Abstract
Acute lymphoblastic leukemia (ALL) is a malignant disorder that originates from one single hematopoietic precursor committed to B- or T-cell lineage. Ordinarily, these cells express CCR5 chemokine receptor, which directs the immune response to a cellular pattern and is involved in cancer pathobiology. The genetic rs333 polymorphism of CCR5 (Δ32), results in a diminished receptor expression, thus leading to impaired cell trafficking. The objective of the present study was to investigate the effect of CCR5 chemokine receptor rs333 polymorphism in the pathogenesis of ALL. The genotype distribution was studied in 79 patients and compared with 80 control subjects, in a childhood population of Southern Brazil. Genotyping was performed using DNA samples amplified by polymerase chain reaction with sequence-specific primers (PCR-SSP). The homozygous (Δ32/Δ32) deletion was not observed in any subject involved in the study. Heterozygous genotype was not associated with ALL risk (OR 0.7%; 95% CI 0.21–2.32; P > 0.05), nor recurrence status of ALL (OR 0.86; 95% CI 0.13–5.48; P > 0.05). This work demonstrated, for the first time, no significant differences in the frequency of the CCR5/Δ32 genotype between ALL and control groups, indicating no effect of this genetic variant on the ALL susceptibility and recurrence risk.
Highlights
Leukemia is the most common childhood cancer, overall incidence is rare
Recurrence risk status of acute lymphoblastic leukemia (ALL) patients was evaluated through the GBTLI Protocol (Brazilian Group of Childhood Leukemia Treatment Protocol-99) which is based on the Cancer Therapy Evaluation Program, proposed by the National Cancer Institute, and takes into account age at diagnosis, leukocyte count, immunophenotyping, involvement of tissues other than bone marrow, and responsiveness to treatment
The chemokine receptor 5 (CCR5) genotypes distribution in ALL patients and controls was stratified by gender
Summary
Leukemia is the most common childhood cancer, overall incidence is rare. Within this population, acute lymphoblastic leukemia (ALL) occurs approximately five times more frequently than acute myelogenous leukemia (AML) and accounts for approximately 78% of all childhood leukemia diagnoses [1]. The specific biological and molecular mechanisms that account for the aggressiveness and poor therapy response of some ALL cases remain to be elucidated. Once chemokines and their receptors have been discovered as essential and selective mediators in leukocyte migration to inflammatory sites and to secondary lymphoid organs, it is reasonable that they play a critical role in tumor initiation, promotion, and progression [3, 4]. Updated research indicates that cancer cells subvert the normal chemokine system, and these molecules and their receptors become important constituents of the tumor microenvironment with very different ways to exert tumor-promoting roles [5]
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