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1 Duke University Medical Center, Durham, North Carolina and 2 Yale-New Haven Medical Center, New Haven, Connecticut
Requests for reprints: Victoria L. Seewaldt, Box 2628, Duke University Medical Center, Durham, NC 27710. Phone: 919-668-2455; Fax: 919-668-2458. E-mail: seewa001{at}mc.duke.edu
Purpose: Currently, we lack biomarkers to predict whether high-risk women with mammary atypia will respond to tamoxifen chemoprevention.
Experimental Design: Thirty-four women with cytologic mammary atypia from the Duke University High-Risk clinic were offered tamoxifen chemoprevention. We tested whether ESR1 promoter hypermethylation and/or estrogen receptor (ER) protein expression by immunohistochemistry predicted persistent atypia in 18 women who were treated with tamoxifen for 12 months and in 16 untreated controls.
Results: We observed a statistically significant decrease in the Masood score of women on tamoxifen chemoprevention for 12 months compared with control women. This was a significant interaction effect of time (0, 6, and 12 months) and treatment group (tamoxifen versus control) P = 0.0007. However, neither ESR1 promoter hypermethylation nor low ER expression predicted persistent atypia in Random Periareolar Fine Needle Aspiration after 12 months tamoxifen prevention.
Conclusions: Results from this single institution pilot study provide evidence that, unlike for invasive breast cancer, ESR1 promoter hypermethylation and/or low ER expression is not a reliable marker of tamoxifen-resistant atypia. (Cancer Epidemiol Biomarkers Prev 2008;17(8):1884–90)
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