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.