A.S. in Medical Laboratory Technology, Indiana University Northwest, 2003
Breast cancer is the second most common cancer-related death among women in the United States. The majority of breast cancer-related deaths are due to tumor metastasis. Several Ets factors have been shown to be dysregulated in breast cancer. Friend leukemia virus integration 1 (Fli1) is an Ets protein that is aberrantly-expressed in retrovirus-induced hematological tumors in mice, and is found to be rearranged in human Ewing's sarcoma and related primitive neuroectodermal tumors characterized by a t(11;22)(q24;q12) translocation. Limited attention has been directed towards elucidating the potential role of Fli1 in epithelial-derived cancers, including breast cancer. Data mining, along with preliminary studies, indicate that Fli1 expression is diminished or lost in human invasive breast cancer tissue specimens. While expressed in non-transformed MCF-10A breast cells, it is absent in invasive breast cancer cell lines. Significantly, re-expression of Fli1 is associated with reduced cellular growth, migration, and invasion. Additionally, the re-expression of Fli1 in the breast cancer cell lines induces cellular senescence. Based upon these observations I hypothesize that the loss of Fli1 is a critical step for breast cancer progression. By defining the unique roles of Fli1 in breast cancer progression, this study hopes to gain invaluable insights into the basis of breast cancer progression and metastasis and potentially identify unique targets of breast cancer therapy.
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