LEADER 03406oam 2200493 450 001 9910137088203321 005 20230621141059.0 010 $a9782889196623 (ebook) 035 $a(CKB)3710000000824755 035 $a(oapen)https://directory.doabooks.org/handle/20.500.12854/42865 035 $a(EXLCZ)993710000000824755 100 $a20191103c2015uuuu uu | 101 0 $aeng 135 $aurmn|---annan 181 $ctxt$2rdacontent 182 $cc$2rdamedia 183 $acr$2rdacarrier 200 10$aCellular and phenotypic plasticity in cancer$b[electronic resource] /$fedited by Petranel Theresa Ferrao, Andreas Behren, Robin Andersonand Erik Thompson 210 $cFrontiers Media SA$d2015 210 1$aFrance :$cFrontiers Media SA,$d2015 215 $a1 online resource (77 pages) $cillustrations 225 1 $aFrontiers Research Topics 320 $aIncludes bibliographical references. 330 $aThe process of Epithelial-Mesenchymal-Transition (EMT) is known to result in a phenotype change in cells from a proliferative state to a more invasive state. EMT has been reported to drive the metastatic spread of various cancers and has also been associated with drug resistance to cytotoxics and targeted therapeutics. Recently phenotype switching akin to EMT has been reported in non-epithelial cancers such as metastatic melanoma. This process involves changes in EMT-Transcription Factors (EMT-TFs), suggesting that phenotype-switching may be common to several tumour types. It remains unclear as to whether the presence of both Epilthelial-like and Mesenchymal-like cells are a pre-requisite for phenotype switching within a tumour, how this heterogeneity is regulated, and if alteration of cell phenotype is sufficient to mediate migratory changes, or whether drivers of cell migration result in an associated phenotype switch in cancer cells. Similarly it has yet to be clarified if cells in an altered phenotype can be refractory to drug therapy or whether mediators of drug resistance induce a concurrent phenotypic change. Little is known today about the underlying genetic, epigenetic and transient changes that accompany this phenotypic switch and about the role for the tumor micro-environment in influencing it. Hence this is currently an area of speculation and keen interest in the Oncology field with wide-ranging translational implications. In this Frontiers Research Topic, we discuss our current understanding of these concepts in various cancer types including breast cancer, colorectal cancer and metastatic melanoma. This topic covers how these processes of cellular and phenotypic plasticity are regulated and how they relate to cancer initiation, progression, dormancy, metastases and response to cytotoxics or targeted therapies. 606 $aCancer 610 $acrosstalk 610 $aImmune System 610 $aPhenotype-switching 610 $aplasticity 610 $aExosomes 610 $aEMT 610 $aTherapy-resistance 610 $asignalling 610 $aheterogeneity 610 $aCancer 615 0$aCancer 700 $aPetranel Theresa Ferrao$4auth$01365478 702 $aAndreas Behren$4auth 702 $aErik Thompson$4auth 702 $aRobin Anderson$4auth 801 0$bUkMaJRU 912 $a9910137088203321 996 $aCellular and phenotypic plasticity in cancer$93387417 997 $aUNINA LEADER 01211nam0 22002771i 450 001 UON00383218 005 20231205104537.708 100 $a20100712d1967 |0itac50 ba 101 $ager 102 $aDE 105 $a|||| 1|||| 200 1 $aˆ"‰Ça" zwischen demonstrativ- und neutralpronomen$eeine sprachvergleichende Untersuchung$fvorgelegt von Siegfried Paul 205 $aBamberg : Rodenbusch$b1967 210 $aXI$d151 p. ; 21 cm 215 $aSul front.: Inaugural-Dissertation zur erlangung des doktorgrades einer Hoen Philosophischen Fakultät der Eberhard-Karls-Universität zu Tübigen 606 $aLingua francese$xPronomi$3UONC070029$2FI 620 $dBamberg$3UONL003068 676 $a448$cLinguistica francese$v21 700 1$aPAUL$bSiegfried$3UONV197627$0704296 712 $aRodenbusch$3UONV277415$4650 801 $aIT$bSOL$c20250627$gRICA 899 $aSIBA - SISTEMA BIBLIOTECARIO DI ATENEO$2UONSI 912 $aUON00383218 950 $aSIBA - SISTEMA BIBLIOTECARIO DI ATENEO$dSI IX PAU $eSI SFR4398 7 $sBuono 996 $aÇa" zwischen demonstrativ- und neutralpronomen$91353055 997 $aUNIOR