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The value of detecting surface and cytoplasmic antigens in acute myeloid leukaemia
A Urbano-Ispizua1, E Matutes, N Villamor
1Postgraduate School of Haematology Farreras Valenti, Hospital Clinic i Provincial de Barcelona, Spain.
Insights
Immunophenotyping acute myeloid leukaemia (AML) cells using monoclonal antibodies (McAb) revealed CD13 as the most sensitive myeloid marker. Lymphoid antigen expression was rare, but CD7 positivity may indicate poor treatment outcomes in AML patients.
Area of Science:
- Hematology
- Immunology
- Oncology
Background:
- Acute myeloid leukaemia (AML) diagnosis relies on morphology and cytochemistry.
- Immunophenotyping offers a more sensitive method for leukaemia cell characterization.
Purpose of the Study:
- To analyze the immunophenotype of AML cells using monoclonal antibodies (McAb).
- To evaluate the diagnostic and clinical relevance of specific myeloid and lymphoid markers in AML.
Main Methods:
- Analysis of 60 AML patient samples using the APAAP technique.
- Application of a panel of anti-myeloid and lymphoid-associated McAb, including CD13, anti-myeloperoxidase (anti-Mpo), CD14, CD68, TdT, CD7, CD19, CD3, CD10, and CD4.
Main Results:
- CD13 was the most sensitive myeloid marker (90% positivity).
- CD14 and CD68 expression were frequent in M4/M5 subtypes (92%).
- Lymphoid antigen expression (TdT, CD7, CD19) was rare; CD4 was expressed in 44% of cases across subtypes.
- CD7 expression correlated with treatment refractoriness or shorter remission duration.
Conclusions:
- Immunophenotyping is crucial for AML diagnosis and classification.
- Specific markers like CD13 and CD14/CD68 aid in identifying AML subtypes.
- CD7 expression warrants further investigation for its prognostic value in AML.
Abstract:
The immunophenotype of leukaemia cells from 60 patients with acute myeloid leukaemia (AML) was analysed with the APAAP technique using a panel of anti-myeloid and lymphoid associated monoclonal antibodies (McAb). Cells from all cases, including three with negative cytochemical features, were labelled by at least one of the anti-myeloid McAb CD13, anti-myeloperoxidase (anti-Mpo), and/or CD14. The most sensitive marker was CD13, since it was positive in 90% of cases. In two out of three AML cases defined as M0-AML, CD13 was expressed in the cytoplasm but not on the membrane; in these three cases peroxidase (Mpo) was not detected by conventional cytochemistry, but could be demonstrated in all of them using the McAb anti-Mpo. The simultaneous expression of CD14 and CD68 McAb was often confined to the M4 and M5 FAB AML subtypes (92% cases) as compared to the others: M1, M2, M3 (18% cases). Lymphoid antigens were rarely positive (TdT+: 13%, CD7+: 15%, CD19+: 5%) and none of the AML cases were CD3+ or CD10+. By contrast, CD4 was expressed in blasts from 44% of cases and this was not restricted to AML with a monocytic component (M4, M5) but also found in other subtypes. There were no significant differences in the clinical or prognostic features according to the positivity or negativity with TdT and CD4. By contrast, expression of CD7 was associated with refractoriness to the treatment or short complete remission duration, although the number of patients is too small to draw firm conclusions. Our findings support the clinical and diagnostic relevance of immunophenotypic studies in AML.
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