Cited 33 times in
Promoter −202 A/C polymorphism of insulin-like growth factor binding protein-3 gene and non-small cell lung cancer risk
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 김성규 | - |
dc.contributor.author | 김세규 | - |
dc.contributor.author | 김영삼 | - |
dc.contributor.author | 문진욱 | - |
dc.contributor.author | 안철우 | - |
dc.contributor.author | 장윤수 | - |
dc.contributor.author | 장준 | - |
dc.date.accessioned | 2015-06-10T12:28:16Z | - |
dc.date.available | 2015-06-10T12:28:16Z | - |
dc.date.issued | 2006 | - |
dc.identifier.issn | 0020-7136 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/109861 | - |
dc.description.abstract | Insulin-like growth factor binding protein-3 (IGFBP-3) inhibits the mitogenic and antiapoptotic activity of insulin-like growth factor (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 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. Therefore, we attempted to ascertain whether the A−202C polymorphic variation of IGFBP-3 gene constitutes a risk factor for non-small cell lung cancer (NSCLC). Our study included 209 NSCLC patients and 209 age-, gender- and smoking status-matched control subjects. The frequencies of each polymorphic variation in the control population were as follows: AA = 95 (45.5%), AC = 91 (43.5%) and CC = 23 (11.0%). In the NSCLC subjects, the genotypic frequencies were as follows: AA = 131 (62.7%), AC = 73 (34.9%) and CC = 5 (2.4%). We detected statistically significant differences in the genotypic distribution between the NSCLC and the control subjects (p < 0.05, Pearson's chi-square test). The NSCLC risk correlated significantly with AA genotype. Using CC genotype as a reference, the odds ratio for the subjects with AC genotype was 2.45 (95% CI = 1.17–5.40) and that for the ones with AA genotype was 4.58 (95% CI = 2.17–10.30). 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. | - |
dc.description.statementOfResponsibility | open | - |
dc.format.extent | 353~356 | - |
dc.relation.isPartOf | INTERNATIONAL JOURNAL OF CANCER | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.subject.MESH | Adult | - |
dc.subject.MESH | Aged | - |
dc.subject.MESH | Carcinoma, Non-Small-Cell Lung/etiology | - |
dc.subject.MESH | Carcinoma, Non-Small-Cell Lung/genetics* | - |
dc.subject.MESH | Case-Control Studies | - |
dc.subject.MESH | Female | - |
dc.subject.MESH | Genotype | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | Insulin-Like Growth Factor Binding Protein 3/genetics* | - |
dc.subject.MESH | Insulin-Like Growth Factor Binding Protein 3/physiology | - |
dc.subject.MESH | Lung Neoplasms/etiology | - |
dc.subject.MESH | Lung Neoplasms/genetics* | - |
dc.subject.MESH | Male | - |
dc.subject.MESH | Middle Aged | - |
dc.subject.MESH | Polymorphism, Genetic* | - |
dc.subject.MESH | Promoter Regions, Genetic | - |
dc.subject.MESH | Risk Factors | - |
dc.title | Promoter −202 A/C polymorphism of insulin-like growth factor binding protein-3 gene and non-small cell lung cancer risk | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Dept. of Internal Medicine (내과학) | - |
dc.contributor.googleauthor | Jin Wook Moon | - |
dc.contributor.googleauthor | Yoon Soo Chang | - |
dc.contributor.googleauthor | Chul Woo Ahn | - |
dc.contributor.googleauthor | Kyeong Nam Yoo | - |
dc.contributor.googleauthor | Ju Hye Shin | - |
dc.contributor.googleauthor | Jee Hyun Kong | - |
dc.contributor.googleauthor | Young Sam Kim | - |
dc.contributor.googleauthor | Joon Chang | - |
dc.contributor.googleauthor | Sung Kyu Kim | - |
dc.contributor.googleauthor | Hee Jung Kim | - |
dc.contributor.googleauthor | Se Kyu Kim | - |
dc.identifier.doi | 10.1002/ijc.21339 | - |
dc.admin.author | false | - |
dc.admin.mapping | false | - |
dc.contributor.localId | A00564 | - |
dc.contributor.localId | A00602 | - |
dc.contributor.localId | A00707 | - |
dc.contributor.localId | A01387 | - |
dc.contributor.localId | A02270 | - |
dc.contributor.localId | A03456 | - |
dc.contributor.localId | A03472 | - |
dc.relation.journalcode | J01092 | - |
dc.identifier.eissn | 1097-0215 | - |
dc.identifier.pmid | 16049980 | - |
dc.identifier.url | http://onlinelibrary.wiley.com/doi/10.1002/ijc.21339/abstract | - |
dc.subject.keyword | insulin‐like growth factor | - |
dc.subject.keyword | insulin‐like growth factor binding protein‐3 | - |
dc.subject.keyword | lung cancer | - |
dc.subject.keyword | polymorphism | - |
dc.contributor.alternativeName | Kim, Sung Kyu | - |
dc.contributor.alternativeName | Kim, Se Kyu | - |
dc.contributor.alternativeName | Kim, Young Sam | - |
dc.contributor.alternativeName | Moon, Jin Wook | - |
dc.contributor.alternativeName | Ahn, Chul Woo | - |
dc.contributor.alternativeName | Chang, Yoon Soo | - |
dc.contributor.alternativeName | Chang, Joon | - |
dc.contributor.affiliatedAuthor | Kim, Sung Kyu | - |
dc.contributor.affiliatedAuthor | Kim, Se Kyu | - |
dc.contributor.affiliatedAuthor | Kim, Young Sam | - |
dc.contributor.affiliatedAuthor | Moon, Jin Wook | - |
dc.contributor.affiliatedAuthor | Ahn, Chul Woo | - |
dc.contributor.affiliatedAuthor | Chang, Yoon Soo | - |
dc.contributor.affiliatedAuthor | Chang, Joon | - |
dc.rights.accessRights | not free | - |
dc.citation.volume | 118 | - |
dc.citation.number | 2 | - |
dc.citation.startPage | 353 | - |
dc.citation.endPage | 356 | - |
dc.identifier.bibliographicCitation | INTERNATIONAL JOURNAL OF CANCER, Vol.118(2) : 353-356, 2006 | - |
dc.identifier.rimsid | 50644 | - |
dc.type.rims | ART | - |
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