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By Marta Cesca


Cancer is the leading killer in the United States, surpassing heart disease in 2004. According to the American Cancer Society, more than 1,500 people die each day from cancer and over 16 million people have been diagnosed with cancer since 1990.\ud In recent years, medical science has taken great strides in understanding and treating cancer. However, prior to 1997, the majority of treatments such as chemotherapy and radiation, were not based on the underlying biology of cancer growth. These treatments are also often associated with serious side effects.\ud Cancer is the result of oncogenic transformation of normal cells to produce cells which have the potential for uncontrolled division, producing a tumour cell mass\ud which invades and destroys the tissue in which it arose, and has the potential to metastatize. It is now recognized that oncogenic transformation is the result of\ud genetic mutations affecting systems controlling the cell cycle and cell death. This has implications for the way in which anti-cancer therapies are developed, because\ud the identification of factors or pathways that are altered in cancer cells may allow the development of specific therapies that target these changes (Hortobagyi, 1999).\ud Growth factors act by binding to cell surface receptors and activating pathways that result in the expression or inhibition of proteins that control cell function. In contrast, tumour suppressor genes are involved in the control of programmed cell death (apoptosis) and prevent uncontrolled proliferation. The balance between the\ud expression of proto-oncogenes and tumour suppressor genes is critical if tissues have to grow and be maintained normally. Research has shown that a series of\ud mutations in these genes is at least partially responsible for the progression from normal breast epithelium to breast cancer and the maintenance of the malignant phenotype (Aaronson, 1991, Harris, 1992). Genes that have been implicated in the pathogenesis of breast cancer include c-myc (Escot, 1986), H-ras (Agnantis, 1986),\ud hst (Lidereau, 1988), int2 (Lidereau, 1988), p53 (Cossman & Schlegel, 1991, Kovach, 1991) and the human epidermal growth factor receptor (HER) gene family (Benz ,1992, Chazin, 1992)

Topics: Tesi di Dottorato, BIO/11 Biologia molecolare, SCIENZE BIOLOGICHE
Year: 2007
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Provided by: CamEPrints

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