Functional characterization of p53 molecules expressed in human squamous cell carcinomas of the head and neck

Molecular Carcinogenesis

Volumn 18, Issue 2, 1997, Pages 89-96

  Yeudall, W Andrew ^a   Jakus, Judit ^a,c   Ensley, John F ^b   Robbins, Keith C ^a  

^a NATIONAL INSTITUTE OF DENTAL AND CRANIOFACIAL RESEARCH   (United States)

^b WAYNE STATE UNIVERSITY   (United States)

^c CTRL RES INSTITUTE FOR CHEMISTRY   (Hungary)

Author keywords

Gene mutation; Oral cancer; p53; Squamous cell carcinoma; Transactivation; Transcription

Indexed keywords

PROTEIN P53;

ARTICLE; CONTROLLED STUDY; GENE MUTATION; GENETIC TRANSCRIPTION; HEAD AND NECK CANCER; HUMAN; HUMAN CELL; PRIORITY JOURNAL; SQUAMOUS CELL CARCINOMA; TRANSACTIVATION;

BLOTTING, WESTERN; CARCINOMA, SQUAMOUS CELL; CELL TRANSFORMATION, NEOPLASTIC; CHLORAMPHENICOL O-ACETYLTRANSFERASE; DNA, COMPLEMENTARY; GENE EXPRESSION REGULATION, NEOPLASTIC; GENES, P53; GENES, REPORTER; HEAD AND NECK NEOPLASMS; HUMANS; MUTATION; PLASMIDS; TRANS-ACTIVATION (GENETICS); TUMOR CELLS, CULTURED;

EID: 0030997982     PISSN: 08991987     EISSN: None     Source Type: Journal    
DOI: 10.1002/(SICI)1098-2744(199702)18:2<89::AID-MC4>3.0.CO;2-L     Document Type: Article

References (43)

