Phenotypic characterization of chronic inflammation in a rare case of endobronchial carcinoma |
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Authors: | Philippe O Gannon Simon Turcotte Jean-Luc Laporte Fred Saad Réjean Lapointe André Duranceau |
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Institution: | 1. Centre de recherche du CHUM (CRCHUM) and Institut du cancer de Montréal, Montreal, QC, Canada 6. Department of Surgery, Centre hospitalier de l’Université de Montréal (CHUM), Université de Montréal, 1560 Sherbrooke East, Montreal, QC, H2L 4M1, Canada 3. Department of Pathology, CHUM, H?pital Notre-Dame, Montreal, QC, Canada 4. Division of Urology, CHUM, Montreal, Canada 5. Faculty of Medicine, Université de Montréal, Montreal, Canada 2. Division of Thoracic Surgery, Department of Surgery, Centre hospitalier de l’Université de Montréal (CHUM), Université de Montréal, 1560 Sherbrooke East, Montreal, QC, H2L 4M1, Canada
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Abstract: | This report presents a phenotypical characterization of the immune cell infiltrate in a rare case of endobronchial carcinoma.
A patient initially treated for an adenocarcinoma of the esophagus developed an endobronchial carcinoma surrounded by gastric
metaplasia distal to a suspected gastrobronchial fistula, 11 years after esophagectomy. Our hypothesis is that the sustained
exposure of the bronchial mucosa to a mixed acid and pancreatobiliary refluxate led to chronic inflammation and promoted malignant
transformation. We performed an immunohistochemical study of the tumor microenvironment evaluating the density of CD3+, CD8+ T lymphocytes, CD20+ B lymphocytes, CD68+ macrophages and FoxP3+ regulatory T cells. Quantification of immune cell density was completed using a novel software-based analysis method. Our
results suggest that, within all the tissues analyzed, FoxP3+ regulatory T cells were present at their highest density in the malignant and metaplastic tissues. The endobronchial metaplasia
biopsied several years prior to the detection of the endobronchial adenocarcinoma was already densely infiltrated by B cells
and macrophages, when compared to the immune cell infiltrate of the endobronchial carcinoma. Altogether, these observations
support the current understanding of carcinogenesis promoted by chronic inflammation. |
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