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Acute myeloid leukemia with t(8;16)(p11.2;p13.3)/KAT6A-CREBBP in adults

Wei Xie1, Shimin Hu1, Jie Xu1

  • 1Departments of Hematopathology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX, 77030-4009, USA.

Annals of Hematology
|February 14, 2019
PubMed

Insights

The rare t(8;16)(p11.2;p13.3) genetic abnormality in acute myeloid leukemia (AML) often presents with monoblastic or myelomonocytic features, frequently arising after prior cancer treatment.

Area of Science:

  • Hematology
  • Cytogenetics
  • Oncology

Background:

  • The t(8;16)(p11.2;p13.3) chromosomal translocation is a rare cytogenetic abnormality associated with acute myeloid leukemia (AML).
  • This specific translocation involves the KAT6A and CREBBP genes.

Purpose of the Study:

  • To characterize the clinical and cytogenetic features of acute myeloid leukemia (AML) associated with the t(8;16)(p11.2;p13.3) abnormality.
  • To evaluate the outcomes and prognostic factors in patients with this specific AML subtype.

Main Methods:

  • Retrospective analysis of 15 adult patients with AML and t(8;16)(p11.2;p13.3).
  • Review of clinical data, including history of malignancy, therapy-related AML (t-AML) versus de novo AML, and presenting AML morphology.
  • Karyotyping and fluorescence in situ hybridization (FISH) to confirm the t(8;16) translocation and assess additional cytogenetic abnormalities.
  • Analysis of treatment response, remission rates, and overall survival.

Main Results:

  • Fifteen adult patients (13 female, 2 male; median age 50) with AML and t(8;16) were identified.
  • Ten patients had therapy-related AML (t-AML), and five had de novo AML.
  • AML subtypes were predominantly monoblastic (12 cases) or myelomonocytic (3 cases); hemophagocytosis was noted in seven patients.
  • The t(8;16) was the sole abnormality in seven cases, with others having additional or complex karyotypes.
  • Thirteen patients achieved complete remission after induction chemotherapy, with a median overall survival of 18.2 months.
  • Patients with de novo AML or non-complex karyotypes showed an undefined survival, suggesting a potentially better prognosis in the absence of adverse factors.

Conclusions:

  • The t(8;16)(p11.2;p13.3) abnormality in AML is frequently associated with monoblastic/myelomonocytic differentiation and often arises in patients with a history of cytotoxic therapy.
  • Patients with de novo AML or t-AML with t(8;16) and a non-complex karyotype may have a favorable outcome.
  • This rare cytogenetic finding warrants further investigation into its specific biological mechanisms and therapeutic implications.
Keywords:
Acute myeloid leukemiaCREBBPKAT6ATherapy-relatedt(8;16)(p11.2;p13.3)

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