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 prior 20 years have witnessed major advances within the therapy of melanoma via surgical procedure and radiation remedy. profits with cytotoxic chemotherapy were even more modest. Of the nearly 900,000 newly clinically determined circumstances of melanoma every year, 50010 lead to demise 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, purely some time past ten years have there been extensive clinical investigations into the mechanisms through which tumor cells metastasize. What has emerged is a fancy technique of host-tumor telephone interactions which has been termed the metastatic cascade. because of the complexity of the metastatic method, the examine of metastasis is multifaceted and consists of parts of such components as differentiation, en­ zymology, genetics, hematology, immunology, membrane biochemistry and molecular biology. the key ambitions of this ebook have been to give the latest advances in our figuring out of ways tumor cells metastasize to secondary websites by means of the top specialists within the biology of tumor invasion and metastasis. we are hoping that this e-book will bring about new ideas for the remedy of subclinical metastatic melanoma. The chapters during this publication tackle either the fundamental technological know-how of metastasis and capability scientific cures directed towards interruption of the metastatic cascade or towards eradication of subclinical metastases. Many proper issues were passed over because of area concerns and hence the themes integrated mirror the prej­ udices of the editors.

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Anatomische untersuchungen ueber die Goldmann EE: verbreitungsweise geschwuelste. Beitr z Klin Chir (Tubingen) 18:595-612, 1891. Iwasaki T: Histological and experimental observations on the destruction of tumour cells in the blood vessels. J. Pathol Bacteriol. 20:85-105. 1915. Griffiths JD, Salsbury AJ: Circulating Cancer Cells. C. Thomas. Springfield. IL, pp. 54-56, 1965. Tarin D, Vass ACR, Kettlewell MGW, Price JE: Absence of metastatic sequelae during long-term treatment of malignant ascites by peritoneo-venous shunting.

Mechanism Example 1. Transport deficiency Methotrexate Melphalan Cytosine arabinoside 2. Increased target enzyme Methotrexate N-phosphono-acetyl-Laspartic acid 3. Decreased drug activation 6-Mercaptopurine 6-Thioguanine Cytosine arabinoside 5-Fluorouracil 4. Increased drug degradation Cytosine arbinoside 6-Mercaptopurine 5. Increased competitive substrate Cytosine arabinoside (dCTP) 6. "Pleotropic" drug resistance (decreased drug accumulation) Adriamycin Actinomycin-D Vinca alkaloids VP-16 m-AMSA 3.

In humans, it is well-recognized that the presence of circulating cancer cells is not synonymous with metastasis (50). Even on morphologic evidence, it appears that most of the cancer cells are killed in the microcirculation (51). Although quantitative data are lacking for humans, published data on the presence of cancer cells in the venous effluent from cancers (52) lead to the reasonable expectation that millions of cancer cells per day are released from primary cancers into the circulation. Even so at autopsy relatively few overt metastases can usually be identified.

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