Rozprawy doktorskie na temat „Tumour suppressor”
Utwórz poprawne odniesienie w stylach APA, MLA, Chicago, Harvard i wielu innych
Sprawdź 50 najlepszych rozpraw doktorskich naukowych na temat „Tumour suppressor”.
Przycisk „Dodaj do bibliografii” jest dostępny obok każdej pracy w bibliografii. Użyj go – a my automatycznie utworzymy odniesienie bibliograficzne do wybranej pracy w stylu cytowania, którego potrzebujesz: APA, MLA, Harvard, Chicago, Vancouver itp.
Możesz również pobrać pełny tekst publikacji naukowej w formacie „.pdf” i przeczytać adnotację do pracy online, jeśli odpowiednie parametry są dostępne w metadanych.
Przeglądaj rozprawy doktorskie z różnych dziedzin i twórz odpowiednie bibliografie.
de, Foy K. "Analysis of candidate tumour suppressor genes in sporadic ovarian tumours". Thesis, University of Cambridge, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.598448.
Pełny tekst źródłaLiu, Lu. "Oncogenes and tumour suppressor genes in human central nervous system tumours /". Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3532-7/.
Pełny tekst źródłaDiscenza, Maria Teresa. "Regulation of expression of the Wilms' tumour 1 tumour suppressor gene". Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=82855.
Pełny tekst źródłaWe have identified a novel trans-acting factor, named complex D, which shows sequence specific binding to the WT1 promoter. By electrophoretic mobility shift assays (EMSA), we demonstrate that the transcription factor Sp1 binds the WT1 promoter at a site overlapping the complex D binding site. Molecular mass determination experiments and in situ UV crosslinking indicate that complex D is approximately 130 kDa and consists of at least two proteins. Transient transfection assays show that the integrity of the complex D binding site is necessary for maximal activation of a reporter gene, suggesting that complex D may function as an activator.
Similar to WT1, the ETS-domain transcription factor Pea3 is expressed in tissues where mesenchymal-epithelial interactions occur and both gene products are implicated in regulating the expression of genes necessary for the epithelialization of common organs. Transient transfection assays using WT1 promoter-reporter gene constructs identified a Pea3 responsive element in the WT1 promoter. Overexpression of Pea3 transactivates the WT1 promoter and the presence of the intact Pea3 responsive element is necessary for the transactivation. We demonstrate, by EMSA, the sequence specific binding of Pea3 to the responsive element.
WT1 and the paired box domain transcription factor Paired box 2 (Pax2) are expressed at the initial stages of metanephric kidney development and are critical for the initiation of nephrogenesis. We generated WT1/Pax2 compound heterozygous mutant mice to provide an in vivo model for studying the interplay between WT1 and Pax2 during nephrogenesis. WT1+/-/Pax2 1Neu/+ kidneys were 50% smaller that wild type kidneys and displayed a more severe underdevelopment of the medulla, renal calyces and renal pelvis compared to Pax21Neu/+ kidneys. We demonstrate that WT1 and Pax2 proteins physically interact in vitro and in vivo. Our data suggest that WT1 is a modifier of the Pax2 mutant phenotype and that both proteins may be implicated in a common pathway in the transcriptional network governing metanephric development.
Judson, Hannah. "Investigation of candidate imprinted tumour suppressor genes". Thesis, University of Edinburgh, 2001. http://hdl.handle.net/1842/28316.
Pełny tekst źródłaMancini, DiNardo Debora. "Methylation-mediated inactivation of tumour suppressor genes". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0021/NQ58149.pdf.
Pełny tekst źródłaPatel, Anjla Chhotubhai. "The role of fat tumour suppressor gene". Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.619808.
Pełny tekst źródłaMarcar, Lynnette Nongkynrih. "Inhibition of p53 tumour suppressor function by tumour associated MAGE-A proteins". Thesis, University of Dundee, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.521696.
Pełny tekst źródłaBurns, Alice Sin Ying Wai. "The role of the p53 tumour suppressor pathway in central primitive neuroectodermal tumours". Thesis, University of Newcastle Upon Tyne, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300357.
Pełny tekst źródłaWang, Yemin. "Role of tumour suppressor ING3 in melanoma pathogenesis". Thesis, University of British Columbia, 2009. http://hdl.handle.net/2429/3850.
Pełny tekst źródłaMarston, Nicola Jane. "Mutational analysis of the tumour suppressor protein, p53". Thesis, Imperial College London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.387679.
Pełny tekst źródłaZabkiewicz, Joanna. "In vivo modelling of tumour suppressor gene function". Thesis, Cardiff University, 2005. http://orca.cf.ac.uk/55388/.
Pełny tekst źródłaHonoÌrio, Sofia Maria Santos Andrade. "Molecular characterisation of candidate 3p21.3 tumour suppressor genes". Thesis, University of Birmingham, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.409070.
Pełny tekst źródłaMarkham, Douglas James. "Acetylation control of the retinoblastoma tumour suppressor protein". Thesis, University of Glasgow, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.433229.
Pełny tekst źródłaNatan, Eviatar. "Why the tumour suppressor p53 is a tetramer". Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609555.
