Figure 1.

Pulmonary fibrosis as field cancerization. Alveolar epithelial cell injury and regeneration failure associated with telomere dysfunction represent a hallmark of pulmonary fibrosis. Pathologically activated TGF-β signaling is involved in altered alveolar epithelial cell features and dysregulated epithelial–mesenchymal interactions. It is postulated that somatic mutations and DNA methylation changes accumulating in pulmonary fibrosis multifocally predispose to lung cancer. TGF-β-mediated fibrotic and immune-suppressive microenvironment in the lung tissue of pulmonary fibrosis may have tumor-promoting features similar to lung cancer stroma.