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Title: Loss of Rb co-operates with Ras to drive biogenesis in mammalian cells
Author: Collins, M. J.
Awarding Body: University College London (University of London)
Current Institution: University College London (University of London)
Date of Award: 2013
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The p53, Rb and Ras/PI3K pathways are implicated in the development of the majority of human cancers. A number of studies have established that these pathways co-operate at the level of the cell cycle leading to loss of normal proliferative controls. For this thesis I have investigated how these signals influence a second critical component of tumour formation – cell growth. I have discovered that while oncogenic Ras is sufficient to drive growth via the canonical growth pathway, PI3K–AKT–TOR, it does so relatively weakly and p53 loss does not drive cell growth at all. Importantly, this work identifies a novel role for the Rb family of tumour suppressors in directing cell growth via a signalling pathway distinct from PI3K–AKT–TOR and via an E2F-independent mechanism. However, I have found that strong, sustained growth requires Rb loss together with Ras signalling, identifying an additional mechanism by which these oncogenic pathways co-operate and a critical role for Ras in preserving the uptake of extracellular nutrients required for biogenesis.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available