Published online May 16, 2022. doi: 10.12998/wjcc.v10.i14.4541
Peer-review started: August 30, 2021
First decision: November 17, 2021
Revised: December 3, 2021
Accepted: March 25, 2022
Article in press: March 25, 2022
Published online: May 16, 2022
The clinicopathological features, immunohistochemical characteristics, and genetic mutation profile of two unusual cases of distal bronchiolar adenoma are retrospectively analyzed and the relevant literature is reviewed.
Case 1 was a 63-year-old female patient who had a mixed ground-glass nodule, with mild cells in morphology, visible cilia, and bilayer structures in focal areas. Immunohistochemical staining for P63 and cytokeratin (CK)5/6 revealed the lack of a continuous bilayer structure in most areas, and no mutations were found in epidermal growth factor receptor, anaplastic lymphoma kinase, ROS1, Kirsten rat sarcoma, PIK3CA, BRAF, human epidermal growth factor receptor-2 (HER2), RET, and neuroblastoma RAS genes. Case 2 was a 58-year-old female patient who presented with a solid nodule, in which most cells were observed to be medium sized, the nuclear chromatin was pale and homogeneous, local cells had atypia, and cilia were found locally. Immunohistochemical staining for P63 and CK5/6 showed no expression of these proteins in mild cell morphology whereas the heteromorphic cells showed a bilayer structure. The same nine genes as above were analyzed, and HER2 gene mutation was identified.
Some unresolved questions remain to be answered to determine whether the lesion is a benign adenoma or a part of the process of malignant transformation from benign adenoma of the bronchial epithelium. Furthermore, whether lesions with atypical bilayer structures are similar to atypical hyperplastic lesions of the breast remains to be elucidated. Moreover, clarity on whether these lesions can be called atypical bronchiolar adenoma and whether they are invasive precursor lesions is needed. Future studies should examine the diagnostic significance of HER2 gene mutation as a prognostic indicator.
Core Tip: In terms of morphology, case 1 had no atypical cells, visible cilia, and bilayer structures in focal areas. Immunohistochemical staining for P63 and cytokeratin (CK)5/6 revealed the lack of a continuous bilayer structure in most areas, and no mutations were found in the genes detected. In case 2, most cells were medium-sized. Furthermore, local cells had atypia, and cilia were found locally. Immunohistochemical staining for P63 and CK5/6 revealed that only heteromorphic cell regions showed a bilayer structure. Human epidermal growth factor receptor-2 gene mutation was identified. Further research is needed to investigate whether these lesions can be called atypical bronchiolar adenoma and whether they are invasive precursor lesions.