The cellular basis of site-specific tumor metastasis

Article Abstract:

Two main theories have been proposed to explain why tumors spread to certain organs and not to others. The 'seed and soil' theory of Stephen Paget, proposed 100 years ago, likened tumor spread to the growth of plants, with survival dependent upon the receptivity of the tissue to which they spread. The mechanical theory, on the other hand, held that tumor metastasis (spread) is the result of blood flow and that cells lodge and multiply in the first organ they arrive at on the way from the primary cancer. Now it seems that both theories are partly correct and that some tumors can spread to almost any other organ, while others are highly selective for certain organs. To form a successful colony at a second site, tumors must grow in the primary site, gain entry to the circulation, adhere to the endothelial wall at the second site, invade the tissue of the organ, and proliferate by cell division. Substances or factors specific to an organ that modulate tumor growth include fibroblast growth factor, located in nervous tissue; transforming growth factor in platelets, cartilage, and bone; and factors inducing the proliferation of blood cells. Growth inhibitors, which can prevent metastasis, are also present in certain organs. Prostatic carcinoma is a leading cause of death in the United States, and when it metastasizes to the spine it grows faster there than in its primary site in the prostate. Researchers have found a growth factor in bone that is not present in other organs that stimulates the growth of prostatic carcinoma cells. In order for cells to come under the influence of growth factors, though, they must successfully invade the organ and establish a blood supply. Organ-specific adhesion molecules are thought to be responsible for selectively trapping circulating tumor cells. Since the cells in circulation 'see' only the basement membrane of the blood vessel, the search for adhesion molecules focussed on endothelial cells, which line the blood vessels. Indeed, tumor cells adhere to endothelial cells derived from blood vessels in their preferred secondary site. Preferential adhesion to cells in the organ itself and to substances outside the cells can also take place. The conditions determining adhesion of tumor cells interact in a complex manner and are regulated by other factors. Once they have attached themselves to a tissue, tumor cells spread in proportion to their ability to degrade the basement membrane or connective tissue that provides support for the organ. This requires secreting enzymes that specifically destroy the proteins located in the tissues, and, although research on this topic is just beginning, it seems likely that this is the case for some lung metastases.

Cancer invasiveness, Tumors, Paget, Stephen

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Chemokines - chemotactic cytokines that mediate inflammation

Article Abstract:

Chemokines are proteins produced by the immune system that can attract immune cells to the site of an injury or inflammation. There are over 40 known chemokines and they attract white blood cells, including T cells, neutrophils and natural killer cells. However, chemokine receptors occur on other tissues, including neurons and epithelial cells but their role in these tissues is unclear. Their most important function is to assist the white blood cell in moving from the blood into the tissues, a process called extravasation. Chemokines have been found in many chronic diseases, so blocking their action may have important therapeutic implications.

Inflammation, Inflammation mediators, Cytokines

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Chemokines and the molecular basis of cancer metastasis

Article Abstract:

Cancer cells may spread to specific organs because those organs contain proteins that bind to specific receptors on the cancer cells. This means the cancer cells would be attracted to those organs but not to other organs. The proteins, which are called chemokines, are also used to direct white blood cells to specific targets.

Development and progression, Cancer

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