Recurrent acute thermal lesion induces esophageal hyperproliferative premalignant lesions in mice esophagus
| Autor: | Christina Barja-Fidalgo, Davy C M Rapozo, R.M. Albano, Bruno Souza Bianchi de Reis, Tania Cristina Moita Blanco, Tatiana de Almeida Simão, L.F. Ribeiro Pinto, Cleber Dario Pinto Kruel, P. Valverde, Isabela Martins Gonzaga, C. Canetti |
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| Rok vydání: | 2016 |
| Předmět: |
Pathology
medicine.medical_specialty Hot Temperature Time Factors Necrosis Clinical Biochemistry Inflammation Respiratory Mucosa Biology Pathology and Forensic Medicine 03 medical and health sciences Cytokeratin Esophagus 0302 clinical medicine medicine Animals Diethylnitrosamine Molecular Biology Thermal lesion Cell Proliferation Mice Inbred BALB C Thermal injury Drinking Water Immunohistochemistry Survival Analysis Ki-67 Antigen medicine.anatomical_structure 030220 oncology & carcinogenesis Concomitant Female 030211 gastroenterology & hepatology medicine.symptom Precancerous Conditions Immunostaining |
| Zdroj: | Experimental and Molecular Pathology. 100:325-331 |
| ISSN: | 0014-4800 |
| DOI: | 10.1016/j.yexmp.2016.02.005 |
| Popis: | Hot beverage consumption is a risk factor for esophageal squamous cell carcinoma, but the underlying mechanisms are still unknown. We developed an experimental mouse model to understand the mechanism of thermal lesion to esophageal carcinogenesis. Female BALB/c mice were treated by gavage with water at different temperatures three times a week and nitrosamines in the drinking water. Water at 70 °C, but not at lower temperatures, initially induced an esophageal necrosis that healed and became resistant to necrosis after further administrations. However, when 70 °C water was associated with N-nitrosodiethylamine at doses above 1 ppm, there was interference in epithelial regeneration, allowing recurrent thermal injury and inflammation. Recurrent thermal injury resulted in hyper proliferative premalignant lesions being induced earlier (at 4 weeks) and at a higher frequency (4-fold increase at 16 weeks) when compared to mice treated with NDEA only. Ki-67 immunostaining revealed that recurrent thermal injury induced basal cell proliferation resulting in the expansion of epithelial basal cells, confirmed by the increase in cytokeratin 14 positive cells with concomitant reduction of differentiated cytokeratin 5 positive cells. We conclude that recurrent thermal lesion may act as a tumor promoter though a strong proliferation stimulus of esophageal epithelial basal cells. |
| Databáze: | OpenAIRE |
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