Tumour-cell invasion and migration: diversity and escape mechanisms

By Peter Friedl, Katarina Wolf. Nature Reviews. Cancer, 2003

3,305 citations recorded by the source corpus.

Subfields: Cancer Research, Cell Biology, Immunology and Allergy

View Paper: https://www.semanticscholar.org/paper/76a34bc8ba09ad251e454034f2e59758aed0d6ec

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Citations in the corpus

Tracking metastatic tumor cell extravasation with quantum dot nanocrystals and fluorescence emission-scanning microscopy (2004, background): “These approaches have generated several hypotheses describing the nature of the processes and have suggested possible therapeutic target”
Intravital imaging of cell movement in tumours (2003, background): “They have not been observed to migrate as collections of attached cells as observed in several in vitro models of invasion (reviewed in Ref”
Research Techniques Made Simple: Analysis of Collective Cell Migration Using the Wound Healing Assay. (2017, background): “Depending on the cell type, cytoskeletal structure, and the context in which it is migrating, the cell can migrate in different morphological variants such as mesenchymal, amoeboid motility modes (Friedl and Wolf, 2003).”
Circulating tumor cells (CTC) detection: clinical impact and future directions. (2007, background): “The importance of the ‘‘collective cells migration’’ has been recently stressed [10,15].”
Tumor metastasis: mechanistic insights and clinical challenges (2006, background): “The engagement of integrins and other attachment molecules is accompanied by the recruitment of proteases to degrade the ECM, providing a pathway for invasio”
Molecular mechanisms of invadopodium formation (2005, positive): “The initial step of cancer cell migration and invasion is the extension of cell protrusions in the direction of cell movement (Friedl and Wolf, 2003).”
Physical forces during collective cell migration (2009, neutral): “dtd" [ ]> Fundamental biological processes including morphogenesis, tissue repair and tumour metastasis require collective cell motion”
Rac and Rho GTPases in cancer cell motility control (2010, background): “Mesenchymal cells are able to move through a matrix-filled space by using proteases, such as MMPs and urokinase-type plasminogen activator (uPA), that degrade ECM proteins and creates the path [61,62].”
Cancer metastasis: building a framework. (2006, neutral): “and focal contact disassembly (Friedl and Wolf, 2003).”
Epithelial-mesenchymal transition in cancer metastasis: mechanisms, markers and strategies to overcome drug resistance in the clinic. (2009, background): “like the type of ECM, the genetic alterations and a potential drug treatment [37,38,158], pointing out the possibility that they could alternatively used as a result of an adaptation of tumour cells to facilitate metastasis.”
Rho GTPases in cancer cell biology (2008, background): “migration to another depending on conditions [17,18].”
Cancer invasion and the microenvironment: plasticity and reciprocity. (2011, positive): “The initial steps of local invasion include the activation of signaling pathways that control cytoskeletal dynamics in tumor cells and the turnover of cellmatrix and cell-cell junctions, followed by active tumor cell migration into the adjacent tissue (Chambers et al., 2002; Friedl and Wolf, 2003; S”