In cancerous cells, mutations in proto-oncogenes cause
these genes to malfunction. When a proto-oncogene mutates, it becomes an oncogene—a gene that instructs the cell to grow and divide repeatedly without stimulation from neighboring cells. Some oncogenes overproduce growth factors, causing the cell to divide too often. Other oncogenes stimulate the cell to reproduce even when no growth factor is present. Cancerresearchers have identified about 100 different types of proto-oncogenes and their cancer-causing oncogene counterparts. A2 Tumor Suppressor Genes Stop Working When runaway cell division occurs, it does not necessarily lead to cancer. Neighboring cells respond by excreting a growth inhibitor. This chemical binds to receptors in the malfunctioning cell, sending a signal to the nucleus that activates tumor suppressor genes. Tumorsuppressor genes are like brakes for cell growth. When activated, these genes halt the cell cycle, preventing further cell division. But if tumor suppressor genes malfunction due to mutations, the rapidly dividing cell ignores messages from its neighbors telling it to stop dividing. Malfunctioning tumor suppressor genes are not enough to cause cancer—the cell still must overcome a host of other safety mechanisms before it can cause truly significant damage. A3 Cell Cycle Clock Malfunctions
The cell nucleus contains a collection of interacting proteins that control cell division. Sometimes called the cell cycle clock, this group of proteins interprets incoming messages at several checkpoints in the cell division cycle. At these checkpoints, the clock evaluates the health of the cell. If conditions are right, the clock activates certain proto-oncogenes, which produce proteins that trigger the cell to enter the next stage of the cell cycle. If conditions are not right, certain tumor suppressor genes produce proteins that prevent the cell from proceeding with cell division.If the cell cycle clock detects DNA damage in a cell, a tumor suppressor gene called p53 prevents the cell from reproducing until the damage is repaired. If the cell is unable to repair the DNA damage, p53 instructs the cell to undergo programmed cell death, or apoptosis, putting a stop to runaway cell division before it starts. Programmed cell death is a normal part of cell life and is tightly controlled by many genes, primarily p53. In a cancerous cell, one or more mutations prevent these genes from doing their jobs. When mutated, p53 allows acell to continue to divide, even with damaged DNA. Thiscan lead to additional mutations in proto-oncogenes or tumor suppressor genes. In some cases, mutations occur in genes that produce proteins to repair damaged DNA. Such mutations can lead to yet other mutations because the faulty DNA cannot duplicate properly during cell division.