Adenocarcinoma in situ of the lung

In situ pulmonary adenocarcinoma (AIS)—previously included in the category of 'bronchioloalveolar carcinoma' (BAC)—is a subtype of lung adenocarcinoma. It tends to arise in the distal bronchioles or alveoli and is defined by a non-invasive growth pattern. This small solitary tumor exhibits pure alveolar distribution (lepidic growth) and lacks any invasion of the surrounding normal lung. If completely removed by surgery, the prognosis is excellent with up to 100% 5-year survival. In situ pulmonary adenocarcinoma (AIS)—previously included in the category of 'bronchioloalveolar carcinoma' (BAC)—is a subtype of lung adenocarcinoma. It tends to arise in the distal bronchioles or alveoli and is defined by a non-invasive growth pattern. This small solitary tumor exhibits pure alveolar distribution (lepidic growth) and lacks any invasion of the surrounding normal lung. If completely removed by surgery, the prognosis is excellent with up to 100% 5-year survival. Although the entity of AIS was formally defined in 2011 (see History), it represents a noninvasive form of pulmonary adenocarcinoma which has been recognized for some time. AIS is not considered to be an invasive tumor by pathologists, but as one form of carcinoma in situ (CIS). Like other forms of CIS, AIS may progress and become overtly invasive, exhibiting malignant, often lethal, behavior. Major surgery, either a lobectomy or a pneumonectomy, is usually required for treatment. The genes mutated in AIS differ based on exposure to tobacco smoke. 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. 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. The criteria for diagnosing pulmonary adenocarcinoma have changed considerably over time. The 2011 IASLC/ATS recommendations, adopted in the 2015 WHO guidelines, use the following criteria for adenocarcinoma in situ: * lepidic = (i.e. scaly covering) growth pattern along pre-existing airway structures