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Novel mechanisms of FAK-dependent immune evasion in pancreatic cancer

  • Full or part time
  • Application Deadline
    Friday, February 14, 2020
  • Competition Funded PhD Project (European/UK Students Only)
    Competition Funded PhD Project (European/UK Students Only)

About This PhD Project

Project Description

Applications are invited from outstanding candidates to join a Cancer Research UK funded PhD programme at the Cancer Research UK Edinburgh Centre, part of the MRC Institute of Genetics and Molecular Medicine (IGMM) at the University of Edinburgh.

For further information on how to apply, please visit:


In the United Kingdom, the 5-year survival rate for patients with pancreatic ductal adenocarcinoma (PDAC) is just 3% (Cancer Research UK statistics), and as a result pancreatic cancer is the 4th most common cause of cancer death in the UK and US. With increasing incidence and only small incremental improvements in treatment it is predicted to become the 2nd most common cause of cancer death within the next decade. Immunotherapy has shown immense promise in the treatment of some cancers. However, it has had limited impact on the treatment of pancreatic cancer and patient prognosis remains poor. Therefore, understanding key molecular pathways that drive resistance to immunotherapy will enable development of new therapeutic strategies for this cancer of high unmet need.

Recently, our own work, and that of others has identified a novel role for the non-receptor protein tyrosine kinase Focal Adhesion Kinase (FAK) in promoting immune evasion and resistance to immunotherapy in multiple tumour types, including pancreatic cancer. These studies have led directly to ongoing clinical trials investigating FAK inhibitors in combination with anti-PD1 immune checkpoint blockade. However, we still lack understanding of how best to utilize FAK inhibitors in combination with other immunotherapies, and which patients are most likely to benefit from targeting FAK.

This project will use a combination of CRISPR gene editing, flow cytometry, proteomics, and in vivo studies to investigate novel mechanisms of FAK-dependent immune regulation in human and mouse models of pancreatic cancer. Specifically, it will focus on better understanding a new role we have uncovered for FAK in regulating mechanisms of cancer cell-intrinsic immune evasion through reprogramming the interferon response. Functional interferon signalling is important for T-cell-mediated anti-tumour immunity and response to immune checkpoint inhibitors. Therefore, this knowledge will further our understanding of how best to utilise FAK inhibitors in combination with immunotherapies.

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