| Literature DB >> 17560245 |
Christina L Roland1, Alden H Harken, Michael G Sarr, Carlton C Barnett.
Abstract
HYPOTHESIS: Solid tumor cells bind to ICAM-1 on endothelial surfaces via MUC-1. Tumor binding to ICAM-1 auto-upregulates tumor ICAM-1 at the leading edge of the tumor and promotes release of chemoattractants for circulating macrophages, and circulating macrophages bind to tumor-expressed ICAM-1, invoking propagation of further chemokines and cytokines that recruit neutrophils. Tight adherence between cell surface ligands on neutrophils and tumor-expressed ICAM-1 activates neutrophils to degranulate, releasing elastases, which break down endovascular and endolymphatic barriers permitting transendothelial tumor cell migration. Consequently, tumor cell ICAM-1 expression dictates metastatic potential and metastatic potential determines cancer lethality.Entities:
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Year: 2007 PMID: 17560245 DOI: 10.1016/j.surg.2007.01.016
Source DB: PubMed Journal: Surgery ISSN: 0039-6060 Impact factor: 3.982