Barsky S H, Rao C N, Grotendorst G R, Liotta L A
Am J Pathol. 1982 Sep;108(3):276-83.
Type V (AB) collagen is present in increased amounts in desmoplasia of human breast carcinoma. Type V collagen occurs as linear deposits in the interstitium (desmoplastic stroma surrounding the tumor), as demonstrated by immunofluorescence and immunoperoxidase techniques utilizing antibodies to Type V collagen. In contrast, no demonstratable Type V occurs in the interstitium of fibroadenoma, fibrocystic disease, or normal breast tissue. As identified and quantitated by pepsin extraction, salt fractionation, and polyacrylamide gel electrophoresis, Type V constitutes 10% +/- 5% of all interstitial collagens (Types I, III, and V) in desmoplasia, compared with 1.5% +/- 0.5% in fibroadenoma and less than 0.1% in all types of fibrocystic disease, including sclerosing adenosis, and less than 0.1% in normal breast tissue. For infiltrating ductal carcinoma, Type V collagen is not secreted by the invasive carcinoma cells, nor is it present in an extracellular basement membrane location. By immunohistologic methods, Type V collagen can be seen exclusively in the desmoplastic stroma. The authors propose that desmoplasia of human breast carcinoma manifests a characteristic collagen profile and that the increased Type V may be produced by specialized cells such as myofibroblasts in the interstitium, which are recruited in response to invasive carcinoma.
V型(AB型)胶原在人乳腺癌的促纤维增生中含量增加。利用抗V型胶原抗体的免疫荧光和免疫过氧化物酶技术显示,V型胶原以线性沉积物的形式存在于间质(肿瘤周围的促纤维增生性基质)中。相比之下,在纤维腺瘤、纤维囊性疾病或正常乳腺组织的间质中未发现可检测到的V型胶原。通过胃蛋白酶提取、盐分级分离和聚丙烯酰胺凝胶电泳鉴定和定量,在促纤维增生中,V型胶原占所有间质胶原(I型、III型和V型)的10%±5%,而在纤维腺瘤中为1.5%±0.5%,在包括硬化性腺病在内的所有类型的纤维囊性疾病中小于0.1%,在正常乳腺组织中小于0.1%。对于浸润性导管癌,V型胶原不是由浸润性癌细胞分泌的,也不存在于细胞外基底膜位置。通过免疫组织学方法,仅在促纤维增生性基质中可见V型胶原。作者提出,人乳腺癌的促纤维增生表现出特征性的胶原谱,V型胶原增加可能是由间质中的特殊细胞如肌成纤维细胞产生的,这些细胞是因浸润性癌而被募集的。