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Published on: July 21, 2018
LKB1 protein expression in the evolution of glandular neoplasia of the lung
Hassan Ghaffar1, Fikret Sahin, Montserrat Sanchez-Cepedes
1Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21231, USA.
Purpose:
About one-third of sporadic lung adenocarcinomas demonstrates biallelic inactivation of the LKB1 gene, but the timing of this event is not known.
Design:
We performed LKB1 immunohistochemistry on 35 primary lung adenocarcinomas and 96 atypical adenomatous hyperplasias (AAH), a form of early glandular neoplasia from which some lung adenocarcinomas arise.
Results:
In all cases, strong cytoplasmic staining was noted in the non-neoplastic epithelium lining the airways from the bronchi to the terminal bronchioles. There was a marked reduction in LKB1 staining in 9 of 35 (26%) adenocarcinomas and in 10 of 96 (10%) AAHs. When the AAHs were subclassified on the basis of cytoarchitectural atypia, loss of LKB1 expression was more frequent in the high-grade lesions (7 of 33, 21%) than low-grade lesions (3 of 63, 5%; P = 0.021). For the 21 adenocarcinomas where the genetic status was known, immunohistochemistry staining reliably reflected the activational state of the LKB1 gene (95% concordancy).
Conclusions:
In AAH, loss of LKB1 expression is strongly associated with severe dysplasia, suggesting that LKB1 inactivation may play a role in the critical transition from premalignant to malignant tumor growth.