The Expression and Structure of p53 Gene Products in Cultured Glioma Cells

  • Toshihiro Mineta
  • Kouzou Fukuyama
  • Tetsuya Shiraishi
  • Kazuo Tabuchi


Previous studies have demonstrated that the allelic deletions of the short arm of chromosome 17 (17p) and the long arm of 10 (10q) are closely associated with tumorigenesis of human malignant gliomas [1,2]. While the allelic deletion in chromosome 10q appears to occur in a relatively late phase associated with the transition from a less malignant to a more malignant state [3], the deletion in chromosome 17p seems to be an early event associated with the occurrence of neoplastic glial cells, suggesting that anti-oncogenes or tumor suppressor genes are important in the development of human gliomas. However, the role of anti-oncogenes in human gliomas has not been studied in detail. Recent studies have demonstrated that the cellular protein p53, which is encoded on chromosome 17p13.1, may function as a suppressor of neoplastic growth and may play an important role in the pathogenesis of human malignant tumors. The p53 protein was first identified through its interaction with the large T antigen of simian virus 40 (SV 40) [4], and had been thought to be a dominant oncogene enabling full transformation of vertebrate somatic cells in combination with an activated ras gene [5]. However, it has recently been shown that the p53 protein observed in the neoplastic cells is entirely mutant and that the wild type p53 suppresses normal cells from transforming [6], which means that the p53 protein may act as a tumor suppressor, like the product of the retinoblastoma susceptibility gene.


Glioma Cell Human Papilloma Virus T98G Cell Human Glioma Cell Line Al72 Cell 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. 1.
    El-Azouzi M, Chung RY, Farmer GE, Maltuza RL, Black PM, Rouleau GA, Hettlich C, Hedley-Whyte ET, Zervas NT, Panagopoulos K, Nakamura Y, Gusella JF, Seizinger BR (1989) Loss of distinct regions on the short arm of chromosome 17 associated with tumorigenesis of human astrocytomas. Proc Natl Acad Sci USA 86: 7186–7190PubMedCrossRefGoogle Scholar
  2. 2.
    Fujimoto M, Fults DW, Thomas GA, Nakamura Y, Heilbrun MP, White R, Story JL, Naylor SL, Kagan-Hallet KS, Sheridan PJ (1989) Loss of heterozygosity on chromosome 10 in human glioblastoma multiforme. Genomics 4: 210–214PubMedCrossRefGoogle Scholar
  3. 3.
    James CD, Carlbom E, Dumanski JP, Hansen M, Nordenskjold M, Collins VP, Cavenee WK (1988) Clonal genomic alterations in glioma malignancy stages. Cancer Res 48: 5546–5551PubMedGoogle Scholar
  4. 4.
    Lane DP, Crawford LV (1979) T antigen is bound to a host protein in SV-40 transformed cells. Nature 278: 261–263PubMedCrossRefGoogle Scholar
  5. 5.
    Parada LF, Land H, Weinberg RA, Wolt D, Rotter V (1984) Cooperation between gene encoding p53 tumour antigen and ras in cellular transformation. Nature 312: 649–651PubMedCrossRefGoogle Scholar
  6. 6.
    Eliyahu D, Michalovitz D, Eliyahu S, Pinhasi-Kimhi O, Oren M (1989) Wild-type p53 can inhibit oncogene-mediated focus formation. Proc Natl Acad Sci USA 86: 8763–8767PubMedCrossRefGoogle Scholar
  7. 7.
    Baker SJ, Fearon ER, Nigro JM, Hamilton SR, Preisinger AC, Jessup JM, van- Tuinen P, Ledbetter DF, Barker DF, Nakamura Y, White R, Vogelstein B (1989) Chromosome 17 deletions and p53 gene mutations in colorectal carcinomas. Science 244: 217–221PubMedCrossRefGoogle Scholar
  8. 8.
    Masuda H, Miller C, Koeffler HP, Battifora H, Cline MJ (1987) Rearrangement of the p53 gene in human osteogenic sarcomas. Proc Natl Acad Sci USA 84: 7716–7719PubMedCrossRefGoogle Scholar
  9. 9.
    Nigro JM, Baker SJ, Preisinger AC, Jessup JM, Hostetter R, Cleary K, Bigner SH, Davidson N, Baylin S, Devilee P, Glover T, Collins FS, Weston A, Modali R, Harris CC, Vogelstein B (1989) Mutations in the p53 gene occur in diverse human tumour types. Nature 342: 705–708PubMedCrossRefGoogle Scholar
  10. 10.
    Takahashi T, Nau MM, Chiba I, Birrer MJ, Rosenberg RK, Vinocour M, Levitte M, Pass H, Gazdar AF, Minna JD (1989) p53: A frequent target for genetic abnormalities in lung cancer. Science 246: 491–494PubMedCrossRefGoogle Scholar
  11. 11.
    Crawford LV, Pirn DC, Gurney EG, Goodfellow P, Papadimitriou JT (1981) Detection of a common feature in several human tumor cell lines—53,000-dalton protein. Proc Natl Acad Sci USA 78: 41–45PubMedCrossRefGoogle Scholar
  12. 12.
    Sarnow, P, Ho YS, Williams J, Levine AJ (1982) Adenovirus Elb-58kd tumor antigen and SV40 large tumor antigen are physically associated with the same 54 kd cellular protein in transformed cells. Cell 28: 387–394PubMedCrossRefGoogle Scholar
  13. 13.
    Werness BA, Levine AJ, Howley PM (1990) Association of human papilloma virus type 16 and 18 E6 protein with p53. Science 248: 76–79PubMedCrossRefGoogle Scholar
  14. 14.
    Bischoff JR, Friedman PN, Marshak DR, Prives C, Beach D (1990) Human p53 is phosphorylated by p60-cdc2 and cyclin B-cdc2. Proc Natl Acad Sci USA 87: 4766–4770PubMedCrossRefGoogle Scholar
  15. 15.
    Milner J, Cook A, Mason J (1990) p53 is associated with p34cdc2 in transformed cells. EMBO J 9: 2885–2889Google Scholar
  16. 16.
    Matlashewski GJ, Tuck S, Pim D, Lamb P, Schneider J, Crawford LV (1987) Primary structure polymorphism at amino acid residue 72 of human p53. Mol Cell Biol 7: 961–963PubMedGoogle Scholar
  17. 17.
    Finlay CA, Hinds PW, Tan T-H, Eliyahu D, Oren M, Levine AJ (1988) Activating mutations for transformation by p53 produce a gene product that forms an hsc70- p53 complex with an altered half-life. Mol Cell Biol 8: 531–539PubMedGoogle Scholar

Copyright information

© Springer-Verlag Tokyo 1991

Authors and Affiliations

  • Toshihiro Mineta
  • Kouzou Fukuyama
  • Tetsuya Shiraishi
  • Kazuo Tabuchi
    • 1
  1. 1.Department of NeurosurgerySaga Medical SchoolSaga, 849Japan

Personalised recommendations