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Chemotaxis in cancer

TLDR
This Review summarizes how chemotaxis directs the different behaviours of tumour cells and stromal cells in vivo, how molecular pathways regulateChemotaxis in tumours and how chemtaxis choreographs cell behaviour to shape the tumour microenvironment and to determine metastatic spread.
Abstract
Chemotaxis of tumour cells and stromal cells in the surrounding microenvironment is an essential component of tumour dissemination during progression and metastasis. This Review summarizes how chemotaxis directs the different behaviours of tumour cells and stromal cells in vivo, how molecular pathways regulate chemotaxis in tumour cells and how chemotaxis choreographs cell behaviour to shape the tumour microenvironment and to determine metastatic spread. The central importance of chemotaxis in cancer progression is highlighted by discussion of the use of chemotaxis as a prognostic marker, a treatment end point and a target of therapeutic intervention.

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Cancer Invasion and the Microenvironment: Plasticity and Reciprocity

TL;DR: The cell-matrix and cell-cell adhesion, protease, and cytokine systems that underlie tissue invasion by cancer cells are described and explained to explain how the reciprocal reprogramming of both the tumor cells and the surrounding tissue structures not only guides invasion, but also generates diverse modes of dissemination.
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Classifying collective cancer cell invasion

TL;DR: A framework for addressing potential mechanisms, experimental strategies and technical challenges to study collective cancer cell invasion is proposed.
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Three-dimensional microfluidic model for tumor cell intravasation and endothelial barrier function

TL;DR: Evidence is provided that the endothelium poses a barrier to tumor cell intravasation that can be regulated by factors present in the tumor microenvironment.
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Differential macrophage programming in the tumor microenvironment.

TL;DR: Targeting molecular pathways regulating TAM polarization holds great promise for anticancer therapy.
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Crossing the endothelial barrier during metastasis

TL;DR: How cancer cells cross the endothelial barrier during extravasation is described and how different receptors, signalling pathways and circulating cells such as leukocytes and platelets contribute to this process are described.
References
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Journal ArticleDOI

Cortactin promotes and stabilizes Arp2/3-induced actin filament network formation.

TL;DR: These results support a model in which cortactin modulates actin filament dendritic nucleation by two mechanisms, (1) direct activation of Arp2/3 complex and (2) stabilization of newly generated filament branch points.
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The inflammatory chemokines CCL2 and CCL5 in breast cancer.

TL;DR: The overall current information suggests that CCL2 and CCL5 are inflammatory mediators with pro-malignancy activities in breast cancer, and that they should be considered as potential therapeutic targets for the limitation of this disease.
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Cancer-associated fibroblasts and tumor growth--bystanders turning into key players.

TL;DR: Clinical studies aiming at CAF-targeting can now be envisioned based on findings from experimental intervention studies with agents targeting, for example FAP or PDGF-, TGF-beta- or hedgehog-signaling.
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Chemokine signaling mediates self-organizing tissue migration in the zebrafish lateral line.

Petra Haas, +1 more
- 01 May 2006 - 
TL;DR: A role for chemokine signaling in mediating the self-organizing migration of tissues during morphogenesis is revealed, and a remarkably small number of SDF1a-responsive cells are able to organize an entire cxcr4b mutant primordium to restore migration and organogenesis in the lateral line.
Journal ArticleDOI

Autologous chemotaxis as a mechanism of tumor cell homing to lymphatics via interstitial flow and autocrine CCR7 signaling.

TL;DR: Computational modeling revealed that transcellular gradients of CCR7 ligand were created under flow to drive this response, illustrating how tumor cells may be guided to lymphatics during metastasis.
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What part of chemotaxis in cancer has not been studied yet?

The text does not provide information about any specific part of chemotaxis in cancer that has not been studied yet.

What part of chemotaxis in breast cancer has not been studied yet?

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