Loss of normal G1 checkpoint control is an early step in carcinogenesis, independent of p53 status

Cancer Research

Volumn 59, Issue 5, 1999, Pages 1008-1014

  Syljuåsen, Randi G ^a   Krolewski, Bozena ^a   Little, John B ^a  

^a HARVARD SCHOOL OF PUBLIC HEALTH   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ANIMAL CELL; ARTICLE; CARCINOGENESIS; CELL CYCLE G1 PHASE; CELL KILLING; CELL TRANSFORMATION; CONTACT INHIBITION; FIBROBLAST; IONIZING RADIATION; MALIGNANT TRANSFORMATION; MOUSE; NONHUMAN; POINT MUTATION; PRIORITY JOURNAL; RADIATION INJURY; RADIOSENSITIVITY; ALPHA RADIATION; ANIMAL; CELL CLONE; CELL CYCLE; CELL DIVISION; CELL LINE; CELL SURVIVAL; EXON; HUMAN; KINETICS; POLYMERASE CHAIN REACTION; RADIATION EXPOSURE; RADIATION RESPONSE; SINGLE STRAND CONFORMATION POLYMORPHISM; TIME; TUMOR SUPPRESSOR GENE; X RAY;

ALPHA PARTICLES; ANIMALS; CELL CYCLE; CELL DIVISION; CELL LINE; CELL SURVIVAL; CELL TRANSFORMATION, NEOPLASTIC; CLONE CELLS; DOSE-RESPONSE RELATIONSHIP, RADIATION; EXONS; G1 PHASE; GENES, P53; HUMANS; KINETICS; MICE; POINT MUTATION; POLYMERASE CHAIN REACTION; POLYMORPHISM, SINGLE-STRANDED CONFORMATIONAL; TIME FACTORS; X-RAYS;

EID: 0033084203     PISSN: 00085472     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Article

References (35)

