Background: Chemokines and their receptors influence carcinogenesis and cysteine-cysteine chemokinereceptor 5 (CCR5) directs spread of cancer to other tissues. A 32 base pair deletion in the coding region of CCR5that might alter the expression or function of the protein has been implicated in a variety of immune-mediateddiseases. The action of antiviral drugs being proposed as adjuvant therapy in cancer is dependent on CCR5wild type status. In the present study, distribution of CCR5Δ32 polymorphism was assessed in North Indianesophageal cancer patients to explore the potential of using chemokine receptors antagonists as adjuvant therapy.Materials and
Methods: DNA samples of 175 sporadic esophageal cancer patients (69 males and 106 females)and 175 unrelated healthy control individuals (69 males and 106 females) were screened for the CCR5Δ32polymorphism by direct polymerase chain reaction (PCR).
Results: The frequencies of wild type homozygous(CCR5/CCR5), heterozygous (CCR5/Δ32) and homozygous mutant (Δ32/Δ32) genotypes were 96.0 vs 97.72%,4.0 vs 1.71% and 0 vs 0.57% in patients and controls respectively. There was no difference in the genotype andallele frequencies of CCR5Δ32 polymorphism in esophageal cancer patients and control group.
Conclusions: TheCCR5Δ32 polymorphism is not associated with esophageal cancer in North Indians. As the majority of patientsexpress the wild type allele, there is potential of using antiviral drug therapy as adjuvant therapy.