1. Levine AJ. The tumor suppressor genes. Ann Rev Biochem 62:623-651, 1993.
2. Clark AR, Purdie CA, Harrison DJ, et al. Thymocyte apoptosis induced by p53-dependent and independent pathways. Nature 362:849-852, 1993.
3. Lowe SW, Schmitt EM, Smith SW, Osborne BA, Jacks T. p53 is required for radiation-induced apoptosis in mouse thymocytes. Nature 362:847-849, 1993.
4. Kastan MB, Zhan Q, El-Deiry WS, et al. A mammalian cell cycle checkpoint pathway utilizing p53 and GADD45 is defective in ataxia-telangiectasia. Cell 71:587-597, 1992.
5. Kuerbitz SJ, Plunkett BS, Walsh WV, Kastan MB. Wild type p53 is a cell cycle checkpoint determinant following irradiation. Proc Natl Acad Sci USA 89:7491-7495, 1992.
6. Eliyahu D, Michaelovitz D, Eliyahu S, Pinhasi-Kimhi O, Oren M. Wild-type p53 can inhibit oncogene-mediated focus formation Proc Natl Acad Sci USA 86:8763-8767, 1989.
7. Finlay CA, Hinds PW, Levine AJ. The p53 proto-oncogene can act as a suppressor of transformation. Cell 57:1083-1093, 1989.
8. Donehower LA, Harvey M, Slagle BL, et al. Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumors. Nature 356:215-221, 1992.
9. El-Deiry WS, Kern SE, Pietenpol JA, Kinzler KW, Vogelstein B. Definition of a consensus binding site for p53. Nat Genet 1:45-49, 1992.
10. Wang P, Reed M, Wang Y, et al. p53 domains: Structure, oligomerization and transformation. Mol Cell Biol 14:5182-5191, 1994.
11. Raycroft L, Wu H, Lozano G. Transcription activation by wildtype but not transforming mutants of the p53 anti-oncogene. Science 249:1049-1051, 1990.
12. Unger T, Nau MM, Segal S, Minna JD. p53: A transdominant regulator of transcription whose function is ablated by mutations occurring in human cancer. EMBO J 11:1383-1390, 1992.
13. Miller CW, Chumakov A, Said J, Chen DL, Aslo A, Koeffler HP. Mutant p53 proteins have diverse intracellular abilities to oligomerize and activate transcription. Oncogene 8:1815-1824, 1993.
14. Zhang W, Shay JW, Deisseroth AB. Inactive p53 mutants may enhance the transcriptional activity of wild-type p53. Cancer Res 53:4772-4775, 1993.
15. Day GL, Blot WJ, Austin DF, et al. Racial differences in risk of oral and pharyngeal cancer: Alcohol, tobacco, and other determinants. J Natl Cancer Inst 85:465-473, 1993.
16. Yeudall WA, Campo MS. Human papillomavirus DNA in biopsies of oral tissues. J Gen Virol 72:173-176, 1991.
17. Blot WJ, Devesa SS, McLaughlin JK, Fraumeni JF Jr. Oral and pharyngeal cancers. Cancer Surv 19-20:23-42, 1994.
18. Macfarlane GJ, Zheng T, Marshall JR, et al. Alcohol, tobacco, diet and the risk of oral cancer: A pooled analysis of three case-control studies. Eur J Cancer B Oral Oncol 31B:181-187, 1995.
19. Somers KD, Merrick MA, Lopez ME, Incognito LS, Schechter GL, Casey G. Frequent p53 mutations in head and neck cancer. Cancer Res 52:5997-6000, 1992.
20. Burns JE, Baird MC, Clark LJ, et al. Gene mutations and increased levels of p53 protein in human squamous cell carcinomas and their cell lines. Br J Cancer 67:1274-1284, 1993.
21. Yeudall WA, Paterson IC, Patel V, Prime SS. Presence of human papillomavirus sequences in tumour-derived human oral keratinocytes expressing mutant p53. Eur J Cancer B Oral Oncol 31B:136-143, 1995.
22. Cardinali M, Pietraskiewicz H, Ensley JF, Robbins KC. Tyrosine phosphorylation as a marker for aberrantly regulated growth promoting pathways in cell lines derived from head and neck malignancies. Int J Cancer 61:98-103, 1995.
23. Rheinwald JG, Beckett MA. Tumorigenic keratinocyte lines requiring anchorage and fibroblast support cultured from human squamous cell carcinomas. Cancer Res 41:1657-1663, 1981.
24. Parkinson EK, Yeudall WA. The epidermis. In: Freshney RI (ed), Culture of Epithelial Cells. Wiley-Liss, New York, 1992, pp. 59-80.
25. Yeudall WA, Crawford RY, Ensley JF, Robbins KC. MTS1/CDK4I is altered in cell lines derived from primary and metastatic oral squamous cell carcinoma. Carcinogenesis 15:2683-2686, 1994.
26. Wigler M, Pellicer A, Silverstein S, Axel R, Urlaub G, Chasin L. DNA-mediated transfer of the adenine phosphoribosyltransferase locus into mammalian cells. Proc Natl Acad Sci USA 76:1373-1376, 1979.
27. Kern SE, Pietenpol JA, Thiagalingam S, Seymour A, Kinzler KW, Vogelstein B. Oncogenic forms of p53 inhibit p53-regulated gene expression. Science 256:827-830, 1992.
28. Sanes JR, Rubenstein JLR, Nicolas JF. Use of a recombinant retrovirus to study post-implantation cell lineage in mouse embryos. EMBO J 5:3133-3142, 1986.
29. Baker SJ, Preisinger AC, Jessup JM, et al. p53 gene mutations occur in combination with 17p allelic deletions as late events in colorectal tumorigenesis. Cancer Res 50:7717-7722, 1990.
30. Rodrigues NR, Rowan A, Smith MEF, et al. p53 mutations in colorectal cancer. Proc Natl Acad Sci USA 87:7555-7559, 1990.
31. Ahomadegbe JC, Barrios M, Fogel S, et al. High incidence of p53 alterations (mutation, deletion, overexpression) in head and neck primary tumors and metastases: Absence of correlation with clinical outcome. Frequent protein overexpression in normal epithelium and in early non-invasive lesions. Oncogene 10:1217-1227, 1995.
32. Hollstein M, Rice K, Greenblatt MS, et al. Database of p53 gene somatic mutations in human tumors and cell lines. Nucleic Acids Res 22:3551-3555, 1994.
33. Sun Y, Hegamyer G, Cheng Y-J, et al. An infrequent point mutation of the p53 gene in human nasopharyngeal carcinoma. Proc Natl Acad Sci USA 89:6516-6520, 1992.
34. Halevy O, Michaelovitz D, Oren M. Different tumor-derived p53 mutants exhibit distinct biological activities. Science 250:113-116, 1990.
35. Day GL, Blot WJ, Austin DF, et al. Racial differences in risk of oral and pharyngeal cancer: Alcohol, tobacco, and other determinants. J Natl Cancer Inst 85:465-473, 1993.
36. Cardinali M, Kratochvil FJ, Ensley JF, Robbins KC, Yeudall WA. Functional characterization in vivo of mutant p53 molecules derived from squamous cell carcinomas of the head and neck. Mol Carcinog 18:78-88, 1997.
37. Sun Y, Nakamura K, Wendel E, Colburn N. Progression toward tumor cell phenotype is enhanced by overexpression of a mutant p53 tumor-suppressor gene isolated from nasopharyngeal carcinoma. Proc Natl Acad Sci USA 90:2827-2831, 1993.
38. Sun Y, Dong Z, Nakamura K, Colburn NH. Dosage-dependent dominance over wild-type p53 of a mutant p53 isolated from nasopharyngeal carcinoma. FASEB J 7:944-950, 1993.
39. Burns JE, Clark LJ, Yeudall WA, et al. The p53 status of cultured human premalignant oral keratinocytes. Br J Cancer 70:591-595, 1994.
40. Edington KG, Loughran OP, Berry IJ, Parkinson EK. Cellular immortality: A late event in the progression of human squamous cell carcinoma of the head and neck associated with p53 alteration and a high frequency of allele loss. Mol Carcinog 13:254-265, 1995.
41. Milner J. Flexibility: The key to p53 function? Trends Biochem Sci 20:49-51, 1995.
42. Pindborg JJ. Oral precancer. In: Barnes I (ed), Surgical Pathology of the Head and Neck, Vol. 1. Marcel Dekker, New York, 1985, pp. 279-331.
43. Min B-M, Baek J-H, Shin K-H, Gujuluva CN, Cherrick HM, Park N-H. Inactivation of the p53 gene by either mutation or HPV infection is extremely frequent in human oral squamous cell carcinoma cell lines. Eur J Cancer B Oral Oncol 30B:338-345, 1994.