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Open AccessJournal ArticleDOI

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

Use of circulating tumor cells (CTC) in peripheral blood of breast cancer patients before and after adjuvant chemotherapy to predict risk for relapse: The SUCCESS trial.

TL;DR: Whether the presence of CTC before and after adjuvant chemotherapy increases the risk of subsequent relapse and death is evaluated and no correlation to tumor size, grading and HR-Status could be found.
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Membrane targeting of WAVE2 is not sufficient for WAVE2-dependent actin polymerization: a role for IRSp53 in mediating the interaction between Rac and WAVE2.

TL;DR: This study indicates that Rac1, along with IRSp53 and Abi1, is involved in a more complex and tight regulation of WAVE2 than one operating solely through membrane localization.
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Mena invasive (MenaINV) and Mena11a isoforms play distinct roles in breast cancer cell cohesion and association with TMEM

TL;DR: It is demonstrated that mouse mammary tumors generated from EGFP-MenaINV expressing tumor cells are significantly less cohesive and have discontinuous cell–cell contacts compared to Mena11a xenografts, suggesting that MenaINV is the isoform associated with breast cancer cell discohesion, invasion and intravasation in mice and in humans.
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The distinct roles of Ras and Rac in PI 3-kinase-dependent protrusion during EGF-stimulated cell migration.

TL;DR: The data show that in EGF-stimulated MTLn3 carcinoma cells, Ras is required for both PtdIns(3,4,5)P3 production and lamellipod extension, whereas Rac1 is needed for formation of adhesive structures, which suggest an unappreciated role for Ras during protrusion, and a crucial role for Rac in the stabilization of protrusions required for cell motility.
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Interleukin-8 secreted by endothelial cells induces chemotaxis of melanoma cells through the chemokine receptor CXCR1.

TL;DR: Antibody inhibition studies indicate that the chemotactic response of melanoma cells is mediated by the CXC‐chemokine receptor CX CR1 and not by the more promiscuous CXCR2, indicating that IL‐8 is the major melanoma chemoattractant secreted by endothelial cells.
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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?

The specific part of chemotaxis in breast cancer that has not been studied yet is not mentioned in the provided information.