delineating an epigenetic continuum for initiation, transformation and progression to breast cancer描述一个后生连续启动,转换和发展为乳腺癌.pdfVIP

Cancers 2011, 3, 1580-1592; doi:10.3390/cancers3021580 OPEN ACCESS cancers ISSN 2072-6694 /journal/cancers Article Delineating an Epigenetic Continuum for Initiation, Transformation and Progression to Breast Cancer Kang Mei Chen 1, Josena K. Stephen 1, Usha Raju 2 and Maria J. Worsham 1,* 1 Department of Otolaryngology/Head and Neck Surgery, Henry Ford Hospital, 1 Ford Place, 1D, Detroit, MI 48202, USA; E-Mails: kchen1@ (K.M.C.); jstephe2@ (J.K.S.) 2 Department of Pathology, Henry Ford Hospital, Detroit, 1 Ford Place, 1D, Detroit, MI 48202, USA; E-Mail: uraju1@ * Author to whom correspondence should be addressed; E-Mail: mworsha1@; Tel.: +1-313-874-3350; Fax: 313-874-1079. Received: 13 January 2011; in revised form: 10 March 2011 / Accepted: 22 March 2011 / Published: 29 March 2011 Abstract: Aberrant methylation of promoter CpG islands is a hallmark of human cancers and is an early event in carcinogenesis. We examined whether promoter hypermethylation contributes to the pathogenesis of benign breast lesions along a progression continuum to invasive breast cancer. The exploratory study cohort comprised 17 breast cancer patients with multiple benign and/or in situ lesions concurrently present with invasive carcinoma within a tumor biopsy. DNA from tumor tissue, normal breast epithelium when present, benign lesions (fibroadenoma, hyperplasia, papilloma, sclerosing adenosis, apocrine metaplasia, atypical lobular hyperplasia or atypical ductal hyperplasia), and in situ lesions