Abstract
Metastasis is an extremely complex process that accounts for most cancer-related deaths. Malignant primary tumors can be removed surgically, but the cells that migrate, invade, and proliferate at distant organs are often the cells that prove most difficult to target therapeutically. There is growing evidence that host factors outside of the primary tumors are of major importance in the development of metastasis. Recently, we have shown that the bromodomain-containing protein 4 or bromodomain 4 (Brd4) functions as an inherited susceptibility gene for breast cancer progression and metastasis. In this paper, we will discuss that host genetic background on which a tumor arises can significantly alter the biology of the subsequent metastatic disease, and we will focus on the role of Brd4 in regulating metastasis susceptibility.
Highlights
Breast cancer is the most common cancer diagnosed in women worldwide
We found that ectopic expression of bromodomain 4 (Brd4) in a highly metastatic mouse mammary tumor cell line reduces both primary tumor growth and metastatic capacity in our mouse model [36]
The genetic background impacts the primary tumor but all of the tissues, which play a role in the establishment of the microenvironment in both primary and metastatic tumor cells
Summary
Breast cancer is the most common cancer diagnosed in women worldwide. In the United States the estimates for 2010 were 209,060 new cases of invasive breast cancer and 40,230 deaths [1]. Metastasis is a multistep complex process that involves the detachment of tumor cells from the primary tumor, migration and invasion through the surrounding tissues and basement membranes, intravasation and survival in the small blood vessels or lymphatic channels, and colonization in a distant target organ. These steps are usually followed by extravasation into the surrounding tissue, survival in the foreign microenvironment, proliferation, and induction of angiogenesis (Figure 1). We will focus on the role that the metastasis susceptibility gene Brd plays in the regulation of extracellular matrix (ECM) gene expression and subsequently metastatic progression
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