Dissertations / Theses: 'Angiogenesis'

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PARMA, LAURA. "INTRAPLAQUE ANGIOGENESIS AND THERAPEUTIC TARGETING OF ANGIOGENESIS." Doctoral thesis, Università degli Studi di Milano, 2020. http://hdl.handle.net/2434/777113.

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In this thesis we have investigated different approaches to block intraplaque angiogenesis in atherosclerosis. Intraplaque angiogenesis is a physiological response to the increased oxygen demand in the plaque but also has adverse effects by facilitating intraplaque hemorrhage and influx of inflammatory mediators, resulting in plaque instability and consequent rupture. To study this phenomenon we used in vitro assays as well as the accelerated atherosclerosis vein graft model in ApoE3*Leiden mice, a unique model in which the formed plaque shows characteristics that highly resemble human atherosclerotic lesions, including intraplaque angiogenesis and hemorrhage and a high inflammatory cell content. We focused on different approaches to restore plaque stability via improving intraplaque oxygen levels as well as via blocking different growth factors signaling. Moreover we studied the effects of our treatments on the interaction between angiogenesis and inflammation both in vitro and in vivo.

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Small, Gary R. "Glucocorticoids and angiogenesis." Thesis, University of Edinburgh, 2005. http://hdl.handle.net/1842/29367.

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It was hypothesised that generation of endogenous glucocorticoids by 11βHSD1 within the vessel wall regulates angiogenesis. In vitro mouse aortic ring cultures established that physiologically-relevant concentrations of glucocorticoids inhibit angiogenesis in a glucocorticoid receptor-dependent manner. In addition 11βHSD1 was found to modulate glucocorticoid-induced angiostasis, for 11dehydrocorticosterone (a substrate for 11βHSD1) although angiostatic in C57B16 aortae did not inhibit angiogenesis in llβHSD1 deficient animals. In vivo using subcutaneous sponge implants in mice, endogenous glucocorticoids were found to inhibit angiogenesis: sponges in adrenalectomised mice grew more vessels compared to sponges from sham-operated animals. 11βHSD1 regulated the angiostatic effects of glucocorticoids, for cortisone (the human equivalent of 11dehydrocorticosterone), although angiostatic in controls did not inhibit angiogenesis in 11βHSD1 deficient mice. In pathology in cutaneous wounds and infracted myocardium endogenous glucocorticoids were found to inhibit angiogenesis. RU38486, (a glucocorticoids receptor antagonist) in comparison to placebo enhanced angiogenesis in both tissues. In similar studies in C57B16 or llβHSD1 deficient mice, 11βHSD1 was found to tonically repress angiogenesis and impair left ventricular remodelling post infarction. Thus 11βHSD1 deficient mice had increased myocardial revascularisation and preserved left ventricular function. In conclusion, by using in vitro, in vivo, and pathological models, endogenous glucocorticoids were seen to inhibit angiogenesis. In addition, 11βHSD1 regeneration of glucocorticoids tonically repressed angiogenesis and influenced left ventricular remodelling post myocardial infarction. Thus 11βHSD1 appears to be an attractive therapeutic target for the management of tissue revascularisation.

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Cunha, Filipa. "Controlling angiogenesis electrically?" Thesis, University of Aberdeen, 2016. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=232613.

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Physiological electrical fields (EFs) can direct some important angiogenic responses of endothelial cells such as directional migration, orientation and proliferation. It has been reported that human umbilical vein endothelial cells (HUVEC) and human microvasculature endothelial cells (HMEC) migrate in opposite directions; to anode and cathode, respectively. Although, in the present study both cell types migrated toward the cathode, HUVEC directedness started at 50mV/mm while HMEC directedness started at 100mV/mm. These results suggest that EFs can promote wound healing by directing endothelial cells to the wound site since EFs of 40 to 100 mV/mm are present in normal healing wounds. EFs also increased cell proliferation and orientated the cleavage plane of dividing cells perpendicular to the EF vector in both endothelial cell lines. The present study showed for the first the time that EFs upregulated the expression of the chemokine receptors CXCR4 and CXCR2 as well as upregulating the levels of phosphorylation of both chemokines in HUVEC and HMEC. It also showed differences of chemokine receptors used by HUVEC and HMEC cells in the early stages of electrotaxis. Ionizing radiation has been shown to directly phosphorylate VEGF receptors in the absence of its ligand VEGF. A question was raised: in the absence of the ligands are EFs able to directly phosphorylate the chemokine receptors? Results showed that in starved HUVEC cells EFs had no effect on the phosphorylation levels of CXCR4 and CXCR2 however in starved HMEC cells an EF may have a direct effect on the phosphorylation levels of CXCR4 and CXCR2. Therefore, EFs represent a physical stimulus that could directly phosphorylate proteins in the absence of its ligand. This work substantiate the importance of endogenous EFs in directing endothelial cells and suggests that EFs might be developed as a component in the clinic to control angiogenesis.

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Järvenpää, J. (Jouko). "Placental angiogenesis and angiogenesis related risk factors in severe pre-eclampsia." Doctoral thesis, University of Oulu, 2008. http://urn.fi/urn:isbn:9789514288760.

