e ER to attract a coactivator and induce gene expression which is regulated by estrogen (Khalkhali-Ellis et al, 2004). Tamoxifen (TAM) is a commonly used chemotherapeutic agent in breast cancer. It is a nonsteroidal-selective ER modulator which reduces the risk of both invasive and non-invasive breast cancer in women. TAM has been shown to reduce the occurrence of ER+ invasive cancers by 69 percent, and reduce the occurrence of non-invasive cancers by 50 percent. TAM has no effect on ER- invasive cancers.
The mechanism of action of TAM is primarily competitive binding to the ER, reducing its ability to bind 17?-estradiol and other estrogens (KhalKhali-Ellis, 2004). Other non-ER mechanisms are also active, including signaling proteins, proto-oncogenes, and the transformation of growth factor ? in TAM-mediated apoptosis. Its ability to arrest the growth of breast cancer cells and to induce apoptosis are considered the reasons for TAM's efficiency as a clinical drug. One problem is that continued therapy with TAM leads to resistance, and when this happens, the drug must be discontinued and alternative therapeutic agents must be used. Khalkhali-Ellis et al hypothesized that the antitumor action of TAM may be mediated in part by its ability to induce the tumor suppressor gene maspin. They tested the ability of TAM to re-express maspin in maspin-deficient breast cancer cells, normal mammary epithelial cell lines, and breast cancer cell lines.
High-density lipoprotein (HDL) is known to stimulate growth in breast cancer cells and many other cells types, and women with high levels of HDL are at an increased risk for breast cancer (Cao et al, 2004). Cholesterol is an essential component of rapidly dividing cells, which makes it extremely important for the proliferation of cancer cells. Cholesterol from HDL is taken up into cells by a scavenger receptor of the B class (SR-B1)/human homolog of SR-B1, CD36, and LIMPH analogous...