Early Lung Cancer With Lepidic Pattern

Adenocarcinoma in Situ, Minimally Invasive Adenocarcinoma, and Lepidic Predominant Adenocarcinoma

Wilko Weichert; Arne Warth

Disclosures

Curr Opin Pulm Med. 2014;20(4):309-316. 

In This Article

Atypical Adenomatous Hyperplasia and Adenocarcinoma in Situ

AAH is a localized, small (usually 0.5 cm or less) lepidic proliferation of mildly to moderately atypical type II pneumocytes and/or Clara cells lining alveolar walls, replacing normal bronchioloalveolar epithelium of the terminal respiratory unit and, sometimes, respiratory bronchioles. AAH is an accepted precursor lesion for ADC and frequently observed as a coincident finding in both neoplastic and nonneoplastic resection specimens. There is a continuum of morphologic changes between AAH and AIS, making a clear-cut distinction of both entities challenging. In AIS, cellular atypia might be more pronounced than in AAH. Overall, cell density, pleomorphism, and cell size can aid in the delineation. Furthermore, AAH must be separated from reactive pneumocyte hyperplasia.

AIS is defined as a small to moderately sized (≤3 cm), solitary neoplastic lesion with pure lepidic growth. Typical cytologic features of AIS include bland, small, monomorphous nuclei with fine chromatin and inconspicuous pinpoint nucleoli. Nuclear groves and nuclear pseudo-inclusions can be prominent. A cell arrangement in orderly strips and small flat monolayers is also a characteristic feature of AIS. Cellular atypia is usually slightly more pronounced than in AAH; in addition, these lesions are usually larger than 0.5 cm. AIS is further subdivided into nonmucinous and mucinous variants, but according to literature and in our own experience virtually all cases are nonmucinous. AIS has been demonstrated to be associated with a 100% 5-year disease-free survival in multiple studies.[3,7,11,13,14,22–26] However, one recent study reported a slightly impaired 5-year overall survival of 98%.[27]

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