Pathogenesis of vertebral metastasis and epidural spinal cord compression

Article Abstract:

The complications that can result from the colonization of other parts of the body by a tumor that has metastasized, or migrated, are numerous. Among them is spinal cord compression, which occurs when a tumor growing outside the dura of the spinal cord increases in size to the point that significant pressure is placed on the cord itself. Spinal cord compression is of major clinical significance; not only does it indicate poor prognosis, but it may result in severe pain, loss of motor function and sphincter control, and perhaps complete paraplegia. Despite the seriousness of cord compression, little is known about its early stages of development. To study spinal cord compression, an animal model has been devised in which tumor cells are injected into mice. Some of these tumor cells will ultimately form tumors pressing against the spinal cord; these tumors may be studied in a step-by-step fashion. First, the tumor cells lodge in the bone marrow, presumably because of the presence of factors suitable for colonization and growth. Rather than invade the bone itself, the cells migrate into the spinal canal by way of the small openings through which the blood vessels pass. Once in the spinal canal, the cells do not necessarily begin forming a tumor mass immediately. They may, indeed, migrate large distances. The cells may migrate posteriorly and begin to form a tumor mass that presses on the cord from the back instead of from the front. It is interesting to note that pressure from the posterior does not necessarily damage the posterior portion of the cord. Even when pressure is placed on the posterior of the cord, the anterior portion of the cord seems to be the first portion damaged. Since motor nerves are located in the anterior portion, motor functions are affected sooner than sensory functions. This effect is also observed in human patients. The extensive migration observed is a strong argument for the inclusion of radiotherapy along with any attempt at surgical removal of a metastatic tumor compressing the spinal cord. (Consumer Summary produced by Reliance Medical Information, Inc.)

Spinal cord compression

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Growth hormone inhibits tumor metastasis

Article Abstract:

The hallmark of cancer, the feature that distinguishes cancers from benign tumors, is the potential for metastasis. This ability to spread throughout the body and seed the growth of new tumors is what makes cancer so deadly. In laboratory experiments using rats, it has now been shown that growth hormone has the ability to inhibit metastasis in cancer. Tumors were surgically implanted into experimental rats, which were divided into four groups. Approximately half the rats were fed a standard protein diet and half were given a diet with the same caloric content but minimal protein. The animals on each diet were further divided; some were given daily injections of growth hormone while others received an inactive placebo (growth hormone group and placebo group). At the end of the experiment, the lungs of the animals were examined for metastatic tumors which had spread from the initial tumors implanted under the skin. More metastatic tumors were found in the rats with the standard protein diet, regardless of treatment. However, among the animals given the standard protein diet, about twice as many metastatic tumors were found in the placebo group, compared with the growth hormone group. Similarly, among the animals fed the protein depleted diet, about half as many metastatic tumors were found in the growth hormone group. Measurements of the implanted tumors revealed no indication that use of the growth hormone accelerated the growth of the initial tumor. The reasons why growth hormone should influence the spread of cancer are not understood. One possibility is that growth hormone stimulates the action of the immune system in some way that helps to destroy potentially metastatic cells. Another possibility is that the growth hormone affects some key step in the process by which a tumor cell becomes metastatic. What this key step might be is unknown. (Consumer Summary produced by Reliance Medical Information, Inc.)

Somatotropin

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Mucin leakage into the cervical stroma may increase lymph node metastasis in mucin-producing cervical adenocarcinomas

Article Abstract:

Adenocarcinomas of the uterine cervix are less common than squamous cell carcinomas; the former type constitutes roughly 3 to 6 percent of all primary cervical cancers. In adenocarcinoma, the prognosis is thought to be worse than in squamous cell carcinoma, primarily due to the greater chance of metastasis (spreading of the cancer). Mucin, which is a set of glycoproteins and polysaccharides, is secreted by a variety of different cancers, as well as by some normal tissues. Cervical adenocarcinomas are among those tumors which can secrete mucin, and an investigation was undertaken to determine if the secretion of mucin is related to the invasiveness of cervical adenocarcinoma. The study was based on surgical specimens obtained from 35 patients with cervical adenocarcinoma. In 14 of those cases, or 40 percent, mucin leakage could be identified. In 10 of the 14 patients with mucin leakage, cancer cells had already migrated to the local lymph nodes, as opposed to only 5 of the 21 patients who did not have mucin leakage. The difference between the groups was statistically significant. Although this significance does not necessarily indicate a causal role, it is possible that the secretion of mucin into the stroma, or supporting tissues of the cervix and uterus, may provide a superior environment for the migration of cells from the original tumor into the lymph nodes. Histologically, mucin secretion was more frequently observed in tumors with greater depths of invasion into the uterine wall. (Consumer Summary produced by Reliance Medical Information, Inc.)

Research, Cervical cancer, Adenocarcinoma, Mucins

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