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    ANALYSIS OF THE HUMAN EPIDERMAL GROWTH FACTOR RECEPTOR GENE AS A PROTO-ONCOGENE (SQUAMOUS CELL CARCINOMA).

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    Author
    HUNTS, JOHN HOWARD.
    Issue Date
    1986
    Keywords
    Oncogenes.
    Cancer -- Genetic aspects.
    Retroviruses.
    Advisor
    Shimizu, Nobuyoshi
    
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    Show full item record
    Publisher
    The University of Arizona.
    Rights
    Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
    Abstract
    The epidermal growth factor receptor (EGFR) gene was examined as a proto-oncogene. Initially, the cellular homolog of the retroviral oncogene erb-B was shown to be localized to the same region of human chromosome 7 as the EGFR gene, giving support to the idea that these genes are closely related. To determine how some cells can over-express the EGFR gene, somatic cell hybrids constructed between a human EGFR-overproducing cell line and a mouse EGFR-deficient cell line were examined. EGFR gene amplification was observed in one of these hybrids along with EGFR gene rearrangement, which is thought to generate an abnormal mRNA. When examining tumor tissue, the EGF receptor (EGFR) was found to be elevated relative to normal adjacent tissue in 9 out of 15 primary human squamous cell carcinomas. Only 2 of these 9 tumors had EGFR gene amplification, suggesting alternative mechanisms potentially involved in increasing EGFR levels. Because placental tissue expresses high levels of EGFR, it was thought that some tissues may normally possess high EGFR levels and that some cancerous tissues inappropriately mimic the mechanisms active in the placenta. From the examination of several tissue samples, EGFR mRNA levels and EGFR protein half-life were also postulated as contributing factors regulating the EGFR levels. The EGFR gene was implicated as a proto-oncogene by evidence which suggests that either a qualitative or a quantitative change in the receptor may be involved in tumorigenesis. Finally, to begin to better understand what role EGFR hyperproduction plays in tumorigenesis, a DNA vector was constructed which produces antisense-RNA for inhibiting EGFR expression.
    Type
    text
    Dissertation-Reproduction (electronic)
    Degree Name
    Ph.D.
    Degree Level
    doctoral
    Degree Program
    Molecular and Cellular Biology
    Graduate College
    Degree Grantor
    University of Arizona
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