作者: Gerhard Hamilton , Barbara Rath
DOI: 10.1007/978-3-319-55947-6_12
关键词:
摘要: Cancer patients die of metastatic disease but knowledge regarding individual steps this complex process intravasation, spread and extravasation leading to secondary lesions is incomplete. Subpopulations tumor cells are supposed undergo an epithelial-mesenchymal transition (EMT), enter the bloodstream eventually establish metastases in a reverse termed mesenchymal-epithelial (MET). Small cell lung cancer (SCLC) represents unique model study due early dissemination relapse, as well availability panel circulating (CTC) lines recently. Additionally, chemosensitive SCLC switch completely resistant phenotype during recurrence. In advanced disease, display extremely high blood counts CTCs contrast other tumors, like breast, prostate colon cancer. Local inflammatory conditions at primary site recruitment macrophages seem increase shedding into circulation processes which may proceed independently EMT. Since millions released by tumors per day, analysis limited number specific time points difficult be related development occur approximately one year later. We have obtained CTC line from with relapsing share characteristic markers malignancy primarily epithelial formation large tumorospheres, containing quiescent hypoxic cells. Although smoking inflammation promote EMT, partial expression vimentin indicates transitional state EMT these most. The exhibit EpCAM , absent phosphorylation β-catenin background levels Snail. Provided that had ever undergone here MET occurred already peripheral circulation. Alternative explanations for mesenchymal heterogeneity cells, cooperative migration or altered gene response microenvironment allowing without EMT/MET.