p16 protein expression is associated with a poor prognosis in squamous cell carcinoma of the lung

被引:32
作者
Huang, CI
Taki, T
Higashiyama, M
Kohno, N
Miyake, M
机构
[1] Kitano Hosp, Tazuke Kofukai Med Res Inst, Dept Thorac Surg, Osaka 5308480, Japan
[2] Kitano Hosp, Tazuke Kofukai Med Res Inst, Dept Oncol 5, Osaka 5308480, Japan
[3] Osaka Med Ctr Canc & Cardiovasc Dis, Dept Surg, Osaka, Japan
[4] Ehime Univ, Sch Med, Dept Internal Med 2, Matsuyama, Ehime 790, Japan
关键词
p16; lung cancer; prognosis; immunohistochemistry;
D O I
10.1054/bjoc.1999.0929
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
An immunohistochemical analysis for p16 protein was performed in 171 patients with non-small-cell lung cancer (NSCLC). Sixty-two carcinomas (36.3%) were classified as p16-negative. p16-negative tumours in squamous cell carcinomas (SCCs) were significantly more than those in adenocarcinomas (P = 0.039). There was no significant difference in survival according to tumour p16 status in patients with NSCLCs or in patients with adenocarcinomas. In contrast,of patients with SCCs, the 5-year survival rate of patients with p16-negative tumours was significantly lower than those with p16-positive tumours (P = 0.001). Especially, the survival of patients with p16-negative tumours was significantly worse than that of patients with p16-positive tumours in the early stage of the SCC, e.g. stage I (P = 0.005). Multivariate analysis showed that p16 status and nodal status were significant prognostic factors for the survival of patients with SCCs of the lung (P = 0.024 and P = 0.008 respectively). In conclusion, our study showed that alteration of p16 was one of the significant factors of a poor prognosis in SCCs of the lung, and that p16 might play an important role in some SCCs of the lung due to its high prevalence and prognostic value. (C) 2000 Cancer Research Campaign.
引用
收藏
页码:374 / 380
页数:7
相关论文
共 49 条
[1]  
Betticher DC, 1997, INT J CANCER, V74, P556, DOI 10.1002/(SICI)1097-0215(19971021)74:5<556::AID-IJC14>3.0.CO
[2]  
2-4
[3]  
Chung GTY, 1995, ONCOGENE, V11, P2591
[4]  
CORDONCARDO C, 1995, AM J PATHOL, V147, P545
[5]  
COX DR, 1972, J R STAT SOC B, V34, P187
[6]   KAI1, A METASTASIS SUPPRESSOR GENE FOR PROSTATE-CANCER ON HUMAN-CHROMOSOME 11P11.2 [J].
DONG, JT ;
LAMB, PW ;
RINKERSCHAEFFER, CW ;
VUKANOVIC, J ;
ICHIKAWA, T ;
ISAACS, JT ;
BARRETT, JC .
SCIENCE, 1995, 268 (5212) :884-886
[7]   WHAT IS THE EVIDENCE THAT TUMORS ARE ANGIOGENESIS DEPENDENT [J].
FOLKMAN, J .
JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE, 1990, 82 (01) :4-6
[8]   K-ras and p53 mutations are an independent unfavourable prognostic indicator in patients with non-small-cell lung cancer [J].
Fukuyama, Y ;
Mitsudomi, T ;
Sugio, K ;
Ishida, T ;
Akazawa, K ;
Sugimachi, K .
BRITISH JOURNAL OF CANCER, 1997, 75 (08) :1125-1130
[9]   Mechanisms of p16INK4A inactivation in non small-cell lung cancers [J].
Gazzeri, S ;
Gouyer, V ;
Vourc'h, C ;
Brambilla, C ;
Brambilla, E .
ONCOGENE, 1998, 16 (04) :497-504
[10]  
Geradts J, 1999, CLIN CANCER RES, V5, P791