Cited 24 times in
Association Between Insulin Resistance and Luminal B Subtype Breast Cancer in Postmenopausal Women
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 김승일 | - |
dc.contributor.author | 남상근 | - |
dc.contributor.author | 박세호 | - |
dc.contributor.author | 박형석 | - |
dc.date.accessioned | 2017-02-24T07:33:43Z | - |
dc.date.available | 2017-02-24T07:33:43Z | - |
dc.date.issued | 2016 | - |
dc.identifier.issn | 0025-7974 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/146454 | - |
dc.description.abstract | Currently, there is limited information on the clinical characteristics of breast cancer patients with insulin resistance. Hence, the purpose of this study was to investigate the association between insulin resistance and clinicopathological factors in newly diagnosed breast cancer patients without diabetes. We assessed 760 patients with breast cancer treated between 2012 and 2014. We compared the clinicopathological characteristics between patients with and without insulin resistance using univariate and multivariate analyses, including after stratification by menopausal status. Insulin resistance was defined according to the homeostatic model assessment of insulin resistance. Of 760 patients, 26.4% had insulin resistance. Age, menopausal status, body mass index, tumor size, histologic grade, Ki-67 expression, and breast cancer subtype significantly differed according to the presence of insulin resistance. Multivariate analysis revealed that postmenopausal status and obesity were significantly associated with insulin resistance. In postmenopausal women, older age, obesity, larger tumor size, advanced stage, and high proliferative luminal B subtype were significantly associated with insulin resistance. In contrast, in premenopausal patients, only obesity was related to insulin resistance. Multivariate analysis indicated that insulin resistance was independently correlated with obesity, larger tumor size, and the luminal B/human epidermal growth factor receptor-2-negative subtype in postmenopausal but not premenopausal patients. Insulin resistance was significantly associated with larger tumors and proliferative luminal B subtype breast cancer in postmenopausal women only. These findings suggest that insulin resistance could mechanistically induce tumor progression and might be a good prognostic factor, and that it could represent a therapeutic target in postmenopausal patients with breast cancer. | - |
dc.description.statementOfResponsibility | open | - |
dc.format | application/pdf | - |
dc.language | English | - |
dc.publisher | Lippincott Williams & Wilkins | - |
dc.relation.isPartOf | MEDICINE | - |
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 | Body Mass Index | - |
dc.subject.MESH | Breast Neoplasms*/epidemiology | - |
dc.subject.MESH | Breast Neoplasms*/metabolism | - |
dc.subject.MESH | Breast Neoplasms*/pathology | - |
dc.subject.MESH | Female | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | Insulin Resistance* | - |
dc.subject.MESH | Medical Records/statistics & numerical data | - |
dc.subject.MESH | Middle Aged | - |
dc.subject.MESH | Neoplasm Staging | - |
dc.subject.MESH | Postmenopause/metabolism* | - |
dc.subject.MESH | Prognosis | - |
dc.subject.MESH | Receptor, ErbB-2 | - |
dc.subject.MESH | Receptors, Estrogen/analysis | - |
dc.subject.MESH | Receptors, Progesterone/analysis | - |
dc.subject.MESH | Republic of Korea/epidemiology | - |
dc.subject.MESH | Risk Factors | - |
dc.subject.MESH | Statistics as Topic | - |
dc.subject.MESH | Tumor Burden | - |
dc.title | Association Between Insulin Resistance and Luminal B Subtype Breast Cancer in Postmenopausal Women | - |
dc.type | Article | - |
dc.publisher.location | United States | - |
dc.contributor.college | College of Medicine | - |
dc.contributor.department | Dept. of Surgery | - |
dc.contributor.googleauthor | Sanggeun Nam | - |
dc.contributor.googleauthor | Seho Park | - |
dc.contributor.googleauthor | Hyung Seok Park | - |
dc.contributor.googleauthor | Sanghwa Kim | - |
dc.contributor.googleauthor | Jee Ye Kim | - |
dc.contributor.googleauthor | Seung Il Kim | - |
dc.identifier.doi | 10.1097/MD.0000000000002825 | - |
dc.contributor.localId | A00658 | - |
dc.contributor.localId | A04558 | - |
dc.contributor.localId | A01524 | - |
dc.contributor.localId | A01753 | - |
dc.relation.journalcode | J02214 | - |
dc.identifier.eissn | 1536-5964 | - |
dc.identifier.pmid | 26945364 | - |
dc.contributor.alternativeName | Kim, Seung Il | - |
dc.contributor.alternativeName | Nam, Sanggeun | - |
dc.contributor.alternativeName | Park, Se Ho | - |
dc.contributor.alternativeName | Park, Hyung Seok | - |
dc.contributor.affiliatedAuthor | Kim, Seung Il | - |
dc.contributor.affiliatedAuthor | Nam, Sanggeun | - |
dc.contributor.affiliatedAuthor | Park, Se Ho | - |
dc.contributor.affiliatedAuthor | Park, Hyung Seok | - |
dc.citation.volume | 95 | - |
dc.citation.number | 9 | - |
dc.citation.startPage | 2825 | - |
dc.identifier.bibliographicCitation | MEDICINE, Vol.95(9) : 2825, 2016 | - |
dc.date.modified | 2017-02-24 | - |
dc.identifier.rimsid | 45098 | - |
dc.type.rims | ART | - |
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.