Detection of the human papillomavirus and analysis of the TP53 polymorphism of exon 4 at codon 72 in penile squamous cell carcinomas

被引:31
作者
Humbey, O
Cairey-Remonnay, S
Guérrini, JS
Algros, MP
Mougin, C
Bittard, H
Aubin, F [1 ]
机构
[1] Univ Hosp Besancon, Dept Cell Biol, EA 3181, Inst Etude & Transfert Genes, F-25030 Besancon, France
[2] Univ Hosp Besancon, Dept Dermatol, F-25030 Besancon, France
[3] Univ Hosp Besancon, Dept Pathol, F-25030 Besancon, France
[4] Univ Hosp Besancon, Dept Urol, F-25030 Besancon, France
关键词
penile squamous cell carcinoma; human papillomavirus; TP53; polymorphism;
D O I
10.1016/S0959-8049(02)00835-3
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Human papillomaviruses (HPV) are thought to be involved in penile squamous cell carcinomas (SCC). A common polymorphism at codon 72 of exon 4 encoding either arginine (Arg) or proline (Pro) has been shown to affect HPV-mediated degradation of p53 in vitro, and may represent a risk factor for HPV-induced carcinogenesis. The presence of HPV DNA as well as the TP53 polymorphism at codon 72 of exon 4 were investigated in a series of 45 penile SCC. HPV detection and typing were carried out by polymerase chain reaction (PCR) with generic primers (MY09-MY11 and FAP59-FAP64), and type-specific DNA probes. TP53 polymorphism was further investigated using Denaturing Gradient Gel Electrophoresis (DGGE). HPV DNA was detected in 67% of penile SCC and 32% of benign lesions (BL) (P<0.05). Among the TP53 amplified samples, the rate of Arg homozygosity in penile SCC was 61% compared with 68% in BL (non-significant (NS)). Our results demonstrate a strong association between penile SCC and the presence of HPV DNA. The TP53 Arg/Arg genotype does not appear to represent a risk factor for the development of genital SCC in men, and no correlation was found between the TP53 polymorphism at codon 72 and the presence of HPV DNA. (C) 2003 Elsevier Science Ltd. All rights reserved.
引用
收藏
页码:684 / 690
页数:7
相关论文
共 43 条
[1]   Genital squamous cell carcinoma in men treated by photochemotherapy. A cancer registry-based study from 1978 to 1998 [J].
Aubin, F ;
Puzenat, E ;
Arveux, P ;
Louvat, P ;
Quencez, E ;
Humbert, P .
BRITISH JOURNAL OF DERMATOLOGY, 2001, 144 (06) :1204-1206
[2]  
BARRASSO R, 1989, CLIN PRACT GYNECOL, V2, P73
[3]  
Bastiaens MT, 2001, MOL CARCINOGEN, V30, P56, DOI 10.1002/1098-2744(200101)30:1<56::AID-MC1013>3.0.CO
[4]  
2-2
[5]   IS P53 POLYMORPHISM MAINTAINED BY NATURAL-SELECTION [J].
BECKMAN, G ;
BIRGANDER, R ;
SJALANDER, A ;
SAHA, N ;
HOLMBERG, PA ;
KIVELA, A ;
BECKMAN, L .
HUMAN HEREDITY, 1994, 44 (05) :266-270
[6]  
Bezerra ALR, 2001, CANCER, V91, P2315, DOI 10.1002/1097-0142(20010615)91:12<2315::AID-CNCR1263>3.0.CO
[7]  
2-C
[8]  
CAIREYREMONNAY S, IN PRESS J INVEST DE
[9]   PREVALENCE OF HUMAN PAPILLOMAVIRUS TYPE-16 AND TYPE-18 IN PENILE CARCINOMA - A STUDY OF 41 CASES USING PCR [J].
CHAN, KW ;
LAM, KY ;
CHAN, ACL ;
LAU, P ;
SRIVASTAVA, G .
JOURNAL OF CLINICAL PATHOLOGY, 1994, 47 (09) :823-826
[10]   Human papillomavirus infections in skin cancers [J].
de Villiers, EM .
BIOMEDICINE & PHARMACOTHERAPY, 1998, 52 (01) :26-33