Genomic changes in progression of low-grade gliomas

J Neurooncol. 2008 Nov;90(2):133-40. doi: 10.1007/s11060-008-9644-z. Epub 2008 Jul 11.

Abstract

Using a one-megabase BAC-based array comparative genomic hybridization technique (aCGH), we have investigated a series of 16 low-grade gliomas (LGGs) and their subsequent progression to higher-grade malignancies. The most frequent chromosome imbalances in primary tumors were gains of chromosomes 7q, 8q, and 22q, and losses of chromosomes 1p, 13q, and 19q. In tumor progression, gains of chromosomes 11q, 7q, 20q, and 21q, and losses of chromosomes 9p, including CDKN2A locus, 19q, 14q, 1p, and 6q were the most frequent genomic disequilibria. Progressive tumors were more imbalanced than primary tumors in terms of altered chromosomal arms (3.8 vs. 6.6 in mean abnormal chromosomal arm) and altered BACs (17 vs. 21%). Interestingly, putative novel candidate genes associated with glioma progression were identified, in particular DOCK8, PTPRD, CER1, TPHO, DHFR, MSH3, ETS1, ACACA, and CSE1L.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Chromosome Deletion
  • Chromosomes
  • Disease Progression
  • Female
  • Genome / genetics*
  • Glioma / genetics*
  • Glioma / metabolism*
  • Humans
  • Male
  • Microsatellite Repeats
  • Middle Aged
  • Nucleic Acid Hybridization / methods