Acute lymphoblastic leukemia (ALL) is a malignant disorder that originates from one single hematopoietic precursor committed\nto B- or T-cell lineage. Ordinarily, these cells express CCR5 chemokine receptor, which directs the immune response to a cellular\npattern and is involved in cancer pathobiology. The genetic rs333 polymorphism of CCR5 (?32), results in a diminished receptor\nexpression, thus leading to impaired cell trafficking. The objective of the present study was to investigate the effect of CCR5\nchemokine receptor rs333 polymorphism in the pathogenesis of ALL. The genotype distribution was studied in 79 patients and\ncompared with 80 control subjects, in a childhood population of Southern Brazil. Genotyping was performed using DNA samples\namplified by polymerase chain reaction with sequence-specific primers (PCR-SSP). The homozygous (?32/?32) deletion was not\nobserved in any subject involved in the study. Heterozygous genotype was not associated with ALL risk (OR 0.7%; 95% CI 0.21ââ?¬â??\n2.32; P > 0.05), nor recurrence status of ALL (OR 0.86; 95% CI 0.13ââ?¬â??5.48; P > 0.05). This work demonstrated, for the first time,\nno significant differences in the frequency of the CCR5/?32 genotype between ALL and control groups, indicating no effect of this\ngenetic variant on the ALL susceptibility and recurrence risk.
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