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CD66c expression in B‐cell acute lymphoblastic leukemia: strength and weakness
Author(s) -
GUILLAUME N.,
PENTHER D.,
VAIDA I.,
GRUSON B.,
HARRIVEL V.,
CLAISSE J .F.,
CAPIOD J. C.,
LEFRERE J. J.,
DAMAJ G.
Publication year - 2011
Publication title -
international journal of laboratory hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.705
H-Index - 55
eISSN - 1751-553X
pISSN - 1751-5521
DOI - 10.1111/j.1751-553x.2010.01254.x
Subject(s) - breakpoint cluster region , cd33 , cd117 , minimal residual disease , abl , myeloid leukemia , myeloid , biology , flow cytometry , antigen , cancer research , microbiology and biotechnology , immunology , leukemia , cd34 , gene , genetics , tyrosine kinase , stem cell , signal transduction
Summary Introduction: In B‐cell acute lymphoblastic leukemia (B‐ALL), testing at diagnosis for BCR/ABL1 gene rearrangements is mandatory for prognostic stratification and treatment decisions. Several diagnostic methods have been proposed using flow cytometry to identify BCR/ABL1 + B‐ALL. Methods: We evaluated expression of the myeloid antigen CD66c by flow cytometry in B‐ALL. We studied 94 patients with B‐ALL. The t (9;22)(q34;q11) or BCR/ABL1 rearrangement was detected by cytogenetic analysis or RT/PCR. Myeloid antigens CD66c, CD13, CD33, CD117, Myeloperoxidase, CD15 and CD65 were determined by flow cytometry. Results: Of these 94 cases, 17 (18%) cases displayed BCR/ABL1 gene rearrangements and 38 (40%) cases were CD66c positive. CD66c was the most common myeloid antigen expressed on malignant lymphoblasts. Its expression was correlated with BCR/ABL1 rearrangements ( P = 0.0001): sensitivity 82%, specificity 69%, positive predictive value 37% and negative predictive value 95%. Co‐expression of CD66c + CD13 + was more frequent in BCR/ABL1 + B‐ALL (29%) than BCR/ABL1 − cases (4%) ( P = 0.0044). Some BCR/ABL1 − B‐ALL cases (including hyperdiploid or cases with normal karyotype) were CD66c positive (31%). Conclusion: CD66c expression is correlated, but not specifically, with BCR/ABL1 rearrangement. It would seem better to interpret the absence of CD66c expression with a lack of BCR/ABL1 rearrangement. This myeloid antigen could be interesting in the detection of minimal residual disease.