Matches in UGent Biblio for { <https://biblio.ugent.be/publication/2976334#aggregation> ?p ?o. }
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- aggregation classification "A1".
- aggregation creator B373599.
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- aggregation date "2012".
- aggregation format "application/pdf".
- aggregation hasFormat 2976334.bibtex.
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- aggregation isPartOf urn:issn:1535-6108.
- aggregation language "eng".
- aggregation rights "I have transferred the copyright for this publication to the publisher".
- aggregation subject "Biology and Life Sciences".
- aggregation title "Endothelial CCR2 signaling induced by colon carcinoma cells enables extravasation via the JAK2-Stat5 and p38MAPK pathway".
- aggregation abstract "Increased expression of the chemokine CCL2 in tumor cells correlates with enhanced metastasis, poor prognosis, and recruitment of CCR2(+)Ly6C(hi) monocytes. However, the mechanisms driving tumor cell extravasation through the endothelium remain elusive. Here, we describe CCL2 upregulation in metastatic UICC stage IV colon carcinomas and demonstrate that tumor cell-derived CCL2 activates the CCR2(+) endothelium to increase vascular permeability in vivo. CCR2 deficiency prevents colon carcinoma extravasation and metastasis. Of note, CCR2 expression on radio-resistant cells or endothelial CCR2 expression restores extravasation and metastasis in Ccr2(-/-) mice. Reduction of CCR2 expression on myeloid cells decreases but does not prevent metastasis. CCL2-induced vascular permeability and metastasis is dependent on JAK2-Stat5 and p38MAPK signaling. Our study identifies potential targets for treating CCL2-dependent metastasis.".
- aggregation authorList BK675572.
- aggregation endPage "105".
- aggregation issue "1".
- aggregation startPage "91".
- aggregation volume "22".
- aggregation aggregates 2976356.
- aggregation isDescribedBy 2976334.
- aggregation similarTo j.ccr.2012.05.023.
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