Kleihues, P., Pietsch, T., and Trojanowski, J.Q. (
Gozzetti, A., and Le Beau, M.M. (
Grant, G., Pathak, S., and Maria, B.L. (
Jay, V., Squire, J., Bayani, J., Alkhani, A.M., Rutka, J.T., and Zielenska, M. (
Kallioniemi, A., Kallioniemi, O.P., Sudar, D., Rutovitz, D., Gray, J.W., Waldman, F., and Pinkel, D. (
Keles, G.E., Berger, M.S., Srinivasan, J., Kolstoe, D.D., Bobola, M.S., and Silber, J.R. (
Lichter, P., Joos, S., Bentz, M., and Lampel, S. (
Lopez-Gines, C., Cerda-Nicolas, M., Gil-Benso, R., Barcia-Salorio, J.L., and Llombart-Bosch, A. (
McDonald, J.D., Daneshvar, L., Willert, J.R., Matsumura, K., Waldman, F., and Cogen, P.H. (
Mitelman, F. (Ed.) (
Reardon, D.A., Michalkiewicz, E., Boyett, J.M., Sublett, J.E., Entrekin, R.E., Ragsdale, S.T., Valentine, M.B., Behm, F.G., Li, H., Heideman, R.L., Kun, L.E., Shapiro, D.N., and Look, A.T. (
Sawyer, J.R., Swanson, C.M., Roloson, G.J., Longee, D.C., Boop, F.A., and Chadduck, W.M. (
Schrock, E., du Manoir, S., Veldman, T., Schoell, B., Wienberg, J., Ferguson-Smith, M.A., Ning, Y., Ledbetter, D.H., Bar-Am, I., Soenksen, D., Garini, Y., and Ried, T. (
Schrock, E., and Padilla-Nash, H. (
Steichen-Gersdorf, E., Baumgartner, M., Kreczy, A., Maier, H., and Fink, F.M. (
Stratton, M.R., Darling, J., Cooper, C.S., and Reeves, B.R. (
Thein, A., Trkova, M., Fox, M., and Parrington, J. (
Tomlinson, F.H., Jenkins, R.B., Scheithauer, B.W., Keelan, P.A., Ritland, S., Parisi, J.E., Cunningham, J., and Olsen, K.D. (
Vagner-Capodano, A.M., Zattara-Cannoni, H., Gambarelli, D., Gentet, J.C., Genitori, L., Lena, G., Graziani, N., Raybaud, C., Choux, M., and Grisoli, F. (
Wiltshire, R.N., Rasheed, B.K.A., Friedman, H.S., Friedman, A.H., and Bigner, S.H. (
Author notes
Departments of Pathology (N.A., R.N.W., R.E.M., D.D.B., S.H.B) andSurgery (H.S.F.), Duke University Medical Center, Durham, NC 27710;Tumor Genetics and Molecular Cytogenetics, Institute for Molecular Biotechnology, Beutenbergstrasse 11, 07745 Jena, Germany (E.S.);National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892 (A.D.)
- chromosome abnormality
- karyotype determination procedure
- fluorescent in situ hybridization
- chromosome rearrangements
- cell lines
- chromosomes
- chromosomes, human, pair 17
- cytogenetics
- diploidy
- isochromosomes
- medulloblastoma
- translocation (genetics)
- transplantation, heterologous
- neoplasms
- comparative genomic hybridization
- spectral karyotyping
- g-banding
- amplification
- chromosome 17q