Original Paper Fas Expression in Non-small Cell Lung Cancer: its Prognostic EVect in Completely Resected Stage III Patients H. Uramoto, T. Osaki, M. Inoue, S. Taga, M. Takenoyama, T. Hanagiri, I. Yoshino, R. Nakanishi, Y. Ichiyoshi and K. Yasumoto Department of Surgery II, School of Medicine, University of Occupational and Environmental Health, 1-1 Iseigaoka Yahatanishi-ku, Kitakyushu, 807-8555 Japan The aim of this study was to examine Fas expression in non-small cell lung cancer (NSCLC) and examine its correlation with clinicopathological features and prognosis. Fas expression was deter- mined by an immunohistochemical analysis using the labelled streptavidin±biotin method from 220 paraYn specimens of completely resected primary stage I±III NSCLC. 80 (36%) of 220 cases were positive for Fas immunostaining. These 80 cases included 44 adenocarcinomas (33%) and 30 squa- mous cell carcinomas (40%). 33 stage I (33%) 13 (43%) stage II and 34 (37%) stage III tumours were Fas positive. No statistically signi®cant diVerences were observed regarding the Fas status with respect to age, sex, histological type, or stage of disease. There was no signi®cant diVerence in survival between early stage (stages I±II) disease pateints with positive Fas expression and those with a negative expression (P = 0.719). However, for patients with completely resected stage III tumours, the patients with positive Fas staining were found to survive for a longer period than those with negative staining (P = 0.026). # 1999 Elsevier Science Ltd. All rights reserved. Key words: Fas protein, non-small cell lung cancer, immunohistochemical analysis, prognostic factor Eur J Cancer, Vol. 35, No. 10, pp. 1462±1465, 1999 INTRODUCTION Fas (also known as APO-1 and CD95) and FasL play a key role in the regulation of apoptosis within the immune system [1]. Both proteins are highly expressed on activated T cells, with low levels of expression seen in resting T cells [2±5]. A ligation of Fas by either activating antibody or by FasL transmits a `death signal' to the target cell, which potentially triggers apoptosis [6±8]. Several investigators have recently reported that colon carcinoma, melanoma, and hepatocel- lular carcinoma cell lines may express FasL and kill Jurkat cells in a Fas-mediated manner [9±11]. However, to our knowledge few reports have investigated its expression on solid tumours including lung cancer. Moreover, the relation- ship between Fas expression and clinical outcome in patients with malignant tumours is still unknown. In this study, we performed an immunohistochemical analysis of Fas in NSCLC to identify any correlation with the clinico- pathological features and prognosis. In addition, we eval- uated the relationship between Fas expression and bcl-2/p53 expression. PATIENTS AND METHODS Patients 220 consecutive patients with completely resected stage I±III NSCLCs in the Department of Surgery II, University of Occupational and Environmental Health, Kitakyushu, Japan, from July 1991 to September 1996 were studied. The patients ranged in age from 38 to 84 years (mean 66.2  9.1 years); 158 were male and 62 were female. All patients pre- operatively underwent diagnostic procedures, including brain computed tomography (CT), body CT, and a bone scinti- gram without mediastinoscopy. The pathological types included 133 adenocarcinomas, 75 squamous cell carcino- mas, 10 large cell carcinomas, and 2 adenosquamous cell carcinomas. According to the new international staging sys- tem for lung cancer [12], following a complete mediastinal lymph node dissection carried out in all patients, staging was as follows: 49 patients were stage IA, 50 patients were stage IB, 17 patients were stage IIA, 13 patients were stage IIB, 59 patients were stage IIIA, and 32 patients were stage IIIB. Of European Journal of Cancer, Vol. 35, No. 10, pp. 1462±1465, 1999 # 1999 Elsevier Science Ltd. All rights reserved. Pergamon Printed in Great Britain PII: S0959-8049(99)00157-4 0959-8049/99/$ - see front matter 1462 Correspondence to H. Uramoto. Received 1 Feb. 1999; revised 17 May 1999; accepted 15 Jun. 1999.