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Apoptosis, or programmed cell death, is linked to cancer in two ways: tumors block the body’s self-destruction mechanisms and cancer cells inactivate genes needed for cell destruction. Chemotherapy damages tumors and marks them for death by exploiting this relationship. Mutations in DNA alter the relationship between apoptosis and cancer, allowing for uncontrolled cell growth. Chemotherapy treatments depend on this relationship and activate different points along the pathway that leads to programmed cell death. Scientists are interested in developing chemotherapies that can directly induce apoptosis.
The programmed death of a cell is called apoptosis, an event usually caused by internal damage or signals from surrounding tissue. Apoptosis and cancer are linked in two important ways. First, tumors cannot grow if the normal security system within the body detects them and triggers their self-destruction, so tumors often block the mechanisms by which the body marks uncontrolled tissue growth for apoptosis. Second, cancer cells inactivate genes that encode proteins needed to destroy malignant cells. Chemotherapies exploit the relationship between apoptosis and cancer by damaging tumors and marking them for death.
Apoptosis occurs when chemical signals initiate a process of self-destruction within a cell, through changes in the membrane, degradation of DNA in the nucleus, and the digestion of cellular proteins by specialized enzymes. There are two types of pathways that will cause a cell to go through apoptosis: the intrinsic, which is initiated by mutations in the DNA, and the extrinsic, which takes its cues from outside the cell. The extrinsic pathway can be triggered by hormones, toxins and other molecules capable of activating special locations on the cell known as death receptors.
During the early stages of tumor formation, mutations occur within the DNA that alter the relationship between apoptosis and cancer allowing for uncontrolled cell growth. Cancer involves pathological changes in the cycle through which cells reproduce and proliferate, events that normally trigger apoptosis when detected within healthy cells. This is sometimes done by suppressing genes that code for important proteins that the body uses to signal cancerous tissue to be eliminated by apoptosis. Tumors can also secrete chemical messengers that confuse or block the process that normally commands cancer cells to self-destruct.
An important gene, p53, encodes messenger proteins that cause apoptosis. Some tumors caused by viruses suppress the activation of this gene and make the tumor cells less sensitive to the activation of death receptors. Whether caused by viruses or not, cellular production of growth-promoting substances is increased in tumors. Normally, the body responds to the uncontrolled proliferation of a particular cell type by causing mass apoptosis, but during oncogenesis – the formation of cancer – the balance between apoptosis and cancer shifts towards cell growth, not death .
Chemotherapy treatments often depend on the relationship between apoptosis and cancer. Most of these drugs also interfere with DNA synthesis and cell division or growth, but these mechanisms ultimately work to destroy cancer cells before they divide and make more copies of themselves. Various drugs activate different points along the pathway that also leads to programmed cell death, sometimes by increasing the sensitivity of death receptors on cancer cells. Since some malignant tumors no longer respond to self-destruct signals, scientists are interested in developing chemotherapies that can directly induce the natural events of apoptosis.
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