Alveolar type II cells are not present in normal epithelium of canine
segmental bronchi but after carcinogen exposure they do occur in intra
-epithelial lesions with all degrees of atypia and in invasive lesions
with different glandular growth patterns. Immunohistochemistry for pr
oliferation markers (PCNA; Ki-67) strongly suggest that such novel typ
e II cells are pluripotential stem cells in canine bronchial carcinoge
nesis. Very likely, bronchial carcinogenesis is subject to an oncofeta
l mechanism of differentiation: bronchial epithelial retrodifferentiat
ion followed by novel differentiation of alveolar tumor stem cells.