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Abstract The incidence of pre-eclampsia (PE) is 2–7% in different populations and in the worst cases PE may threaten the survival of both mother and newborn; its pathogenesis is not resolved. Field literature today considers PE an angiogenic disorder. Coordinated vascularization is essential for placental development. We wanted to find novel factors in the etiology of PE, and focused our attention on angiogenesis, inherited thrombophilia and folate-homocysteine metabolism. Homocysteine inhibits endothelial cell proliferation, which is closely related to angiogenesis. We performed gene expression profiling of placental tissue using microarray chips, studied the prevalence of factor V Leiden (FVL), prothrombin (F5) G20210A and methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism in patients with severe pregnancy complications and normal controls, compared the expression of the placental adiponectin, leptin and their receptor genes and the relationship of each to trophoblast apoptosis and further, studied the effect of folic acid fortified mineral water on plasma homocysteine concentration during pregnancy. Gene expression profiling revealed downregulation of nine and upregulation of four genes. Interestingly, in one PE patient with cord compression during delivery the profile resembled that observed in normals. The expression level of the leptin and the adiponectin receptor 1 (ADIPOR1) genes was significantly higher in PE. No other significant expression changes were observed. The rate of apoptosis was higher in patients with PE. The FVL prevalence was 9.5%, in PE cases and 1.8% in the controls; a difference of 7.7%, (95% CI 2.0–13.4%). No statistical difference was found in other polymorphisms.. Maternal serum folate concentration increased in our intervention group, but decreased in the control group (p < 0.05). The plasma homocysteine concentrations decreased more in the intervention group (p < 0.001). The expression of angiogenesis-related placental genes can be altered in PE and cord compression cases. The activity of adipocytokine genes in PE may mean that they have a role in placental angiogenesis and apoptosis. Women with FVL may have an increased risk of PE. Fortified mineral water will help us to ensure that especially pregnant women achieve adequate folate intake.

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Sköldenberg, Erik. "Angiogenesis in childhood malignancies." Doctoral thesis, Uppsala University, Department of Surgical Sciences, 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3481.

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Angiogenesis is necessary for the growth and spread of solid tumors. In these studies angiogenesis was measured in childhood malignancies in general and in Wilms’ tumor in particular, and cutting needle biopsy (CNB) specimens were evaluated for diagnosis in childhood renal tumors.

In 33 patients with Wilms’ tumor, tumor capillaries were quantified, expression of angiogenic growth factors in tumor tissue investigated, and concentrations of angiogenic growth factors in serum measured. Reference values for angiogenic growth factors were obtained in 80 healthy adults (fibroblast growth factor 2 [FGF-2], vascular endothelial growth factor A [VEGF-A]) and 94 healthy children (angiogenin [ANG], epidermal growth factor [EGF], FGF-2, hepatocyte growth factor [HGF], tumor necrosis factor alpha [TNFA] and VEGF-A) aged 0.5-18 years. These reference values were compared with values in sera taken at diagnosis in 268 children with tumors and leukemias. CNB specimens were evaluated in 25 children with renal tumors.

A large number of capillaries was an independent prognostic factor for a poor outcome in Wilms’ tumor. Angiogenic growth factors were expressed in Wilms’ tumor tissue, and elevated concentrations of HGF and VEGF-A were found in both benign and malignant tumors. HGF was increased in leukemia, and TNFA was increased in leukemia, lymphoma and neuroblastoma. CNB, which proved to be a safe procedure, had a sensitivity of 76%.

These studies have demonstrated that quantification of capillaries is a prognostic factor in Wilms’ tumor and that HGF, TNFA and VEGF-A are frequently elevated in sera from children with cancer. Quantification of capillaries in tumor tissue and of circulating angiogenic growth factors would therefore seem to be of clinical relevance in managing children with cancer.

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Mellberg, Sofie. "Molecular Regulation of Angiogenesis." Doctoral thesis, Uppsala universitet, Institutionen för genetik och patologi, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-9418.

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Angiogenesis, de novo formation of blood vessels from the pre-existing vasculature, is crucial in embryo development, and in processes in the adult such as wound healing and ovulation. Angiogenesis is also involved in pathological conditions such as cancer and chronic inflammatory diseases, which are propagated by dysregulated, excess angiogenesis. On the other hand, lack of functional vessels and poor blood flow is a major problem in myocardial and peripheral ischemia. A detailed understanding of the molecular mechanisms underlying angiogenesis is of vital importance for the development of drugs to regulate angiogenesis. The aim of this thesis has been to identify genes involved in regulation of angiogenesis. We have investigated gene expression over time in endothelial cells (ECs), using different in vitro models. We show that the proteoglycan endocan is upregulated in ECs invading a fibrin matrix in response to vascular endothelial growth factor (VEGF)-A. There was increased expression of endocan in renal tumour cells and tumour vessels compared to normal renal tissues, indicating that endocan might have a role in tumour growth and tumour angiogenesis. We also show that vascular endothelial protein tyrosine phosphatase (VE-PTP) is induced in ECs during differentiation into vessel structures in a three dimensional collagen matrix. Silencing of VE-PTP disrupts vessel formation and increases the activity of VEGF receptor-2 (VEGFR-2) and downstream signalling, leading to increased EC proliferation. This presents a possible mechanism for the failure of vessel formation, as EC morphogenesis requires growth arrest of the cells. We also show that VE-PTP and VEGFR-2 are closely associated in resting ECs. VEGF-A stimulation leads to rapid loss of association, coinciding with increased phosphorylation of VEGFR-2. The function of VE-PTP in vivo was investigated using the zebrafish model. We demonstrate specific expression of a zebrafish VE-PTP orthologue (zVE-PTP) in the developing vasculature. Silencing of zVE-PTP leads to defective vessel sprouting and branching, indicating a critical role for zVE-PTP in development of the zebrafish vasculature. In conclusion, this thesis presents gene regulation during endothelial cell morphogenesis and details the expression pattern of endocan and the function of VE-PTP in regulation of VEGFR-2-driven angiogenesis.

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Zetterberg, Eva. "Angiogenesis in myeloproliferative disorders /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-383-3/.

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Sköldenberg, Erik. "Angiogenesis in childhood malignancies /." Uppsala : Institutionen för kirurgiska vetenskaper, Uppsala universitet, 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3481.

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O'Brien, Timothy Stephen. "Angiogenesis in bladder cancer." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.388846.

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Chan, Hock Yee. "Studies on tumour angiogenesis." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.299162.

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Peirsis, Pages Maria. "Anti-Angiogenesis in neuroblastoma." Thesis, University of Bristol, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.529877.

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Patel, Neel. "Radionuclide imaging of angiogenesis." Thesis, University of Oxford, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.600030.

