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

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).

• Authors: Nozomu Kawashima, Akira Shimada, Takeshi Taketani, Yasuhide Hayashi, Nao Yoshida, Kimikazu Matsumoto, Yoshiyuki Takahashi, Seiji Kojima, Koji Kato
• Journal: International journal of hematology (Int J Hematol) Vol. 95 Issue 5 Pg. 577-80 (May 2012) ISSN: 1865-3774 [Electronic] Japan
• PMID: 22403058 (Publication Type: Case Reports, Journal Article)

Chemical References

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

Topics

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