ArticleThe American journal of pathology2007
The host inflammatory response promotes liver metastasis by increasing tumor cell arrest and extravasation.
Article in The American journal of pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
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Who cites it
81 citing papers in PubMed, 175 citations in OpenAlex.
- Role of Organ-Specific Endothelial Cells in Melanoma Adhesion Patterns.Biomedicines · 2026Article
- Functions and clinical implications of the liver microenvironment in hepatic uveal melanoma metastases.Cancer metastasis reviews · 2025Review
- Endothelial activation during the diapedesis of cancer cells: between the kiss of death and therapeutic breakthrough.Cellular & molecular biology letters · 2025Review
- Unveiling the Involvement of Extracellular Vesicles in Breast Cancer's Organotrophic Metastasis: Molecular Mechanisms and Translational Prospects.International journal of molecular sciences · 2025Review
- The pan-immune-inflammation value predicts prognosis and chemotherapy-related adverse events in Wilms' tumor patients.BMC cancer · 2025Article
- Macrophages in the premetastatic and metastatic niche: key functions and therapeutic directions.Journal of translational medicine · 2025Review
- Tumor microbiome: roles in tumor initiation, progression, and therapy.Molecular biomedicine · 2025Review
- Cancer stem cells and tumor-associated macrophages as mates in tumor progression: mechanisms of crosstalk and advanced bioinformatic tools to dissect their phenotypes and interaction.Frontiers in immunology · 2025Review
- The Role of Myeloid Cells on the Development of Hepatic Metastases in Gastrointestinal Cancer.Gastro hep advances · 2025Review
- Small cell lung cancer with liver metastases: from underlying mechanisms to treatment strategies.Cancer metastasis reviews · 2024Review
- Article
- Altered lipid metabolism as a predisposing factor for liver metastasis in MASLD.Molecules and cells · 2024Review
- Review
- Identification of potential classes of glycoligands mediating dynamic endothelial adhesion of human tumor cells.Glycobiology · 2023Article
- Metastasis organotropism in colorectal cancer: advancing toward innovative therapies.Journal of translational medicine · 2023Review
- Roles of macrophages in tumor development: a spatiotemporal perspective.Cellular & molecular immunology · 2023Review
- Methylation across the central dogma in health and diseases: new therapeutic strategies.Signal transduction and targeted therapy · 2023Review
- Analysis of the metastatic mechanism and progress in the treatment of breast cancer liver metastasis: a narrative review.Translational cancer research · 2023Review
- Aptamer‑based therapy for targeting key mediators of cancer metastasis (Review).International journal of oncology · 2022Review
- Review
21 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammation can play a regulatory role in cancer progression and metastasis. Previously, we have shown that metastatic tumor cells entering the liver trigger a proinflammatory response involving Kupffer cell-mediated release of tumor necrosis factor-alpha and the up-regulation of vascular endothelial cell adhesion receptors, such as E-selectin. Here, we analyzed spatio-temporal aspects of the ensuing tumor-endothelial cell interaction using human colorectal carcinoma CX-1 and murine carcinoma H-59 cells and a combination of immunohistochemistry, confocal microscopy, and three-dimensional reconstruction. E-selectin expression was evident mainly on sinusoidal vessels by 6 and 10 hours, respectively, following H-59 and CX-1 inoculation, and this corresponded to a stabilization of the number of tumor cells within the sinuses. Tumor cells arrested in E-selectin(+) vessels and appeared to flatten and traverse the vessel lining, away from sites of intense E-selectin staining. This process was evident by 8 (H-59) and 12 (CX-1) hours after inoculation, coincided with increased endothelial vascular cell adhesion molecule-1 expression, and involved tumor cell attachment in areas of intense vascular cell adhesion molecule-1 and platelet endothelial cell adhesion molecule-1 expression. Nonmetastatic (human) MIP-101 and (murine) M-27 cells induced a weaker response and could not be seen to extravasate. The results show that metastatic tumor cells can alter the hepatic microvasculature and use newly expressed endothelial cell receptors to arrest and extravasate.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.