Hogg, Alison (2011) A study of the NF-κB signalling pathway in human acute myeloid leukaemia. Masters thesis, University of East Anglia.
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Abstract
The transcription factor NF-κB can play both a protective and destructive role in cells. NF-κB protects by signalling for the immune system when cells fall under attack from pathogens. NF-κB signalling becomes a danger to cells when signalling becomes constitutive and can promote excessive inflammation and tumourigenesis. Constitutive NF-κB signalling occurs within acute myeloid leukaemia cells, promoting cell survival. This provides reason to investigate the NF-κB signalling pathway in greater detail. Prevention of NF-κB signalling should lead to cell apoptosis of AML cells but this outcome may be affected by any one of the many signalling components that make up the extremely complex NF-κB signalling pathway. A range of the NF-κB signalling components within AML cells are investigated in detail this study. It was uncovered that although p50 NF-κB levels were consistent in AML and control cell samples, IκB levels were markedly reduced, leading to greater basal NF-κB activity in AML cancer cells compared to control non-cancer cells. Furthermore, this inhibited IκB level observed in AML cells, appeared to be maintained by autocrine TNF production, as anti-TNF treatment impaired the observed response. These findings indicate that IκB levels underlie the high basal NF-κB activity that is observed in AML cancer cells, and possibly other types of NF-κB-dependent cancers. Targetting IκB may help improve cancer chemotherapeutic effectiveness in AML.
Item Type: | Thesis (Masters) |
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Faculty \ School: | Faculty of Science > School of Pharmacy |
Depositing User: | Nicola Veasy |
Date Deposited: | 04 Mar 2015 12:45 |
Last Modified: | 04 Mar 2015 12:45 |
URI: | https://ueaeprints.uea.ac.uk/id/eprint/52530 |
DOI: |
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