Madri J A, Carter D
Hum Pathol. 1984 Jul;15(7):625-31. doi: 10.1016/s0046-8177(84)80286-5.
The relation between scarring and the development of pulmonary neoplasia has been a topic of interest for some time. One current concept suggests that the scar is a predisposing factor in the development of a cancer. In contrast, the scar or desmoplasia observed in breast, stomach, pancreatic, and colonic neoplasms is presumed to be a host response to the neoplasm. In the present study type-specific collagen antibodies were used in an immunofluorescence assay. By taking advantage of the collagen heterogeneity present in the lung and the changes in relative amounts of different collagen types during the fibrotic response, the fibrotic processes in tumorous and nontumorous areas of individual specimens were assessed qualitatively. The findings are consistent with the notion that the scar or desmoplasia in and around pulmonary tumors is not "mature" and inactive but rather represents an active, ongoing process, as evidenced by the continued presence of type III collagen. In contrast, areas of fibrosed lung parenchyma at some distance from the neoplasm revealed a mature, late stage of the fibrotic process, as evidenced by a decrease in type III and increases in types I and V collagen. Thus, the findings support the notion that the scarring associated with pulmonary neoplasia appears to be a host response to the tumor.
瘢痕形成与肺部肿瘤发生之间的关系一直是人们关注的话题。当前一种观点认为，瘢痕是癌症发生的一个易感因素。相反，在乳腺、胃、胰腺和结肠肿瘤中观察到的瘢痕或促纤维增生反应被认为是机体对肿瘤的一种反应。在本研究中，使用了类型特异性胶原抗体进行免疫荧光测定。利用肺中存在的胶原异质性以及纤维化反应过程中不同胶原类型相对含量的变化，对单个标本的肿瘤和非肿瘤区域的纤维化过程进行了定性评估。研究结果与以下观点一致：肺部肿瘤内部及周围的瘢痕或促纤维增生反应并非“成熟”且无活性，而是一个活跃的、持续进行的过程，Ⅲ型胶原的持续存在证明了这一点。相比之下，距肿瘤一定距离的肺实质纤维化区域显示出纤维化过程的成熟晚期阶段，这表现为Ⅲ型胶原减少，Ⅰ型和Ⅴ型胶原增加。因此，研究结果支持这样一种观点，即与肺部肿瘤相关的瘢痕形成似乎是机体对肿瘤的一种反应。
