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Low-Intensity CD66c Expression Orchestrates an Immunosuppressive Niche Promoting Residual Disease in Pediatric ProB
Gabriela Zamora-Herrera1,2, Rubí Romo-Rodríguez1,3, Jebea A López-Blanco1
1Laboratory of Oncoimmunology and Cytomics of Childhood Cancer, Centro de Investigación Biomédica de Oriente, Instituto Mexicano del Seguro Social, Puebla 74360, Mexico.
Insights
Low CD66c expression in pediatric B-cell acute lymphoblastic leukemia (B-ALL) may indicate immune evasion, leading to increased relapse risk and treatment failure. This finding offers insights into disease aggressiveness and treatment response.
Area of Science:
- Pediatric Hematology Oncology
- Immunology
- Cancer Biology
Background:
- B-cell precursor acute lymphoblastic leukemia (B-ALL) is the most common pediatric leukemia.
- Aberrant antigen expression, including myeloid antigen CD66c, is common in B-ALL and linked to prognosis.
- CD66c's role in disease aggressiveness and treatment response warrants investigation in diverse populations.
Purpose of the Study:
- To evaluate the expression of CD66c in Mexican pediatric B-ALL patients.
- To correlate CD66c expression with measurable residual disease (MRD), mortality, and survival.
- To investigate the impact of CD66c on mesenchymal stromal cells (MSCs) and disease biology.
Main Methods:
- Immunophenotyping of 128 pediatric B-ALL patients and control bone marrow samples.
- Assessment of aberrant antigen expression in hematopoietic cells.
- Phenotyping of bone marrow microenvironment stroma, including MSCs.
Main Results:
- 84.38% of B-ALL patients showed aberrant myeloid antigen expression.
- Low CD66c expression was associated with detectable MRD, increased mortality, and reduced survival.
- MSCs from patients with varying CD66c expression levels exhibited inflammatory profiles.
Conclusions:
- Low CD66c expression may facilitate immune evasion and persistence, increasing relapse risk.
- CD66c expression serves as a potential marker for disease aggressiveness and therapeutic response in pediatric B-ALL.
- Understanding CD66c's role can inform diagnostic and prognostic strategies for pediatric leukemia.
Abstract:
Background/Objectives: B-cell precursor acute lymphoblastic leukemia (B-ALL), the most common pediatric acute leukemia (AL), is frequently characterized by aberrant antigen expression, which aids diagnosis and prognosis. The myeloid antigen CD66c is notably frequent in B-ALL and has been proposed as a marker of disease aggressiveness and treatment response. Evaluating CD66c in Mexican pediatric patients may provide insights into disease biology. Methods: A cohort of 128 pediatric patients was referred to the Laboratory of Oncoimmunology and Cytomics of Childhood Cancer (OCL) at Instituto Mexicano del Seguro Social (IMSS) for immunophenotyping tests between March 2022 and November 2023. Additionally, control bone marrow (BM) samples were assessed. Aberrant antigen expression in hematopoietic populations and BM microenvironment stroma phenotyping were performed. Results: In total, 84.38% of B-ALL patients exhibited aberrant expression of ≥1 myeloid antigen. Among CD66c-positive patients, 13.79% had detectable measurable residual disease (MRD) during follow-up and 20.69% died. Mesenchymal stromal cells (MSCs) from patients with positive or low CD66c expression displayed inflammatory profiles. ProB leukemias with low CD66c expression were more likely to exhibit detectable MRD, increased mortality, and reduced survival. Conclusions: Low CD66c expression induces molecular stealth that could favor immune evasion and niche persistence, thereby increasing the risk of relapse and therapeutic failure.
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