1887

Abstract

This study aimed to assess the role of specific human papillomavirus type 16 (HPV-16) variants, in combination with p53 codon 72 polymorphism genotypes, in cervical carcinogenesis. An initial sequence analysis of HPV-16 long control, E6 and E7 regions of 53 well-defined cervical samples containing HPV-16 revealed that a T to G transition at nucleotide position 350 within the E6 open reading frame was the most common variation, the frequency of which seemed to decrease with increasing severity of the lesion. Therefore, a total of 246 cervical samples of residents of The Netherlands was specifically analysed for HPV-16 350G/T variants and/or p53 codon 72 genotypes. These comprised HPV-negative normal cervical scrapes (=40), normal cervical scrapes containing HPV-16 (=46), scrapes containing HPV-16 from women with abnormal cervical cytology participating in a non-intervention follow-up study without (=38) and with (=51) a histologically proven cervical intraepithelial neoplasia (CIN) III lesion at the end of the study, and cervical squamous cell carcinomas (=71). Neither specific HPV-16 350G/T variants nor specific p53 genotypes were associated with a higher risk of developing CIN III or cervical cancer. However, HPV-16 350T variants were significantly over-represented in p53 Arg homozygous women with cervical cancer. This suggests that, in p53 Arg/Arg women, infection with HPV-16 350T variants confers a higher risk of cervical cancer.

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2000-02-01
2024-04-26
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References

  1. Beckman, G., Birgander, R., Själander, A., Saha, N., Holmberg, P. A., Kivelä, A. & Beckman, L. (1994). Is p53 polymorphism maintained by natural selection? Human Heredity 44, 266-270.[CrossRef] [Google Scholar]
  2. Bontkes, H. J., Van Duin, M., DeGruijl, T. D., Duggan-Keen, M. F., Walboomers, J. M. M., Stukart, M. J., Verheijen, R. H. M., Helmerhorst, T. J. M., Meijer, C. J. L. M., Scheper, R. J., Stevens, F. R. A., Dyer, P. A., Sinnott, P. & Stern, P. L. (1998). HPV-16 infection and progression of cervical intra-epithelial neoplasia: analysis of HLA polymorphism and HPV-16 E6 sequence variants. International Journal of Cancer 78, 166-171.[CrossRef] [Google Scholar]
  3. Conrad Stöppler, M., Ching, K., Stöppler, H., Clancy, K., Schlegel, R. & Icenogle, J. P. (1996). Natural variants of the human papillomavirus type 16 E6 protein differ in their abilities to alter keratinocyte differentiation and to induce p53 degradation. Journal of Virology 70, 6987-6993. [Google Scholar]
  4. de Roda Husman, A.-M., Walboomers, J. M. M., van den Brule, A. J. C., Meijer, C. J. L. M. & Snijders, P. J. F. (1995). The use of general primers GP5 and GP6 elongated at their 3′ ends with adjacent highly conserved sequences improves human papillomavirus detection by PCR. Journal of General Virology 76, 1057-1062.[CrossRef] [Google Scholar]
  5. Giannoudis, A., Graham, D. A., Southern, S. A. & Herrington, C. S. (1999). The p53 codon 72 Arg/Pro polymorphism is not related to HPV type or lesion grade in low and high grade squamous intraepithelial lesions and invasive squamous carcinoma of the cervix. International Journal of Cancer 83, 66-69.[CrossRef] [Google Scholar]
  6. Hayes, V. M., Hofstra, R. M. W., Buys, C. H. C. M., Hollema, H. & Van Der Zee, A. G. J. (1998). Homozygous arginine-72 in wild type p53 and risk of cervical cancer. Lancet 352, 1756. [Google Scholar]
  7. Helland, A., Langerod, A., Johnsen, H., Olsen, A. O., Skovlund, E. & Borresen-Dale, A. L. (1998). p53 polymorphism and risk of cervical cancer. Nature 396, 530-531.[CrossRef] [Google Scholar]
  8. Hildesheim, A., Schiffman, M., Brinton, L. A., Fraumeni, J. F., Herrero, R., Bratti, M. C., Schwartz, P., Mortel, R., Barnes, W., Greenberg, M., McGowan, L., Scott, D. R., Martin, M., Herrera, J. E. & Carrington, M. (1998). p53 polymorphism and risk of cervical cancer. Nature 396, 531-532. [Google Scholar]
  9. Hultman, T., Bergh, S., Moks, T. & Uhlen, M. (1991). Bidirectional solid phase sequencing of in vitro amplified plasmid DNA. BioTechniques 10, 84-93. [Google Scholar]
  10. IARC (1995).IARC monographs on the evaluation of the carcinogenic risks to humans. Lyon, France: IARC Scientific Publications.
