Journal
CANCER IMMUNOLOGY IMMUNOTHERAPY
Volume 64, Issue 1, Pages 41-50Publisher
SPRINGER
DOI: 10.1007/s00262-014-1615-y
Keywords
Cancer; Complement system; Lectin pathway; Biomarkers
Categories
Funding
- Danish Council for Independent Research, Medical Sciences
- Kornerup Fund
- Aase and Ejnar Danielsen Fund
- Aage and Johanne Louis-Hansen Fund
- Kathrine and Vigo Skovgaard Fund
- Vissing Fond
- Henrik Henriksen Fund
- Obel Foundation
- Hede-Nielsen Family Fund
- Midtjyske Bladfond
- Jochum Foundation
- Bjarne Jensen Fund
- Inger Bonnen Fund
- Arvid Nilsson Fund
- Erna Hamilton Fund
- Dagmar Marshall Fund
- Oda and Hans Svenningsen Fund
- Walter and O. Kristiane Christensen Fund
- Knud Hojgaard Fund
- Spar Nord Fund
- Axel Muusfeldt Fund
- Einar Willumsen Fund
- Frimodt-Heineke Fund
- H.C. Bechgaard Fund
- KID Fund
- Leif Rasmussen Fund
- Sophus and Astrid Jacobsen Fund
- Thora and Viggo Grove Fund
- Torben and Alice Frimodt Fund
- Hvidovre Hospital
- Novo Nordisk Fonden [NNF13OC0007989] Funding Source: researchfish
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Colorectal cancer (CRC) is a leading cause of cancer death worldwide. Lack of symptoms results in late detection and increased mortality. Inflammation, including complement activation, plays an important role in tumorigenesis. The concentrations of nine proteins of the lectin pathway of the complement system were determined using time-resolved immunofluorometric assays. The first cohort investigated comprised a matched case-control study of 95 patients with CRC, 48 patients with adenomas and 48 individuals without neoplastic findings. Based on the results, Collectin-liver 1 (CL-L1), M-ficolin and MAp44 were determined as the most promising biomarkers and were subsequently evaluated in a case-control study of 99 CRC patients, 196 patients with adenomas and 696 individuals without neoplastic bowel lesions. Using logistic regression, we found that CL-L1, M-ficolin and MAp44 levels could significantly distinguish between patients with CRC, patients with adenomas and individuals without neoplastic bowel lesions. Higher levels of CL-L1 or MAp44 were associated with lower odds of CRC (OR 0.42 (0.25-0.70) p = 0.0003 and OR 0.39 (0.23-0.65) p = 0.0003, respectively), whereas higher levels of M-ficolin were associated with higher odds of CRC compared to individuals without CRC (OR 1.94 (1.46-2.59) p < 0.0001). The combination of CL-L1, M-ficolin and MAp44 in a test of CRC versus individuals without CRC resulted in 36 % sensitivity at 83 % specificity. CL-L1, M-ficolin and MAp44 in combination discriminate between CRC and patients without cancer. The markers did not have sufficient discriminatory value for CRC detection, but may prove useful for screening when combined with other markers.
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