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Angiogenesis is a fundament al process in the survival, growth and spread of cancers. In recent years several therapies have been developed to interfere with this process. Despite initial optimism these agents have rarely provided durable clinical responses. Methods capable 0f assessing angiogenesis are required to help develop effective anti-angiogenic approaches Radionuclide imaging is one potential method of assessing angiogenesis. VEGF and integrin expression are two key factors in regulation of angiogenesis in tumours and provide potential targets for radionuclide imaging of angiogenesis. This thesis investigates whether targeting of VEGF and integrins can be performed to image angiogenesis and if treatment with antiangiogenic therapy can be detected via such imaging. VEGF imaging was successfully performed by radiolabelling bevacizumab, a monoclonal antibody directed against all isoforms of VEGF, with 111 indium for SPECT imaging. This agent was validate in vitro and in vivo mouse xenograft models, and appears to bind to matrix and cell membrane associated VEGF within tumours. lntegrin imaging was attempted using 99Tc-maraciclatide, another SPECT imaging agent. This is a commercial agent based on the RGD tripeptide sequence and binds primarily to α,β3 and α,β5 integrins. It was assessed in a clinical trial and compared with histological markers of angiogenes' in patients with colorectal, renal and breast tumours. There was an inverse relationship between 99mTc•maraciclatide uptake and β13 vascular density but no correlation with other angiogenic markers. Both tracers were investigated in a preclinical xenograft model with antiangiogenic therapies Rapamycin, an mTOR inhibitor, increased uptake of 111ln-bnDTPA-bevacizumab and decrease uptake of 99"'Tc-maraciclatide. These responses corresponded with an increase in VEGF an decrease in β3 integrin levels in the tumours. Rapamycin therapy was also associated with reduction in blood vessel number and changes in perfusion as demonstrated by DCE•MRI. The effect of bevacizumab therapy on 99Tc•maraciclatide uptake was also investigated. Bevacizumab had no significant effect on either 99mTc-maraciclatide uptake or β3 integrin levels. These preliminary results demonstrate that both radiotracers have potential for imagin, angiogenesis and detecting response to angiogenic therapies. They also highlight the complex nature of the angiogenic process and that further work is necessary to determine the clinical usefulness of these agents.

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Fox, Stephen B. "Angiogenesis in human cancer." Thesis, University of Oxford, 1996. http://ora.ox.ac.uk/objects/uuid:da4c4e35-7203-4efe-8716-109b5b1c4941.

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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.

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Scott, A. "Modulators of retinal angiogenesis." Thesis, University College London (University of London), 2014. http://discovery.ucl.ac.uk/1427875/.

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Angiogenesis is the sprouting of new capillaries from pre-existing vessels and is driven by hypoxia. While physiological hypoxia in the retina is paramount to regulating physiological angiogenesis, pathological ischemia is a cause of pathological neovascularisation and a large proportion of blindness worldwide. The aim of this thesis is to explore ways of redirecting neovascularisation towards healthy revascularisation. I do this by looking at ways of modulating angiogenesis at an early stage in Oxygen-induced retinopathy (OIR) in mice. This model is based on vessel depletion by exposure to hyperoxia, which results in acute retinal hypoxia upon return to room air. This hypoxia then triggers neovascularisation in the remaining vessels after 5 days. Vascular endothelial growth factor (Vegf) plays a critical role in development and disease of the retinal vasculature. Genetic ablation of astrocyte-derived Vegf surprisingly showed minor impacts on retinal vasculature development. However, it had a vessel stabilizing role during the hyperoxic phase and also promoted vessel regeneration in the hypoxic phase. In other experiments, it was shown that C3H/HeJ mice, which contain the retinal degeneration 1 (Rd1) mutation (Pde6bRd1) and have abnormally thin retinas, do not become ischemic despite vaso-obliteration and do not develop neovascularisation. This demonstrates that maintaining a balance between oxygen demand and supply at the onset of ischemia critically influences the angiogenesis outcome. Using this model, vascular tortuosity was established as an early phenotype of OIR possibly predictive of neovascularisation. Finally, in other experiments, it was shown that inflammation can modulate hypoxia. Subcutaneous injection of lipopolysaccharide (LPS) in mice with hypoxic retinas, led to bilateral reduction of hypoxia, reduction of VEGF and healthy revascularization. From a conceptual point of view, this is a paradigm changer because it shows for the first time that it is possible to change hypoxia in the retina without changing the oxygen (i.e. vascular) supply.

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Trouillon, Raphael. "Electrochemical biosensors and angiogenesis." Thesis, Imperial College London, 2010. http://hdl.handle.net/10044/1/6120.

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Electrochemical methods provide attractive sensing techniques for biology. Electrochemical devices can be easily manufactured, miniaturized and are sometimes the only direct sensing method available. However, stability of these sensors is problematic, as foreign-body type reactions may induce distortions of the signal (biofouling). As a consequence, investigating the interactions with the biological matrix is of paramount importance to achieve reliable sensing. Different types of electrodes (boron doped diamond and different preparations of glassy carbon) and various electrode coatings were tested, in the presence of biological molecules. The results showed that boron doped diamond and fibronectin coated sensors offer good stability, even in the presence of high concentrations of proteins. A generally applicable protocol to assess the quality of electrode materials in biofouling conditions is also presented. Fibronectin has also been found to be a highly biocompatible coating, perfectly suited for cell-based measurements. This fibronectin coating was used on an electrode array to study the pathway leading to angiogenic factor induced nitric oxide release. Vascular endothelial growth factor, a well known angiogenic factor, was initially used and allowed me to setup a reliable and robust protocol for the use of electrode arrays in biology. It was then demonstrated that angiogenin, another angiogenic factor, leads to nitric oxide exocytosis through PI-3 kinase transduction.

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Elstow, S. F. "The angiogenesis factors of the eye and their relationship to tumour derived angiogenesis factors." Thesis, University of Manchester, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.355902.

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Jackson, Shaun William. "Purinergic angiogenesis : an investigation of the role of extracellular nucleotide mediated signaling in angiogenesis." Master's thesis, University of Cape Town, 2006. http://hdl.handle.net/11427/9506.