  11. Jacobs, M. V., De Roda Husman, A. M., Van Den Brule, A. J. C., Snijders, P. J. F., Meijer, C. J. L. M. & Walboomers, J. M. M. (1995). Group-specific differentiation between high and low risk human papillomavirus genotypes by general primer-mediated PCR and two cocktails of oligonucleotide probes. Journal of Clinical Microbiology 33, 901-905. [Google Scholar]
  12. Josefsson, A. M., Magnusson, P. K. E., Ylitalo, N., Quarforth-Tubbin, P., Ponten, J., Adami, H. O. & Gyllensten, U. B. (1998). p53 polymorphism and risk of cervical cancer. Nature 396, 531. [Google Scholar]
  13. Klaes, R., Ridder, R., Schaefer, U., Benner, A. & Doeberitz, M. V. (1999). No evidence of p53 allele-specific predisposition in human papillomavirus-associated cervical cancer. Journal of Molecular Medicine 77, 299-302.[CrossRef] [Google Scholar]
  14. Lanham, S., Campbell, I., Watt, P. & Gornall, R. (1998). p53 polymorphism and risk of cervical cancer. Lancet 352, 1631. [Google Scholar]
  15. Londesborough, P., Ho, L., Terry, G., Cuzick, J., Wheeler, C. & Singer, A. (1996). Human papillomavirus genotype as a predictor of persistence and development of high-grade lesions in women with minor cervical abnormalities. International Journal of Cancer 69, 364-368.[CrossRef] [Google Scholar]
  16. Minaguchi, T., Kanamori, Y., Matsushima, M., Yoshikawa, H., Taketani, Y. & Nakamura, Y. (1998). No evidence of correlation between polymorphism at codon 72 of p53 and risk of cervical cancer in Japanese patients with human papillomavirus 16/18 infection. Cancer Research 58, 4585-4586. [Google Scholar]
  17. Mullokandov, M. R., Kholodilov, N. G., Atkin, N. B., Burk, R. D., Johnson, A. B. & Klinger, H. P. (1996). Genomic alterations in cervical carcinoma: losses of chromosome heterozygosity and human papillomavirus tumor status. Cancer Research 56, 197-205. [Google Scholar]
  18. Myers, G., Delius, H., Icenogle, J. P., Bernard, H. U., Baker, C., Halpern, A. & Wheeler, C. (1995). HPV and animal PV nucleic acid sequences. In Human Papillomavirus Compendium. A Compilation and Analysis of Nucleic Acid and Amino Acid Sequences.Los Alamos, NM: Los Alamos National Laboratory.
