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

Persistent Link:
http://hdl.handle.net/10150/183865
Title:
ANALYSIS OF THE HUMAN EPIDERMAL GROWTH FACTOR RECEPTOR GENE AS A PROTO-ONCOGENE (SQUAMOUS CELL CARCINOMA).
Author:
HUNTS, JOHN HOWARD.
Issue Date:
1986
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)
Keywords:
Oncogenes.; Cancer -- Genetic aspects.; Retroviruses.
Degree Name:
Ph.D.
Degree Level:
doctoral
Degree Program:
Molecular and Cellular Biology; Graduate College
Degree Grantor:
University of Arizona
Advisor:
Shimizu, Nobuyoshi

Full metadata record

DC FieldValue Language
dc.language.isoenen_US
dc.titleANALYSIS OF THE HUMAN EPIDERMAL GROWTH FACTOR RECEPTOR GENE AS A PROTO-ONCOGENE (SQUAMOUS CELL CARCINOMA).en_US
dc.creatorHUNTS, JOHN HOWARD.en_US
dc.contributor.authorHUNTS, JOHN HOWARD.en_US
dc.date.issued1986en_US
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © 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.en_US
dc.description.abstractThe 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.en_US
dc.typetexten_US
dc.typeDissertation-Reproduction (electronic)en_US
dc.subjectOncogenes.en_US
dc.subjectCancer -- Genetic aspects.en_US
dc.subjectRetroviruses.en_US
thesis.degree.namePh.D.en_US
thesis.degree.leveldoctoralen_US
thesis.degree.disciplineMolecular and Cellular Biologyen_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.grantorUniversity of Arizonaen_US
dc.contributor.advisorShimizu, Nobuyoshien_US
dc.identifier.proquest8623854en_US
dc.identifier.oclc697656065en_US
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