Abstract
Abstract Over the past few decades, multiple trials have warranted the benefits of using prevention as an effective strategy for lowering breast cancer incidence. The Breast Cancer Prevention Trial (BCPT) and Study of Tamoxifen and Raloxifene (STAR) conducted by National Cancer Institute demonstrated the effectiveness of tamoxifen and raloxifene as preventive agents in reducing diagnoses of invasive breast cancer. Another prevention study the VITAL cohort study demonstrated that omega-3 supplementation reduces breast cancer incidence in postmenopausal women. In vivo studies have produced results that demonstrated a delay in onset of breast cancer in transgenic mice model. However, current in vitro effort did not have a system that closely resembles the linear progression of breast cancer and therefore stalls the molecular investigation of breast cancer prevention. Majority of in vitro preventive studies have been conducted using cancer cell lines that do not represent precancerous status of mammary tissues and do not mirror the observation of delayed onset or reduced incidence in in vivo and clinical trials. A recent report has suggested the use of a new series of mammary cells that represent hyperplasia, ductal carcinoma in situ (DCIS) and invasive carcinoma in nude mice. In this study we propose the use of 21T series breast cancer cells as a model for breast cancer prevention study using omega-3 ethyl esters. Preliminary data using this model has shown that omega-3 ethyl esters derived from Omacor® reduce proliferation only in 21NT (DCIS) and 21MT-1 (Invasive Carcinoma) and not in 21PT cells (hyperplasic). Suppression of proliferation is most optimal in the presence of estrogen. Survival of cells is inhibited in all cell lines and Ki67 index is reduced in the presence of treatments. Targets of omega-3 ethyl esters may include Akt, ER and NF-kB. Current studies are conducted to investigate the effect of omega-3 ethyl esters on these targets. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 5444. doi:1538-7445.AM2012-5444
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