Abstract
BACKGROUND
The regulation of programmed cell death, or apoptosis, is crucial for normal development and for the maintenance of homeostasis. It has been shown that the novel antiapoptotic protein Bax inhibitorโ1 (BIโ1) represents a new type of regulator of cell death pathways controlled by Bclโ2 and Bax.
METHODS
Surgically resected lung specimens were obtained from 32 patients with peripheral adenocarcinomas, and BIโ1 gene expression was examined and compared with expression of the p53, bclโ2 and Bax genes.
RESULTS
Fourteen of 32 tumors (43.8%) were positive for BIโ1 gene expression by in situ hybridization. BIโ1 gene expression in tumor specimens was significantly higher in adenocarcinomas with bronchioloalveolar carcinoma (BAC) and in adenocarcinomas of mixed subtypes with bronchioloalveolar spreading (14 of 17 tumors; 82.4%) than in carcinomas without it spreading. Patients who had BIโ1โpositive adenocarcinoma showed a relatively favorable prognosis compared with patients who had BIโ1โnegative adenocarcinoma. Eleven of 32 tumors (34.4%) were positive for the p53 protein, only 1 of 32 tumors (3.1%) was positive for the Bclโ2 protein, and 26 of 32 tumors (81.3%) were positive for the Bax protein. Protein expressions of p53, Bclโ2, and Bax, as detected by immunohistochemistry, were not associated with BIโ1 gene expression.
CONCLUSIONS
BIโ1 gene expression was restricted to tumor cells with lepidic growth and was a prognostic factor for peripheralโtype adenocarcinoma. It is believed that BIโ1 gene expression is conserved evolutionarily and may act as a key regulator of the apoptotic pathway in BAC. Cancer 2006. ยฉ 2005 American Cancer Society.