【摘 要】
：
Epithelial-mesenchymal transition (EMT) is a critical mechanism which contributes to body plan formation in most metazoans.We have made the hypothesis that
【机 构】
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IMCB A*STAR Experimental Therapeutic Centre Singapore
【出 处】
：
BIT‘s2nd Annual World Cancer Congess-2009 (2009第二届癌症大会)
论文部分内容阅读
Epithelial-mesenchymal transition (EMT) is a critical mechanism which contributes to body plan formation in most metazoans.We have made the hypothesis that EMT can also play a major role in the local and distant dissemination of carcinoma.Phenotypic analyses of human carcinoma show that dedifferentiated tumors exhibit a number of EMT features.Regulation of cell adhesion is one of the critical mechanisms driving EMT.Biophysical approaches have been developed to unravel the basis of cadherin mediated adhesion strengthening.The shift from type 1 E-cadherin to N-cadherin or to type 2 cadherins is observed during EMT of carcinoma cells.An initial adhesion not exceeding several nanonewtons is reinforced only following cortical actin polymerization.E-cadherin mediated adhesion is significantly higher than N-cadherin mediated adhesion.Much weaker adhesion is observed in cells expressing type 2 cadherins.In an attempt to further characterize EMT in carcinoma we have focused on micrometastasis in breast carcinoma.Carcinoma ceils can be detected in blood and bone marrow of breast cancer patients.Bone marrow micrometastasis was found to be an independent prognostic factor for disease progression.We recently investigated whether micrometastasis is already observed at an early stage of the disease.
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