Evaluation of CD66c expression for minimal residual disease in precursor B acute lymphoblastic leukemia

Background: Acute lymphoblastic leukemia (ALL) is a malignant clonal expansion of lymphoid hematopoietic precursors that exhibit developmental arrest at varying stages of differentiation. Two subtypes are defined, according to which lymphoid progenitor is affected: B-cell-precursor ALL (B-ALL) and T-cell ALL (T-ALL). The incidence of ALL differs with age; there is an early peak at 4 to 5 years, a decline in young adults, followed by a slight increase after 50 years of age. Minimal residual disease (MRD) is the name attributed to the very low number of blast cells remaining in the patient during or after treatment (in the remission period). MRD detected in early phases of therapy is shown to provide prognostic information. MRD has proven to be the strongest prognostic factor. MRD-based treatment strategies further improve outcome in the involved patients.
Aim of the study: 1) To evaluate CD66c as a marker for minimal residual disease by flow cytometry in B-ALL patients. 2) To assess the effect of CD66c on the treatment outcomes and overall survival of patients with B-ALL.
Methodology: This is a prospective study which was conducted at Clinical Pathology department, South Egypt Cancer Institute, Assiut University in the period between January 2019 and December 2020. Patients included in the study underwent the standard clinical examination and laboratory evaluation followed by bone marrow aspiration. Sixty B-ALL patients (n=60) underwent flowcytometric analysis for CD66c. Out of the sixty patients (n=60) included at the first time, forty patients (n=40) were re-evaluated at the post-induction phase.
Results: This study included 60 patients, 36 (60%) males and 24 (40%) females. The patients’ ages ranged between 2 and 25 years with median age of 6 years. CD66 was expressed in 70% of our B-ALL patients. There was statistically significant difference between the level of expression of CD66c both before and after treatment (p=0.000). No significant correlations were found between level of expression of CD66c and WBCs, PB blasts or BM blast cells. There was no significant correlation found between CD66c and OS. Bone marrow aspirate samples analysed on the post-induction phase showed that CD66c was still stably expressed.
Conclusion: CD66c is highly expressed in our B-ALL patients and is stably expressed after induction of treatment, so its addition in MRD panels can contribute to increasing the sensitivity of the assay. As regard its prognostic value, we couldn’t precise its use for evaluation of overall survival in B-ALL patients.