The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.
Progression of human papillomavirus type 18-immortalized human keratinocytes to a malignant phenotype
Abstract
We have developed a model system for progression of human epithelial cells to malignancy, using a human papillomavirus type 18 (HPV-18)-immortalized human keratinocyte cell line. Cells of cell line FEP-1811 were nontumorigenic in athymic mice through at least 12 passages in culture, but after 32 passages were weakly tumorigenic, producing tumors that regressed. After 62 passages they produced invasive squamous cell carcinomas that grew progressively. The progression to malignancy was associated with an increase in the efficiency of forming colonies in soft agar and with altered differentiation properties. In an organotypic culture system, FEP-1811 cells at passages 12 and 32 exhibited features typical of premalignant intraepithelial neoplasia in vivo, and cells at passage 68 exhibited features consistent with squamous cell carcinomas. No change in copy number of the transfected HPV-18 genome or in the level of expression of the viral transforming gene products E6 and E7 was detected between tumorigenic and nontumorigenic cells. Cytogenetic analysis of cells at early, middle, and late passage levels and cells cultured from tumors revealed that several chromosomal abnormalities segregated with the tumorigenic cell populations.
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“Despite the fact that expression of high-risk oncogenes in primary human keratinocytes can cause cellular immortalization, with the cells exhibiting many characteristics of premalignant lesions, these cells do not form tumours when injected into nude mice.”
From The Not-So-Good, the Bad and the Ugly: HPV E5, E6 and E7 Oncoproteins in the Orchestration of Carcinogenesis (2021) · cites this paper as [309]
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“Additional oncogenic events are necessary for malignant progression to occur, such as expression of oncogenes like ras or fos, or accumulation of oncogenic mutations over prolonged passaging in culture [307,308,309,310]”
From The Not-So-Good, the Bad and the Ugly: HPV E5, E6 and E7 Oncoproteins in the Orchestration of Carcinogenesis (2021) · cites this paper as [309]
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Cites
The human papilloma virus-16 E7-oncoprotein is able to bind to the retinoblastoma gene product
Dyson, N., Howley, P. M., Münger, K., & Harlow, E. (1989) · Science · doi:10.1126/science.2537532 · Cited by 3,017
Research works printed but not linked: 3
- [19]McCance, D. J., Kopan, R., Fuchs, E. & Laimins, L. A. (1988) Proc. Natl. Acad. Sci. USA 85, 7169–7173.
- [21]Pecoraro, G., Morgan, D. & Defendi, V. (1989) Proc. Natl. Acad. Sci. USA 86, 563–567.
- [31]Steinberg, M. L. & Defendi, V. (1979) Proc. Natl. Acad. Sci. USA 76, 801–805.
Cited by
Genetic and Epigenetic Changes in Human Epithelial Cells Immortalized by Telomerase
Farwell, D. G., Shera, K. A., Koop, J. I., Bonnet, G. A., Matthews, C. P., Reuther, G. W., Coltrera, M. D., McDougall, J. K., & Klingelhutz, A. J. (2000) · The American Journal of Pathology · doi:10.1016/s0002-9440(10)65025-0 · Cited by 196
Self-citationBasukala, O., & Banks, L. (2021) · Viruses · doi:10.3390/v13101892 · Cited by 137
Metadata
- Authors
- Hurlin, P. J., Kaur, P., Smith, P. P., Perez-Reyes, N., Blanton, R. A., & McDougall, J. K.
- Affiliations
- Fred Hutchinson Cancer Research Center, Seattle, WA 98104.
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 1991-01-15
- Volume
- 88
- Issue
- 2
- Pages
- 570-574
- ISSN
- 0027-8424
- 1091-6490
- Cited by
- 124
- References
- 1
- Language
- en
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- Hurlin, P. J., Kaur, P., Smith, P. P., Perez-Reyes, N., Blanton, R. A., & McDougall, J. K. (1991). Progression of human papillomavirus type 18-immortalized human keratinocytes to a malignant phenotype. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.88.2.570