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Includes bibliographical references.
Angiogenesis refers to the growth and maturation of new vessels from pre-existing differentiated blood vessels. Co-ordination of angiogenic responses is crucial for a wide range of physiological and pathological processes. In particular, angiogenesis is hypothesized to facilitate tumour growth and promote metastasis, prompting research into anti-angiogenesis based cancer therapies. CD39/NTPDasel is an ectoenzyme expressed by vascular endothelium that hydrolyses extracellular nucleoside di- and triphosphates to the monophosphate derivatives. As such, this enzyme has a role in modulating endothelial responses to mucleotides that bind specific receptors termed Purinergic-type 2(P2) receptors. Since a number proliferation and migration in vitro, we propose that nucleotide signalling influences the process of angiogenesis in vivo.

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Vitaliti, Alessandra. "Inhibition of tumor induced angiogenesis /." [S.l.] : [s.n.], 1999. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=13409.

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Dixelius, Johan. "Endothelial differentiation and angiogenesis regulation." Doctoral thesis, Uppsala University, Department of Genetics and Pathology, 2002. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3009.

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Angiogenesis can be defined as the formation of new blood vessels from pre-existing ones. Angiogenesis is required for development and maintenance of our vascular system and thus of fundamental importance to our existence. The endothelial cells that line the inside of the vessels de-differentiate, migrate, proliferate and re-differentiate during angiogenesis. Angiogenesis is tightly regulated, controlled by several angiogenic factors of various classes that promote angiogenesis but also by anti-angiogenic factors that counteract the effect of the pro-angiogenic factors. We have examined three factors involved in angiogenesis regulation, Vascular endotelial growth factor (VEGFR) -3, the matrix protein laminin-1 and the collagen XVIII derived fragment endostatin.

Five tyrosine phosphorylation sites in the cytoplasmic tail of VEGFR-3 were identified by phosphopeptide mapping (PPM). The data was confirmed by PPM using point-mutated receptors generated by site-directed mutagenesis.

Laminin-1 was found to promote angiogenesis in the chicken chorioallantoic membrane assay and in a synergistic fashion together with suboptimal levels of fibroblast growth factor 2 (FGF-2) in embryoid bodies. Laminin-1 also promoted endothelial tubular morphogenesis in vitro, and upregulated the expression of the endothelial differentiation marker Jagged-1.

Endostatin was shown to affect endothelial FGF-2-induced cell survival and morphogenesis. This was a result of direct binding to endothelial cells and induction of tyrosine phosphorylation of many proteins including the adaptor protein Shb. The apoptotic and morphogenic responses induced by endostatin was shown to be dependent on Shb. Further, endostatin inhibited endothelial migration and affected molecules implicated in migration. In particular, FGF-2 induced actin reorganization, and β-catenin regulation was modulated by endostatin.

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Wahlquist, Hanna. "Hypoxia and Angiogenesis in IUGR." Thesis, Uppsala University, Department of Medical Biochemistry and Microbiology, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-9316.

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BACKGROUND: Intrauterine growth restriction (IUGR) is a condition where the infant fails to reach its genetic growth potential due to numerous factors. IUGR foetuses are associated with high perinatal mortality and morbidity. This study investigated if hypoxia might be involved during gestation, and whether if hypoxia may have an impact on the development of the placenta, through regulation of various angiogenic factors, such as HIF-1_, VEGF, PIGF, VEGFR-1 and CD31. METHOD: Each sample of placental tissue was stained by immunohistochemisty for HIF-1_, VEGF, PIGF, VEGFR-1 and CD31. The intensity of staining was graded and the difference between the normal term placentas and the IUGR term placentas were evaluated. RESULTS: HIF-1_ was found to be upregulated in the normal term placental tissue, and VEGFR-1 was found to be upregulated in the IUGR term placental tissue. The other antibodies did not show any significant difference and PIGF failed to show any positive staining. CONCLUSIONS: Further studies on hypoxia in IUGR would be beneficial.

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Barendsz-Janson, A. F. "Predictive models of tumor angiogenesis." [Maastricht : Maastricht : Universiteit Maastricht] ; University Library, Maastricht University [Host], 1998. http://arno.unimaas.nl/show.cgi?fid=8524.

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Hellebrekers, Debby Maria Elisabeth Ida. "Epigenetic regulation of tumor angiogenesis." Maastricht : Maastricht : Universiteit Maastricht ; University Library, Universiteit Maastricht [host], 2006. http://arno.unimaas.nl/show.cgi?fid=5612.

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Bråkenhielm, Ebba. "Angiogenesis in obesity and cancer /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-578-6/.

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Zhang, Li Lyna. "Mechanistic studies of endometrial angiogenesis." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.339028.

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Mavrou, Athina. "Targeting angiogenesis in prostate cancer." Thesis, University of Bristol, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.654119.

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Angiogenesis, primarily induced by vascular endothelial growth factor (VEGF). has been shown to be required for prostate cancer development and metastasis. Alternatively spliced isoforms associated with cancer progression have been described in all of the hallmarks of cancer, including angiogenesis. VEGF mRNA is alternatively spliced at the terminal exon, to produce two families of isoforms. The pro- angiogenic family, VEGFxxx. has been shown to be up-regulated in several cancer types including prostate cancer, whereas the antiangiogenic family is preferentially expressed in normal non-angiogenic tissues, but down-regulated in prostate cancer. One of the molecules shown to be involved in the regulation of VEGF alternative splicing is SRPK1. This is a protein kinase that phosphorylates the splicing factor SRSF1 and favours the production of the proangiogenic VEGF isoform. I therefore tested the hypothesis that SRPK1 regulates VEGF mRNA splicing in prostate cancer and that down-regulation of this kinase would increase the production of the anti-angiogenic isoform, preventing angiogenesis and tumour growth. I also tested the hypothesis that SRPK1 and SRSF1 are up-regulated in prostate cancer, given the extensive mis-regulation of splicing events in this malignancy. Studies on prostatectomy samples from patients with prostate cancer showed an up -regulation of SRPK1 and SRSF1 in malignant compared to benign tissues. In addition, a panel of prostate cancer cell lines showed increased expression of SRPK1 when compared with primary prostate epithelial cells. Stable SRPK1 knock-down in PC-3 and LnCap prostate cancer cells and inhibition of SRPK1 using small molecule inhibitors caused a reduction in the pro - angiogenic VEGF expression and splice factor phosphorylation . In vivo, inhibition of SRPK1 by lentiviral knockdown and a small molecule inhibitor resulted in a reduction of prostate tumour growth and decreased vascular density. This study identifies a molecular mechanism that regulates angiogenesis in prostate cancer and provides evidence for the potential use of an SRPK1 inhibitor in the treatment of prostate cancer.

