Acute myeloid leukemia with translocation t(8;16) presents with features which mimic acute promyelocytic leukemia and is associated with poor prognosis

Adi Diab, Lynette Zickl, Omar Abdel-Wahab, Suresh Jhanwar, Manjit A. Gulam, Katherine S. Panageas, Jay P. Patel, Joseph Jurcic, Peter Maslak, Elisabeth M. Paietta, James K. Mangan, Martin Carroll, Hugo F. Fernandez, Julie Teruya-Feldstein, Selina M. Luger, Dan Douer, Mark R. Litzow, Hillard M. Lazarus, Jacob M. Rowe, Ross L. Levine & 1 others Martin S. Tallman

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

Previous small series have suggested that acute myeloid leukemia with t(8;16) is a distinct morphologic and clinical entity associated with poor prognosis. We describe 18 patients with t(8;16) AML, including their clinical, cytomorphologic, immunophenotypic and cytogenetic features. Half of the patients had extramedullary disease, most commonly leukemia cutis, which often preceded bone marrow involvement and six had therapy-related AML. Patients with t(8;16) AML commonly present with clinical and pathological features that mimic APL, with promyelocytes and promyeloblast-like cells and coagulopathy in most patients. Several patients also presented with marrow histiocytes with hemophagocytosis and erythrophagocytosis. Comprehensive molecular analysis for co-occurring genetic alterations revealed a somatic mutation in RUNX1 in 1 of 6 t(8;16) patients with no known AML mutation in the remaining five t(8;16) patients. This suggests that the t(8;16) translocation could be sufficient to induce hematopoietic cell transformation to AML without acquiring other genetic alteration. These data further support classifying t(8;16) AML as a clinically and molecularly defined subtype of AML marked by characteristic clinical and cytomorphologic features that mimic APL, and is associated with very poor survival.

Original languageEnglish (US)
Pages (from-to)32-36
Number of pages5
JournalLeukemia Research
Volume37
Issue number1
DOIs
StatePublished - Jan 2013

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Acute Promyelocytic Leukemia
Acute Myeloid Leukemia
Bone Marrow
Granulocyte Precursor Cells
Mutation
Histiocytes
Cytogenetics
Leukemia
Survival

Keywords

  • AML
  • APL
  • Leukemia
  • T(8;16)
  • Therapy-related AML

ASJC Scopus subject areas

  • Cancer Research
  • Hematology
  • Oncology

Cite this

Acute myeloid leukemia with translocation t(8;16) presents with features which mimic acute promyelocytic leukemia and is associated with poor prognosis. / Diab, Adi; Zickl, Lynette; Abdel-Wahab, Omar; Jhanwar, Suresh; Gulam, Manjit A.; Panageas, Katherine S.; Patel, Jay P.; Jurcic, Joseph; Maslak, Peter; Paietta, Elisabeth M.; Mangan, James K.; Carroll, Martin; Fernandez, Hugo F.; Teruya-Feldstein, Julie; Luger, Selina M.; Douer, Dan; Litzow, Mark R.; Lazarus, Hillard M.; Rowe, Jacob M.; Levine, Ross L.; Tallman, Martin S.

In: Leukemia Research, Vol. 37, No. 1, 01.2013, p. 32-36.

