C17-ORF37 AND HER2 RELATIONSHIP: MOLECULAR AND FUNCTIONAL STUDIES

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