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Bourghardt, Peebo Beatrice. "Angiogenesis from a new perspective." Doctoral thesis, Linköpings universitet, Oftalmiatrik, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-73137.

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Angiogenesis is the emergence of new blood and lymph vessels from existing ones. In the pathologic form it contributes to the onset and progression of numerous different human disorders such as cancer, inflammation, atherosclerosis and blinding eye diseases. There exist a number of models to study angiogenesis, both in vitro and in vivo, but there is no single perfect model so far. Consequently there is a need to develop new angiogenesis assays for evaluating blood and lymph vessel behaviour in different physiologic settings. The aim of this thesis was to gain insight into in vivo angiogenesis introducing a new technique in an inflammatory corneal model. The method involved in vivo examination of the cornea and subsequent comparison of in vivo findings with ex vivo immunohistochemical analysis of the same tissue samples. An existing suture model for inflammatory angiogenesis in the cornea was modified for in vivo observations with a clinically-approved corneal confocal microscope. In this thesis, corneal lymph vessels were characterized for the first time in vivo and findings from the experimental bench could be applied in a clinical setting, where presumed lymphatics were observed in a corneal transplant patient with rejection. Furthermore, the technique was extended to investigate time-lapse processes in sprouting and regressing capillaries, and led to a number of new observations. CD11b+ myeloid cells constitute the first bulk of infiltrating inflammatory cells and contribute to inflammatory sprouting and regression in numerous ways including pre-patterning of the corneal stroma and guiding of capillary sprouts. Newly formed hemangiogenic sprouts are perfused with a slow-moving fluid and have a lumen. In blood vessel regression, capillary remodeling occurred by abandonment of sprout tips in close association with macrophages and vascular loops formed by presumed intussusceptive angiogenesis. In addition, a network of pericyte- and endothelium-free basement membrane tubes was formed after desertion or degradation of vascular endothelium in former corneal capillaries. In conclusion, we introduce a new in vivo technique for investigating angiogenesis in a corneal model were in vivo findings can be interpreted with ex vivo definitions of specific cell types by immunohistochemistry. Findings from pre-clinical experiments have been possible to apply in a clinical setting when examining patients with corneal pathology.

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Bainbridge, James William Braithwaite. "Gene therapy for ocular angiogenesis." Thesis, University College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.409631.

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Ahmed, Shahzada Khuram. "Angiogenesis in the nasal mucosa." Thesis, University of Birmingham, 2013. http://etheses.bham.ac.uk//id/eprint/4032/.

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Nasal polyposis is a common disease affecting 2-4% of the general population. The aetiology and pathogenesis are far from clear. Recent publications have suggested up-regulation of several pro-angiogenic factors including VEGF. The aim of this study was to assess and quantify the degree of angiogenesis in nasal polyposis and to determine if angiogenesis was the driving force behind polyposis. We started by developing a novel triple stain to assess remodelling in the nasal mucosa. For the first time we were able to categorically refute the common belief of angiogenesis driven polyposis. We then carried out genomic studies and identified upregulation of genes controlling the cell cycle and apoptosis, suggesting cell turnover is an important part of the pathogenesis of nasal polyps. Our gene expression data was confirmed by TUNEL staining, indicating an increased level of apoptosis in nasal polyp tissue, counterbalancing the increased cell proliferation. Inflammatory genes are also upregulated, however the data collected so far cannot distinguish between different types of inflammatory response. We carried out proteomic studies using the lu minex system but this did not clarify the situation despite using matched samples that were used in the gene array. They highlight the protein differences occurring in the polyps themselves. We have shown chemoattractants for eosinophils & macrophages (which are found in polyps), and significantly in iNOS, which is novel.

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Ferguson, Mary L. "Angiogenesis in human lung tumours." Thesis, University of Oxford, 2008. http://ora.ox.ac.uk/objects/uuid:865de25c-1ac3-4a30-85fa-a9fc677bfcc2.

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Angiogenesis, the growth of new blood vessels, is vital to tumour growth. Prevailing dogma has been that tumours cannot grow without angiogenesis. Based on this premise, anti-angiogenic drugs are used clinically. However, the principle of angiogenesis as an absolute requirement for tumour growth has been challenged with reports that many tumours are entirely or partially non-angiogenic. This study describes and quantifies characteristics of non-angiogenic non-small cell lung tumours, demonstrates non-angiogenic growth in small-cell/neuroendocrine lung tumours and investigates the underlying pathogenetic processes by comparison with angiogenic lung tumours. Hypoxia is an important stimulus for angiogenesis. Differences in response to hypoxia may determine whether a tumour produces new vessels. In order to test this, levels of. necrosis, often considered a surrogate marker of hypoxic stress, were quantified but no difference in quantity of necrosis was found Moreover, immunohistochemical investigation of hypoxia and angiogenesis factors provided no unambiguous explanation for the differences in angiogenesis. Significant differences were seen, however, in fibrosis and inflammation, which were both greater in angiogenic tumours. Differences were greater for lymphocytes rather than cells of the ‘innate’ immune system. This provided an alternative hypothesis: angiogenesis occurs during wound healing and in the growth of granulation tissue, so it is possible that tumour angiogenesis is a response to factors produced by immune cells rather than the tumour itself. A tumour’s angiogenic status may, therefore, be determined by the response it provokes from the immune system. Further work to test this theory would compare levels of immunogenic factors such as Tumour Necrosis Factor and tumour cell surface antigens such as the HLA class I molecules. The study concludes with an investigation into the molecular basis of non-angiogenic growth using the technique of comparative genomic hybridisation (CGH) which allows amplifications and deletions of areas of DNA to be calculated. High-resolution array CGH was evaluated against conventional CGH, and the results compared with previous RNA studies from our laboratory. These revealed a set of genes with consistent changes in both RNA and DNA, several of which form part of known angiogenic and inflammatory pathways.

