title: DNA hypermethylation and clinicopathological features in breast cancer: the Western New York Exposures and Breast Cancer (WEB) Study.
abstract: Aberrant DNA hypermethylation of gene promoter regions has been increasingly recognized as a common molecular alteration in carcinogenesis. We evaluated the association between major clinicopathological features and hypermethylation of genes in tumors among 803 incidence breast cancer cases from a large population-based case-control study conducted in Western New York State. DNA samples were isolated from archive paraffin embedded tumor tissue and were analyzed for hypermethylation status of the E-cadherin, p16, and RAR-beta(2) genes using real time methylation-specific polymerase chain reaction. The frequencies of hypermethylation were 20.0% for E-cadherin, 25.9% for p16, and 27.5% for RAR-beta(2) genes. For postmenopausal women, hypermethylation of E-cadherin tended to be more likely in progesterone receptor (PR) negative than in PR-positive tumors (odds ratio (OR), 1.41; 95% confidence interval (CI), 0.91-2.18). Hypermethylation of p16 tended to be more frequent among estrogen receptor (ER) negative cases than ER-positive cases (OR, 1.51; 95% CI, 1.01-2.32). Hypermethylation of RAR-beta(2) gene was inversely associated with histological and nuclear grade of breast cancer.
authors.affiliation: Department of Social and Preventive Medicine, School of Public Health and Health Professions, University at Buffalo, 270 Farber Hall, Buffalo, NY 14214, USA. mtao@buffalo.edu
authors.forename: Meng Hua
authors.initials: MH
authors.lastname: Tao
authors.forename: Peter G
authors.initials: PG
authors.lastname: Shields
authors.forename: Jing
authors.initials: J
authors.lastname: Nie
authors.forename: Amy
authors.initials: A
authors.lastname: Millen
authors.forename: Christine B
authors.initials: CB
authors.lastname: Ambrosone
authors.forename: Stephen B
authors.initials: SB
authors.lastname: Edge
authors.forename: Shiva S
authors.initials: SS
authors.lastname: Krishnan
authors.forename: Catalin
authors.initials: C
authors.lastname: Marian
authors.forename: Bin
authors.initials: B
authors.lastname: Xie
authors.forename: Janet
authors.initials: J
authors.lastname: Winston
authors.forename: Dominica
authors.initials: D
authors.lastname: Vito
authors.forename: Maurizio
authors.initials: M
authors.lastname: Trevisan
authors.forename: Jo L
authors.initials: JL
authors.lastname: Freudenheim
mesh_terms: D000328:Adult; D000368:Aged; D001943:Breast Neoplasms / Q000453:epidemiology / Q000209:etiology* / Q000235:genetics*; D015820:Cadherins / Q000096:biosynthesis / Q000235:genetics; D016022:Case-Control Studies; D019941:Cyclin-Dependent Kinase Inhibitor p16; D019175:DNA Methylation; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D008875:Middle Aged; D009362:Neoplasm Metastasis; D009363:Neoplasm Proteins / Q000096:biosynthesis / Q000235:genetics; D009518:New York; D017698:Postmenopause; D011980:Receptors, Progesterone / Q000096:biosynthesis / Q000235:genetics; D018168:Receptors, Retinoic Acid / Q000096:biosynthesis / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: C000614131:CDKN2A protein, human; D015820:Cadherins; D019941:Cyclin-Dependent Kinase Inhibitor p16; D009363:Neoplasm Proteins; C533416:RARB2 protein, human; D011980:Receptors, Progesterone; D018168:Receptors, Retinoic Acid