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Blood, 1 June 2001, Vol. 97, No. 11, pp. 3574-3580

NEOPLASIA

High frequency of immunophenotype changes in acute myeloid leukemia at relapse: implications for residual disease detection (Cancer and Leukemia Group B Study 8361)

Maria R. Baer, Carleton C. Stewart, Richard K. Dodge, Gail Leget, Norbert Sulé, Krzysztof Mrózek, Charles A. Schiffer, Bayard L. Powell, Jonathan E. Kolitz, Joseph O. Moore, Richard M. Stone, Frederick R. Davey, Andrew J. Carroll, Richard A. Larson, and Clara D. Bloomfield

From the Roswell Park Cancer Institute, Buffalo, New York; CALGB Statistical Center, Durham, North Carolina; Southeastern Cancer Center, Lumberton, North Carolina; The Ohio State University Medical Center, Columbus, Ohio; Wayne State University School of Medicine, Detroit, Michigan; Wake Forest University School of Medicine, Winston-Salem, North Carolina; North Shore University Hospital, Manhasset, New York; Duke University Medical Center, Durham, North Carolina; Dana-Farber Cancer Institute, Boston, Massachusetts; State University of New York Upstate Medical University, Syracuse, New York; University of Alabama at Birmingham; University of Chicago Medical Center, Chicago, Illinois.

Multiparameter flow cytometry (MFC) has the potential to allow for sensitive and specific monitoring of residual disease (RD) in acute myeloid leukemia (AML). The use of MFC for RD monitoring assumes that AML cells identified by their immunophenotype at diagnosis can be detected during remission and at relapse. AML cells from 136 patients were immunophenotyped by MFC at diagnosis and at first relapse using 9 panels of 3 monoclonal antibodies. Immunophenotype changes occurred in 124 patients (91%); they consisted of gains or losses of discrete leukemia cell populations resolved by MFC (42 patients) and gains or losses of antigens on leukemia cell populations present at both time points (108 patients). Antigen expression defining unusual phenotypes changed frequently: CD13, CD33, and CD34, absent at diagnosis in 3, 33, and 47 cases, respectively, were gained at relapse in 2 (67%), 15 (45%), and 17 (36%); CD56, CD19, and CD14, present at diagnosis in 5, 16, and 20 cases, were lost at relapse in 2 (40%), 6 (38%), and 8 (40%). Leukemia cell gates created in pretreatment samples using each 3-antibody panel allowed identification of relapse AML cells in only 68% to 91% of cases, but use of 8 3-antibody panels, which included antibodies to a total of 16 antigens, allowed identification of relapse AML cells in all cases. Thus, the immunophenotype of AML cells is markedly unstable; nevertheless, despite this instability, MFC has the potential to identify RD in AML if multiple antibody panels are used at all time points.

© 2001 by The American Society of Hematology.
 

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