Thesis (M.S.)--University of Hawaii at Manoa, 2007. / Includes bibliographical references (leaves 45-55). / i, 92 leaves, bound ill. 29 cm

Errata pages inserted behind leaf 293. / Includes bibliography (leaves 255-293). / xv, 293, [60] leaves, [33] leaves of plates : ill. (some col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Aims to determine the molecular mechanism by which expression of Fas is lost in colorectal tumours and investigates the effects of re-introducing Fas into colon cancer cells. An animal study was undertaken in addition to the studies of colorectal cancer, to investigate the role of Fas signalling in hormone-dependent involution of the prostate gland. / Thesis (Ph.D.)--University of Adelaide, Dept. of Surgery, 1998?

Bibliography: leaves [127-137] / 126 [78] leaves, [26] leaves of plates : ill ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis (Ph.D.)--University of Adelaide, Dept. of Biochemistry, 1985

Errata pages inserted behind leaf 293. / Includes bibliography (leaves 255-293). / xv, 293, [60] leaves, [33] leaves of plates : ill. (some col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Aims to determine the molecular mechanism by which expression of Fas is lost in colorectal tumours and investigates the effects of re-introducing Fas into colon cancer cells. An animal study was undertaken in addition to the studies of colorectal cancer, to investigate the role of Fas signalling in hormone-dependent involution of the prostate gland. / Thesis (Ph.D.)--University of Adelaide, Dept. of Surgery, 1998?

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.

No description available.

published_or_final_version / Medicine / Doctoral / Doctor of Philosophy

published_or_final_version / abstract / Biochemistry / Master / Master of Philosophy

published_or_final_version / abstract / Pathology / Master / Master of Philosophy

published_or_final_version / abstract / Pathology / Doctoral / Doctor of Philosophy