Title page, table of contents and introduction only. The complete thesis in print form is available from the University of Adelaide Library. / Apoptosis and inflammation have been considered to be linked mechanisms. Defective apoptosis may result in cell accumulation and prolonged half life of inflammatory cells in rheumatoid arthritis (RA). A similar phenomenon is seen in malignancy. Therefore, defects in apoptosis pathways that have been proposed to contribute to the pathogenesis of malignancy may also be seen in RA. It has been reported by many studies that treatments that induce apoptosis of malignant cells are advantageous for cancer treatment and this suggests that targeting apoptosis pathways may be important in the management of a variety of pathologies that involve abnormalities in cell proliferation. While apoptosis induction has been a common mechanism in the treatment of cancer, it has only recently been seriously considered to be effective in regulating proliferative cells in inflammation. This thesis provides important information regarding the TRAIL mediated pathway of apoptosis and possible factors that modulate the ability of this pathway to induce apoptosis in RA. / http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1286764 / Thesis (Ph.D.) -- University of Adelaide, School of Medical Sciences, 2007

Title page, table of contents and introduction only. The complete thesis in print form is available from the University of Adelaide Library. / Apoptosis and inflammation have been considered to be linked mechanisms. Defective apoptosis may result in cell accumulation and prolonged half life of inflammatory cells in rheumatoid arthritis (RA). A similar phenomenon is seen in malignancy. Therefore, defects in apoptosis pathways that have been proposed to contribute to the pathogenesis of malignancy may also be seen in RA. It has been reported by many studies that treatments that induce apoptosis of malignant cells are advantageous for cancer treatment and this suggests that targeting apoptosis pathways may be important in the management of a variety of pathologies that involve abnormalities in cell proliferation. While apoptosis induction has been a common mechanism in the treatment of cancer, it has only recently been seriously considered to be effective in regulating proliferative cells in inflammation. This thesis provides important information regarding the TRAIL mediated pathway of apoptosis and possible factors that modulate the ability of this pathway to induce apoptosis in RA. / http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1286764 / Thesis (Ph.D.) -- University of Adelaide, School of Medical Sciences, 2007

Title page, table of contents and introduction only. The complete thesis in print form is available from the University of Adelaide Library. / Apoptosis and inflammation have been considered to be linked mechanisms. Defective apoptosis may result in cell accumulation and prolonged half life of inflammatory cells in rheumatoid arthritis (RA). A similar phenomenon is seen in malignancy. Therefore, defects in apoptosis pathways that have been proposed to contribute to the pathogenesis of malignancy may also be seen in RA. It has been reported by many studies that treatments that induce apoptosis of malignant cells are advantageous for cancer treatment and this suggests that targeting apoptosis pathways may be important in the management of a variety of pathologies that involve abnormalities in cell proliferation. While apoptosis induction has been a common mechanism in the treatment of cancer, it has only recently been seriously considered to be effective in regulating proliferative cells in inflammation. This thesis provides important information regarding the TRAIL mediated pathway of apoptosis and possible factors that modulate the ability of this pathway to induce apoptosis in RA. / http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1286764 / Thesis (Ph.D.) -- University of Adelaide, School of Medical Sciences, 2007