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

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

The previous 20 years have witnessed major advances within the remedy of melanoma by way of surgical procedure and radiation treatment. profits with cytotoxic chemotherapy were even more modest. Of the nearly 900,000 newly clinically determined situations of melanoma every year, 50010 bring about loss of life of the sufferer. the first reason for those deaths is metastasis. even if the time period metastasis used to be first coined by way of Recamier in 1829, in basic terms long ago ten years have there been extensive clinical investigations into the mechanisms during which tumor cells metastasize. What has emerged is a fancy strategy of host-tumor mobile interactions which has been termed the metastatic cascade. as a result complexity of the metastatic approach, the learn of metastasis is multifaceted and comprises parts of such components as differentiation, en­ zymology, genetics, hematology, immunology, membrane biochemistry and molecular biology. the most important goals of this ebook have been to provide the newest advances in our figuring out of ways tumor cells metastasize to secondary websites by means of the prime specialists within the biology of tumor invasion and metastasis. we are hoping that this ebook will bring about new options for the therapy of subclinical metastatic melanoma. The chapters during this ebook handle either the fundamental technological know-how of metastasis and capability medical remedies directed towards interruption of the metastatic cascade or towards eradication of subclinical metastases. Many correct themes were passed over as a result of house concerns and therefore the subjects incorporated replicate the prej­ udices of the editors.

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Extra resources for Mechanisms of Cancer Metastasis: Potential Therapeutic Implications

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Interactions between cancer cells and their environments, particularly their microenvironments which include other cells, can also produce changes in cancer host cell properties which are expected to be relevant to metastasis (9). The extent to which metastasis is dependent on transient, dynamic cancer cell properties as exemplified above, and on "pre-existing" metastatic subpopulations must be determined by experimentation. Recent studies have tended to support the concept of "transient metastatic compartments" based on genetic (10) and epigenetic events (7,11) and indicate that metastatic capacity is an unstable property.

The relationship of enzymes to invasion is discussed elsewhere in this volume (see Chapters 18-22). However, there is not always a simple relationship between enzyme production by cancer cells and their invasive capacities either in vivo (29) or in vitro (30), and the critical issue may be the degre;-of inhibition of enzyme activity. Thus, Hakala et al. (29) showed that invasiveness in a series of intracranial tumors does not correlate with enzyme production, but rather that the invasive tumors tend to produce less tissue inhibitor of metalloproteinases (TIMP) than non-invasive tumors.

Prominent among these are: differences in body size and lifespan; species variation in the anatomy and physiology of major organ systems; variation in the contribution of different elements of host immune and non-immune reactions in combating neoplasia; and significant species variation in the absorption, distribution, metabolism and excretion of therapeutic agents. The incidence of spontaneous tumors arising in specific cell types also varies significantly in man and animals. Similarly, the risk of tumor formation occurring in the same target organ after exposure to carcinogens varies among species and this is recognized as a serious limiting factor in using animals to predict the carcinogenic liability of food additives, chemicals or drugs.

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