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Published on: December 28, 2015
Immunophenotypic changes between diagnosis and relapse in childhood acute lymphoblastic leukemia
E R van Wering1, A Beishuizen, E T Roeffen
1Dutch Childhood Leukemia Study Group, The Hague, The Netherlands.
Childhood acute lymphoblastic leukemia (ALL) relapses show frequent immunophenotypic shifts, particularly in precursor B-ALL. These changes, involving marker expression, can alter leukemia classification and necessitate comprehensive monitoring strategies.
Area of Science:
- Hematology
- Oncology
- Immunology
Background:
- Childhood acute lymphoblastic leukemia (ALL) is a heterogeneous disease.
- Understanding phenotypic changes at relapse is crucial for treatment and prognosis.
- Previous studies have indicated potential shifts in leukemia cell markers during relapse.
Purpose of the Study:
- To investigate morphological and immunophenotypic changes in childhood ALL at relapse compared to diagnosis.
- To identify specific marker shifts and their implications for leukemia classification.
- To evaluate the correlation between morphological and immunophenotypic alterations.
Main Methods:
- Morphological and immunophenotypic analysis of 40 childhood ALL cases (32 precursor B-ALL, 8 T-ALL) at diagnosis and relapse.
- Expression patterns of non-lineage, B-lineage, T-lineage, and myeloid markers were assessed.
- Double labeling and marker shift definitions (> or = 50% change) were employed.
Main Results:
- Morphological differences were observed in 34% of precursor B-ALL and 14% of T-ALL.
- Immunophenotypic shifts occurred in 72% of precursor B-ALL and 75% of T-ALL, involving minor marker changes.
- Intra-lineage shifts occurred in 10% of precursor B-ALL, and inter-lineage shifts in 5%, with some cases reclassified as acute non-lymphocytic leukemia.
Conclusions:
- Immunophenotypic shifts are common at relapse in childhood ALL, affecting both precursor B-ALL and T-ALL.
- These shifts can lead to intra-lineage or inter-lineage changes, impacting diagnostic classification.
- Monitoring minimal residual disease in ALL should utilize multiple marker combinations and potentially molecular techniques.
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