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Chen, Wei. "Modelling of tumour-induced angiogenesis." Thesis, Northumbria University, 2015. http://nrl.northumbria.ac.uk/30235/.

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Controlled by extracellular signals, tumour-induced angiogenesis is a crucial step in the development of tumours. Among the many cell signals already identified, the VEGF and Notch signalling pathways play a critical role in controlling endothelial cells (ECs) during angiogenesis. Although this regulatory mechanism has become a current research focus in biology, its computational modelling is still rare. We focus on developing a computational model to simulate the VEGF and Notch signalling regulatory mechanism to perceive the micro procedure of angiogenesis in silico and fill the gap between biology and computer engineering. We first developed a mathematical model with nonlinear partial differential equations (PDEs) to describe the migration of endothelial tip cells during tumour-induced angiogenesis. The simulation results show that both chemotaxis and haptotaxis have impacts on the migration of ECs in velocity and density, and the impacts depend on the gradient and direction of tumour angiogenenic factor (TAF), and fibronectin, implying a possible malignant mechanism for some subgroups of tumour. We then developed the model further to simulate the regression, recurrence or clearance of tumours due to tumour cytotoxic factors, including the immune system and drugs delivered through the vessels formed during angiogenesis, providing a broader understanding of tumours. Based on the PDE model which provided parameters of continuum mathematical model, we finally developed an enzymatic catalysed regulating model in the form of ordinary differential equations (ODEs) with agent-based modelling (ABM) using Java and MATLAB languages, to visually realise the sprouting regulated by VEGF and Notch signalling during angiogenesis. The simulation describes the process of how an endothelial stalk cell becomes an endothelial tip cell, and sprouts under the influence of VEGF and Notch signalling, revealing the relationship between sprouting and branching. As the simulation results are consistent with reported in vitro and in vivo assays, the study bridges angiogenesis research and computer modelling from the dynamic regulatory mechanism perspective, offering a huge leap over previous studies in computationally simulating tumour-induced angiogenesis. It is hoped that the results will assist researchers in both the experimental and theoretical angiogenesis communities to improve understanding of the complexity and identify the fundamental principles of angiogenesis, whilst also using modelling approaches that will enrich knowledge for computational scientists in this field.

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Dennie, Joëlle 1970. "NMR imaging of tumor angiogenesis." Thesis, Massachusetts Institute of Technology, 1997. http://hdl.handle.net/1721.1/43595.

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Thesis (S.M.)--Massachusetts Institute of Technology, Dept. of Nuclear Engineering, 1997.
Includes bibliographical references (leaves 66-69).
Cancer remains a major medical problem accounting for over 500,000 deaths in the US annually. A common feature of most human tumors is their ability to induce the proliferation of new blood vessels, i.e. angiogenesis. Considerable evidence now exists which demonstrates that these tumor vessels are associated with a distinct range of morphological and physiological properties which are not present in normal tissue vasculature. Several studies now document that in a wide variety of tumor models, average tumor vessels have diameters two times those of normal tissue vessels. NMR techniques based on magnetic susceptibility mechanisms are sensitive to varying sizes of blood vessels. By using gradient echo (GE) and spin echo (SE) pulse sequences and different concentrations of an exogenous contrast agent, it is possible to determine the signal contribution from small versus large vessels by examining the change in T2 and T2* rates ([delta]R2 and [delta]R2*), i.e. the ratio of [delta]R2* to [delta]R2 increases with vessel size. This ratio provides an index for the average size of vessels within a voxel. The central goal of this research was to utilize such a tool in order to obtain a regional picture of the tumor vascular bed. Rats, inoculated with C6 glial cells, underwent an MR imaging series nineteen days after implantation, which comprised conventional SE and GE images prior to and following serial injections of an equilibrium iron oxide contrast agent (MION). Regions within the tumor and in the contralateral normal gray matter were identified. The change in the T2 rate and T2* rate ([delta]R2 and [delta]R2*) were calculated for each region. Since susceptibility contrast mechanisms designed to study the distribution of vessel sizes rely entirely on the compartmentalization of the contrast agent within the vasculature, the first set of experiments was designed to demonstrate the stability of MION to remain within the vasculature, despite the disruption in the blood brain barrier. The second experiments measured [delta]R2 and [delta]R2* as a function of contrast agent concentration and TE. The MR measurements were compared with predicted values of [delta]R2 and [delta]R2* made from histological assessment of vessel sizes and theoretical Monte Carlo simulation results. The steady state measurements of [delta]R2 and [delta]R2* in the first experiments demonstrated that once the maximum contrast agent concentration had been reached, the values of [delta]R2 and [delta]R2* remained stable over 90 minutes, suggesting that MION remains within the vasculature. In the second experiments, significant differences were observed between the tumor and contralateral deep gray matter. Specifically, the ratio of ([delta] R2*/ ([delta]R2 was greater in the tumor than the normal brain, by a factor of 1.9 ± 0.2. From histologic sections and numerical simulations, the corresponding ratio was predicted to be 1.9 ± 0.1. These ratios are suggestive of a greater relative density of large vs small vessels. Maps of the ratio [delta]R2*/[delta]R2 were also produced on a pixel by pixel basis. Regions of high intensity on these maps (indicating a higher ratio of [delta]R2*/[delta]R2) corresponded well with the location of the tumor as determined using conventional images.
by Joëlle Dennie.
S.M.

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Parsonson, Louis. "Modelling angiogenesis in three dimensions." Thesis, University of Nottingham, 2015. http://eprints.nottingham.ac.uk/29075/.

