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Advances in Hematology
Volume 2014 (2014), Article ID 924030, 5 pages
Research Article

Absence of Association between CCR5 rs333 Polymorphism and Childhood Acute Lymphoblastic Leukemia

1Laboratory of Study and Application of DNA Polymorphisms, Department of Pathological Sciences, Biological Sciences Center, State University of Londrina, Rodovia Celso Garcia Cid, (PR 445), Km 380, 86051-970 Londrina, PR, Brazil
2Laboratory of Hematology, Department of Pathology, Clinical and Toxicological Analysis, Health Sciences Center, State University of Londrina, Londrina, PR, Brazil

Received 27 January 2014; Revised 19 March 2014; Accepted 21 March 2014; Published 13 April 2014

Academic Editor: Helen A. Papadaki

Copyright © 2014 Carlos Eduardo Coral de Oliveira et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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; ), nor recurrence status of ALL (OR 0.86; 95% CI 0.13–5.48; ). 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.