Akanksha Upadhyaya1, Robert A Smith1, Diego Chacon-Cortes1, Gwladys Revêchon1, Claire Bellis2, Rod A Lea2, Larisa M Haupt1, Suzanne K Chambers3, Philippa H Youl4, Lyn R Griffiths5. 1. Genomics Research Centre, Institute of Health and Biomedical Innovation, Queensland University of Technology, Queensland, Australia; Griffith Health Institute, Griffith University, Queensland, Australia. 2. Genomics Research Centre, Institute of Health and Biomedical Innovation, Queensland University of Technology, Queensland, Australia. 3. Griffith Health Institute, Griffith University, Queensland, Australia; Cancer Council Queensland, Brisbane, Queensland, Australia; The Prostate Cancer Foundation of Australia, New South Wales, Australia; Health and Wellness Institute, Edith Cowan University, Western Australia, Australia; Centre for Clinical Research, University of Queensland, Queensland, Australia. 4. Griffith Health Institute, Griffith University, Queensland, Australia; Cancer Council Queensland, Brisbane, Queensland, Australia; School of Public Health, Queensland University of Technology, Queensland, Australia. 5. Genomics Research Centre, Institute of Health and Biomedical Innovation, Queensland University of Technology, Queensland, Australia; Griffith Health Institute, Griffith University, Queensland, Australia. Electronic address: lyn.griffiths@qut.edu.au.
Abstract
BACKGROUND: Breast cancer (BC) is primarily considered a genetic disorder with a complex interplay of factors including age, gender, ethnicity, family history, personal history and lifestyle with associated hormonal and non-hormonal risk factors. The SNP rs2910164 in miR146a (a G to C polymorphism) was previously associated with increased risk of BC in cases with at least a single copy of the C allele in breast cancer, though results in other cancers and populations have shown significant variation. METHODS: In this study, we examined this SNP in an Australian sporadic breast cancer population of 160 cases and matched controls, with a replicate population of 403 breast cancer cases using High Resolution Melting. RESULTS: Our analysis indicated that the rs2910164 polymorphism is associated with breast cancer risk in both primary and replicate populations (p=0.03 and 0.0013, respectively). In contrast to the results of familial breast cancer studies, however, we found that the presence of the G allele of rs2910164 is associated with increased cancer risk, with an OR of 1.77 (95% CI 1.40-2.23). CONCLUSIONS: The microRNA miR146a has a potential role in the development of breast cancer and the effects of its SNPs require further inquiry to determine the nature of their influence on breast tissue and cancer.
BACKGROUND:Breast cancer (BC) is primarily considered a genetic disorder with a complex interplay of factors including age, gender, ethnicity, family history, personal history and lifestyle with associated hormonal and non-hormonal risk factors. The SNP rs2910164 in miR146a (a G to C polymorphism) was previously associated with increased risk of BC in cases with at least a single copy of the C allele in breast cancer, though results in other cancers and populations have shown significant variation. METHODS: In this study, we examined this SNP in an Australian sporadic breast cancer population of 160 cases and matched controls, with a replicate population of 403 breast cancer cases using High Resolution Melting. RESULTS: Our analysis indicated that the rs2910164 polymorphism is associated with breast cancer risk in both primary and replicate populations (p=0.03 and 0.0013, respectively). In contrast to the results of familial breast cancer studies, however, we found that the presence of the G allele of rs2910164 is associated with increased cancer risk, with an OR of 1.77 (95% CI 1.40-2.23). CONCLUSIONS: The microRNA miR146a has a potential role in the development of breast cancer and the effects of its SNPs require further inquiry to determine the nature of their influence on breast tissue and cancer.
Authors: T P McVeigh; R J Mulligan; U M McVeigh; P W Owens; N Miller; M Bell; F Sebag; C Guerin; D S Quill; J B Weidhaas; M J Kerin; A J Lowery Journal: Endocr Connect Date: 2017-09-12 Impact factor: 3.335