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The process through which new blood vessels are formed within the body is known as angiogenesis. An essential part of our survival, it has also been implicated more recently in many diseases both in terms of induced growth, and abnormal vascular structure. Angiogenesis is characterized as two processes, the development of a vascular network during embryonic growth and the production of new blood vessels. This work focuses on the latter, and seeks to develop a robust, three-dimensional model for simulating blood vessel growth and the attendant processes of blood flow and mass transfer within the simulated system. A system was developed which utilises medical imaging scan data (specifically, MicroCT) as the initial conditions from which a network of vessels is grown. This is combined with GPU accelerated simulations of fluid dynamics, with the intention of providing a technique for future use in predictive medicine and therapeutic simulation.

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Yi, Ming. "Extracellular matrix proteins and angiogenesis /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2003. http://wwwlib.umi.com/cr/ucsd/fullcit?p3091204.

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Åkerman, Maria E. "Targeting and inhibiting tumor angiogenesis /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2005. http://wwwlib.umi.com/cr/ucsd/fullcit?p3166405.

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Zhao, Yang. "Novel Regulators of Tumour Angiogenesis." Thesis, The University of Sydney, 2015. http://hdl.handle.net/2123/15496.

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The work in this thesis describes two novel inhibitors of tumour angiogenesis, both of which target the vasculature. One is a first-in-class oligonucleotide-based inhibitor (Blockmir CD5-2) that normalises tumour angiogenic vessels, the other, an endogenously expressed gene (ARHGAP18) that is essential for the stabilisation of blood vessels. CD5-2 is an oligonucleotide based drug that inhibits the binding of miR-27a to a specific target in endothelial cells, VE-cadherin, resulting in a modest increase in its expression. CD5-2 administration to tumour bearing mice induces structural and functional normalisation of tumour vasculature and results in retardation of tumour growth likely through enhanced distribution of CD8+ T cells within the tumour parenchyma, and increased tumour cell apoptosis. The strength of the effects of CD5-2 in vivo are postulated to lead to significant and broad range of downstream pathways activated as a result of enhancing the expression of VE-Cadherin. ARHGAP18, a member of the RhoGTPase family, acts as a negative regulator of vessel generation and maturation in endothelial cells. However, in tumour cells ARHGAP18 has opposite effects where overexpression results in promotion of proliferation and migration. Thus, ARHGAP18 may impact tumour growth through its action on two of the major compartments.

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Twomey, Catherine T. "Novel cytoskeletal regulators of angiogenesis." Thesis, University of Bristol, 2017. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.742988.

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Axelsson, Hans. "Prostaglandins and angiogenesis in experimental cancer /." Göteborg : Department of Surgery, Institute of Clinical Sciences at Sahlgrenska Academy, University of Gothenburg, 2010. http://hdl.handle.net/2077/21933.

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Cabrerizo, Granados David 1993. "Endothelial Snail1 in angiogenesis and tumorigenesis." Doctoral thesis, Universitat Pompeu Fabra, 2020. http://hdl.handle.net/10803/670305.

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Snail1 is a transcriptional factor with a great relevance in tumor development as it is required for epithelial to mesenchymal transition and activation of cancer-associated fibroblasts (CAF). In this thesis, we reported that tumor endothelial cells did also express Snail1, being key for angiogenesis, by promoting endothelial cell migration, invasion and tubulogenesis in vitro. Those roles are associated to Snail1 induction by FGF2 and VEGFA, leading to gene expression profile change in endothelial cells and modulation of their activation status. Specific Snail1 depletion in the endothelium of adult mice does not promote an overt phenotype; however, it controls angiogenesis and vessel morphology in Matrigel plug assay. Moreover, endothelium-specific Snail1 depletion in the MMTVPyMT breast cancer murine model delays the initiation of neoplasms, being less advanced and with a papillary morphology, which was corroborated by orthotopic breast tumor inoculation model. These in vivo effects are associated to the inability of Snail1-deficient endothelial cells to promote a full in vitro and in vivo activation of fibroblasts through a reduced FGF2 and CXCL12 signaling; as well as to sustain a complete in vivo angiogenesis, with wider and less invasive neo-vessels. Similar changes on tumor onset and morphology are observed by pretreatment on MMTV-PyMT mice with the angiogenic inhibitor bevacizumab. Checking those results in human breast tumor samples, we could recapitulate most of the findings of our mouse models. Altogether, these findings establish a new role for Snail1 in endothelial cells, not only in angiogenesis but also in tumor onset, development and phenotype
Snail1 es un factor de transcripción con gran relevancia en el desarrollo tumoral, siendo necesario para la transición epitelio-mesénquima y la activación de fibroblastos asociados al cáncer (CAF). En esta tesis, hemos reportado la expresión de Snail1 en células endoteliales de tumor, jugando un papel fundamental en angiogénesis, promoviendo su migración, invasión y tubulogenesis in vitro. Estas funciones están asociadas a la inducción de Snail1 por FGF2 y VEGF-A, que generan un cambio en el perfil de expresión génica en las células endoteliales y modulan su estado de activación. La depleción específica de Snail1 en el endotelio de ratones adultos no supone un cambio fenotípico evidente; sin embargo, sí controla la angiogénesis y la morfología de los vasos en ensayos de plugs de Matrigel. Además, la eliminación específica de Snail1 en el endotelio del modelo murino de tumores de mama espontáneos MMTV-PyMT provoca el retraso en la iniciación de tumores, siendo éstos menos avanzados y con una morfología papilar. Estos efectos in vivo están asociados a la incapacidad de las células endoteliales sin Snail1 de promover una activación completa de fibroblastos in vitro e in vivo, debido a una señalización reducida de las vías de FGF2 y CXCL12; ni de generar una angiogénesis completa in vivo, con neovasos más anchos y menos invasivos. Cambios similares en la aparición de tumores y en su morfología se observaron en ratones MMTV-PyMT pretratados con el antiangiógenico bevacizumab. En muestras humanas de cáncer de mama pudimos recapitular la mayoría de los descubrimientos de los modelos animales usados. En resumen, estos hallazgos establecen un nuevo papel para Snail1 en las células endoteliales, no solo en angiogénesis, sino también en la aparición tumoral, el desarrollo y el fenotipo del tumor.

