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Related Experiment Videos

Clonal analysis of gliomas

M M Kattar1, W J Kupsky, R K Shimoyama

  • 1Department of Pathology, Harper Hospital, Wayne State University, Detroit, MI 48201, USA.

Human Pathology
|October 29, 1997
PubMed
Summary

Low-grade and malignant gliomas are typically monoclonal, originating from a single precursor cell. Gliomatosis cerebri may present as oligoclonal, suggesting multiple origins or collisions.

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Area of Science:

  • Neuro-oncology
  • Cancer Genetics
  • Molecular Biology

Background:

  • Malignant gliomas exhibit heterogeneity and diffuse spread, raising questions about their clonal origin (monoclonal vs. polyclonal).
  • Understanding the clonality of low-grade gliomas, potential precursors to malignant gliomas, is limited.
  • Surgical samples may not fully represent the clonal diversity seen in autopsy tissues.

Purpose of the Study:

  • To investigate the clonality of low-grade and malignant gliomas.
  • To compare clonality in surgical versus autopsy materials.
  • To utilize a Polymerase chain reaction (PCR)-based assay for X chromosome inactivation patterns.

Main Methods:

  • Analysis of archival surgical and autopsy tissues from female patients with low-grade and malignant gliomas.

Related Experiment Videos

  • Microdissection of tumor areas followed by PCR amplification of the HUMARA locus.
  • Assay using a methylation-sensitive restriction enzyme (HhaI) to detect nonrandom X chromosome inactivation.
  • Densitometric scanning of PCR products to measure allele band intensities.

    • Main Results:

    • Most low-grade and malignant gliomas analyzed were monoclonal (15/19 in surgical group A, 8/13 in autopsy group S).
    • Gliomatosis cerebri samples showed opposite X inactivation skewing in distant areas, suggesting oligoclonal derivation.
    • Focal loss of heterozygosity (LOH) and microsatellite instability were observed in some malignant gliomas.
    • Biphasic gliomas demonstrated monoclonal origin.

    Conclusions:

    • Low-grade and malignant gliomas are predominantly monoclonal, with extensive spread attributed to cell migration.
    • Gliomatosis cerebri may arise from oligoclonal processes or collision of distinct gliomas.
    • Biphasic gliomas likely originate from a single precursor cell.
    • LOH at the HUMARA locus suggests X chromosome deletion during malignant glioma evolution.