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Isolation of Circulating Tumor Cells in an Orthotopic Mouse Model of Colorectal Cancer
Published on: July 18, 2017
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Prediagnostic circulating markers of inflammation and risk of oesophageal adenocarcinoma: a study within the National
Michael B Cook1, Matthew J Barnett2, Cathryn H Bock3
1Division of Cancer Epidemiology and Genetics, NIH, DHHS, National Cancer Institute, Rockville, Maryland, USA.
Gut
|August 20, 2018
Summary
Systemic inflammation markers, including soluble tumor necrosis factor receptor 2 (sTNFR2), are linked to esophageal adenocarcinoma risk. Obesity and smoking increase this risk, partly through inflammation pathways, highlighting potential therapeutic targets.
Area of Science:
- Oncology
- Inflammation Biology
- Epidemiology
Background:
- Systemic inflammation is implicated in esophageal adenocarcinoma (EAC) development.
- Previous studies suggest a link, but prospective data on specific inflammation markers are limited.
Purpose of the Study:
- To investigate associations between prediagnostic circulating inflammation markers and EAC risk.
- To determine the extent to which inflammation mediates the relationship between obesity, smoking, and EAC risk.
Main Methods:
- Nested case-control study within seven prospective cohorts (296 EAC cases, 296 controls).
- Quantification of 69 circulating inflammation markers using multiplex assays.
- Conditional logistic regression and mediation analyses were employed.
Main Results:
- Soluble tumor necrosis factor receptor 2 (sTNFR2) showed a significant association with EAC (ORs, quartile 4 vs 1 = 2.67).
- Other markers like C-reactive protein and resistin were also associated.
- Mediation analysis indicated sTNFR2 explained 33% of the association between waist circumference and EAC risk. Plasminogen activator inhibitor 1 mediated smoking-related risk.
Conclusions:
- This prospective study confirms a link between systemic inflammation and EAC risk.
- Provides novel evidence that obesity and smoking increase EAC risk indirectly through systemic inflammation.
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