Nonmucinous AIS is thought to derive from a transformed cell in the distal airways and terminal respiratory units, and often shows features of club cell or Type II pneumocyte differentiation. Mucinous AIS, in contrast, probably derives from a transformed glandular cell in distal bronchioles. A multi-step carcinogenesis hypothesis suggests a progression from pulmonary atypical adenomatous hyperplasia (AAH) through AIS to invasive adenocarcinoma (AC), but to date this has not been formally demonstrated. Type-I cystic adenomatoid malformation (CAM) has recently been identified as a precursor lesion for the development of mucinous AIS, but these cases are rare. Rarely, AIS may develop a rhabdoid morphology due to the development of dense perinuclear inclusions.
Adenocarcinoma in situ of the lung
Epithelial-myoepithelial carcinoma of the lung
Salivary gland–like carcinoma of the lung
Minimally invasive adenocarcinoma of the lung
Sarcomatoid carcinoma of the lung
Mucinous cystadenocarcinoma of the lung
Adenocarcinoma of the lung
Pulmonary sclerosing pneumocytoma