The presence of leukaemia-associated phenotypes is an independent predictor of induction failure in acute myeloid leukaemia

被引:8
作者
Al-Mawali, A. [1 ,2 ]
To, L. B. [3 ]
Gillis, D.
Hissaria, P.
Mundy, J.
Lewis, I. [4 ]
机构
[1] Univ Adelaide, Hanson Inst, Div Haematol, IMVS, Adelaide, SA 5000, Australia
[2] Univ Adelaide, Hanson Inst, Div Human Immunol, IMVS, Adelaide, SA 5000, Australia
[3] Royal Adelaide Hosp, IMVS, Div Haematol, Adelaide, SA 5000, Australia
[4] IMVS, Hanson Ctr Canc Res, Div Haematol, Adelaide, SA, Australia
关键词
Acute myeloid leukaemia; leukaemia-associated phenotypes; multiparameter flow cytometry; immunophenotyping; lineage infidelity; MINIMAL RESIDUAL DISEASE; SURFACE-MARKER ANALYSIS; ABERRANT PHENOTYPES; EXPRESSION; ANTIGENS; CELLS; AML; DAUNORUBICIN; CD7;
D O I
10.1111/j.1751-553X.2007.01003.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Immunophenotyping of acute myeloid leukaemia (AML) has controversial implications with regards to prognosis. The aims of the present study were to determine the frequency of leukaemia-associated phenotypes (LAP) in AML and to correlate their presence with response to induction chemotherapy. We analysed bone marrow samples at diagnosis from 84 AML patients using triple staining flow cytometry with routine standard panel of monoclonal antibodies. The association of LAP and response to induction chemotherapy was evaluated retrospectively. LAP were observed in 54 (64%) patients: lineage infidelity in 19 (35%), asynchronous antigen expression in 28 (52%), and lack of expected lineage specific antigens in 19 (35%). Significant correlation was found between LAP and responses to induction chemotherapy. Response to induction chemotherapy was more frequent in the absence of LAP (P < 0.05, estimated risk ratio of 1.6, 95%CI, 1.0-2.6) in a multivariate analysis. In conclusion, our data show the presence of LAP in AML is an independent predictor for response to induction chemotherapy and risk of relapse and should be considered for counselling patients and planning therapy.
引用
收藏
页码:61 / 68
页数:8
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