Mechanisms of Cancer Metastasis: Potential Therapeutic by William E. Powers (auth.), Kenneth V. Honn, William E.

By William E. Powers (auth.), Kenneth V. Honn, William E. Powers, Bonnie F. Sloane (eds.)

The earlier two decades have witnessed major advances within the remedy of melanoma via surgical procedure and radiation remedy. earnings with cytotoxic chemotherapy were even more modest. Of the nearly 900,000 newly clinically determined instances of melanoma every year, 50010 lead to loss of life of the sufferer. the first reason behind those deaths is metastasis. even supposing the time period metastasis used to be first coined through Recamier in 1829, merely some time past ten years have there been in depth clinical investigations into the mechanisms through which tumor cells metastasize. What has emerged is a posh strategy of host-tumor phone interactions which has been termed the metastatic cascade. end result of the complexity of the metastatic procedure, the learn of metastasis is multifaceted and comprises components of such parts as differentiation, en­ zymology, genetics, hematology, immunology, membrane biochemistry and molecular biology. the foremost goals of this publication have been to provide the latest advances in our knowing of ways tumor cells metastasize to secondary websites through the major specialists within the biology of tumor invasion and metastasis. we are hoping that this booklet will result in new ideas for the remedy of subclinical metastatic melanoma. The chapters during this e-book deal with either the elemental technology of metastasis and capability medical cures directed towards interruption of the metastatic cascade or towards eradication of subclinical metastases. Many correct themes were passed over because of house concerns and therefore the subjects incorporated mirror the prej­ udices of the editors.

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Neurosurg. 59:461-466, 1983. Turner GA, Weiss L: Differential cell migration into stromal and protein-impregnated synthetic membranes and the effects of tumor necrotic extracts. Invasion Metastasis 2:361-368, 1982. Kuettner KE, Pauli BU: Resistance of cartilage to invasion. ) Bone Metastasis. K. Hall, Boston, pp. 131-165, 1981. Wallace AC, Chew EC, Jones DS: Arrest and extravasation of cancer cells in the lung. ) Pulmonary Metastasis. K. Hall, Boston, pp. 26-42, 1978. Weiss L, Glaves D: Cancer cell damage at the vascular endothelium.

It is beyond the scope of this chapter to discuss the broad range of biological approaches now under development for cancer treatment. Suffice it to say that these approaches are certain to complement, if not displace conventional chemotherapy. This field, which once suffered from lack of biochemical characterization of immune factors, has rapidly progressed from the level of phenomenology to the isolation, purification and production (by genetic engineering) of lymphokines such as IL-2, lymphotoxins, tumor necrosis factor, interferons and others (see Chapters 13-16).

It must be emphasized, however, that toxicity mediated by oxygen-dependent pathways is not the only mechanism involved. The localization of activity of the oxygen metabolites and other leukocyte products to regions close to their targets serves to both potentiate their target cytotoxicity and to limit their generalized toxicity. In addition, as a variety of cancer cells examined usually have lower levels of superoxide dismutase than their normal counterparts (43), these metabolites may well play an important role in killing cancer cells in the post-arrest phase of metastasis.

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