Detection and typing of human papillomavirus DNA in uterine cervices with coexistent grade I and grade III intraepithelial neoplasia: biologic progression or independent lesions?

被引:33
作者
Agorastos, T
Miliaras, D [1 ]
Lambropoulos, AF
Chrisafi, S
Kotsis, A
Manthos, A
Bontis, J
机构
[1] Aristotle Univ Thessaloniki, Lab Histol Embryol & Anthropol, Sch Med, GR-54006 Thessaloniki, Greece
[2] Aristotle Univ Thessaloniki, Fac Med, Univ Clin Obstet & Gynecol 1, Papageorgiou Hosp, GR-54006 Thessaloniki, Greece
[3] Dept Pathol, Gen Clin, Thessaloniki, Greece
[4] Aristotle Univ Thessaloniki, Fac Med, Dept Mol Biol, Lab Gen Biol, GR-54006 Thessaloniki, Greece
关键词
cervical intraepithelial neoplasia; human papillomavirus; clonality;
D O I
10.1016/j.ejogrb.2004.11.024
中图分类号
R71 [妇产科学];
学科分类号
100211 ;
摘要
Objective: To examine the HPV type infection of cervical cone specimens with coexistent CIN1 and CIN3 lesions, in order to define if coexistence of low- and high-grade lesions in the same cervix represent different stages of evolution in a continuing process that is caused by a single viral type or independent lesions induced by different HPV types. Study design: The examined material included 43 cases with coexistent CIN1 and CIN3 in the cone biopsy specimen. Detection and typing of HPV was made by RFLP-PCR. Results: All CIN1 lesions were HPV positive, while three CIN3 lesions were HPV-negative. The proportion of agreement of the HPV type in the two lesions, excluding negative cases (n = 40), was 60% (95% confidence interval: 43.3-75. 1). HPV 16 was the most common type in both CIN3 (56.8%) and CIN1 (46.5%). Conclusions: The so-called morphologic progression of CIN is not always synonymous with biologic progression, since many coexistent CIN lesions are caused by different HPV types, and so represent different cell clones. Clonality of coexistent CIN lesions may be implicated in the evolution of CIN as other recent studies have shown. (c) 2004 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:99 / 103
页数:5
相关论文
共 30 条
  • [1] Human papillomavirus infection among women in South and North Vietnam
    Anh, PTH
    Hieu, NT
    Herrero, R
    Vaccarella, S
    Smith, JS
    Thuy, NT
    Nga, NH
    Duc, NB
    Ashley, R
    Snijders, PJF
    Meijer, CJLM
    Muñoz, N
    Parkin, DM
    Franceschi, S
    [J]. INTERNATIONAL JOURNAL OF CANCER, 2003, 104 (02) : 213 - 220
  • [2] The causal relation between human papillomavirus and cervical cancer
    Bosch, FX
    Lorincz, A
    Muñoz, N
    Meijer, CJLM
    Shah, KV
    [J]. JOURNAL OF CLINICAL PATHOLOGY, 2002, 55 (04) : 244 - 265
  • [3] CRUM CP, 1983, GYNECOL ONCOL, P88
  • [4] Duggan MA, 1998, EUR J GYNAECOL ONCOL, V19, P338
  • [5] Guo ZM, 2000, INT J CANCER, V86, P518, DOI 10.1002/(SICI)1097-0215(20000515)86:4<518::AID-IJC12>3.3.CO
  • [6] 2-P
  • [7] TUMOR SUPPRESSOR GENES - NEW PROSPECTS FOR CANCER-RESEARCH
    HOLLINGSWORTH, RE
    LEE, WH
    [J]. JOURNAL OF THE NATIONAL CANCER INSTITUTE, 1991, 83 (02) : 91 - 96
  • [8] Clonality analysis of synchronous lesions of cervical carcinoma based on X chromosome inactivation polymorphism, human papillomavirus type 16 genome mutations, and loss of heterozygosity
    Hu, XR
    Pang, TY
    Asplund, A
    Pontén, J
    Nistér, M
    [J]. JOURNAL OF EXPERIMENTAL MEDICINE, 2002, 195 (07) : 845 - 854
  • [9] Natural history of cervical human papillomavirus lesions
    Katase, K
    Teshima, H
    Hirai, Y
    Hasumi, K
    [J]. INTERVIROLOGY, 1995, 38 (3-4) : 192 - 194
  • [10] Detection of human papillomavirus DNA in cytologically normal women and subsequent cervical squamous intraepithelial lesions
    Liaw, KL
    Glass, AG
    Manos, MM
    Greer, CE
    Scott, DR
    Sherman, M
    Burk, RD
    Kurman, RJ
    Wacholder, S
    Rush, BB
    Cadell, DM
    Lawler, P
    Tabor, D
    Schiffman, M
    [J]. JOURNAL OF THE NATIONAL CANCER INSTITUTE, 1999, 91 (11) : 954 - 960