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Immunophenotypic dysplasia and aberrant T-cell antigen expression in acute myeloid leukaemia with complex karyotype and TP53 mutations
  1. Katelyn C Dannheim1,
  2. Olga Pozdnyakova2,
  3. Paola Dal Cin2,
  4. Olga K Weinberg3
  1. 1 Department of Pathology, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA
  2. 2 Department of Pathology, Brigham and Women’s Hospital, Boston, Massachusetts, USA
  3. 3 Department of Pathology, Boston Children’s Hospital, Boston, Massachusetts, USA
  1. Correspondence to Dr Olga K Weinberg , Department of Pathology, Boston Children’s Hospital, Boston, MA 02115, USA ; olga.weinberg{at}


Aims Cytogenetic and molecular aberrations are the strongest factors in determining outcome in acute myeloid leukaemia (AML). AML with complex karyotype confers a particularly poor prognosis and is associated with morphologic dysplasia. Flow cytometric immunophenotyping (FCI) has been investigated in defining dysplasia within myelodysplastic syndromes, but little is known about immunophenotypic dysplasia in AML and correlation with genetic abnormalities. This study aimed to explore differences in antigen expression by FCI in AML with complex karyotype (AML-CK) and AML with complex karyotype and TP53 mutations (AML-TP53) compared with AML with normal karyotype (AML-NK).

Methods Twenty-five cases of AML-CK, 13 of which had abnormalities of TP53, were compared with 83 cases of AML-NK using FCI.

Results Our findings demonstrated brighter expression of CD34 with decreased CD33 and aberrant expression of CD5 in blasts of AML-CK, while AML-TP53 blasts exhibited brighter expression of CD13. Granulocytes in AML-CK exhibited brighter expression of CD5, CD7, CD10 and CD14, with brighter CD3 also seen in AML-TP53.

Conclusions Our results suggest that immunophenotypic dysplasia correlates with complex karyotype and TP53 mutation, including increased expression of T-cell antigens.

  • leukaemia, flow cytometry, myelodysplasia, immunophenotyping of leukaemias
  • lymphomas, genetics

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  • Handling editor Mary Frances McMullin.

  • Contributors KD and OKW developed the hypothesis and designed the study. All authors assisted in collecting the clinical data for analysis. KD performed the statistical analysis and wrote the manuscript with support from OW, OP and PDC.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Patient consent Not required.

  • Provenance and peer review Not commissioned; externally peer reviewed.