Enzyme Inhibitors in Breast Cancer Therapy Coursework

Enzyme Inhibitors in Breast Cancer Therapy - Coursework Example Among all of the different types of cancer, breast cancer is the highest cause of death in women between the ages 20 and 59, having been responsible for 32 percent of all new cancer cases in 2003. In most patients, the metastases at distant sites of the body become the main cause of death. The rates of metastasis and mortality in breast cancer patients have recently decreased with the aid of early diagnosis by mammographic screening and the implementation of adjuvant therapy. Aromatase inhibitors may be used as adjuvant therapy, first-line, second-line or even third- line therapy (Cunnick et al 2001). Third-line therapy uses the medicine if patients relapse after the second treatment, which followed an initial treatment. Adjuvant therapy, on the other hand, aids in the eradication of breast tumor cells that might have already metastasized to different organ systems by the time of diagnosis. Cancer cells are characterized as having the ability to be viable under stressful conditions. Growth and survival factors activate a variety of intracellular signal transduction pathways; these pathways play a critical role in the regulating growth, differentiation, and senescence, and have been found to prevent apoptosis under many circumstances (Ripple et al 2005). The ability of cancer cells to metastasize to other organ systems results in smaller chances of curing the disease. Common phenotypes of metastatic cancer cells have been found to be (1) unregulated growth and survival, (2) decreased cell to cell adhesion, (3) increased ability in degrading the extracellular matrix, and (4) increased motility (Zhang et al 2005). Cancer cells have been found to possess altered apoptosis signals, which are transduced by the p53 tumor suppressor gene. The said gene regulates the expression of multiply apoptosis-inducing proteins that act upon the mitochondria. Normal cells are induced to apoptosis through the intrinsic pathway, where cytochrome c is released from the mitochondria. The liberated cytochrome c binds to apoptotic protease, activating dactor-1 (apad-1), which assembles into an oligomer called the apoptosome. The apoptosome then recruits and activates caspase-9, which triggers a proteolytic cascade, resulting in cell death. In cancer cells, excessive mitotic signals activate the intrinsic pathway, as a result of mutations within signaling pathways (Mashima et al 2005; Ripple et al 2005).