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[Infant leukemia with t(1;22) presenting proliferation of erythroid and megakaryocytic cell lineages]

M Oshima1, T Fukushima, K Koike

  • 1Department of Pediatrics, Ibaraki Children's Hospital.

Insights

This infant leukemia case shows blasts expressing both red blood cell and platelet precursor markers, suggesting a common origin. This dual marker expression occurred during bone marrow relapse.

Area of Science:

  • Hematology
  • Pediatric Oncology
  • Molecular Biology

Background:

  • Infant leukemia presents unique diagnostic challenges.
  • Distinguishing between different myeloid leukemia subtypes is crucial for treatment.
  • Lineage infidelity in leukemia blasts can complicate diagnosis.

Observation:

  • A 9-month-old girl presented with anemia, splenomegaly, and thrombocytopenia.
  • Bone marrow examination revealed erythroblasts and megakaryoblasts.
  • Flow cytometry showed distinct CD41 and glycophorin A positive populations initially.

Findings:

  • At relapse, leukemia blasts became double-positive for erythroblastic and megakaryoblastic surface markers.
  • Chromosomal analysis revealed a t(1;22)(p13;q13) translocation, specific for infant acute megakaryoblastic leukemia (M7).
  • The findings suggest leukemia originated from a common progenitor cell of both erythroid and megakaryocytic lineages.

Implications:

  • This case highlights the potential for lineage plasticity in infant leukemia.
  • Understanding progenitor cell abnormalities is key to diagnosing and treating infant myeloid leukemias.
  • The t(1;22) translocation serves as a critical diagnostic marker for this specific infant leukemia subtype.

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