Phenotypic changes in acute myeloid leukaemia: implications in the detection of minimal residual disease

AIM: To explore the role of phenotypic changes as possible limiting factors in the immunological detection of minimal residual disease in patients with acute myeloid leukaemia (AML). METHODS: 20 relapses were evaluated, with special attention to changes in the criteria used for the definition of a p...

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Published inJournal of clinical pathology Vol. 49; no. 1; pp. 15 - 18
Main Authors Macedo, A, San Miguel, J F, Vidriales, M B, López-Berges, M C, García-Marcos, M A, Gonzalez, M, Landolfi, C, Orfão, A
Format Journal Article
LanguageEnglish
Published London BMJ Publishing Group Ltd and Association of Clinical Pathologists 01.01.1996
BMJ
BMJ Publishing Group LTD
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Summary:AIM: To explore the role of phenotypic changes as possible limiting factors in the immunological detection of minimal residual disease in patients with acute myeloid leukaemia (AML). METHODS: 20 relapses were evaluated, with special attention to changes in the criteria used for the definition of a phenotype as "aberrant". In all cases the same monoclonal antibody and fluorochrome were used at diagnosis and in relapse. RESULTS: Six out of the 16 patients showed aberrant phenotypes at diagnosis. At relapse, no changes in the aberrant phenotypes were detected in most of the patients; nevertheless, in two of the four patients with asynchronous antigen expression this aberration disappeared at relapse. At diagnosis in both cases there were already small blast cell subpopulations showing the phenotype of leukaemic cells at relapse. Ten out of the 16 cases analysed showed significant changes in the expression of at least one of the markers analysed. CONCLUSIONS: At relapse in AML the "leukaemic phenotypes" usually remained unaltered, while other phenotypic features--not relevant for distinguishing leukaemic blast cells among normal progenitors--changed frequently; however, they were not a major limitation in the immunological detection of minimal residual disease.
Bibliography:istex:53F6526B7D51501505078025B9AB72C8F79387C5
PMID:8666678
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ISSN:0021-9746
1472-4146
DOI:10.1136/jcp.49.1.15