Increased phospho-AKT (Ser(473)) expression in bronchial dysplasia: implications for lung cancer prevention studies.

Tsao AS, McDonnell T, Lam S, Putnam JB, Bekele N, Hong WK, Kurie JM
Cancer Epidemiol Biomarkers Prev. 2003 12 (7): 660-4

PMID: 12869408

AKT, a downstream mediator of phosphatidylinositol 3'-kinase, is activated in non-small cell lung cancer (NSCLC), but we have not yet defined the stage of malignant transformation at which AKT is activated in the bronchial epithelium. We performed immunohistochemical analysis of activated AKT [phosphorylated (p)-AKT Ser(473)] in tissue specimens of normal bronchial epithelium, bronchial hyperplasia and squamous metaplasia ("reactive" epithelium), bronchial dysplasia, and NSCLC. Among NSCLC specimens, immunohistochemical findings were correlated with patient demographics, tumor stage, histology, and survival. We observed p-AKT expression in 12 of 44 (27.3%) normal bronchial biopsy specimens, 4 of 9 (44.4%) reactive epithelium specimens, 22 of 25 (88%) dysplastic specimens, and 25 of 76 (33%) NSCLC specimens. Among patients with resected early-stage or locally advanced NSCLC, p-AKT expression had no effect on tumor stage, histology, or survival. Of the histological groups examined, bronchial dysplasia specimens expressed p-AKT most frequently, supporting AKT activation as an early event in lung cancer progression. Given its role as a mediator of malignant transformation, p-AKT should be investigated as a potential target in future lung cancer prevention studies.

MeSH Terms (16)

Biomarkers Bronchi Bronchial Neoplasms Bronchoscopy Carcinoma, Non-Small-Cell Lung Epithelium Female Humans Lung Neoplasms Male Middle Aged Phosphatidylinositol 3-Kinases Protein-Serine-Threonine Kinases Proto-Oncogene Proteins Proto-Oncogene Proteins c-akt Respiratory Mucosa

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