Myeloid lineage involvement in acute lymphoblastic leukemia: a morphology antibody chromosomes (MAC) study

M Larramendy1, W el-Rifai, U Saarinen

  • 1Department of Medical Genetics, University of Helsinki, Finland.

Experimental Hematology
|December 1, 1995
PubMed

Insights

Chromosomal abnormalities in acute lymphoblastic leukemia (ALL) were investigated in myeloid cells. Aberrations were found in lymphoid cells and, in one case, in nonleukemic erythroblasts, suggesting shared clonal origins.

Area of Science:

  • Pediatric Hematology Oncology
  • Cancer Genetics
  • Cell Biology

Background:

  • Acute lymphoblastic leukemia (ALL) is a heterogeneous cancer.
  • Understanding the cellular origins and genetic landscape of ALL is crucial for diagnosis and treatment.
  • Clonal chromosomal abnormalities are hallmarks of cancer, but their presence in non-leukemic cell lineages in ALL is not fully understood.

Purpose of the Study:

  • To investigate the presence of clonal chromosomal abnormalities in myeloid cell lineages within bone marrow aspirates of children diagnosed with ALL.
  • To determine if these abnormalities extend beyond the leukemic lymphoid blasts to other hematopoietic cell types.

Main Methods:

  • Utilized a combination of Morphology, Antibody staining, and Chromosome analysis (MAC) techniques.
  • Employed in situ hybridization procedures for detailed genetic analysis.
  • Analyzed bone marrow aspirates from six pediatric patients with ALL.

Main Results:

  • Chromosomal aberrations were identified in CD10- and CD20/22-positive lymphoid cells of patients with lymphoid-only ALL.
  • Mature lymphocytes (CD22+ and CD3+) did not exhibit these chromosomal aberrations.
  • In one patient with mixed lymphoid and myeloid-associated antigen expression, clonal aberrations were present in CD10+ and CD19+ blasts, as well as in glycophorin A-positive, morphologically nonleukemic erythroblasts.

Conclusions:

  • Clonal chromosomal abnormalities in pediatric ALL can be present in lymphoid progenitor cells.
  • The findings suggest a potential shared clonal origin or early divergence event between lymphoid and myeloid lineages in some ALL cases.
  • Further research is needed to elucidate the implications of these findings for ALL pathogenesis and clinical management.

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