  19. Nindl, I., Rindfleisch, K., Lotz, B., Schneider, A. & Dürst, M. (1999). Uniform distribution of HPV-16 E6 and E7 variants in patients with normal histology, cervical intra-epithelial neoplasia and cervical cancer. International Journal of Cancer 82, 203-207.[CrossRef] [Google Scholar]
  20. Nobbenhuis, M. A. E., Walboomers, J. M. M., Helmerhorst, T. H. J. M., Rozendaal, L., Remmink, A. J., Risse, E. K. J., van der Linden, H. C., Voorhorst, F. J., Kenemans, P. & Meijer, C. J. L. M. (1999). Relation of human papillomavirus status to cervical lesions and consequences for cervical cancer screening: a prospective study. Lancet 354, 20-25.[CrossRef] [Google Scholar]
  21. Remmink, A. J., Walboomers, J. M. M., Helmerhorst, T. H. J. M., Voorhorst, F. J., Rozendaal, L., Risse, E. K. J., Meijer, C. J. L. M. & Kenemans, P. (1995). The presence of persistent high-risk HPV genotypes is associated with progressive disease: natural history up to 36 months. International Journal of Cancer 61, 306-311.[CrossRef] [Google Scholar]
  22. Rosenthal, A. N., Ryan, A., Al-Jehani, R. M., Storey, A., Harwood, C. A. & Jacobs, I. J. (1998). p53 codon 72 polymorphism and risk of cervical cancer in UK. Lancet 352, 871-872.[CrossRef] [Google Scholar]
  23. Sang Song, Y., Kee, H. S., Kim, J. W., Park, N. H., Kang, S. B., Chang, W. H. & Lee, H. P. (1997). Major sequence variants in E7 gene of human papillomavirus type 16 from cervical cancerous and noncancerous lesions of Korean women. Gynecologic Oncology 66, 275-281.[CrossRef] [Google Scholar]
  24. Scheffner, M., Werness, B. A., Huibregtse, J. M., Levine, A. J. & Howley, P. M. (1990). The E6 oncoprotein encoded by the human papillomavirus type 16 and 18 promotes degradation of p53. Cell 63, 1129-1136.[CrossRef] [Google Scholar]
  25. Snijders, P. J. F., Van Duin, M., Walboomers, J. M. M., Steenbergen, R. D. M., Risse, E. K. J., Helmerhorst, T. J. M., Verheijen, R. H. M. & Meijer, C. J. L. M. (1998). Telomerase activity exclusively in cervical carcinomas and a subset of cervical intraepithelial neoplasia grade III lesions: strong association with elevated messenger RNA levels of its catalytic subunit and high-risk human papillomavirus DNA. Cancer Research 58, 3812-3818. [Google Scholar]
  26. Storey, A., Thomas, M., Kalita, A., Harwood, C., Gardiol, D., Mantovani, F., Breuer, J., Leigh, I. M., Matlashewski, G. & Banks, L. (1998). Role of a p53 polymorphism in the development of human papillomavirus-associated cancer. Nature 393, 229-234.[CrossRef] [Google Scholar]
  27. Van Ranst, M. A., Tachezy, R., Delius, H. & Burk, R. D. (1993). Taxonomy of the human papillomaviruses. Papillomavirus Reports 4, 61-65. [Google Scholar]
  28. Walboomers, J. M. M., Jacobs, M. V., Manos, M. M., Bosch, F. X., Kummer, J. A., Shah, K. V., Snijders, P. J. F., Peto, J., Meijer, C. J. L. M. & Munoz, N. (1999). Human papillomavirus is a necessary cause of invasive cervical cancer worldwide. Journal of Pathology 189, 12-19.[CrossRef] [Google Scholar]
  29. Werness, B. A., Levine, A. J. & Howley, P. M. (1990). Association of human papillomavirus type 16 and 18 E6 proteins with p53. Science 248, 76-79.[CrossRef] [Google Scholar]
  30. Xi, L. F., Koutsky, L. A., Galloway, D. A., Kuypers, J., Hughes, J. P., Wheeler, C. M., Holmes, K. K. & Kiviat, N. B. (1997). Genomic variation of human papillomavirus type 16 and risk for high grade cervical intraepithelial neoplasia. Journal of the National Cancer Institute 89, 796-802.[CrossRef] [Google Scholar]
  31. Yamada, T., Manos, M. M., Peto, J., Greer, C. E., Munoz, N., Bosch, F. X. & Wheeler, C. M. (1997). Human papillomavirus type 16 sequence variation in cervical cancers: a worldwide perspective. Journal of Virology 71, 2463-2472. [Google Scholar]
  32. Zehbe, I., Voglino, G., Delius, H., Wilander, E. & Tommasino, M. (1998a). Risk of cervical cancer and geographical variations of human papillomavirus 16 E6 polymorphisms. Lancet 352, 1441-1442.[CrossRef] [Google Scholar]
  33. Zehbe, I., Wilander, E., Delius, H. & Tommasino, M. (1998b). Human papillomavirus 16 E6 variants are more prevalent in invasive cervical cancer than the prototype. Cancer Research 58, 829-833. [Google Scholar]
  34. Zehbe, I., Voglino, G., Wilander, E., Genta, F. & Tommasino, M. (1999). Codon 72 polymorphism of p53 and its association with cervical cancer. Lancet 354, 218-219.[CrossRef] [Google Scholar]
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