Abstract
Abstract Observable infiltration of immune cells in stages of early breast cancer progression mirrors two recently conceptualized factors of carcinogenesis: tumor microenvironment and tumor-promoting inflammation. Clinical studies using immunohistochemical staining for CD45 in patient-derived breast tissue demonstrate the involvement of leukocytes in breast cancer development, but the lack of an appropriate in vitro model has hindered molecular studies thus far. However, the 21T series cell lines effectively mimic breast cancer progression. This cell line series was obtained from the same breast cancer patient and consists of three cell lines representing atypical hyperplasia (21PT), ductal carcinoma in situ (21NT) and invasive carcinoma (21MT-1). This unique cell line series is used in our molecular study of omega-3 ethyl esters as breast cancer preventive agents. Preliminary invasion assays have described varying degrees of monocyte recruitment according to stages of progression. 21PT cells when plated on the bottom chamber failed to mobilize monocytes as effectively as 21NT or 21MT-1 and the addition of omega-3 ethyl esters suppressed the baseline invasion capacity of monocytes by 30%. Epidemiologic studies suggest that omega-3 fatty acids can act as potent cancer preventive agents and are possibly more potent when used in an ethyl ester form. Based on this, we hypothesize that omega-3 ethyl esters may prohibit early breast cancer progression through inhibiting immune cell infiltration and disrupting the formation of a tumor-promoting inflammatory and oxidative microenvironment. Phenotypic studies aim to interrogate the effect of omega-3 ethyl esters on tumor microenvironment including chemokine secretion and MMP production whereas molecular experiments probe into the importance of the Wnt pathway as a key player in the transition from ADH to DCIS. This study will demonstrate how omega-3 ethyl esters may function as breast cancer preventive agents as well as provides a model of study to test the efficacy of cancer preventive agents in vitro. Citation Information: Cancer Res 2011;71(24 Suppl):Abstract nr P3-10-04.
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