Pełny tekst źródłaRohrig, A. E. "Role for tumour suppressor Merlin in gene expression". Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1415770/.
Pełny tekst źródłaShahid, Taha. "Structure and mechanism of the BRCA2 tumour suppressor". Thesis, Imperial College London, 2014. http://hdl.handle.net/10044/1/25538.
Pełny tekst źródłaSeng, Tzer Jing. "Identification of candidate tumour suppressor genes on chromosome 22 in central nervous system tumours". Thesis, University of Cambridge, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.615650.
Pełny tekst źródłaFogel, Valentina. "Regulation of the tumour suppressor p53 by E2F-1". Thesis, Imperial College London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.409008.
Pełny tekst źródłaBruce, Christopher Kenneth. "Investigations of putative tumour suppressor loci in human malignancy". Thesis, Keele University, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.394629.
Pełny tekst źródłaGarvin, Alexander. "Post-translational regulation of the tumour suppressor IRF-1". Thesis, University of Nottingham, 2010. http://eprints.nottingham.ac.uk/13893/.
Pełny tekst źródłaAl-Azraqi, Abdulla Ali. "The P53 tumour suppressor pathway in human ovarian carcinoma". Thesis, University of Newcastle Upon Tyne, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.264421.
Pełny tekst źródłaBurbidge, Owen David. "Developing nanobodies to stabilise the tumour suppressor protein p16INK4a". Thesis, University of Cambridge, 2019. https://www.repository.cam.ac.uk/handle/1810/288375.
Pełny tekst źródłaWoodward, Emma Roisin. "Molecular genetic studies of the VHL tumour suppressor gene". Thesis, University of Cambridge, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624312.
Pełny tekst źródłaBhullar, Punamdip Kaur. "Egr2/Egr3 are essential tumour suppressor genes for lymphomagenesis". Thesis, Brunel University, 2013. http://bura.brunel.ac.uk/handle/2438/8319.
Pełny tekst źródłaZeqiraj, Elton. "Structure of the LKB1-STRAD-MO25 tumour suppressor complex". Thesis, University of Dundee, 2009. https://discovery.dundee.ac.uk/en/studentTheses/eb957e54-7f2a-4d08-ba2b-7838d71c25b9.
Pełny tekst źródłaCrosland, Rachel. "Studies of the PTEN tumour suppressor in endometrial cancer". Thesis, Sheffield Hallam University, 2004. http://shura.shu.ac.uk/19515/.
Pełny tekst źródłaMilner, Ben J. "The role of tumour suppressor genes in ovarian cancer". Thesis, University of Aberdeen, 1993. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU555006.
Pełny tekst źródłaSvärd, Jessica. "Repressing the hedgehog signalling pathway : functional analysis of the tumour suppressors patched1 and suppressor of fused /". Stockholm : Karolinska institutet, 2007. http://diss.kib.ki.se/2007/978-91-7357-380-1/.
Pełny tekst źródłaMcKenna, Sarah Mary Michelle. "The role played by BRCA1 in mediating the cytotoxic effect of antimicrotubule agents". Thesis, Queen's University Belfast, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.246470.
Pełny tekst źródłaAsimakopoulos, Fotios A. "Molecular analysis of chromosome 20q deletions associated with myeloproliferative disorders and myelodysplastic syndromes". Thesis, University of Cambridge, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.388490.
Pełny tekst źródłaChinswangwatanakul, Wimol. "Role of p16 in chronic myeloid leukaemia and normal haemopoiesis". Thesis, Imperial College London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.313953.
Pełny tekst źródłaJowsey, Paul Andrew. "The role of poly(ADP-ribose) polymerase-1 in the MDM2-p53 DNA damage response pathway". Thesis, University of Newcastle Upon Tyne, 2003. http://hdl.handle.net/10443/1005.
Pełny tekst źródłaStrickson, Amanda J. "Analysis of expressed sequence tags mapping to the critical region of the 5q syndrome". Thesis, Open University, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.250497.
Pełny tekst źródłaAndrews, H. N. "Role played by BRCA1 in regulating the interferon gamma mediated antiproliferative response". Thesis, Queen's University Belfast, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.269159.
Pełny tekst źródłaMcWilliams, Stewart. "BRCA1 regulates the interferon gamma mediated antiproliferative response". Thesis, Queen's University Belfast, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.246464.
Pełny tekst źródłaBright-Thomas, Rachel Marie. "Corrective gene therapy in a murine model of familial adenomatous polyposis : a study of the efficacy of gene transfer and the resultant phenotypic effects". Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.274918.
Pełny tekst źródłaSchweighoffer, Edina. "The role of Syk protein tyrosine kinase in B cell development and function". Thesis, Open University, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.250493.
Pełny tekst źródłaFidler, Carrie. "Molecular analysis of the 5q- syndrome". Thesis, Open University, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.338608.
Pełny tekst źródłaGornall, Robert J. "TP53 polymorphisms and haplotypes in breast, cervical and ovarian cancer". Thesis, University of Southampton, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.310562.
