This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Bigner, S. H. Articles by Bigner, D. D. Search for Related Content PubMed PubMed Citation Articles by Bigner, S. H. Articles by Bigner, D. D.

Specific Chromosomal Abnormalities in Malignant Human Gliomas¹

Preuss Laboratory for Brain Tumor Research [D. D. B.], Department of Pathology [S. H. B., P. C. B., D. D. B.], Surgery [D. E. B.] and Community and Family Medicine [L. H. M.], Duke University Medical Center, Durham, North Carolina 27710; Central Hospital, Skövde, Sweden [J. M.]; and Department of Neurosurgery, University of Alabama Medical Center, Birmingham, Alabama 35294 [M. S. M.]

Karyotypic analysis of 54 malignant human gliomas (5 anaplastic astrocytomas, 43 glioblastoma multiformes, 3 gliosarcomas, 2 giant cell glioblastomas, 1 anaplastic mixed glioma) has demonstrated that 12 tumors contained normal stemlines or only lacked one sex chromosome. The 42 tumors with abnormal karyotypes included 38 tumors which could be completely analyzed. Six of these 38 cases had near-triploid or near-tetraploid stemlines and 32 had near-diploid stemlines. Statistically significant numerical deviations in the near-diploid group were gains of chromosome 7 (26 of 32; P < 0.001), and losses of chromosome 10 (19 of 32; P < 0.001). Double minutes occurred in 18 of 32 near diploid tumors. The distribution of structural abnormalities was analyzed statistically by comparing the incidence of breakpoints in each chromosomal arm to the expected value based on chromosomal arm length. This analysis demonstrated that structural abnormalities of 9p and 19q were significant statistically (P < 0.005 and P = 0.02, respectively). Although chromosome 1, 6p, the centromeric region of chromosome 11, 13q, and 15q were also frequently involved in structural abnormalities, the incidence of these breaks did not reach statistical significance. This demonstration of specific chromosomal abnormalities in near-diploid gliomas provides the basis for the investigation of genes which may be quantitatively or qualitatively altered in these neoplasms.

¹ This investigation was supported in part by CA-11898 and CA-43722 from the National Cancer Institute, P01-NS-20023 from NINCDS, and the Swedish Cancer Society.

² To whom requests for reprints should be addressed.

Received 6/26/87. Revised 10/ 1/87. Accepted 10/26/87.

This article has been cited by other articles:

				K. Ueki, R. Nishikawa, Y. Nakazato, T. Hirose, J. Hirato, N. Funada, T. Fujimaki, S. Hojo, O. Kubo, T. Ide, et al. Correlation of Histology and Molecular Genetic Analysis of 1p, 19q, 10q, TP53, EGFR, CDK4, and CDKN2A in 91 Astrocytic and Oligodendroglial Tumors Clin. Cancer Res., January 1, 2002; 8(1): 196 - 201. [Abstract] [Full Text] [PDF]

				J. S. Smith, I. Tachibana, S. M. Passe, B. K. Huntley, T. J. Borell, N. Iturria, J. R. O'Fallon, P. L. Schaefer, B. W. Scheithauer, C. D. James, et al. PTEN Mutation, EGFR Amplification, and Outcome in Patients With Anaplastic Astrocytoma and Glioblastoma Multiforme J Natl Cancer Inst, August 15, 2001; 93(16): 1246 - 1256. [Abstract] [Full Text] [PDF]

				J. M. Nigro, M. A. Takahashi, D. G. Ginzinger, M. Law, S. Passe, R. B. Jenkins, and K. Aldape Detection of 1p and 19q Loss in Oligodendroglioma by Quantitative Microsatellite Analysis, a Real-Time Quantitative Polymerase Chain Reaction Assay Am. J. Pathol., April 1, 2001; 158(4): 1253 - 1262. [Abstract] [Full Text] [PDF]

				R. N. Wiltshire, B.K. A. Rasheed, H. S. Friedman, A. H. Friedman, and S. H. Bigner Comparative genetic patterns of glioblastoma multiforme: Potential diagnostic tool for tumor classification Neuro-oncol, July 1, 2000; 2(3): 164 - 173. [Abstract] [PDF]

				D. W. Lee, K. Zhang, Z.-Q. Ning, E. H. Raabe, S. Tintner, R. Wieland, B. J. Wilkins, J. M. Kim, R. I. Blough, and R. J. Arceci Proliferation-associated SNF2-like Gene (PASG): A SNF2 Family Member Altered in Leukemia1 Cancer Res., July 1, 2000; 60(13): 3612 - 3622. [Abstract] [Full Text]

				J. A. Biegel Cytogenetics and molecular genetics of childhood brain tumors Neuro-oncol, April 1, 1999; 1(2): 139 - 151. [Abstract] [PDF]

				F. B. Furnari, H. Lin, H.-J. S. Huang, and W. K. Cavenee Growth suppression of glioma cells by PTEN requires a functional phosphatase catalytic domain PNAS, November 11, 1997; 94(23): 12479 - 12484. [Abstract] [Full Text] [PDF]

				J. Li, C. Yen, D. Liaw, K. Podsypanina, S. Bose, S. I. Wang, J. Puc, C. Miliaresis, L. Rodgers, R. McCombie, et al. PTEN, a Putative Protein Tyrosine Phosphatase Gene Mutated in Human Brain, Breast, and Prostate Cancer Science, March 28, 1997; 275(5308): 1943 - 1947. [Abstract] [Full Text]

				E Solomon, J Borrow, and A. Goddard Chromosome aberrations and cancer Science, November 22, 1991; 254(5035): 1153 - 1160. [Abstract] [PDF]

				Y. Wu, D. Dowbenko, S. Spencer, R. Laura, J. Lee, Q. Gu, and L. A. Lasky Interaction of the Tumor Suppressor PTEN/MMAC with a PDZ Domain of MAGI3, a Novel Membrane-associated Guanylate Kinase J. Biol. Chem., July 7, 2000; 275(28): 21477 - 21485. [Abstract] [Full Text] [PDF]