Cell proliferation and apoptosis culminate in early stages of oral oncogenesis

被引:47
作者
Derka, S.
Vairaktaris, E.
Papakosta, V.
Vassiliou, S.
Acil, Y.
Vylliotis, A.
Spyridonidou, S.
Lazaris, A. C.
Mourouzis, C.
Kokkori, A.
Moulavasili, P.
Perrea, D.
Donta, I.
Yapijakis, C.
Patsouris, E.
机构
[1] Univ Athens, Sch Med, Dept Neurol, Eginition Hosp, Athens 11528, Greece
[2] Univ Athens, Sch Med, Dept Expt Surg, Athens 11527, Greece
[3] Univ Athens, Sch Med, Dept Pathol, Athens 11527, Greece
[4] Univ Kiel, Dept Maxillofacial Surg, Klin & Poliklin Mund Kiefer Gesischtschirurg, D-24105 Kiel, Germany
[5] Univ Athens, Sch Med, Dept Oral & Maxillofacial Surg, Athens 11521, Greece
关键词
oral cancer; Bcl-2; Bax; Ki-67; immunohistochemistry; histological grade;
D O I
10.1016/j.oraloncology.2005.10.008
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Markers of cell proliferation (Ki-67 antigen) and apoptosis (Bax, Bcl-2) were studied in an experimental system of induced oral carcinogenesis in Syrian golden hamsters. Thirty-seven animals were divided into one control group and three experimental groups, which were treated with a carcinogen and sacrificed at 10, 14 and 19 weeks after treatment. The histological status of the lesions in the three experimental groups corresponded well with tumour advancement (from oral mucosal dysplasia to moderately differentiated squamous cell carcinoma). Tumour sections were studied using monoclonal antibodies against Bax, Bcl-2 and Ki-67 proteins. Pro-apoptotic Bax expression maintained high levels during all stages of oral carcinogenesis. Anti-apoptotic Bcl-2 expression decreased significantly in dysptastic and early invasion lesions and consequently increased almost to normal tissue level in consequent stages. Finally, Ki-67 expression increased sharply in initial stages of oral carcinogenesis, but significantly decreased in later stages. (c) 2005 Elsevier Ltd. All rights reserved.
引用
收藏
页码:540 / 550
页数:11
相关论文
共 31 条
[1]   Bax and other pro-apoptotic Bcl-2 family "killer-proteins" and their victim, the mitochondrion [J].
Antonsson, B .
CELL AND TISSUE RESEARCH, 2001, 306 (03) :347-361
[2]   APOPTOSIS AND DISEASE [J].
CARSON, DA ;
RIBEIRO, JM .
LANCET, 1993, 341 (8855) :1251-1254
[3]   Dysregulated expression of bcl-2 and bax in oral carcinomas:: evidence of posttranscriptional control [J].
Chen, Y ;
Kayano, T ;
Takagi, M .
JOURNAL OF ORAL PATHOLOGY & MEDICINE, 2000, 29 (02) :63-69
[4]   BCL-2 BLOCKS P53-DEPENDENT APOPTOSIS [J].
CHIOU, SK ;
RAO, L ;
WHITE, E .
MOLECULAR AND CELLULAR BIOLOGY, 1994, 14 (04) :2556-2563
[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]  
GERDES J, 1984, J IMMUNOL, V133, P1710
[7]   Cancer statistics, 2000 [J].
Greenlee, RT ;
Murray, T ;
Bolden, S ;
Wingo, PA .
CA-A CANCER JOURNAL FOR CLINICIANS, 2000, 50 (01) :7-33
[8]   BCL-2 family members and the mitochondria in apoptosis [J].
Gross, A ;
McDonnell, JM ;
Korsmeyer, SJ .
GENES & DEVELOPMENT, 1999, 13 (15) :1899-1911
[9]   Co-expression of p53 and Ki67 and lack of EBV expression in oral squamous cell carcinoma [J].
Iamaroon, A ;
Khemaleelakul, U ;
Pongsiriwet, S ;
Pintong, J .
JOURNAL OF ORAL PATHOLOGY & MEDICINE, 2004, 33 (01) :30-36
[10]   Differential expression of bcl-2 and bax in squamous cell carcinomas of the oral cavity [J].
Jordan, RCK ;
Catzavelos, GC ;
Barrett, AW ;
Speight, PM .
ORAL ONCOLOGY, 1996, 32B (06) :394-400