Control subjects were 2 years older than case patients, on average, but had a similar gender ratio and ethnic background (Table 2). Compared to case patients, control subjects were less likely to be cigarette smokers, to have a history of COPD or environmental tobacco smoke exposure, or to have a positive family history of lung cancer in their first-degree relatives.
Deficient PI1 types were significantly overrepresented among case patients compare to control subjects (p < 0.05) [Table 3]. For the two ELA2 SNP sites, the frequency distribution of alleles and genotypes at Rep_a was similar between case patients and control subjects, but differed at Rep_b. Specifically, the allele G at Rep_b was overrepresented among case patients. We then compared intragenic haplotypes between case patients and control subjects (Table 3, lower portion) using the haplotype score test. There was an overall strong association (judged by global and simulated p values) between the two SNPs and lung cancer risk, particularly with haplotypes T-G and G-A. These two SNPs showed a strong LD in the case patients (D’ approximately equal to 1.0) and a weak LD in the control group (D’ = 0.81), suggesting that they may have different functionality toward the development of lung cancer. No correlation existed between the two SNPs in case patients or control subjects (r2 = 0.01), reflecting the disparate allele frequencies of the two markers in the study population. All that you need about medicine on Canadian Neighbor Pharmacy. This information will be usful for you.