Expression of the Bax inhibitor-1 gene in pulmonary adenocarcinoma

Authors

  • Ryota Tanaka M.D.,

    1. Department of Thoracic Surgery, Gunma Prefectural Cancer Center, Gunma, Japan
    2. Department of Pathology, Institute of Basic Medical Sciences, University of Tsukuba, Ibaraki, Japan
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  • Tadashi Ishiyama M.S.,

    1. Department of Pathology, Institute of Basic Medical Sciences, University of Tsukuba, Ibaraki, Japan
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  • Teruhito Uchihara M.D.,

    1. Department of Pathology, Institute of Basic Medical Sciences, University of Tsukuba, Ibaraki, Japan
    2. First Department of Internal Medicine, University of the Ryukyus, Okinawa, Japan
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  • Yukinori Inadome M.D.,

    1. Department of Clinical Pathology, Institute of Clinical Medicine, University of Tsukuba, Ibaraki, Japan
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  • Tatsuo Iijima M.D.,

    1. Department of Pathology, Institute of Basic Medical Sciences, University of Tsukuba, Ibaraki, Japan
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  • Yukio Morishita M.D.,

    1. Department of Clinical Pathology, Institute of Clinical Medicine, University of Tsukuba, Ibaraki, Japan
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  • Junko Kano M.D.,

    1. Department of Pathology, Institute of Basic Medical Sciences, University of Tsukuba, Ibaraki, Japan
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  • Tomoyuki Goya M.D.,

    1. Department of Surgery II, Institute of Medical Sciences, Kyorin University, Tokyo, Japan
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  • Masayuki Noguchi M.D.

    Corresponding author
    1. Department of Pathology, Institute of Basic Medical Sciences, University of Tsukuba, Ibaraki, Japan
    • Department of Pathology, Institute of Basic Medical Sciences, Graduate School of Comprehensive Human Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba-shi, Ibaraki 305-8575, Japan
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    • Fax: (011) 81 298533150


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 inhibitor-1 (BI-1) represents a new type of regulator of cell death pathways controlled by Bcl-2 and Bax.

METHODS

Surgically resected lung specimens were obtained from 32 patients with peripheral adenocarcinomas, and BI-1 gene expression was examined and compared with expression of the p53, bcl-2 and Bax genes.

RESULTS

Fourteen of 32 tumors (43.8%) were positive for BI-1 gene expression by in situ hybridization. BI-1 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 BI-1-positive adenocarcinoma showed a relatively favorable prognosis compared with patients who had BI-1-negative adenocarcinoma. Eleven of 32 tumors (34.4%) were positive for the p53 protein, only 1 of 32 tumors (3.1%) was positive for the Bcl-2 protein, and 26 of 32 tumors (81.3%) were positive for the Bax protein. Protein expressions of p53, Bcl-2, and Bax, as detected by immunohistochemistry, were not associated with BI-1 gene expression.

CONCLUSIONS

BI-1 gene expression was restricted to tumor cells with lepidic growth and was a prognostic factor for peripheral-type adenocarcinoma. It is believed that BI-1 gene expression is conserved evolutionarily and may act as a key regulator of the apoptotic pathway in BAC. Cancer 2006. © 2005 American Cancer Society.

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