p53 polymorphism, human papillomavirus infection in the oral cavity, and oral cancer

被引:57
作者
Summersgill, KF
Smith, EM
Kirchner, HL
Haugen, TH
Turek, LP
机构
[1] Univ Iowa, Dept Oral Pathol Radiol & Med, Coll Dent, Iowa City, IA 52242 USA
[2] Univ Iowa, Coll Publ Hlth, Dept Epidemiol, Iowa City, IA 52242 USA
[3] Univ Iowa, Coll Publ Hlth, Dept Biostat, Iowa City, IA 52242 USA
[4] Univ Iowa, Coll Med, Iowa City, IA 52242 USA
[5] Vet Affairs Med Ctr, Dept Pathol, Iowa City, IA 52242 USA
来源
ORAL SURGERY ORAL MEDICINE ORAL PATHOLOGY ORAL RADIOLOGY AND ENDODONTOLOGY | 2000年 / 90卷 / 03期
关键词
D O I
10.1067/moe.2000.107359
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
Objectives. Human papillomavirus (HPV) infection has emerged as a risk factor in oral carcinogenesis. An arginine-coding polymorphism of the tumor suppressor protein p53 at codon 72 is more readily degraded by the HPV oncoprotein EG. Our objective was to evaluate the association between p53 polymorphism at codon 72 and HPV infection In the oral cavity, as well as its association with oral cancer. Study design. Oral squamous cells from 202 patients with oral cancer and 333 age-sex frequency matched controls were evaluated by polymerase chain reaction for the presence and type of HPV and for alleles of codon 72 in p53. Fisher exact test and chi(2) tests were used to evaluate the data, Results, The p53 codon 72 polymorphism is not associated with HPV infection, whether comparing HPV-negative controls with HPV-positive controls or comparing HPV-negative cases with HPV-positive cases. Additionally, we round no association with the codon 72 polymorphism and oral cancer, whether comparing HPV-negative controls with HPV-negative cases or comparing HPV-positive controls with HPV-positive cases. Conclusions. There is no association between p53 codon 72 polymorphism and HPV infection or between the p53 polymorphism and the risk of oral cancer.
引用
收藏
页码:334 / 339
页数:6
相关论文
共 62 条
  • [41] THE E6 ONCOPROTEIN ENCODED BY HUMAN PAPILLOMAVIRUS TYPE-16 AND TYPE-18 PROMOTES THE DEGRADATION OF P53
    SCHEFFNER, M
    WERNESS, BA
    HUIBREGTSE, JM
    LEVINE, AJ
    HOWLEY, PM
    [J]. CELL, 1990, 63 (06) : 1129 - 1136
  • [42] Oral cancer risk in relation to sexual history and evidence of human papillomavirus infection
    Schwartz, SM
    Daling, JR
    Doody, DR
    Wipf, GC
    Carter, JJ
    Madeleine, MM
    Mao, EJ
    Fitzgibbons, ED
    Huang, SX
    Beckmann, AM
    McDougall, JK
    Galloway, DA
    [J]. JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE, 1998, 90 (21): : 1626 - 1636
  • [43] Do human papillomavirus infections cause oral cancer?
    Shah, KV
    [J]. JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE, 1998, 90 (21): : 1585 - 1586
  • [44] Tumor surveillance via the ARF-p53 pathway
    Sherr, CJ
    [J]. GENES & DEVELOPMENT, 1998, 12 (19) : 2984 - 2991
  • [45] Human papillomavirus and risk of oral cancer
    Smith, EM
    Hoffman, HT
    Summersgill, KS
    Kirchner, HL
    Turek, LP
    Haugen, TH
    [J]. LARYNGOSCOPE, 1998, 108 (07) : 1098 - 1103
  • [46] p53 and genetic susceptibility to cervical cancer
    Sonoda, Y
    Saigo, PE
    Boyd, J
    [J]. JOURNAL OF THE NATIONAL CANCER INSTITUTE, 1999, 91 (06) : 557 - 557
  • [47] Role of a p53 polymorphism in the development of human papillomavirus-associated cancer
    Storey, A
    Thomas, M
    Kalita, A
    Harwood, C
    Gardiol, D
    Mantovani, F
    Breuer, J
    Leigh, IM
    Matlashewski, G
    Banks, L
    [J]. NATURE, 1998, 393 (6682) : 229 - 234
  • [48] Szarka K, 1999, ANTICANCER RES, V19, P2377
  • [49] Prognostic value of mutations and a germ line polymorphism of the p53 gene in non-small cell lung carcinoma:: association with clinicopathological features
    Tagawa, M
    Murata, M
    Kimura, H
    [J]. CANCER LETTERS, 1998, 128 (01) : 93 - 99
  • [50] Thomas M, 1999, MOL CELL BIOL, V19, P1092