1. Okada, S. Radiation effects on cell cycle progress through the life cycle. In: Radiation Biochemistry, Vol. 1, pp. 189-246. New York: Academic Press, 1970.
2. Little, J. B. Delayed initiation of DNA synthesis in irradiated human diploid cells. Nature (Lond.), 218: 1064-1065, 1968.
3. Nagasawa, H., and Little, J. B. Comparison of kinetics of x-ray-induced cell killing in normal, ataxia telangiectasia and hereditary retinoblastoma fibroblasts. Mutat. Res., 109: 297-308, 1983.
4. 1 arrest and long-term induction of Cipl in normal human fibroblasts. Genes Dev., 8: 2540-2551, 1994.
5. Li, C. Y., Nagasawa, H., Tsang, N. M., and Little, J. B. Radiation-induced reversible G(0)/G(1) block is abolished in human diploid fibroblasts transfected with the human papilloma virus E6 gene: implication of the p53-Cipl/WAFI pathway. Int. J. Oncol., 6: 233-236, 1995.
6. Tsang, N. M., Nagasawa, H., Li, C., and Little, J. B. Abrogation of p53 function by transfection of HPVI6 E6 gene enhances the resistance of human diploid fibroblasts to ionizing radiation. Oncogenc. 10: 2403-2408, 1995.
7. Linke, S. P., Clarkin, K. C., and Wahl, G. M. p53 mediates permanent arrest over multiple cell cycles in response to y-irradiation. Cancer Res., 57: 1171-1179, 1997.
8. 1 arrest in established human tumor cell lines. Oncogene, 11: 1885-1892, 1995.
9. 1S arrest in p53+ human tumor cells synchronized by mitotic selection. Cancer Res., 58: 2036-2041, 1998.
10. 1 phase arrest and p53 function in human tumor cells. Cancer Res., 55: 1842-1846, 1995.
11. Kastan, M. B., Onyekwere, O., Sidransky, D., Vogelstein, B., and Craig, R. W. Participation of p53 protein in the cellular response to DNA damage. Cancer Res., 51: 6304-6311, 1991.
12. Kuerbitz, S. J., Plunkett, B. S., Walsh, W. V., and Kastan, M. B. Wild-type p53 is a cell cycle checkpoint determinant following irradiation. Proc. Natl. Acad. Sci. USA, 89: 7491-7495, 1992.
13. O'Connor, P. M., Jackman, J., Bae, I., Myers, T. G., Fan, S., Mutoh, M., Scudiero, D. A., Monks, A., Sausville, E. A., Weinstein, J. N., Friend, S., Fornace, A. J. J., and Kohn, K.W. Characterization of the p53 tumor suppressor pathway in cell lines of the National Cancer Institute anticancer drug screen and correlations with the growth-inhibitory potency of 123 anticancer agents. Cancer Res., 57: 4285-4300, 1997.
14. Yount, G. L., Haas-Kogan, D. A., Vidair, C. A., Haas, M., Dewey, W. C., and Israel, M. A. Cell cycle synchrony unmasks the influence of p53 function on radiosensitivity of human glioblastoma cells. Cancer Res., 56: 500-506, 1996.
15. Reznikoff, C. A., Bertram, J. S., Brankow, D. W., and Heidelberger, C. Quantitative and qualitative studies of chemical transformation of cloned C3H mouse embryo cells sensitive to postconfluence inhibition of cell division. Cancer Res., 33: 3239-3249, 1973.
16. Krolewski, B., and Little, J. B. Application of denaturing gradient gel blots to detect p53 mutations in x-ray-transformed mouse C3H 10T1/2 clones. Mol. Carcinog., 7: 190-196, 1993.
17. Miller, S. A., Dykes, D. D., and Polesky, H. F. A simple salting out procedure for extracting DNA from human nucleated cells. Nucleic Acids Res., 16: 1215, 1988.
18. Terhune, P. G., Memoli, V. A., and Longnecker, D. S. Evaluation of p53 mutation in pancreatic acinar cell carcinomas of humans and transgenic mice. Pancreas, 16: 6-12, 1998.
19. Bienz, B., Zakut-Houri, R., Givol, D., and Oren, M. Analysis of the gene coding for the murine cellular tumour antigen. p53. EMBO J., 3: 2179-2183, 1984.
20. Paquette, B., Wagner, R., and Little, J. B. In vitro reversion of transformed phenotype in mouse C3H/10T1/2 cells: modification in genomic 5-methylcytosine content. Int. J. Onc., 8: 727-734, 1998.
21. Crompton, N. E., Emery, G. C., Shi, Y., Sigg, M., and Blattmann, H. Radiation-induced genetic instability: no association with changes in radiosensitivity or cell cycle checkpoints in C3H 10T1/2 mouse fibroblasts. Radiat. Environ. Biophys., 36: 255-259, 1998.
22. Raaphorst, G. P., Vadasz, J. A., Azzam, E. I., Sargent, M. D., Borsa, J., and Einspenner, M. Comparison of heat and/or radiation sensitivity and membrane composition of seven x-ray-transformed C3H 10T1/2 cell lines and normal C3H 10T1/2 cells. Cancer Res., 45: 5452-5456, 1985.
23. Fearon, E. R., and Vogelstein, B. A genetic model for colorectal tumorigenesis. Cell. 61: 759-767, 1990.
24. Kadohama, T., Tsuji, K., and Ogawa, K. Indistinct cell cycle checkpoint after UV damage in H-ras-transformed mouse liver cells despite normal p53 gene expression. Oncogene, 9: 2845-2852, 1994.
25. Sherr, C. J. Cancer cell cycles. Science (Washington DC), 274: 1672-1677, 1996.
26. El-Deiry, W. S., Tokino, T., Velculescu, V. E., Levy, D. B., Parsons, R., Trent, J. M., Lin, D., Mercer, W. E., Kinzler, K. W., and Vogelstein, B. WAFI, a potential mediator of p53 tumor suppression. Cell, 75: 817-825, 1993.
27. 1 arrest. Cell. 76: 1013-1023, 1994.
28. WAFI/Cipl in human brain tumors. Oncogene, 11: 2021-2028, 1995.
29. 1 checkpoint does not decrease cell survival following DNA damage. Cancer Res., 53: 4164-4168, 1993.
30. Huang, H., Li, C. Y., and Little, J. B. Abrogation of p53 function by transfection of HPV16 E6 gene does not enhance resistance of human tumour cells to ionizing radiation. Int. I. Radiat. Biol., 70: 151-160, 1996.
31. Lowe, S. W., Bodis, S., McClatchey, A., Remington, L., Ruley, H. E., Fisher, D. E., Housman, D. E., and Jacks. T. p53 status and the efficacy of cancer therapy in vivo. Science (Washington DC), 266: 807-810, 1994.
32. McIlwrath, A. J., Vasey, P. A., Ross, G. M., and Brown, R. Cell cycle arrests and radiosensitivity of human tumor cell lines: dependence on wild-type p53 for radio-sensitivity. Cancer Res., 54: 3718-3722, 1994.
33. Fan, S., El-Deiry, W. S., Bae, I., Freeman, J., Jondle, D., Bhatia, K., Fomace, A. J. J., Magrath, I., Kohn, K. W., and O'Connor, P. M. p53 gene mutations are associated with decreased sensitivity of human lymphoma cells to DNA damaging agents. Cancer Res., 54: 5824-5830, 1994.
34. Soussi, T., de Fromentel, C. C. and May, P. Structural aspects of the p53 protein in relation to gene evolution. Oncogene, 5: 945-952, 1990.
35. Greenblatt, M. S., Bennett, W. P., Hollstein, M., and Harris, C. C. Mutations in the p53 tumor suppressor gene: clues to cancer etiology and molecular pathogenesis. Cancer Res., 54: 4855-4878, 1994.