Childhood acute myeloid leukemia with bone marrow eosinophilia caused by t(16;21)(q24;q22)

Int J Hematol. 2012 May;95(5):577-80. doi: 10.1007/s12185-012-1044-7. Epub 2012 Mar 9.

Abstract

Acute myeloid leukemia with abnormal bone marrow eosinophilia (AML-M4Eo) is often reported in core binding factor (CBF) leukemia, with translocations such as inv(16)(p13q22), t(16;16)(p13;q22) or t(8;21)(q22;q22); however, it is rarely reported with t(16;21)(q24;q22), which produces the RUNX1-CBFA2T3 (AML1-MTG16) chimera. The similarity between this chimera and RUNX1-RUNXT1 (AML1-MTG8) by t(8;21)(q22;q22) remains controversial. Adult leukemia with t(16;21)(q24;q22) was primarily therapy related, and shows poor prognosis; however, pediatric AML with this translocation was quite rare and tended to be de novo AML. We present here a 4-year-old boy with de novo AML-M4Eo and t(16;21)(q24;q22). He received chemotherapy and survived for more than 70 months without transplantation. We speculated that pediatric AML with t(16;21)(q24;q22) showed favorable prognosis, as with t(8;21)(q22;q22).

Publication types

  • Case Reports

MeSH terms

  • Antineoplastic Agents / therapeutic use
  • Bone Marrow / metabolism
  • Bone Marrow / pathology
  • Child
  • Chromosomes, Human, Pair 16
  • Chromosomes, Human, Pair 21
  • Core Binding Factor Alpha 2 Subunit / genetics*
  • Eosinophilia / complications*
  • Eosinophilia / genetics
  • Eosinophilia / pathology
  • Humans
  • Leukemia, Myeloid, Acute / complications*
  • Leukemia, Myeloid, Acute / drug therapy
  • Leukemia, Myeloid, Acute / genetics
  • Leukemia, Myeloid, Acute / pathology
  • Male
  • Repressor Proteins / genetics*
  • Translocation, Genetic
  • Tumor Suppressor Proteins / genetics*

Substances

  • Antineoplastic Agents
  • CBFA2T3 protein, human
  • Core Binding Factor Alpha 2 Subunit
  • Repressor Proteins
  • Tumor Suppressor Proteins