biochemical studies aimed at determining the factors causing the proliferation and the restriction of growth of breast cancer cells abound in the literature. In this paper, three such studies are analyzed. One looks at the tumor suppressor gene, maspin. and how it may be recruited to help fight cell proliferation. A second looks at the role of high-density lipoprotein in breast cancer cell proliferation and how it can be counteracted, and the third looks at a novel way of killing breast cancer cells through a CD47 mediated Gi protein-dependent protein kinase A pathway.
Biochemical Approaches in Breast Cancer Treatment
Breast cancer is the most common cancer found in women and in Western societies it is the leading cause of early death in women (Cao et al 2004). Most human breast cancers require estrogen for their continued growth, and these cancers have been shown to respond to antiestrogen therapy alone or when it is used in combination with other forms of chemotherapy (Khalkhali-Ellis et al, 2004). Because a large number of women who may be at risk for breast cancer receive hormone therapy, there is a pressing need to discover the role played by estrogen in promoting breast cancer. The tumor suppressor gene maspin is known to be present in high concentrations in normal mammary epithelial cells, which also require estrogen for continued growth. However, maspin is down-regulated in primary breast cancer cells, and is entirely absent in aggressive mammary carcinoma lines. When mammary carcinoma cell line MDA-MB-435 is transected with maspin cDNA, the growth and metastatic ability of these cells in severely inhibited in nude mice. Treatment of human breast cancer cells and prostate cancer cells with recombinant maspin has been shown to reduce the motility of these cells.
When estrogen binds to the estrogen receptor (ER) on mammary epithelial cells or breast cancer cells, a conformational change occurs which allows th...