Human papilloma virus type 16 E6 gene expression in oral exophytic epithelial lesions as detected by in situ rtPCR

被引:22
作者
Al-Bakkal, G
Ficarra, G
McNeill, K
Eversole, LR
Sterrantino, G
Birek, C [1 ]
机构
[1] Univ Manitoba, Fac Dent, Dept Oral Biol, Winnipeg, MB, Canada
[2] Univ Florence, Inst Stomatol, Florence, Italy
[3] Univ Pacific, Sch Dent, Los Angeles, CA USA
[4] Univ Manitoba, Fac Dent, Dept Dent Diagnost, Winnipeg, MB, Canada
[5] Univ Manitoba, Fac Dent, Dept Surg Sci, Winnipeg, MB, Canada
来源
ORAL SURGERY ORAL MEDICINE ORAL PATHOLOGY ORAL RADIOLOGY AND ENDODONTOLOGY | 1999年 / 87卷 / 02期
关键词
D O I
10.1016/S1079-2104(99)70273-8
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
Objective. We adopted an in situ reverse transcriptase polymerase chain reaction method of detecting and determining the frequency of early (E6) gene expression of human papilloma virus type 16 at the individual cell level in a sample of oral exophytic lesions with various degrees of epithelial hyperplasia and dysplasia in immunosuppressed and immunocompetent patients. Study design. The significance of differences between the study groups was determined by Mantel-Haenszel chi-square analysis and calculation of odds ratios, accounting for immunosuppression and degree of dysplasia, respectively. Results. Grouped together, the lesions of dysplasia (mild to severe) and squamous cell carcinoma were found to be 16 rimes more likely to express human papilloma virus E6 mRNA than the benign lesions (P =.0013); in the lesions of immunosuppressed patients, human papilloma virus 16 E6 was roughly 10 times more likely to be expressed than in those of the immunocompetent patients (P =.0008, accounting for dysplasia). Conclusions. Our data indicate that human papilloma virus 16 E6 gene expression, and perhaps integration of the virus in the host genome, might play a role in the development of oral neoplasia in association with immunosuppression.
引用
收藏
页码:197 / 208
页数:12
相关论文
共 83 条
[1]   MOLECULAR-BIOLOGY OF HUMAN PAPILLOMAVIRUS INFECTION AND ONCOGENESIS [J].
ANDROPHY, EJ .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1994, 103 (02) :248-256
[2]   PROGRESSIVE SQUAMOUS EPITHELIAL NEOPLASIA IN K14-HUMAN PAPILLOMAVIRUS TYPE-16 TRANSGENIC MICE [J].
ARBEIT, JM ;
MUNGER, K ;
HOWLEY, PM ;
HANAHAN, D .
JOURNAL OF VIROLOGY, 1994, 68 (07) :4358-4368
[3]   PAPILLOMAVIRUSES AND HUMAN CANCER [J].
ARENDS, MJ ;
WYLLIE, AH ;
BIRD, CC .
HUMAN PATHOLOGY, 1990, 21 (07) :686-698
[4]   LOSS OF P53 PROTEIN IN HUMAN PAPILLOMAVIRUS TYPE-16 E6-IMMORTALIZED HUMAN MAMMARY EPITHELIAL-CELLS [J].
BAND, V ;
DECAPRIO, JA ;
DELMOLINO, L ;
KULESA, V ;
SAGER, R .
JOURNAL OF VIROLOGY, 1991, 65 (12) :6671-6676
[5]  
BRESLOW N, 1980, IARC SCI PUBL, V1, P137
[6]   DETECTION OF MULTIPLE HUMAN PAPILLOMAVIRUS TYPES IN CONDYLOMATA ACUMINATA FROM IMMUNOSUPPRESSED PATIENTS [J].
BROWN, DR ;
BRYAN, JT ;
CRAMER, H ;
KATZ, BP ;
HANDY, V ;
FIFE, KH .
JOURNAL OF INFECTIOUS DISEASES, 1994, 170 (04) :759-765
[7]  
BUONAGURO FM, 1994, ANTIBIOT CHEMOTHER, V46, P102
[8]  
Chen Z, 1997, CANCER RES, V57, P1614
[9]  
Choo KB, 1996, J MED VIROL, V49, P15, DOI 10.1002/(SICI)1096-9071(199605)49:1<15::AID-JMV3>3.3.CO
[10]  
2-4