ArticleInternational journal of colorectal disease2011
Local calprotectin production in colorectal cancer and polyps--active neutrophil recruitment in carcinogenesis.
Article in International journal of colorectal disease, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- Duodenal and colonic mucosal S100A8/A9 (calprotectin) expression is increased and correlates with the severity of select histologic lesions in dogs with chronic inflammatory enteropathy.BMC veterinary research · 2024Article
- Tumor-Associated Neutrophils in Colorectal Cancer Development, Progression and Immunotherapy.Cancers · 2022Review
- Tissue mRNA for S100A4, S100A6, S100A8, S100A9, S100A11 and S100P Proteins in Colorectal Neoplasia: A Pilot Study.Molecules (Basel, Switzerland) · 2021Article
- Neutrophil Extracellular Traps in Digestive Cancers: Warrior or Accomplice.Frontiers in oncology · 2021Review
- Improving the diagnosis of high grade and stage bladder cancer by detecting increased urinary calprotectin expression in tumor tissue and tumor-associated inflammatory response.Investigative and clinical urology · 2019Article
- Faecal Calprotectin.The Clinical biochemist. Reviews · 2018Review
- Response to Infliximab in Crohn's Disease: Genetic Analysis Supporting Expression Profile.Mediators of inflammation · 2015Article
- Clinical and histopathological correlations of fecal calprotectin release in colorectal carcinoma.World journal of gastroenterology · 2014Article
- Expression of neutrophil gelatinase-associated lipocalin in colorectal neoplastic progression: a marker of malignant potential?British journal of cancer · 2013Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimThe aim of this study is to examine the expression level and localization of calprotectin in cancer tissue, tumor-adjacent mucosa, and polyps in colonic biopsies. Calprotection expression was correlated with neutrophil infiltration, markers of bacteremia, and systemic inflammation. MATERIALS AND
methodsPatients with colorectal cancer (n = 28) and adenoma (n = 38) were compared with healthy controls (n = 33). Calprotectin expression levels were measured by ELISA, and its localization was visualized by immunohistochemistry and correlated with the degree of neutrophil infiltration (visualized by Esterase staining). The expression of tumor necrosis factor (TNF)-alpha, procalcitonin, endotoxemia, carcinoembryonic antigen (CEA), and C-reactive protein was also investigated.
resultsMucosal calprotectin was expressed in significantly higher concentrations in carcinoma (94.2 ± 31.2 ng/mg total protein) and adenoma (122.8 ± 60.3 ng/mg total protein) in comparison with mucosal biopsies from healthy controls (20.4 ± 5.4 ng/mg total protein), tumor-adjacent mucosa from patients with colorectal carcinoma (21.6 ± 5.1 ng/mg total protein), and adenoma (45 ± 14.6 ng/mg total protein, all p < 0.05). Immunohistochemistry showed calprotectin reactivity mainly in granulocytes and macrophages with only singular reactive epithelial cells. Positive staining (quantified by the number of positive cells per square millimeter) was markedly increased in carcinoma tissue (85 ± 21.5) and in adenoma (67.5 ± 20) as compared with tumor-adjacent epithelia (18.8 ± 4.3, p = 0.0007, p = 0.003, respectively), and there was a highly significant correlation, r = 0.89, p = 0.001) between calprotectin staining and neutrophil infiltration. No significant differences were found in the systemic levels of TNF-alpha, procalcitonin, and endotoxemia, whereas CEA and C-reactive protein levels were significantly higher in the cancer group (p < 0.05).
conclusionOur results support the evidence that increased calprotectin expression is an early step in the neoplastic transformation during colorectal carcinogenesis. Moreover, its expression is closely related to an inflammatory response and points out a possible biological link between inflammation and neoplastic transformation in colorectal cancer.
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