published_or_final_version / Dentistry / Master / Master of Orthodontics

published_or_final_version / Medicine / Master / Doctor of Medicine

The Best M.Phil Thesis in the Faculties of Dentistry, Engineering, Medicine and Science (University of Hong Kong), Li Ka Shing Prize,1997-1999 / published_or_final_version / Pathology / Master / Master of Philosophy

No description available.

Angiogenesis is the formation of new vessels from existing vasculature and is essential for tumour growth and metastasis. It is controlled by angiogenic factors secreted by the tumour which regulate the matrix remodelling, endothelial cell (EC) proliferation, and capillary differentiation necessary for establishing a blood supply. This thesis has examined angiogenesis in human tumours. Immunohistochemically highlighted vessels in tumours were quantified using different methods to develop a rapid and objective method for measuring tumour angiogenesis. Significant associations between Chalkley counting, microvessel density, vascular area and perimeter were demonstrated; the Chalkley technique gave independent prognostic information and was suitable for a diagnostic service. Studies on the frequency EC of S-phase showed proliferation (labelling index 2.2%) occurs mostly at the tumour margin suggesting the growth factors controlling ECs are different from those regulating tumour cells and that remodelling the existing vasculature might play a more important role than previously recognised. To investigate further ECtumour matrix interactions, the expression of cell adhesion molecules (CAMs) was examined. CAM expression mirrored that of EC proliferation with preferential expression on endothelium at the tumour periphery: expression of CAMs was also present on neoplastic cells. Thus, acquisition of CAMs by tumour cells together with EC phenotypic modulation might promote angiogenesis and metastasis. The angiogenic factor thymidine phosphorylase (TP) was examined in normal tissues and tumours. Although TP was expressed in ECs there was no correlation between expression in normal or neoplastic tissue and vascularity. Nevertheless, TP was elevated in small low grade tumours, in accordance with TP being chemotactic but non-mitogenic for ECs. A monoclonal antibody to flt-4, a candidate angiogenic factor receptor was generated and characterised. In contrast to the in-situ mRNA expression profile, a restricted pattern of protein expression was observed in normal tissues and variable expression in tumours.

Angiogenesis is an essential physiological process involved in wound repair, endometrial growth and embryogenesis and is tightly regulated in normal tissues. However, angiogenesis is also associated with some pathological conditions; in these conditions, angiogenesis eludes regulation and presents as either unabated (as in diabetic retinopathy and neoplasia), or as an inefficient process (as in ischaemic coronary disease). Regardless of this, all angiogenic mechanisms have a common biological basis, ergo, the shift of anti-angiogenic research has been towards biologically-based angiogenesis inhibitors; it is well established that these anti-angiogenic paradigms can be applied to inhibit the growth of solid neoplasms. / Antagonists of tumour-associated angiogenesis from a diverse range of sources have been identified and analysed, including agents capable of eliciting an apoptotic response in the endothelial cells lining the tumour vasculature. Tumour-associated microvascular endothelial cells, although derived from normal, host endothelial cells, exhibit differential characteristics which are able to be exploited, in order to induce endothelial cell apoptosis in tumour vessels, while normal, host vessels remain unaffected. / Thesis (PhDBiomedicalScience)--University of South Australia, 2005.

Angiogenesis is an essential physiological process involved in wound repair, endometrial growth and embryogenesis and is tightly regulated in normal tissues. However, angiogenesis is also associated with some pathological conditions; in these conditions, angiogenesis eludes regulation and presents as either unabated (as in diabetic retinopathy and neoplasia), or as an inefficient process (as in ischaemic coronary disease). Regardless of this, all angiogenic mechanisms have a common biological basis, ergo, the shift of anti-angiogenic research has been towards biologically-based angiogenesis inhibitors; it is well established that these anti-angiogenic paradigms can be applied to inhibit the growth of solid neoplasms. / Antagonists of tumour-associated angiogenesis from a diverse range of sources have been identified and analysed, including agents capable of eliciting an apoptotic response in the endothelial cells lining the tumour vasculature. Tumour-associated microvascular endothelial cells, although derived from normal, host endothelial cells, exhibit differential characteristics which are able to be exploited, in order to induce endothelial cell apoptosis in tumour vessels, while normal, host vessels remain unaffected. / Thesis (PhDBiomedicalScience)--University of South Australia, 2005.

Thesis (Ph. D.)--School of Pharmacy and School of Biological Sciences. University of Missouri--Kansas City, 2006. / "A dissertation in pharmaceutical sciences and molecular biology and biochemistry." Advisor: Joyce Tombran-Tink. Typescript. Vita. Title from "catalog record" of the print edition Description based on contents viewed Oct. 31, 2007. Includes bibliographical references (leaves 193-234). Online version of the print edition.

Thesis (Ph. D.)--University of Hong Kong, 2008. / Non-Latin script record

Thesis (M.Orth.)--University of Hong Kong, 2002. / Includes bibliographical references (leaves 122-142). Also available in print.