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  Mechanisms dysregulating canonical Wnt signalling in AML


   Cardiff School of Medicine

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Prof Alex Tonks, Prof R Darley  No more applications being accepted  Funded PhD Project (European/UK Students Only)

About the Project

PhD studentship opportunities in the Department of Haematology, Cardiff
Applications are sought from outstanding and enthusiastic UK/EU science graduates ideally with relevant laboratory experience. The project will be undertaken in the Department of Haematology, one of the largest centres for the study of blood diseases in the UK. The student will be required to integrate knowledge of tumour biology, cell signalling and haematopoietic development. Techniques will include subcloning, retroviral gene transduction, flow cytometry, western blotting, gene expression and cell biology.
The successful candidates will join a group of 10 members (PhD students, post-docs and technicians) based in the Tonks/Darley AML Research Group. This group has an excellent track record centred on integrating fundamental research on haematopoietic development and leukaemia with translational and preclinical studies aimed at drug targeting of molecular abnormalities.

Project descriptions:-
Acute Myeloid Leukemia (AML) is a blood cancer arising from disruption of normal blood cell development. With conventional treatment over half of AML patients die from this disease, so the aim of these projects is to understand the complex and highly heterogeneous molecular mechanisms underlying AML to allow the development of targeted therapies. The project will examine Wnt signalling, a frequent abnormality that we have identified in AML.

Mechanisms dysregulating canonical Wnt signalling in AML
This is a Cancer Research Wales funded studentship. Wnt signalling is a key developmental regulator and is one of the most frequently dysregulated processes in AML. The key to Wnt signalling is the entry of a protein, called β-catenin, into the nucleus of the cell where it effects changes in gene expression. Normal blood cells resist entry of β-catenin into the nucleus. In contrast, in AML high levels of β-catenin accumulate in the nucleus in a large proportion of patients. The key defect shown by AML blasts is the nuclear entry of β-catenin. Blocking the entry of β-catenin into the nucleus would be a key therapeutic axis in this disease. This project therefore seeks to identify the factors influencing nuclear localisation of β-catenin in AML

Applications are sought from outstanding and enthusiastic individuals with an interest in cancer biology. Laboratory experience will be an advantage especially in tissue culture, molecular biology or protein analysis.

Please submit a CV and covering letter to [Email Address Removed]

Funding Notes

UK/EU tuition fees only (if applicable, any eligible non-EU candidates must fund the remainder of the overseas fee)
Doctoral Stipend matching UK Research Council National Minimum (£13,726 p.a. for 2012/13, updated each year)

Where will I study?