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Chromosome aberrations in mesoblastic nephroma

D E Schofield1, E J Yunis, J A Fletcher

  • 1Department of Pathology, Brigham and Women's Hospital, Boston, Massachusetts.

The American Journal of Pathology
|September 1, 1993
PubMed
Summary

Mesoblastic nephroma (MN), a common infant kidney tumor, shows extra copies of chromosome 11 in cellular and mixed types. Gains of chromosomes 8 and 17 also appear linked to MN development.

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Area of Science:

  • Pediatric Oncology
  • Cytogenetics
  • Molecular Pathology

Background:

  • Mesoblastic nephroma (MN) is the most frequent renal tumor in infants.
  • Histological subtypes include classic, cellular, and mixed, differentiated by cellularity.
  • Previous studies suggested a potential link between extra chromosome 11 copies and MN.

Purpose of the Study:

  • To investigate the role of chromosome copy number in the development of mesoblastic nephroma.
  • To determine if extra copies of chromosome 11 are specifically associated with certain MN histological subtypes.
  • To explore additional nonrandom cytogenetic events in cellular and mixed MN.

Main Methods:

  • Analysis of nuclear suspensions from 17 formalin-fixed, paraffin-embedded MN tumors.
  • Fluorescence in situ hybridization (FISH) using probes for chromosome 11 (D11Z1) and other chromosomes (7, 8, 9, 12, 17, 20).
  • DNA aneuploidy assessment via image analysis.

Main Results:

  • Extra copies of D11Z1 (chromosome 11) were found in 7/10 cellular or mixed MNs, but not in classic MNs (P < 0.05).
  • Additional gains of D8Z1 (chromosome 8) and D17Z1 (chromosome 17) were observed in 5/10 and 4/10 cellular/mixed MNs, respectively.
  • DNA aneuploidy was present in 3 tumors, all exhibiting more than four chromosomal aberrations by FISH.

Conclusions:

  • Increased copy number of chromosome 11 is associated with cellular and mixed types of mesoblastic nephroma.
  • Gains of chromosomes 8 and 17 represent potential nonrandom cytogenetic events in MN evolution.
  • Cytogenetic analysis, including FISH, is crucial for understanding MN pathogenesis and potential progression markers.

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