International Journal of Hematology

, Volume 95, Issue 5, pp 577–580 | Cite as

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

  • Nozomu KawashimaEmail author
  • Akira Shimada
  • Takeshi Taketani
  • Yasuhide Hayashi
  • Nao Yoshida
  • Kimikazu Matsumoto
  • Yoshiyuki Takahashi
  • Seiji Kojima
  • Koji KatoEmail author
Case Report


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).


AML Pediatric Eosinophilia t(16;21)(q24;q22) RUNX1-CBFA2T3 


Conflict of interest

The authors declare no conflict of interest.


  1. 1.
    Schnittger S, Bacher U, Haferlach C, Kern W, Haferlach T. Rare CBFB-MYH11 fusion transcripts in AML with inv(16)/t(16;16) are associated with therapy-related AML M4eo, atypical cytomorphology, atypical immunophenotype, atypical additional chromosomal rearrangements and low white blood cell count: a study on 162 patients. Leukemia. 2007;21(4):725–31.PubMedGoogle Scholar
  2. 2.
    Tobal K, Johnson PR, Saunders MJ, Harrison CJ, Liu Yin JA. Detection of CBFB/MYH11 transcripts in patients with inversion and other abnormalities of chromosome 16 at presentation and remission. Br J Haematol. 1995;91(1):104–8.PubMedCrossRefGoogle Scholar
  3. 3.
    Delaunay J, Vey N, Leblanc T, Fenaux P, Rigal-Huguet F, Witz F, et al. Prognosis of inv(16)/t(16;16) acute myeloid leukemia (AML): a survey of 110 cases from the French AML Intergroup. Blood. 2003;102(2):462–9.PubMedCrossRefGoogle Scholar
  4. 4.
    Balgobind BV, Hollink IH, Arentsen-Peters ST, Zimmermann M, Harbott J, Beverloo HB, et al. Integrative analysis of type-I and type-II aberrations underscores the genetic heterogeneity of pediatric acute myeloid leukemia. Haematologica. 2011;96(10):1478–87.PubMedCrossRefGoogle Scholar
  5. 5.
    Raimondi SC, Kalwinsky DK, Hayashi Y, Behm FG, Mirro J, Williams DL. Cytogenetics of childhood acute nonlymphocytic leukemia. Cancer Genet Cytogenet. 1989;40(1):13–27.PubMedCrossRefGoogle Scholar
  6. 6.
    Kondoh K, Nakata Y, Furuta T, Hosoda F, Gamou T, Kurosawa Y, et al. A pediatric case of secondary leukemia associated with t(16;21)(q24;q22) exhibiting the chimeric AML1-MTG16 gene. Leuk Lymphoma. 2002;43(2):415–20.PubMedCrossRefGoogle Scholar
  7. 7.
    Frascella E, Zampieron C, Sainati L, Casula L, Pasquali F, Mura R, et al. AML1-MTG16 gene rearrangement in a pediatric therapy related AML after Ewing sarcoma: a case discussion and review of literature. Cancer Therapy. 2005;3(A):285–92.Google Scholar
  8. 8.
    Park IJ, Park JE, Kim HJ, Jung HJ, Lee WG, Cho SR. Acute myeloid leukemia with t(16;21)(q24;q22) and eosinophilia: case report and review of the literature. Cancer Genet Cytogenet. 2010;196(1):105–8.PubMedCrossRefGoogle Scholar
  9. 9.
    De Braekeleer E, Douet-Guilbert N, Le Bris MJ, Morel F, Férec C, De Braekeleer M. RUNX1-MTG16 fusion gene in acute myeloblastic leukemia with t(16;21)(q24;q22): case report and review of the literature. Cancer Genet Cytogenet. 2008;185(1):47–50.PubMedCrossRefGoogle Scholar
  10. 10.
    Tsukimoto I, Tawa A, Horibe K, Tabuchi K, Kigasawa H, Tsuchida M, et al. Risk-stratified therapy and the intensive use of cytarabine improves the outcome in childhood acute myeloid leukemia: the AML99 trial from the Japanese Childhood AML Cooperative Study Group. J Clin Oncol. 2009;27(24):4007–13.PubMedCrossRefGoogle Scholar
  11. 11.
    Gamou T, Kitamura E, Hosoda F, Shimizu K, Shinohara K, Hayashi Y, et al. The partner gene of AML1 in t(16;21) myeloid malignancies is a novel member of the MTG8(ETO) family. Blood. 1998;91(11):4028–37.PubMedGoogle Scholar
  12. 12.
    Ito Y. Oncogenic potential of the RUNX gene family: ‘overview’. Oncogene. 2004;23(24):4198–208.PubMedCrossRefGoogle Scholar
  13. 13.
    Kitabayashi I, Ida K, Morohoshi F, Yokoyama A, Mitsuhashi N, Shimizu K, et al. The AML1-MTG8 leukemic fusion protein forms a complex with a novel member of the MTG8(ETO/CDR) family, MTGR1. Mol Cell Biol. 1998;18(2):846–58.PubMedGoogle Scholar
  14. 14.
    Monma F, Nishii K, Lorenzo F, Usui E, Ueda Y, Watanabe Y, et al. Molecular analysis of PDGFRalpha/beta genes in core binding factor leukemia with eosinophilia. Eur J Haematol. 2006;76(1):18–22.PubMedCrossRefGoogle Scholar
  15. 15.
    Agarwal R, Vishnubhatla S, Gupta R, Bakhshi S. Diagnostic and follow-up eosinophilia is not predictive of outcome in childhood acute myeloid leukemia. J Pediatr Hematol Oncol. 2011;33(2):e51–3.PubMedCrossRefGoogle Scholar

Copyright information

© The Japanese Society of Hematology 2012

Authors and Affiliations

  • Nozomu Kawashima
    • 1
    Email author
  • Akira Shimada
    • 2
  • Takeshi Taketani
    • 3
  • Yasuhide Hayashi
    • 4
  • Nao Yoshida
    • 1
  • Kimikazu Matsumoto
    • 1
  • Yoshiyuki Takahashi
    • 2
  • Seiji Kojima
    • 2
  • Koji Kato
    • 1
    Email author
  1. 1.Division of Hematology/Oncology, Children’s Medical CenterJapanese Red Cross Nagoya First HospitalNagoyaJapan
  2. 2.Department of PediatricsNagoya University Graduate School of MedicineNagoyaJapan
  3. 3.Division of Blood TransfusionShimane University HospitalIzumoJapan
  4. 4.Department of Hematology/OncologyGunma Children’s Medical CenterShibukawaJapan

Personalised recommendations