Metastasis of Breast Cancer (Cancer Metastasis - Biology and by R.E. Mansel (Editor), Oystein Fodstad (Editor), W.G. Jiang

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

Metastasis (spread of melanoma within the physique) is the most explanation for loss of life for sufferers with breast melanoma, the prime woman tumour within the industrialised international locations and constructing nations alike. The biology and therapy of breast melanoma metastasis is still an energetic quarter of medical and scientific research. Written via specialists within the topic sector, the publication has lined a vast variety of subject matters within the metastasis of breast melanoma, from genetics, biology to medical administration. major themes contain genetic keep watch over, biology, development elements, telephone adhesion, mobilephone motility and invasion, natures of bone metastasis, sentinel node cures, hormonal hyperlinks, new biomarkers and detection of micrometastasis, and prognosis The publication additionally covers the present cures together with surgical administration, chemotherapy and hormonal remedies. This well timed booklet presents the present wisdom within the sector of breast melanoma metastasis and should be of vital analyzing fabric for oncologists, radiologists, melanoma researchers, biologists and medical expert.

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Extra resources for Metastasis of Breast Cancer (Cancer Metastasis - Biology and Treatment)

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Hepatocyte growth factor enhances adhesion of breast cancer cells to endothelial cells in vitro through up-regulation of CD44. Exp Cell Res 2003, 288(1):189–197. Martin TA, Watkins G, Mansel RE, Jiang WG. Hepatocyte growth factor disrupts tight junctions in human breast cancer cells. Cell Biol Int 2004, 28(5):361–371. Parr C, Jiang WG. Hepatocyte growth factor activation inhibitors (HAI-1 and HAI-2) regulate HGF-induced invasion of human breast cancer cells. Int J Cancer 2006, 119(5):1176–1183.

Once immortalized, the BRCA1 null MEFs proliferated at a significantly greater rate and exhibited greater metastatic potential than immortalized control MEFs. The results from these studies begin to reconcile the seeming paradox between the accepted function of BRCA1 as a tumor suppressor and the slow growth phenotype of BRCA1 mutant/null cells in culture. Consistent with the findings from the laboratory research, studies of human clinical samples indicate that BRCA1 mutation-associated breast cancers exhibit 3.

Demonstrated that the exogenous expression of BRCA1 resulted in downregulation of estrogen-stimulated expression of an estrogen-responsive reporter construct in human breast, prostate, and cervical carcinoma cell lines (72). Additional studies by this and other groups have shown that BRCA1 is physically associated with ERα-regulated promoters such as pS2 and regulates expression of the corresponding endogenous gene expression in breast cancer cell lines (40, 55, 73). Additional in vitro characterization has indicated that BRCA1 and ERα physically interact with each other through the aminoterminal region of BRCA1 and the ligand-binding domain (LBD) of ER-α in an estrogen-independent manner (40).

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