Allelic Losses in Oligodendroglial and Oligodendroglioma-like Neoplasms: Analysis Using Microsatellite Repeats and Polymerase Chain Reaction

Mahlon Johnson, Cindy L. Vnencak-Jones, Steven A. Toms, Paul M. Moots, Robert Weil

Research output: Contribution to journalArticle

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Abstract

Context.-Oligodendroglial tumors are heterogenous neoplasms with histologic features shared with other central nervous system tumors, such as dysembryoplastic neuroepithelial tumors. Objective.-We examined a series of tumors, identified as possessing oligodendroglial components at the time of intraoperative examination, to see if molecular subsets based on the oligodendroglial component could be recognized. Design.-DNA was extracted from fresh brain tumor tissue and corresponding peripheral blood or normal tissues. Genotypes for multiple loci were determined by polymerase chain reaction amplification using fluorescent-labeled primers for markers on chromosomes 1p, 17p, and 19q. Results.-Of the 12 oligodendrogliomas, 6 (60%) of 10 informative cases for 1p exhibited loss of heterozygosity (LOH). Six (50%) of 12 informative cases for 19q exhibited LOH. Each case also showed LOH at 1p. Three (25%) of 12 informative cases exhibited LOH at 17p for the dinucleotide repeat within the TP53 gene. In oligoastrocytomas, none of 4 informative cases showed LOH at 1p, 1 (25%) showed LOH at 19q, and 2 (50%) at 17p. One case also displayed microsatellite instability at 3 of 8 markers. In the 3 anaplastic oligodendrogliomas, 1 was not informative for 1p and none of the informative tumors exhibited LOH at 1p or 17p; 1 case (33%) exhibited LOH at 19q. Of the 14 informative anaplastic oligoastrocytomas, LOH was seen in 5 (36%) at both 1p and 19q and in 2 (14%) at 17p. Those with allelic loss at TP53 were astrocytoma predominant. No dysembryoplastic neuroepithelial tumors exhibited LOH at any marker on 1p, 17p, or 19q. Conclusions.-These findings suggest that routine screening for allelic losses, in samples intraoperatively determined to have an oligodendroglial component, will reveal prognostically or therapeutically relevant information in the majority of cases.

Original languageEnglish (US)
Pages (from-to)1573-1579
Number of pages7
JournalArchives of Pathology and Laboratory Medicine
Volume127
Issue number12
StatePublished - Dec 1 2003
Externally publishedYes

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Oligodendroglioma
Loss of Heterozygosity
Microsatellite Repeats
Polymerase Chain Reaction
Neoplasms
Neuroepithelial Neoplasms
Dinucleotide Repeats
Central Nervous System Neoplasms
Microsatellite Instability
p53 Genes
Astrocytoma
Genetic Markers
Brain Neoplasms

All Science Journal Classification (ASJC) codes

  • Pathology and Forensic Medicine
  • Medical Laboratory Technology

Cite this

Allelic Losses in Oligodendroglial and Oligodendroglioma-like Neoplasms : Analysis Using Microsatellite Repeats and Polymerase Chain Reaction. / Johnson, Mahlon; Vnencak-Jones, Cindy L.; Toms, Steven A.; Moots, Paul M.; Weil, Robert.

In: Archives of Pathology and Laboratory Medicine, Vol. 127, No. 12, 01.12.2003, p. 1573-1579.

Research output: Contribution to journalArticle

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abstract = "Context.-Oligodendroglial tumors are heterogenous neoplasms with histologic features shared with other central nervous system tumors, such as dysembryoplastic neuroepithelial tumors. Objective.-We examined a series of tumors, identified as possessing oligodendroglial components at the time of intraoperative examination, to see if molecular subsets based on the oligodendroglial component could be recognized. Design.-DNA was extracted from fresh brain tumor tissue and corresponding peripheral blood or normal tissues. Genotypes for multiple loci were determined by polymerase chain reaction amplification using fluorescent-labeled primers for markers on chromosomes 1p, 17p, and 19q. Results.-Of the 12 oligodendrogliomas, 6 (60{\%}) of 10 informative cases for 1p exhibited loss of heterozygosity (LOH). Six (50{\%}) of 12 informative cases for 19q exhibited LOH. Each case also showed LOH at 1p. Three (25{\%}) of 12 informative cases exhibited LOH at 17p for the dinucleotide repeat within the TP53 gene. In oligoastrocytomas, none of 4 informative cases showed LOH at 1p, 1 (25{\%}) showed LOH at 19q, and 2 (50{\%}) at 17p. One case also displayed microsatellite instability at 3 of 8 markers. In the 3 anaplastic oligodendrogliomas, 1 was not informative for 1p and none of the informative tumors exhibited LOH at 1p or 17p; 1 case (33{\%}) exhibited LOH at 19q. Of the 14 informative anaplastic oligoastrocytomas, LOH was seen in 5 (36{\%}) at both 1p and 19q and in 2 (14{\%}) at 17p. Those with allelic loss at TP53 were astrocytoma predominant. No dysembryoplastic neuroepithelial tumors exhibited LOH at any marker on 1p, 17p, or 19q. Conclusions.-These findings suggest that routine screening for allelic losses, in samples intraoperatively determined to have an oligodendroglial component, will reveal prognostically or therapeutically relevant information in the majority of cases.",
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