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Cancers are characterized by uncontrolled growth and spread of abnormal cells. The most fundamental characteristic of cells is their ability to reproduce themselves. They do this simply by dividing. One cell becomes two, the two become four, and so on. The division of normal cells occurs in a regulated fashion. In most parts of the body, the cells continually divide and form new cells to supply the material for growth or to replace worn-out or injured cells. For example, when you cut your finger, certain cells divide rapidly until the tissue is healed and the skin is repaired. They will then go back to their normal rate of division. In contrast, cancer cells divide in a haphazard manner. The result is that they typically pile up into a non-structured mass or tumor. A benign tumor does not spread to other parts of the body, but cancers are capable of spreading throughout the body by two mechanisms: invasion and metastasis. Invasion refers to the direct migration and penetration by cancer cells into neighboring tissues. Metastasis refers to the ability of cancer cells to penetrate into lymphatic and blood vessels, circulate through the bloodstream, and then invade normal tissues elsewhere in the body.
A gene encodes information for the production of a specific protein molecule. It is made up of a nucleotide sequence on a section of chromosomal DNA. When the gene sequence is altered (mutated), it may produce an abnormal protein. Cell division is regulated by a network of proteins. If one or more of these proteins become abnormal, a cell may continue to divide when it should stop. The genes implicated in cancer development are classified into three types:
One particular tumor suppressor gene codes for a protein called "p53" that can trigger cell suicide (apoptosis). In cells that have undergone DNA damage, the p53 protein acts like a brake pedal to halt cell growth and division. If the damage cannot be repaired, the p53 protein eventually initiates cell suicide, thereby preventing the genetically damaged cell from growing out of control.
Cancer Tends to Involve Multiple Mutations Cancer may begin because of the accumulation of mutations involving oncogenes, tumor suppressor genes, and DNA repair genes. For example, colon cancer can begin with a defect in a tumor suppressor gene that allows excessive cell proliferation. The proliferating cells then tend to acquire additional mutations involving DNA repair genes, other tumor suppressor genes, and many other growth-related genes. Over time, the accumulated damage can yield a highly malignant, metastatic tumor. In other words, creating a cancer cell requires that the brakes on cell growth (tumor suppressor genes) be released at the same time that the accelerators for cell growth (oncogenes) are being activated.
Abnormal genes may be inherited at the birth or acquired after birth. The normal operation of our physiological system continuously produces free radicals, which could damage DNA, thereby resulting in gene mutations. DNA may also be damaged by exposure to radiation or chemicals (carcinogens).
Because a number of mutations usually must occur for cancer to arise, the chances of developing cancer increase as a person gets older since more time has been available for mutations to accumulate. For example, a 75-year-old person is a hundred times more likely to develop colon cancer than a 25-year-old, because the older person has a longer exposure time to factors that may promote gene mutations linked to cancer.
Reference: National Cancer Institute, USA.
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