Research output: Contribution to journalArticle

Diab, A, Zickl, L, Abdel-Wahab, O, Jhanwar, S, Gulam, MA, Panageas, KS, Patel, JP, Jurcic, J, Maslak, P, Paietta, EM, Mangan, JK, Carroll, M, Fernandez, HF, Teruya-Feldstein, J, Luger, SM, Douer, D, Litzow, MR, Lazarus, HM, Rowe, JM, Levine, RL & Tallman, MS 2013, 'Acute myeloid leukemia with translocation t(8;16) presents with features which mimic acute promyelocytic leukemia and is associated with poor prognosis', Leukemia Research, vol. 37, no. 1, pp. 32-36. https://doi.org/10.1016/j.leukres.2012.08.025
Diab, Adi ; Zickl, Lynette ; Abdel-Wahab, Omar ; Jhanwar, Suresh ; Gulam, Manjit A. ; Panageas, Katherine S. ; Patel, Jay P. ; Jurcic, Joseph ; Maslak, Peter ; Paietta, Elisabeth M. ; Mangan, James K. ; Carroll, Martin ; Fernandez, Hugo F. ; Teruya-Feldstein, Julie ; Luger, Selina M. ; Douer, Dan ; Litzow, Mark R. ; Lazarus, Hillard M. ; Rowe, Jacob M. ; Levine, Ross L. ; Tallman, Martin S. / Acute myeloid leukemia with translocation t(8;16) presents with features which mimic acute promyelocytic leukemia and is associated with poor prognosis. In: Leukemia Research. 2013 ; Vol. 37, No. 1. pp. 32-36.
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abstract = "Previous small series have suggested that acute myeloid leukemia with t(8;16) is a distinct morphologic and clinical entity associated with poor prognosis. We describe 18 patients with t(8;16) AML, including their clinical, cytomorphologic, immunophenotypic and cytogenetic features. Half of the patients had extramedullary disease, most commonly leukemia cutis, which often preceded bone marrow involvement and six had therapy-related AML. Patients with t(8;16) AML commonly present with clinical and pathological features that mimic APL, with promyelocytes and promyeloblast-like cells and coagulopathy in most patients. Several patients also presented with marrow histiocytes with hemophagocytosis and erythrophagocytosis. Comprehensive molecular analysis for co-occurring genetic alterations revealed a somatic mutation in RUNX1 in 1 of 6 t(8;16) patients with no known AML mutation in the remaining five t(8;16) patients. This suggests that the t(8;16) translocation could be sufficient to induce hematopoietic cell transformation to AML without acquiring other genetic alteration. These data further support classifying t(8;16) AML as a clinically and molecularly defined subtype of AML marked by characteristic clinical and cytomorphologic features that mimic APL, and is associated with very poor survival.",
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AU - Diab, Adi

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AU - Jhanwar, Suresh

AU - Gulam, Manjit A.

AU - Panageas, Katherine S.

AU - Patel, Jay P.

AU - Jurcic, Joseph

AU - Maslak, Peter

AU - Paietta, Elisabeth M.

AU - Mangan, James K.

AU - Carroll, Martin

AU - Fernandez, Hugo F.

AU - Teruya-Feldstein, Julie

AU - Luger, Selina M.

AU - Douer, Dan

AU - Litzow, Mark R.

AU - Lazarus, Hillard M.

AU - Rowe, Jacob M.

AU - Levine, Ross L.

AU - Tallman, Martin S.

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N2 - Previous small series have suggested that acute myeloid leukemia with t(8;16) is a distinct morphologic and clinical entity associated with poor prognosis. We describe 18 patients with t(8;16) AML, including their clinical, cytomorphologic, immunophenotypic and cytogenetic features. Half of the patients had extramedullary disease, most commonly leukemia cutis, which often preceded bone marrow involvement and six had therapy-related AML. Patients with t(8;16) AML commonly present with clinical and pathological features that mimic APL, with promyelocytes and promyeloblast-like cells and coagulopathy in most patients. Several patients also presented with marrow histiocytes with hemophagocytosis and erythrophagocytosis. Comprehensive molecular analysis for co-occurring genetic alterations revealed a somatic mutation in RUNX1 in 1 of 6 t(8;16) patients with no known AML mutation in the remaining five t(8;16) patients. This suggests that the t(8;16) translocation could be sufficient to induce hematopoietic cell transformation to AML without acquiring other genetic alteration. These data further support classifying t(8;16) AML as a clinically and molecularly defined subtype of AML marked by characteristic clinical and cytomorphologic features that mimic APL, and is associated with very poor survival.

AB - Previous small series have suggested that acute myeloid leukemia with t(8;16) is a distinct morphologic and clinical entity associated with poor prognosis. We describe 18 patients with t(8;16) AML, including their clinical, cytomorphologic, immunophenotypic and cytogenetic features. Half of the patients had extramedullary disease, most commonly leukemia cutis, which often preceded bone marrow involvement and six had therapy-related AML. Patients with t(8;16) AML commonly present with clinical and pathological features that mimic APL, with promyelocytes and promyeloblast-like cells and coagulopathy in most patients. Several patients also presented with marrow histiocytes with hemophagocytosis and erythrophagocytosis. Comprehensive molecular analysis for co-occurring genetic alterations revealed a somatic mutation in RUNX1 in 1 of 6 t(8;16) patients with no known AML mutation in the remaining five t(8;16) patients. This suggests that the t(8;16) translocation could be sufficient to induce hematopoietic cell transformation to AML without acquiring other genetic alteration. These data further support classifying t(8;16) AML as a clinically and molecularly defined subtype of AML marked by characteristic clinical and cytomorphologic features that mimic APL, and is associated with very poor survival.

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