作者: Yvonne Chao , Qian Wu , Marie Acquafondata , Rajiv Dhir , Alan Wells
DOI: 10.1007/S12307-011-0085-4
关键词:
摘要: Epithelial to mesenchymal transition (EMT) is an oft-studied mechanism for the initiation of metastasis. We have recently shown that once cancer cells disseminate a secondary organ, epithelial reverting (MErT) may occur, which we postulate enable metastatic colonization. Despite wealth in vitro and vivo studies, evidence supportive MErT human specimens rare difficult document because clinically detectable metastases are typically past micrometastatic stage at this most likely evident. obtained paired primary tumors from breast prostate patients evaluated expression various markers by immunohistochemistry. The exhibited increased membranous E-cadherin compared tumors, consistent with EMT site site. However, re-emergence phenotype was only partial or incomplete. Expression connexins 26 and/or 43 also on majority metastases, particularly those brain. upregulation vimentin FSP1 mostly unchanged. examined carcinoma varied sizes found while lesion, inversely correlated size This not suggests second occur ectopic tumor growth seed further but provides basis failure discern phenotypes macrometastases. In summary, report persistence readily allows Our results suggest continue display phenotypic plasticity beyond initiates