PMC:3492652 / 8085-9838 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/3492652","sourcedb":"PMC","sourceid":"3492652","source_url":"https://www.ncbi.nlm.nih.gov/pmc/3492652","text":"Results\nTable 1 shows the clinicopathological features of cases and controls. All the clinical characteristics, except for smoking status, were not significantly different between the cases and controls. This difference of smoking status was controlled in the multiple logistic regression analysis, adjusted for age, gender, and smoking status.\nBy direct sequencing of the AKT2 promoter region in 24 lung cancer patient samples, we identified 1 novel polymorphism (-9826 C/G) and 4 known polymorphisms (-9473 C/T, -9151 C/T, -9025 C/T, and -8618 G/A). Also, we identified 1 novel polymorphism (-811 A/G) and 2 known polymorphisms (-675 A/- and -244 C/T) by direct sequencing in the AKT3 promoter region (Table 2). The genotype distributions of the polymorphisms were in HWE. Also, LD and haplotypes in the polymorphisms of AKT2 were calculated. However, the LD and haplotype block in AKT3 polymorphisms were unidentified because of the low frequency of the AKT3-811 G allele and AKT3-244 T allele (2.1% and 2.2%, respectively) (Fig. 1). Accordingly, we focused on the -675 A/- polymorphism in the AKT3 promoter region. Further analyses were then performed on the samples from 460 lung cancer patients and 460 controls.\nAssociation of lung cancer risk with AKT polymorphisms was then analyzed, revealing no association of the polymorphisms with the risks of lung cancer (Table 3). The association of the polymorphisms with the risk of lung cancer was further examined after stratifying the subjects according to gender and smoking status. However, the subsequent analysis revealed no significant association. Furthermore, the haplotypes of the AKT2 polymorphisms were not associated with the risks of lung cancer in 3 alternative models (data not shown).","divisions":[{"label":"Title","span":{"begin":0,"end":7}}],"tracks":[]}