Scientists have discovered that cells transform to ehir malignant state through a series of mutations (changes) to specific genes. Two classes of genes are known as cancer-triggering genes. These are proto-oncogenes, which encourage growth and tumor suppressor genes, which retard growth. When a proto-oncogene mutates, it encourages cell multiplication beyond the norm. On the reverse side, when a tumor suppressor gene mutates, it loses its ability to prevent cell growth.
For a cancerous tumor to form, several of the genes in a cell have to mutate. A normal cell population sustains a genetic mutation and continues to grow when it should be resting. This is known as a genetically altered cell. This cell looks normal, but reproduces too much. This is known as hyperplasia. Once these cells start to look abnormal in shape and location, the tissue now takes on the characterisic of dysplasia. When the cells continue to appear more abnormal in growth and appearance, but stay within the boundaries of the tissues where they began, this is known as in situ cancer. When the cells invade the surrounding tissue, break through the original boundaries, and perhaps break off and migrate through the blood or lymph fluid, this is known as invasive cancer.
About 20% of breast cancers are the result of a family-inherited gene mutation. All breast cancers involve some type of gene mutation. Here are some of the genes involved in breast cancer:
Oncogenes - erb-B - codes for the epidermal growth factor receptor erb-B2 - also known as HER-2 or HER-2-neu - also related to growth factor Bcl-1 - codes for cyclin D1, a stimulator of the cell cycle clock
Tumor Suppressor genes - RB - genes for proteins in the nucleus of the cell - Think of it as a brake in the cell cycle p53- codes for the p53 protein which can stop cell division and induce abnormal cells to commit suicide BRCA1 - unsure of cell location - breast and ovarian cancer BRCA2 - unsure of cell location - breast cancer
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