Use this URL to cite or link to this record in EThOS: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.647643
Title: Role of HR23B, HDAC6 and Myd88 and their interplay in response to HDAC inhibitor treatment
Author: New, Maria
Awarding Body: University of Oxford
Current Institution: University of Oxford
Date of Award: 2014
Availability of Full Text:
Access through EThOS:
Full text unavailable from EThOS. Restricted access.
Access through Institution:
Abstract:
Abnormal epigenetic control is a common early event in tumour progression, and aberrant acetylation in particular has been implicated in tumourigenesis. Histone deacetylases (HDACs) are enzymes that regulate acetylation of chromatin and a variety of other non-histone substrates. Significantly, HDAC inhibitors are potent anti-proliferative agents and exhibit clinical activity in lymphoproliferative and haematological maligancy. However, the mechanistic details by which HDAC inhibitors affect proliferation remain to be elucidated. I have explored the cellular processes affected by HDAC inhibitors, and begun to illuminate a new pathway, regulated by HDAC, which impinges on the cellular effect of HDAC inhibitors. My results suggest that the proteins HR23B and Myd88 are important sensitivity determinants for HDAC inhibitor treatment, and that their interplay with HDAC6 dictates cell fate choice between survival by autophagy or apoptosis.
Supervisor: La Thangue, Nicholas Sponsor: Leukaemia and Lymphoma Research
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.647643  DOI: Not available
Keywords: Oncology ; Myd88 ; biomarker
Share: