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[Cancer Research 54, 321-326, January 15, 1994]
© 1994 American Association for Cancer Research

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Activation of p53 Gene Expression in Premalignant Lesions during Head and Neck Tumorigenesis1

Dong M. Shin2, Jhingook Kim, Jae Y. Ro, Jason Hittelman, Jack A. Roth, Waun K. Hong and Walter N. Hittelman

Department of Thoracic/Head and Neck Medical Oncology [D. M. S., W. K. H.], Thoracic Surgery [J. K., J. A. R.], Pathology [J. Y R.], and Clinical Investigation [J. H.,W. N. H.], The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030

2 To whom requests for reprints be addressed, at The University of Texas M. D. Anderson Cancer Center, Department of Thoracic/Head and Neck Medical Oncology, 1515 Holcombe Boulevard, Box 80, Houston, TX 77030.

With the goal of identifying a potential intermediate biomarker in the multistep process of head and neck cancer development, we conducted immunohistochemical analyses for p53 expression in 33 patients with head and neck squamous cell carcinomas whose tissue sections contained adjacent normal epithelium, hyperplastic, and/or dysplastic lesions. Fifteen of 33 (45%) squamous cell carcinomas of the head and neck expressed p53, but none of four normal control patients (cancer-free nonsmokers) expressed detectable p53 in oral mucosa specimens. To determine when p53 expression is initiated during head and neck tumorigenesis, we examined the normal and premalignant lesions adjacent to the tumors. Five of 24 (21%) samples of normal epithelium adjacent to tumors, 7 of 24 (29%) samples of hyperplasia, and 9 of 20 (45%) samples of dysplasia expressed p53. Quantitative image analysis demonstrated not only a gradual increase in the amount of p53 expression as tissue abnormalities progressed but also a topological change in expression. Whereas p53 expression, when present, was limited to the basal layer in normal epithelium adjacent to tumor, the expression of p53 expanded into the parabasal and superficial layers in hyperplasia and dysplasia. We conclude that p53 expression can be altered in very early phases of head and neck tumorigenesis. Thus, it may be an excellent candidate for risk assessment and may serve as an intermediate biomarker in chemoprevention trials.

1 Supported in part by NIH Grants CA-52501, CA-48364, and CA-45746. D. M. S. is a recipient of the Clinical Oncology Career Development Award (ACS 91-271) from the American Cancer Society.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Received 9/27/93. Accepted 11/24/93.




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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1994 by the American Association for Cancer Research.