The ability to invade and metastasize are the defining characteristics of a cancer. Invasion refers to the ability of cancer cells to penetrate through the membranes that separate them from healthy tissues and blood vessels. Metastasis can refer either to the spread of cancer cells to other parts of the body, or to the condition produced by this spread. The English word metastasis (plural, metastases) comes from a Greek word that means "a change." The tumors produced by metastasis are sometimes called secondary tumors. Metastasis is responsible for 90% of the deaths caused by cancer.
Metastasis is a complex multi-step process that begins with changes in the genetic material of a cell (carcinogenesis) followed by the uncontrolled multiplication of altered cells. It continues with the development of a new blood supply for the tumor (angiogenesis), invasion of the circulatory system, dispersal of small clumps of tumor cells to other organs or parts of the body, and the growth of secondary tumors in those sites.
Carcinogenesis and genetic mutations
The first step in cancer development is a change or mutation of the DNA in the chromosomes of a cell. Mutations can be triggered by a number of different factors, including:
Environmental carcinogens. Ultraviolet radiation from the sun is known to cause skin cancer. Chemical carcinogens include tobacco smoke, asbestos, and benzene. Ionizing radiation from x-ray therapy or atomic fallout, or industrial exposure to uranium or thorium are also associated with an increased risk of cancer.
Chromosomal rearrangement or damage. Oncogenes are genes found in the chromosomes of tumor cells whose activation is associated with the conversion of normal cells into cancer cells. Oncogenes are sometimes activated by chromosomal rearrangements. The so-called Philadelphia chromosome, an abnormality that involves a transposition of genetic material between the long arms of human chromosomes 9 and 22, is found in about 80% of patients with chronic myelocytic leukemia.
Loss of tumor suppressor genes. Another type of genetic alteration that can lead to cancer is the inactivation of anti-oncogenes, or tumor suppressor genes. Under normal circumstances, tumor suppressor genes act like a brake on cell growth and division. If these genes are altered or lost, oncogenes can stimulate cells to multiply uncontrollably without any opposition. In colorectal cancer, deletion of the DCC gene, which is a tumor suppressor gene located on the long arm of human chromosome 18, lowers the patient's chances of five-year survival by 30%.
Other mutations in a cell's DNA occur for reasons that are not yet fully understood.
Rebecca J. Frey PhD, The Gale Group Inc., Gale, Detroit,