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Proto-oncogene analysis in multiple myeloma.

M Ladanyi1, S Wang, R Niesvizky

  • 1Department of Pathology (Cytogenetics Service), Memorial Sloan-Kettering Cancer Center, New York, NY 10021.

The American Journal of Pathology
|October 1, 1992
PubMed
Summary
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This study investigated genetic alterations in multiple myeloma (MM), finding no evidence of BCL2 or MYC proto-oncogene translocations. These results suggest alternative mechanisms drive MM pathogenesis.

Area of Science:

  • Hematology
  • Oncology
  • Molecular Biology

Background:

  • The genetic basis of multiple myeloma (MM) is poorly understood due to challenges in cytogenetic analysis.
  • Known chromosomal abnormalities in MM involve proto-oncogenes BCL1 and MYC.
  • BCL2 protein overexpression suggests potential translocation-mediated deregulation, but its configuration in MM is undefined.

Purpose of the Study:

  • To investigate the role of BCL2 and MYC proto-oncogene rearrangements in multiple myeloma (MM).
  • To define the configuration of the BCL2 gene in MM using various breakpoint probes.
  • To assess the frequency of rearrangements distal to the MYC gene in MM.

Main Methods:

  • Southern blotting was used to analyze DNA from 17 patients with plasma cell dyscrasias (16 MM, 1 plasmacytoma).

Related Experiment Videos

  • Specific probes targeting BCL2 breakpoint regions (MBR, MCR, 5' cDNA), BCL1 MTC, and the MYC-associated MLVI-4 region were employed.
  • Rearrangement of immunoglobulin heavy chain genes confirmed the presence of tumor DNA.

    • Main Results:

    • No BCL2 gene rearrangements were detected using MBR, MCR, or 5' cDNA probes in any of the MM cases.
    • No rearrangements were found with the BCL1 MTC probe or the MLVI-4 probe targeting the MYC-associated region.
    • Immunoglobulin heavy chain gene rearrangements confirmed the validity of the tumor DNA samples.

    Conclusions:

    • Translocation-mediated deregulation of BCL2 is unlikely to be the primary mechanism in most MM cases.
    • Rearrangements distal to the MYC gene, detected by the MLVI-4 probe, may be less frequent in MM than previously reported.
    • The BCL1 MTC probe may not detect all translocation breakpoints within band 11q13 in MM, similar to observations in lymphomas.