Pełny tekst źródłaGallagher, Stuart John. "The Role of the p14ARF Tumour Suppressor in Promoting Apoptosis". Thesis, The University of Sydney, 2008. http://hdl.handle.net/2123/3597.
Pełny tekst źródłaGallagher, Stuart John. "The Role of the p14ARF Tumour Suppressor in Promoting Apoptosis". University of Sydney, 2008. http://hdl.handle.net/2123/3597.
Pełny tekst źródłaThe incidence of melanoma has risen dramatically during the past three decades, yet there has been little improvement in effective treatments for this intractable and aggressive disease. Melanoma tumours are notoriously resistant to apoptosis, a cell suicide program that is activated by most cancer therapies. This thesis explores the role of the melanoma susceptibility gene product p14ARF in promoting cell cycle arrest and apoptosis, in order to resolve the impact of this tumour suppressor in melanomagenesis and melanoma susceptibility. The p14ARF tumour suppressor gene is mutated in almost half of all cancers, and germline mutations in p14ARF confer a greatly increased risk of developing melanoma. The primary function of p14ARF is to relay oncogenic signals to p53, a central regulator of cellular response to stress. There is conflicting evidence regarding the role of p14ARF in promoting apoptosis. Much of the current evidence is based on murine studies, which may not translate accurately to humans due to important differences in animal physiology and the primary sequence and functions of the mouse and human ARF proteins. Furthermore, results from previous studies are often compounded by supra-physiological expression of p14ARF, and are complicated by the fact that p14ARF shares its genomic sequence with the p16INK4a tumour suppressor gene. This study demonstrates that p14ARF expression in human cancer and primary cell lines promotes rapid p53-dependent cell cycle arrest, rather than apoptosis. As p14ARF expression did not induce apoptosis, we investigated if p14ARF could modulate the sensitivity of a cell to apoptosis induced by cytotoxic agents. Using a p14ARF-inducible U2OS osteosarcoma cell line model, we examined the impact of p14ARF expression on the apoptotic response of the cell to a panel of thirteen cytotoxic agents. p14ARF expression increased apoptosis caused by a sub-set of agents, including trichostatin A, sodium butyrate, DRB, Adriamycin and UVB radiation. p14ARF-mediated chemosensitivity was p53- and caspase-dependent, and involved the loss of mitochondrial potential. While loss of mitochondrial potential was dependent on p53, it was not blocked by caspase inhibition, demonstrating that caspases play a role downstream of mitochondrial depolarisation. Inhibition of individual components of the apoptotic program showed that p14ARF-mediated chemosensitivity was not strictly dependent on the pro-apoptotic Bax or Fas proteins. We also investigated whether p14ARF could sensitise melanoma to chemotherapeutics in vivo. We investigated the expression level of p14ARF, p16INK4a and MITFm and mutation status of B-RAF, N-RAS and PTEN in melanomas from 30 patients that had undergone isolated limb infusion - a palliative therapeutic strategy that results in much higher response rates than systemic treatment. Expression of p14ARF did not predict response to the drugs actinomycin D and melphalan . Instead, high expression of p16INK4a and presence of activating N-RAS mutation were independent predictors of response to high doses of these chemotherapeutic drugs. This work suggests that p14ARF analogues may be beneficial adjuncts in cancer therapy, but are unlikely to be effective as single agents. Additionally, p14ARF mimetics will only be effective in tumours with intact p53 signalling. Melanomas frequently carry functional p53, and may be susceptible to this mode of treatment providing the apoptotic pathway downstream of p53 is intact or can be restored.
McArdle, Stephanie. "p53 epitopes as potential tumour targets for immunotherapy programmes against cancers". Thesis, University of Sheffield, 2000. http://etheses.whiterose.ac.uk/14459/.
Pełny tekst źródłaGaentzsch, Peer Christian. "The role of the human tumour suppressor CYLD in Drosophila". Thesis, University of Oxford, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.491496.
Pełny tekst źródłaTang, Kit Shing. "Stability, folding and evolution of the tumour suppressor protein p16". Thesis, University of Cambridge, 2001. https://www.repository.cam.ac.uk/handle/1810/251785.
Pełny tekst źródłaKhoo, Kian Hoe. "Thermodynamic analysis of the stability of the tumour suppressor, p53". Thesis, University of Cambridge, 2010. https://www.repository.cam.ac.uk/handle/1810/252185.
Pełny tekst źródłaDuarte, Antonio. "Regulation of gene expression by the Wilms' tumour suppressor, WT1". Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.389178.
Pełny tekst źródłaJones, Rebecca May. "Regulation and function of the INK4a/ARF tumour suppressor locus". Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1444810/.
Pełny tekst źródłaNarayan, Nisha. "Functional regulation of the Discs Large Tumour Suppressor by phosphorylation". Thesis, Open University, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.495581.
Pełny tekst źródłaMartin, Rosalind J. L. "Mapping of putative tumour suppressor genes in epithelial ovarian cancer". Thesis, Queen's University Belfast, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287363.
Pełny tekst źródłaBrandt, Tobias. "Molecular mechanisms of DNA recognition by the tumour suppressor p53". Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609611.
Pełny tekst źródła