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Related Experiment Videos

Karyotypic patterns in acute mixed lineage leukemia.

Y Hayashi1, K Sugita, S Nakazawa

  • 1Division of Hematology/Oncology, Saitama Children's Medical Center, Japan.

Leukemia
|February 1, 1990
PubMed
Summary

Cytogenetic analysis of acute mixed lineage leukemia (AMLL) in children reveals distinct patterns. Chromosome alterations like 11q23 translocations and t(9;22) correlate with specific antigen expressions, aiding in disease classification.

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Area of Science:

  • Pediatric Hematology/Oncology
  • Cancer Cytogenetics
  • Immunophenotyping

Background:

  • Acute mixed lineage leukemia (AMLL) presents a diagnostic challenge due to its mixed myeloid and lymphoid features.
  • Accurate classification of AMLL is crucial for determining appropriate treatment strategies and predicting patient outcomes.
  • Understanding the underlying genetic and immunophenotypic profiles can refine AMLL classification.

Purpose of the Study:

  • To investigate cytogenetic and immunologic characteristics of blast cells in pediatric AMLL.
  • To identify patterns of chromosome alterations and antigen expression that can aid in AMLL classification.
  • To correlate specific karyotypic abnormalities with distinct immunophenotypes in AMLL.

Main Methods:

  • Performed cytogenetic studies to analyze chromosome alterations in blast cells from 13 children with AMLL.

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  • Conducted immunologic studies to assess antigen expression (e.g., CD19, HLA-DR, CD10, CD13) on blast cells.
  • Correlated cytogenetic findings with immunophenotypic data and clinical features (age, hyperleukocytosis).

    • Main Results:

    • Six patients with 11q23 translocations (including t(11;19), t(9;11), t(1;11)) were younger and had hyperleukocytosis; blasts expressed CD19 and HLA-DR, with only one case positive for CD10 (CALLA).
    • Four patients with t(9;22)(q34;q11) were older and had hyperleukocytosis; blasts expressed CD13, CD19, and HLA-DR, with three cases positive for CD10 (CALLA).
    • 11q23 translocations were associated with CD10-negative ALL with a myeloid phenotype, while t(9;22) occurred in CD10-positive AML with a lymphoid phenotype. One case showed a 7q35-q36 translocation.

    Conclusions:

    • Karyotypic alterations, specifically 11q23 translocations and t(9;22), are associated with distinct immunophenotypes in pediatric AMLL.
    • The findings suggest that cytogenetic analysis can refine the classification of AMLL, differentiating between lymphoid and myeloid phenotypes.
    • These correlations provide valuable insights for improved diagnostic and therapeutic approaches in pediatric AMLL.