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In vivo clonal evolution of pre-B to B-cell acute lymphoblastic leukemia in childhood
1Institute of Hematology, Chaim Sheba Medical Center, Tel-Hashomer, Israel.
Insights
Clonal evolution in pre-B-cell acute lymphoblastic leukemia (ALL) was observed in two infants. Relapse showed distinct L3 morphology and surface immunoglobulins, suggesting a significant shift in leukemia cell characteristics.
Area of Science:
- Hematology
- Oncology
- Pediatric Oncology
Background:
- Pre-B-cell acute lymphoblastic leukemia (ALL) is a common childhood cancer.
- Understanding the mechanisms of relapse and treatment resistance is crucial for improving outcomes.
- Clonal evolution, the genetic diversification of cancer cells over time, is implicated in disease progression.
Observation:
- Two infants with pre-B-cell ALL (L1 morphology, specific immunophenotype) achieved remission.
- Both infants relapsed with distinct L3 morphology and the emergence of surface immunoglobulins.
- One patient developed Burkitt's lymphoma, a distinct entity often associated with L3 morphology.
Findings:
- These cases provide further evidence for clonal evolution in pre-B-cell ALL.
- The observed phenotypic changes (morphology, surface immunoglobulin expression) indicate significant cellular adaptation during relapse.
- This represents a rare instance of documented clonal evolution with surface immunoglobulin emergence in relapsed ALL.
Implications:
- Clonal evolution may drive treatment resistance and disease relapse in pediatric ALL.
- Monitoring immunophenotypic and morphologic changes during relapse is important for accurate diagnosis and treatment.
- Further research into the genetic underpinnings of these evolutionary changes could reveal new therapeutic targets.
Abstract:
Two cases are described that provide further evidence for clonal evolution in pre-B-cell acute lymphoblastic leukemia. Two infants, whose lymphoblasts at diagnosis were morphologically subtyped as L1 and immunophenotyped as HLA DR+, CD19+, CD10+/- and C mu-, were induced and maintained in remission. One child relapsed 6 months after initiation of therapy. This time his lymphoblasts had L3 morphology and immunophenotyping demonstrated the appearance of surface immunoglobulins. The second child relapsed 18 months after initiation of therapy with a lymphomatous picture. He also had peripheral and bone marrow blasts with L3 morphology and surface immunoglobulins. A lymph node biopsy showed diffuse small non-cleaved lymphoma with a 'starry sky' appearance compatible with Burkitt's lymphoma. Only one case with a similar clonal evolution has been reported in the literature, but no surface immunoglobulins were demonstrated. The significance of clonal evolution in these cases and its potential practical implications are discussed.