This small solitary tumor exhibits pure alveolar distribution (lepidic growth) and lacks any invasion of the surrounding normal lung.

Non-smokers with AIS commonly have mutations in EGFR (a driver) or HER2 (an important oncogene), or a gene fusion with ALK or ROS1 as one of the elements.

[5] 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.

[6] 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.

[10][11] The 2011 IASLC/ATS recommendations, adopted in the 2015 WHO guidelines, use the following criteria for adenocarcinoma in situ: [12] * lepidic = (i.e. scaly covering) growth pattern along pre-existing airway structures By this standard, AIS cannot be diagnosed according to core biopsy or cytology sampling.

[15] AIS may be further subclassified by histopathology, by which there are two major variants: This information is mostly in reference to the now outdated entity of BAC, which included some invasive forms of disease.

The treatment of choice in any patient with BAC is complete surgical resection, typically via lobectomy or pneumonectomy, with concurrent ipsilateral lymphadenectomy.

[16] Non-mucinous BAC are highly associated with classical EGFR mutations, and thus are often responsive to targeted chemotherapy with erlotinib and gefitinib.

[27] In non-mucinous BAC, neither club cell nor type II pneumocyte differentiation appears to affect survival or prognosis.

[23] An analysis of Surveillance epidemiology and End results registry ( SEER) by Read et al. revealed that although the incidence of BAC has increased over the past two decade it still constitutes less than 4% of NSCLC in every time interval.