d and rodent models, and their mammalian counterparts in normal functioning cells are termed proto-oncogenes. These proto-oncogenes play a major role in signaling pathways which regulate embryonic development, differentiation, cell renewal in the adult and cell death. More than 50 oncogenes have been identified in human cancers. Oncogenes stimulate the uncontrolled growth of cancer cells. By contrast, the tumor-suppressor genes do just the opposite and inhibit cancer cell growth. These genes also play a role in growth, differentiation, regulation, and preprogrammed cell death. Another group of tumor-suppressor genes is involved with DNA repair.
Cancer cells exhibit several genetic changes from normal cells and a limited number of genetic alterations can give rise to uncontrolled cell proliferation (Haber and Fearon, 1998). Families can have an inherited cancer syndrome, but this is often difficult to detect because of incomplete penetrance and the occurrence of phenocopies. Tumor-suppressor gene defects are most predominant in inherited cancer syndromes.
About five to 10 percent of breast cancer is thought to occur because of genetic predisposition (Haber and Fearon, 1998). Two genes have been identified which are associated with an increased risk for breast cancer BRCA1 and BRCA2.sup.10, which both encode for a large protein believed to act in the cellular response to DNA damage. A mutation of either of these genes leads to a lifetime risk of developing breast cancer. BRCA1 also increases the risk of ovarian cancer, and BRCA2 mutations increase the risk of breast cancer in males and pancreatic cancer in both sexes.
In 1997, the National Human Genome Research Institute discovered a new gene that is of great importance in a major metabolic pathway in the growth and progression of breast cancer in humans (New gene, 1999). The gene is expressed in abnormally high levels in tumor cells in most patients with breast ...