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Promoter -202 A/C Polymorphism of Insulin-like Growth Factor Binding Protein-3 Gene and Non-small Cell Lung Cancer Risk  

Moon, Jin Wook (Department of Internal Medicine, Yonsei University College of Medicine)
Chang, Yoon Soo (Department of Internal Medicine, Yonsei University College of Medicine)
Han, Chang Hoon (Department of Internal Medicine, Yonsei University College of Medicine)
Kang, Shin Myung (Department of Internal Medicine, Yonsei University College of Medicine)
Park, Moo Suk (Department of Internal Medicine, Yonsei University College of Medicine)
Byun, Min Kwang (Department of Internal Medicine, Yonsei University College of Medicine)
Chung, Wou Young (Department of Internal Medicine, Yonsei University College of Medicine)
Park, Jae Jun (Department of Internal Medicine, Yonsei University College of Medicine)
Yoo, Kyeong Nam (Brain Korea 21 Project for Medical Sciences, Yonsei University College of Medicine)
Shin, Ju Hye (Cancer Metastasis Research Center, Yonsei University College of Medicine)
Kim, Young Sam (Department of Internal Medicine, Yonsei University College of Medicine)
Chang, Joon (Department of Internal Medicine, Yonsei University College of Medicine)
Kim, Sung Kyu (Department of Internal Medicine, Yonsei University College of Medicine)
Kim, Hee Jung (Department of Laboratory Medicine, Yonsei University College of Medicine)
Kim, Se Kyu (Department of Internal Medicine, Yonsei University College of Medicine)
Publication Information
Tuberculosis and Respiratory Diseases / v.58, no.4, 2005 , pp. 359-366 More about this Journal
Abstract
Background : IGFBP-3 inhibits the mitogenic and anti-apoptotic activity of IGF by blocking the binding of IGF to its receptor. However, under certain circumstances, IGFBP-3 can enhance the activity of IGF by protecting IGF from its degradation. More than half of the interindividual variations in IGFBP-3 levels are known to be genetically determined by the polymorphism at -202 locus of IGFBP-3 gene. Method : We attempted to ascertain whether A-202C polymorphic variation of IGFBP-3 gene constitutes a risk factor for non-small cell lung cancer (NSCLC), using PCR-restriction fragment length polymorphism (RFLP). Our study included 104 NSCLC patients and 104 age-, gender-, and smoking status-matched control subjects. Result : In the 104 NSCLC subjects, the genotypic frequencies at the -202 site were as follows: AA = 67 (64.4%), AC = 35 (33.7%), and CC = 2 (1.9%). We did detect significant differences in the genotypic distribution between the NSCLC and the control subjects (p<0.05), and the NSCLC risk correlated significantly with AA genotype at the -202 locus (AA>AC>CC). Using CC genotype as a reference, the odds ratio (OR) for the subjects with AC genotype was 2.60 (95% CI: 0.89 - 8.60), and the OR associated with AA genotype was 5.89 (95% CI: 1.92 - 21.16). Conclusion : These results indicate that the dysregulation of IGF axis should now be considered as another important risk factor for NSCLC, and a potential target for novel antineoplastic therapies and/or preventative strategies in high-risk groups.
Keywords
Insulin-like growth factor (IGF); Insulin-like growth factor binding protein-3 (IGFBP-3); Non-small cell lung cancer (NSCLC); Promoter -202 A/C polymorphism; Restriction fragment length polymorphism (RFLP);
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