Abstract

Aim The clinical behavior of the human urinary bladder papillary transitional cell carcinoma (TCC) probably results from a complex interaction between carcinogenic insults and host resistance during the patient’s life. While the main recognized risk factor is smoking, little information exists about the susceptibility to TCC development. The human leukocyte antigen E (HLA-E) molecule plays an important role both as a modulator of natural killer (NK) cell activity by interacting with CD94-NKG2A receptor in the innate immunity pathway and as an antigen-presenting molecule triggering a specific immune response, thus it may influence tumor immune surveillance. The aim of this study was to explore a possible influence of five HLA-E variation sites, one in exon 2 at position 424 (rs1059510), three at exon 3 in the positions 756 (rs1264457), 887 (rs41560815) and 906 (rs41562314) and one in exon 4 at the position 1691 (rs17875370), on the susceptibility to urinary bladder TCC development and progression in Brazilian subjects. Methods These variation sites were evaluated by means of direct sequencing of PCR products using an ABI3100 Genetic Analyzer. On this bases, 105 healthy donors and 73 patients with historical of TCC, both from Ribeirao Preto City, Southeast Brazil, were evaluated for the variation sites described above. Results Only two of the five variation sites evaluated were polymorphic in an admixed population such as Brazilians, i.e., positions +424 and +756. Considering these, the allele and genotype distributions in patients and controls were very similar and no significant difference was detected, even when patients were compared as a whole or stratified into high and low grade tumor patients. Conclusions In conclusion, although previous associations have been described evolving neighboring genes such as HLA-A and HLA-G, the HLA-G locus seems to be not associated with TCC susceptibility and/or progression to aggressive tumors.

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