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Tumor suppressors and oncogenes in the development of Xenopus laevis /Wallingford, John Beckett. January 1998 (has links)
Thesis (Ph. D.)--University of Texas at Austin, 1998. / Vita. Includes bibliographical references (leaves 139-163). Available also in a digital version from Dissertation Abstracts.
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Aberrant methylation of E-cadherin gene (ECAD) in invasive ductal breast carcinoma /Lui, Lik-hang, Eric. January 2005 (has links)
Thesis (M. Med. Sc.)--University of Hong Kong, 2005.
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Genetic analysis on the EPHB2 gene in breast cancer /Cheng, Wan-biu. January 2005 (has links)
Thesis (M. Med. Sc.)--University of Hong Kong, 2005.
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The role of p16 tumor suppressor gene in the diagnosis of thyroid disease /Leung, Pui-ling, Pauline. January 2006 (has links)
Thesis (M. Med. Sc.)--University of Hong Kong, 2006.
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Investigating the link between cancer-related genes and autophagyToh, Pei Chern Pearl January 2014 (has links)
No description available.
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Subcellular localisation of growth suppressor protein deleted in livercancer 2 (DLC2)Ng, Chi-heng, David., 吳志恒. January 2005 (has links)
published_or_final_version / abstract / Biochemistry / Master / Master of Philosophy
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Identification and characterization of a novel tumor suppressor gene, delected in liver cancer 2, (DLC2)Leung, Ho-yin, Thomas, 梁浩然 January 2005 (has links)
published_or_final_version / abstract / Pathology / Doctoral / Doctor of Philosophy
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Study of the role of the tumor suppressor phosphatase and tensin homolog (PTEN) in hepatocellular carcinomaWong, Lai-ting, 王麗婷 January 2008 (has links)
published_or_final_version / Pathology / Master / Master of Philosophy
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Molecular regulations of deleted in liver cancer (DLC) protein familyKo, Chi-fat., 高自發. January 2009 (has links)
published_or_final_version / Pathology / Doctoral / Doctor of Philosophy
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The functions of p53 during an adenovirus infectionCampbell, Hamish George, n/a January 2008 (has links)
p53 is a pivotal tumour suppressor in mammalian cells. It protects the integrity of a number of cellular pathways, preventing the malignant transformation of cells. There is however perhaps nothing more efficient at disrupting cellular pathways than a virus. Viruses infiltrate cells commandeering the normal growth and survival pathways for their narcissistic needs. While the association between viral infections and the induction of p53 has long been recognised, there is controversy surrounding the ultimate role of p53 during a virus infection. The classical model of p53 in an adenovirus infection is that p53 is a formidable obstacle which needs to be overcome. Adenoviruses overcome p53 by degrading the protein and removing its ability to transactivate its target genes. However the degradation is not immediate and there is increasing evidence which would suggest p53 is actually beneficial to an adenovirus infection. In the introductory chapter, I review what is known about p53 and virus infections. What emerges from this review is the sheer number of interactions that occur between viruses and p53, indicating its importance in an infection. Additionally it shows that adenoviruses are not the only virus shown to benefit from the presence of p53.
What beneficial role p53 may be fulfilling in an adenovirus infection is unclear. The experiments reported in this thesis investigate the functions of p53 in an adenovirus infection. In Chapter Three, immunoblots on a panel of adenovirus infected cells reveal that p53 levels do not correlate with the level of the classical p53 target proteins. This indicates that p53 is disconnected from its target genes during an infection. Promoter/reporter assays carried out on infected cells show that adenovirus can directly regulate p53 target genes independently of p53. In Chapter Five, I show this regulation is dependent on E1a, with transient transfection of E1a resulting in the marked activation of p53 target promoters. E1a mediated transactivation appears to be reliant on the largest splice variant of E1a (E1a-289R) and the presence of pRB. Electrophoresis mobility shift assays reveal that the transcription factor Sp1 is involved.
In Chapter Four, p53 transcription in an adenovirus infection was directly assayed by using an artificial p53 consensus response element. The results show that p53 is unable to activate its consensus response element during an infection. However, I show that p53 is transcriptionally competent in an infection, and is able to transactivate a mutant derivative of the p53 consensus sequence. This shows that p53 is not only transcriptional competent but has a gain-of-function in an infection. This gain-of-function requires E1a, and appears not to be due to a change in the DNA binding affinity of p53.
The data in this thesis show that adenoviruses not only appear to inhibit and control the normal transcriptional profile of p53 but appear to modify p53, giving it a new transcriptional profile. This provides a possible mechanism by which p53 could aid an adenovirus infection.
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