Researchers have found that cancer develops from mutations within the genes of cells. Thus, cancer is a genetic disease. Cancer susceptibility genes are of two types. Some are oncogenes, which activate cell division and influence embryonic development, and some are tumor suppressor genes, which halt cell division.

These genes are typically found in normal human cells, but certain kinds of mutations may transform the normal cells. Inherited defects may cause a genetic mutation, whereas exposure to a carcinogen may cause an acquired mutation. Current evidence indicates that carcinogenesis results from a complex interaction of carcinogens and accumulated mutations in several genes.

In animal studies of the ability of viruses to transform cells, some human viruses exhibit carcinogenic potential. For example, the Epstein-Barr virus, the cause of infectious mononucleosis, has been linked to Burkitt\'s lymphoma and nasopharyngeal cancer.

High-frequency radiation, such as ultraviolet and ionizing radiation, damages the genetic material known as deoxyribonucleic acid (DNA), possibly inducing genetically transferable abnormalities. Other factors, such as a person\'s tissue type and hormonal status, interact to potentiate radiation\'s carcinogenic effect. Examples of substances that may damage DNA and induce carcinogenesis include:

❑alkylating agents — leukemia

❑aromatic hydrocarbons and benzopyrene (from polluted air) — lung cancer

❑asbestos — mesothelioma of the lung

❑tobacco — cancer of the lung, oral cavity and upper airways, esophagus, pancreas, kidneys, and bladder

❑vinyl chloride — angiosarcoma of the liver.

Diet has also been implicated, especially in the development of GI cancer as a result of a high animal fat diet. Additives composed of nitrates and certain methods of food preparation — particularly charbroiling — are also recognized factors.

The role of hormones in carcinogenesis is still controversial, but it seems that excessive use of some hormones, especially estrogen, produces cancer in animals. Also, the synthetic estrogen diethylstilbestrol causes vaginal cancer in some daughters of women who were treated with it. It\'s unclear, however, whether changes in human hormonal balance retard or stimulate cancer development.

Some forms of cancer and precancerous lesions result from genetic predisposition either directly (as in Wilms\' tumor and retinoblastoma) or indirectly (in association with inherited conditions such as Down syndrome or immunodeficiency diseases). Expressed as autosomal recessive, X-linked, or autosomal dominant disorders, their common characteristics include:

❑early onset of malignant disease

❑increased incidence of bilateral cancer in paired organs (breasts, adrenal glands, kidneys, and eighth cranial nerve [acoustic neuroma])

❑increased incidence of multiple primary malignancies in nonpaired organs

❑abnormal chromosome complement in tumor cells.

READ BOOK EXCERPT ONLINE » Malignant spinal neoplasms: Causes and incidence (Professional Guide to Diseases (Eighth Edition))

Primary tumors of the spinal cord may be extramedullary (occurring outside the spinal cord) or intramedullary (occurring within the cord itself). Extramedullary tumors may be intradural (meningiomas and schwannomas), which account for 60% of all primary malignant spinal cord neoplasms, or extradural (metastatic tumors from breasts, lungs, prostate, leukemia, or lymphomas), which account for 25% of these malignant neoplasms.

Intramedullary tumors, or gliomas (astrocytomas or ependymomas), are comparatively rare, accounting for only about 10%. In children, they\'re low-grade astrocytomas.

Spinal cord tumors are rare compared with intracranial tumors (ratio of 1:4). They occur equally in men and women, with the exception of meningiomas, which occur mostly in women. Spinal cord tumors can occur anywhere along the length of the cord or its roots.

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Treatment of spinal cord tumors generally includes decompression or radiation. Laminectomy is indicated for primary tumors that produce spinal cord or cauda equina compression; it isn\'t usually indicated for metastatic tumors. If the tumor is slowly progressive or if it\'s treated before the cord degenerates from compression, symptoms are likely to disappear, and complete restoration of function is possible. In a patient with metastatic carcinoma or lymphoma who suddenly experiences complete transverse myelitis with spinal shock, functional improvement is unlikely, even with treatment, and his outlook is ominous. If the patient has incomplete paraplegia of rapid onset, emergency surgical decompression may save cord function. Steroid therapy with dexamethasone minimizes cord edema and temporarily relieves symptoms until surgery can be performed. Partial removal of intramedullary gliomas, followed by radiation, may alleviate symptoms for a short time. Metastatic extradural tumors can be controlled with radiation, analgesics and, in the case of hormone-mediated tumors (breast and prostate), appropriate hormone therapy. Transcutaneous electrical nerve stimulation (TENS) may control radicular pain from spinal cord tumors and is a useful alternative to opioid analgesics. In TENS, an electrical charge is applied to the skin to stimulate large-diameter nerve fibers and thereby inhibit transmission of pain impulses through small-diameter nerve fibers. Chemotherapy generally hasn\'t proven effective against most spinal tumors, but may be recommended in some cases.

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