Stromal cells and extracellular matrix components in spontaneous canine transmissible venereal tumour at different stages of growth.
Stromal cells and extracellular matrix (ECM) components are important for tumour cell behaviour. Little is known about the role of stromal cells and ECM components in the progression and regression of spontaneous canine transmissible venereal tumour (CTVT). In this study, the stromal cell type was determined by immunohistochemical labelling with antibodies to desmin, vimentin and alpha-smooth muscle actin (alpha-SMA) during the progressive and regressive stages of spontaneous CTVT. The distribution of ECM components tenascin-C, chondroitin sulphate and versican were determined immunohistochemically, and hyaluronan distribution was determined using a biotinylated protein complex with specific affinity for hyaluronan. Stromal cells of tumours in both the progressive and regressive stage were positive for vimentin and negative for desmin. The number of stromal cells expressing alpha-SMA was significantly higher (P=0.001) in regressing tumours, than progressing tumours. These results suggest that the modulation of stromal cells that occurs during the regression of CTVT is similar to that occurring during wound healing. Tenascin-C was weakly expressed in the stroma of tumours in the progressive stage and in regions of the regressing tumours with tumour infiltrating lymphocytes (TILs), but intensely expressed in the stroma of tumours in late regressive stage. In addition, tenascin-C was also expressed in the cytoplasm of some tumour cells in the late regressive stage. A strong stromal tenascin-C intensity was significantly associated with regressing tumours (P=0.001). Strong stromal hyaluronan intensity and a high proportion of hyaluronan-positive tumour cells were significantly associated with progressing tumours (P=0.001). This suggests that hyaluronan is involved in the growth of the tumour. There was no significant difference in the expression of chondroitin sulphate and versican in progressing and regressing tumours.
Mukaratirwa
S
S
Department of Pathobiology, Utrecht University. tmukaratirwa@vet.uz.ac.zw
Chimonyo
M
M
Obwolo
M
M
Gruys
E
E
Nederbragt
H
H
D000199:Actins / Q000378:metabolism; D000818:Animals; D011508:Chondroitin Sulfate Proteoglycans / Q000378:metabolism; D002809:Chondroitin Sulfates / Q000378:metabolism; D003893:Desmin / Q000378:metabolism; D004283:Dog Diseases / Q000378:metabolism* / Q000473:pathology*; D004285:Dogs; D005109:Extracellular Matrix / Q000378:metabolism / Q000473:pathology; D005260:Female; D006820:Hyaluronic Acid / Q000378:metabolism; D007150:Immunohistochemistry; D037181:Lectins, C-Type; D016246:Lymphocytes, Tumor-Infiltrating / Q000473:pathology; D008297:Male; D009365:Neoplasm Regression, Spontaneous / Q000473:pathology / Q000503:physiopathology; D017154:Stromal Cells / Q000378:metabolism / Q000473:pathology; D019063:Tenascin / Q000378:metabolism; D014685:Venereal Tumors, Veterinary / Q000378:metabolism* / Q000473:pathology*; D053675:Versicans; D014746:Vimentin / Q000378:metabolism
D000199:Actins; D011508:Chondroitin Sulfate Proteoglycans; D003893:Desmin; D037181:Lectins, C-Type; D019063:Tenascin; D014746:Vimentin; D053675:Versicans; D006820:Hyaluronic Acid; D002809:Chondroitin Sulfates