Download Cancer Metastasis, Molecular and Cellular Mechanisms and by W.G. Jiang (Editor), R.E. Mansel (Editor) PDF

By W.G. Jiang (Editor), R.E. Mansel (Editor)

This ebook covers the molecular and mobile facets of melanoma metastasis, and discusses the medical element of micro- and macro-metastases, which lead to the loss of life of the vast majority of sufferers with melanoma. the present variation makes an attempt to check the present prestige of the elemental medical and medical study within the sector, and is a really precious reference for clinicians, oncologists, and biologists. it really is meant for undergraduates in addition to postgraduates within the quarter of medication, oncology, and melanoma biology.

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Additional resources for Cancer Metastasis, Molecular and Cellular Mechanisms and Clinical Intervention, Volume 1: Biology and Treatment (Cancer Metastasis - Biology and Treatment)

Sample text

In contrast over expression of wild type FAK induced an increase in cyclin D1 and a decrease in p21(104). Thus integrin-dependent activation of FAK can have a profound affect on cell proliferation by promoting activation of MAPKs and also modulating the cell-cycle machinery. Over activity in either of these pathways could contribute to a tumourigenic phenotype. For example, expression of a membrane bound constitutively active FAK prevented non-adherent MDCK epithelial cells from entering apoptosis (88).

Coinjection of small peptides, which include the RGD motif, can significantly impair the lung colonising ability of melanoma cells (118) as well as reduce the formation of spontaneous metastases (119). The principal mechanism for these results was believed to be as a consequence of the ability of RGD peptides to disrupt integrin-ligand interactions and therefore prevent integrin-dependent processes including adhesion and migration. Although these conclusions may have been true, recent data from Buckley et al have demanded that we may need to interpret data generated by use of RGD peptides a little more cautiously (120).

Examination of the tumours of the thymus and liver in these mice showed loss of the single remaining wild-type allele of PTEN. Interestingly the mice also developed non-neoplastic hyperplasia of the lymph nodes caused by a defective apoptosis pathway in B cells and macrophages (141). Thus PTEN regulated pathways include suppression of cancer and also regulation of apoptosis. Since 41 many of these pathways are driven by integrin ligation these data confirm that deregulated integrin signalling can promote the metastatic phenotype.

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