Prognostic value of Bak expression in oral tongue squamous cell carcinomas

被引:4
作者
Xie, X [1 ]
Clausen, OPF
Boysen, M
机构
[1] Univ Oslo, Rikshosp, Dept Otolaryngol, N-0027 Oslo, Norway
[2] Univ Oslo, Rikshosp, Inst Pathol, N-0027 Oslo, Norway
关键词
apoptosis; Bak; prognosis; tongue squamous cell carcinoma;
D O I
暂无
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Bak is a pro-apoptotic member of the Bcl-2 family of genes that are involved in regulation of programmed cell death. By means of immunohistochemical methods, Bak expression was evaluated in formalin-fixed, paraffin-embedded diagnostic specimens from 83 patients with T1-T4 oral tongue squamous cell carcinomas (SCC). The fractions of tumor cells expressed Bak and their staining intensities were given an expression score. Bak expression was compared with our previous investigated apoptosis-related parameters such as apoptotic index (AI), Bax and Bcl-2 expression, and p53 accumulation. Bak expression correlated positively with Bcl-2 expression (p=0.0001). No significant correlation was found between Bak expression and Bax expression, AI, or p53 accumulation. Patients with Bak expression exceeding the mean value had poorer disease-specific survival when compared with those with values below the mean Bak expression (p=0.01). Cox proportional hazards regression analysis revealed that Bak expression was a significant, independent prognostic variable (p=0.0325). A two-parameter combination of Bak expression and Bax expression, AI, or p53 accumulation revealed an enhanced prognostic potential (p<0.0001) when compared with single parameters. We conclude that Bak expression, particularly in combination with Bax expression, as well as in combination with AI, or p53 accumulation, has prognostic value in tongue SCC.
引用
收藏
页码:369 / 374
页数:6
相关论文
共 39 条
[1]  
Bairey O, 1999, CLIN CANCER RES, V5, P2860
[2]   Expression of apoptosis regulatory proteins of the Bcl-2 family and p53 in primary resected non-small cell lung cancer [J].
Borner, MM ;
Brousset, P ;
Pfanner-Meyer, B ;
Bacchi, M ;
Vonlanthen, S ;
Hotz, MA ;
Altermatt, HJ ;
Schlaifer, D ;
Reed, JC ;
Betticher, DC .
BRITISH JOURNAL OF CANCER, 1999, 79 (5-6) :952-958
[3]   INDUCTION OF APOPTOSIS BY THE BCL-2 HOMOLOG BAK [J].
CHITTENDEN, T ;
HARRINGTON, EA ;
OCONNOR, R ;
FLEMINGTON, C ;
LUTZ, RJ ;
EVAN, GI ;
GUILD, BC .
NATURE, 1995, 374 (6524) :733-736
[4]   A CONSERVED DOMAIN IN BAK, DISTINCT FROM BH1 AND BH2, MEDIATES CELL-DEATH AND PROTEIN-BINDING FUNCTIONS [J].
CHITTENDEN, T ;
FLEMINGTON, C ;
HOUGHTON, AB ;
EBB, RG ;
GALLO, GJ ;
ELANGOVAN, B ;
CHINNADURAI, G ;
LUTZ, RJ .
EMBO JOURNAL, 1995, 14 (22) :5589-5596
[5]   New members of the Bcl-2 family and their protein partners [J].
Farrow, SN ;
Brown, R .
CURRENT OPINION IN GENETICS & DEVELOPMENT, 1996, 6 (01) :45-49
[6]   CLONING OF A BCL-2 HOMOLOG BY INTERACTION WITH ADENOVIRUS E1B 19K [J].
FARROW, SN ;
WHITE, JHM ;
MARTINOU, I ;
RAVEN, T ;
PUN, KT ;
GRINHAM, CJ ;
MARTINOU, JC ;
BROWN, R .
NATURE, 1995, 374 (6524) :731-733
[7]  
Frederick MJ, 1999, CLIN CANCER RES, V5, P361
[8]  
Friedman M, 1997, ANN OTO RHINOL LARYN, V106, P445
[9]   The central executioners of apoptosis: caspases or mitochondria? [J].
Green, D ;
Kroemer, G .
TRENDS IN CELL BIOLOGY, 1998, 8 (07) :267-271
[10]   Enforced dimerization of BAX results in its translocation, mitochondrial dysfunction and apoptosis [J].
Gross, A ;
Jockel, J ;
Wei, MC ;
Korsmeyer, SJ .
EMBO JOURNAL, 1998, 17 (14) :3878-3885