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Elevated Levels of the P53 Tumour Suppressor Protein in the Basal Layer of Recurrent Laryngeal Papillomas

  • Louise J. Clark
  • Kenneth MacKenzie
  • E. Kenneth Parkinson

Abstract

A viral aetiology for recurrent respiratory papillomatosis (RRP) has long since been postulated and the human papilloma virus (HPV) types 6,11,16 and 18 have been detected reproducibly in laryngeal papillomas and squamous cell carcinomas of the head and neck (SCCs of the H & N). Whilst the underlying mechanism(s) for the abnormal proliferation of respiratory epithelial cells leading to the formation of papillomas is unknown, it is known that the above HPV types, transform keratinocytes in culture with potencies which correlate with their ability to inactivate the p53 tumour suppressor protein. The E6 proteins of HPVs 16 and 18 complex and degrade the p53 protein1,2, whereas HPV6 and 11 E6 proteins have been reported to only weakly bind p53 without degradation2.

Keywords

Human Papilloma Virus Human Papilloma Virus Type Respiratory Epithelial Cell Basal Epithelial Cell Recurrent Respiratory Papillomatosis 
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.

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References

  1. 1.
    M. Scheffner, B.A. Werness, J.M. Humbregtse, A.J. Levine and P.M. Howley, The E6 oncoprotein encoded by human papillomavirus types 16 and 18 promotes the degradation of p53, Cell 63:1129 (1990).PubMedCrossRefGoogle Scholar
  2. 2.
    T. Crook, J.A. Tidy and K.H. Vousden, Degradation of p53 can be targeted by HPV sequences distinct from those required for p53 binding and trans-activation, Cell 67:547 (1991).PubMedCrossRefGoogle Scholar
  3. 3.
    J.E. Burns, M.C. Baird, L.J. Clark, P. Burns, K. Edington, C. Chapman, R. Mitchell, G. Robertson, D. Soutar and E.K. Parkinson, Gene mutations and elevated protein levels in human squamous cell carcinomas and their cell lines, Br J Cancer 67:1274 (1993).PubMedCrossRefGoogle Scholar
  4. 4.
    M.J. Arends, Y.K. Donaldson, E. Duvall, A.H. Wyllie and C. Bird, HPV in full thickness cervical biopsies: high prevalence in CIN 2 and CIN 3 detected by a sensitive PCR method, J Pathol 165:301 (1991).PubMedCrossRefGoogle Scholar
  5. 5.
    G.R. Ogden, R.A. Kiddie, D.P Lunny and D.A. Lane, Assessment of p53 protein in normal, benign and malignant oral mucosa, J Pathol. 166:389 (1992).PubMedCrossRefGoogle Scholar
  6. 6.
    S.W. Lowe and H. Ruley, Stabilization of the p53 tumor suppressor is induced by adenovirus 5 El A and accompanies apoptosis, Gene Devel 7:535 (1993).CrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media New York 1994

Authors and Affiliations

  • Louise J. Clark
    • 1
  • Kenneth MacKenzie
    • 2
  • E. Kenneth Parkinson
    • 1
  1. 1.The Beatson Institute for Cancer ResearchGarscube EstateBearsden, GlasgowUK
  2. 2.Department of OtolaryngologyGlasgow Royal InfirmaryGlasgowUK

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