Tenascin expression in relation to stromal tumour cells in canine gastrointestinal epithelial tumours.
The expression of tenascin, alpha-smooth muscle actin (alpha-SMA), desmin and vimentin was investigated immunohistochemically in the stroma of normal canine stomach, small intestine and colon, and in 30 epithelial tumours of the canine stomach, small intestine or colon. In addition, "co-localization" of tenascin and alpha-SMA was investigated by double immunohistochemistry. Tenascin was absent in the normal gastric mucosa but present in the normal intestine, with a gradual increase in immunolabelling intensity from the cryptal glands to the surface epithelium. Tenascin expression was greater in all adenomas and carcinomas than in normal tissues. Two different patterns of tenascin expression were observed in all carcinomas, irrespective of their site. In well-differentiated tumour regions of both gastric and intestinal tumours, a fibrillary sub-glandular expression was observed; in poorly differentiated tumour regions, however, the expression pattern was diffuse. Incomplete invasion of the muscularis mucosae was accompanied by thickening and increased tenascin expression. In normal stomach and intestines, alpha-SMA and desmin were demonstrated in pericryptal myofibroblasts and smooth muscle cells of the muscle layers. In colonic adenomas and gastric and intestinal carcinomas, alpha-SMA was demonstrated in all stromal cells surrounding tumour cells. In contrast to alpha-SMA labelling, desmin labelling was negative in tumour stromal cells (in both gastric and intestinal tumours), except in tumour regions close to the muscularis mucosae. This suggested that myofibroblasts in gastric and intestinal tumours originated from pre-existing fibroblasts, except in tumour regions close to the muscularis mucosae, where the myofibroblasts seemed to originate from smooth muscle cells of the muscularis mucosae. There was a strong co-localization of tenascin and alpha-SMA-expressing myofibroblasts, suggesting that myofibroblasts are responsible for tenascin secretion.
Mukaratirwa
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Department of Pathology, Faculty of Veterinary Medicine, Utrecht University, PO Box 80158, Yalelan 1, 3508 TD Utrecht, The Netherlands.
de Witte
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van Ederen
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Nederbragt
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H
D000230:Adenocarcinoma / Q000378:metabolism / Q000473:pathology / Q000662:veterinary*; D000236:Adenoma / Q000378:metabolism / Q000473:pathology / Q000662:veterinary*; D000818:Animals; D014408:Biomarkers, Tumor / Q000378:metabolism; D003893:Desmin / Q000378:metabolism; D004283:Dog Diseases / Q000473:pathology*; D004285:Dogs; D005347:Fibroblasts / Q000378:metabolism / Q000473:pathology; D005770:Gastrointestinal Neoplasms / Q000378:metabolism / Q000473:pathology / Q000662:veterinary*; D007124:Immunoenzyme Techniques / Q000662:veterinary; D017154:Stromal Cells / Q000378:metabolism* / Q000473:pathology; D019063:Tenascin / Q000378:metabolism*; D014746:Vimentin / Q000378:metabolism
D014408:Biomarkers, Tumor; D003893:Desmin; D019063:Tenascin; D014746:Vimentin