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Open AccessJournal ArticleDOI

Keeping Out the Bad Guys: Gateway to Cellular Target Therapy

Takanori Kitamura, +1 more
- 01 Nov 2007 - 
- Vol. 67, Iss: 21, pp 10099-10102
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TLDR
It is shown that lack of CCR1 prevents the accumulation of M MP-expressing cells at the invasion front and suppresses tumor invasion, providing the possibility of a novel therapeutic strategy for advanced cancer--prevention of the recruitment of MMP- expressing cells by chemokine receptor antagonist.
Abstract
Tumor-stromal interaction is implicated in many stages of tumor development, although it remains unclear how genetic lesions in tumor cells affect stromal cells. We have recently shown that inactivation of transforming growth factor-beta family signaling within colon cancer epithelium increases chemokine CC chemokine ligand 9 (CCL9) and promotes recruitment of the matrix metalloproteinase (MMP)-expressing stromal cells that carry CC chemokine receptor 1 (CCR1), the cognate receptor for CCL9. We have further shown that lack of CCR1 prevents the accumulation of MMP-expressing cells at the invasion front and suppresses tumor invasion. These results provide the possibility of a novel therapeutic strategy for advanced cancer--prevention of the recruitment of MMP-expressing cells by chemokine receptor antagonist.

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Mouse models of colon cancer.

TL;DR: What models have been developed most recently and what they have taught us about colon cancer formation, progression, and possible treatment strategies are discussed.
Journal ArticleDOI

Inactivation of chemokine (C-C motif) receptor 1 (CCR1) suppresses colon cancer liver metastasis by blocking accumulation of immature myeloid cells in a mouse model

TL;DR: It is suggested that CCR1 antagonists can provide antimetastatic therapies for patients with disseminated colon cancer in the liver because of their role in tumor invasion and metastasis.
Journal ArticleDOI

Genetic Engineering of Mesenchymal Stem Cells and Its Application in Human Disease Therapy

TL;DR: The current understanding of the use of genetically engineered mesenchymal stem cells in human disease therapy with emphasis on genetic modifications aimed to improve survival, homing, angiogenesis, and heart function after myocardial infarction is presented.
References
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Journal ArticleDOI

Pivotal role of CXCR3 in melanoma cell metastasis to lymph nodes.

TL;DR: It is shown that mouse B16F10 melanoma cells constitutively express chemokine receptor CXCR3, and that its ligands CXCL9/Mig, CxCL10/IP-10, and CX CL11/I-TAC induce cellular responses in vitro, such as actin polymerization, migration, invasion, and cell survival.
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Hyperplastic gastric tumors induced by activated macrophages in COX-2/mPGES-1 transgenic mice

TL;DR: Results indicate that an increased level of PGE2 enhances macrophage infiltration, and that they are activated through epithelial cells by the gastric flora, resulting in gastric metaplasia and tumorous growth.
Journal ArticleDOI

Chemokine receptor CXCR3 promotes colon cancer metastasis to lymph nodes

TL;DR: It is shown that some human colon cancer cell lines express CXCR3 constitutively, and activation of CX CR3 with its ligands stimulates colon cancer metastasis preferentially to the draining lymph nodes with poorer prognosis.
Journal ArticleDOI

Identification and characterization of a potent, selective, and orally active antagonist of the CC chemokine receptor-1.

TL;DR: This study is the first to demonstrate that a non-peptide chemokine receptor antagonist is efficacious in an animal model of an autoimmune disease and identified a potent, selective, and orally available CCR1 antagonist that may be useful in the treatment of chronic inflammatory diseases.
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