Abstract
Chemokines and their receptors influence carcinogenesis and cysteine-cysteine chemokine receptor 5 (CCR5) directs spread of cancer to other tissues. A 32 base pair deletion in the coding region of CCR5 that might alter the expression or function of the protein has been implicated in a variety of immune-mediated diseases. The action of antiviral drugs being proposed as adjuvant therapy in cancer is dependent on CCR5 wild type status. In the present study, distribution of CCR5Δ32 polymorphism was assessed in North Indian esophageal cancer patients to explore the potential of using chemokine receptors antagonists as adjuvant therapy. 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 CCR5Δ32 polymorphism by direct polymerase chain reaction (PCR). 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 and allele frequencies of CCR5Δ32 polymorphism in esophageal cancer patients and control group. The CCR5Δ32 polymorphism is not associated with esophageal cancer in North Indians. As the majority of patients express the wild type allele, there is potential of using antiviral drug therapy as adjuvant therapy.
Highlights
Tumor growth and metastatic dissemination develop through a complex molecular dysregulation involving cell migration, invasion, resistance to apoptosis, and immune escape mechanisms
Distribution of CCR5Δ32 polymorphism was assessed in North Indian esophageal cancer patients to explore the potential of using chemokine receptors antagonists as adjuvant therapy
Chemokines belong to the family of chemotactic cytokines that are considered to be the main regulators of leukocyte trafficking under homeostatic and inflammatory conditions
Summary
Tumor growth and metastatic dissemination develop through a complex molecular dysregulation involving cell migration, invasion, resistance to apoptosis, and immune escape mechanisms. Apart from GIT cancers, the association of CCR5Δ32 has been evaluated in other cancers like skin cancer and bladder cancer (Zafiropoulos et al, 2004), cervical cancer (Zheng et al, 2006), osteosarcoma (von Luettichau et al, 2008), breast cancer (Manes et al, 2003; Zafiropoulos et al, 2004; Degerli et al, 2005; Aoki et al, 2009; Guleria et al, 2012; Eskandari-Nasab et al, 2014) and prostate cancer (Balistreri et al, 2009) Chemokines and their receptors influence carcinogenesis and cysteine-cysteine chemokine receptor 5 (CCR5) directs spread of cancer to other tissues. As the majority of patients express the wild type allele, there is potential of using antiviral drug therapy as adjuvant therapy
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