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39

Powolny, Anna Aleksandra. "Diet, nutrition and prostate cancer angiogenesis." Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1148992965.

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Murohara, Toyoaki. "Angiogenesis and vasculogenesis for therapeutic neovascularization." Nagoya University School of Medicine, 2003. http://hdl.handle.net/2237/5392.

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Marsh, Howard Piers. "Genetic polymorphisms in bladder cancer angiogenesis." Thesis, University of Bristol, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.428513.

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Sutton, Christopher Derek. "Angiogenesis in resected colorectal liver metastases." Thesis, University of Leicester, 2003. http://hdl.handle.net/2381/29870.

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Aims: To assess the prognostic significance of angiogenesis using microvessel density (MVD) and angiogenesis-modulating cytokines, in a consecutive series of patients undergoing liver resection for colorectal metastases. Methods: 5 microm sections from formalin-fixed, paraffin-embedded tissue blocks were immunohistochemically stained for microvessels, vascular endothelial growth factor (VEGF) thrombospondin-1 (TSP-1), thymidine phosphorylase (TP) and p53. MVD was measured using a computerised image analysis system. At the edge of the tumour, areas of highest vessel counts or hotspots, and the mean of contiguous x200 high power fields were counted. Within the tumour, hotspots and the random cumulative mean of vessel counts were analysed. The percentage expression of VEGF, TSP-1, TP and p53 was recorded. MVD and the cytokines were correlated using the test. The Kaplan-Meier method, the log rank test, and the Cox proportional hazard model were used to correlate MVD, the cytokines and clinico- pathological variables with patient survival. Results: 182 patients, age range 25-81 (mean 61) were included. On univariate analysis, bilobar disease (p=0.003), tumour edge hotspot (p= 0.005), lymphocytic TP (p=0.02), stromal TSP-1 (p=0.01) and perivascular TSP-1 (p=0.03) significantly correlated with poor prognosis. High expression of TP correlated with high MVD (p=0.04 for hotspots, p=0.001 for contiguous vessels). On multivariate analysis tumour edge hotspot, and bilobar disease were independent prognostic factors (p= 0.038, and p= 0.04 respectively). Conclusion: Thymidine phosphorylase is an important cytokine associated with high tumour edge microvessel density. Tumour edge hotspot and bilobar disease are independent prognostic markers of poor survival in patients who have undergone liver resection for colorectal liver metastases.

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Lichtenbeld, Hera Henrica Corine. "Tumor angiogenesis: an in vitro study." Maastricht : Maastricht : Universitaire Pers Maastricht ; University Library, Maastricht University [Host], 1993. http://arno.unimaas.nl/show.cgi?fid=6017.

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Beijnum, Judith Rosina van. "Gene expression profiling of tumor angiogenesis." Maastricht : Maastricht : Universiteit Maastricht ; University Library, Maastricht University [Host], 2006. http://arno.unimaas.nl/show.cgi?fid=7710.

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Levchenko, Tetyana. "The role of angiomotin in angiogenesis /." Stockholm, 2003. http://diss.kib.ki.se/2004/91-7349-761-4/.

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Veitonmäki, Niina. "Angiostatic mechanisms of endogenous angiogenesis inhibitors /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-555-7/.

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Hillen, Femke. "Tumor cell plasticity: vascularisation beyond angiogenesis." Maastricht : Maastricht : Universiteit Maastricht ; University Library, Universiteit Maastricht [host], 2008. http://arno.unimaas.nl/show.cgi?fid=9514.

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Sluimer, Judith Christina. "Hypoxia, HIF and angiogenesis in atherosclerosis." Maastricht : Maastricht : Universitaire pers Maastricht ; University Library, Universiteit Maastricht [host], 2008. http://arno.unimaas.nl/show.cgi?fid=10707.

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Fawcett, Jonathan. "Molecular aspects of angiogenesis and metastasis." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.386753.

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Duncan, Timothy Jake. "Immunoediting and angiogenesis in ovarian cancer." Thesis, University of Nottingham, 2010. http://eprints.nottingham.ac.uk/11326/.

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Advances in the treatment of ovarian cancer have had a limited impact on prognosis over recent decades. Alternatives to the traditional surgical and chemotherapeutic approach are being sought. Many novel therapies relate to a greater understanding of the molecular changes which occur during carcinogenesis and the development of targeted therapies to exploit these abnormalities. The aim of this thesis was to investigate the prognostic significance of markers relating to tumour immunology, angiogenesis and apoptosis, through the use of Tissue Microarray Technology. 339 cases of ovarian cancers diagnosed between 1982 and 1997 were assessed. Tumours were analysed immunohistochemically for expression of components of the IFNy (IFNGR1, STAT1, p27, caspase 1), TRAIL (DR4 and DR5) and angiogenic (VEGF) pathways. Loss of expression of IFNGR1 was an independent predictor of poor prognosis, although STAT 1 was not. High levels of cytoplasmic and nuclear p27 expression were associated with a reduced survival; cytoplasmic was independently prognostic. Tumours with reduced levels of caspase 1 had improved survival. These results suggest that only patients expressing IFNGR1 may benefit from IFNy therapy and provides evidence of immunoediting in ovarian cancer. DR4 and DR5 did not predict prognosis suggesting that the TRAIL pathway may not be significant in ovarian cancer apoptosis with implications for TRAIL-related therapy. High levels of VEGF occurred infrequently, being an independent marker of poor prognosis. This may identify a group of patients who may preferentially benefit from anti-angiogenic therapy. The thesis illustrates that ovarian cancers are heterogeneous and variations in expression of protein markers can predict tumour behaviour and stratify for therapy. Future targeted therapies may be selected on the basis of an immunohistochemical profile which predicts the pathways that are still functioning. New therapies as they arise should be trialed and targeted to tumours expressing the appropriate molecular markers.

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Dissertations / Theses on the topic 'Angiogenesis'

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