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Discovery Research

Cancer ResearchGenetic instability and death in cancer cells

The integrity of the genetic information in cells is protected by elaborate mechanisms to ensure that an accurate DNA copy is passed from generation to generation. These mechanisms repair errors in DNA sequence or stop growth if DNA structure is compromised. If the level of DNA damage is too severe, cells may die rather than attempt repair. The purpose of this project is to understand the role of these mechanisms in the maintenance of gene stability and the commitment of cancer cells to death, how these mechanisms are altered in cancer, and how they can be exploited to improve therapy.


  • Principle investigator: Professor Mark Meuth
  • University of Sheffield
  • Award amount: £3,939,496
  • September 2009 – August 2014



Cancer ResearchAnalysis of a human cyclin-dependent kinase (CDK), as a novel regulator of genomic stability

Many cancers do not respond well to chemotherapy. Understanding why chemotherapy does not work as well for these cancers will allow us to develop better treatment options, and hopefully lead to further increases in patient survival. This project has shown that a specific protein, CDK18, can influence whether a cancer cell will live or die after being treated with chemotherapy. Some breast cancers have particularly high amounts of this protein, which may make them resistant to chemotherapy. This knowledge could help predict how an individual patient’s tumour would respond to specific chemotherapeutic drugs.


  • Principle investigator: Dr Spencer Collis
  • University of Sheffield
  • Award amount: £156,036
  • March 2012 – March 2015



Cancer ResearchDefining and exploiting signalling pathways in natural killer cells

It is now known that the immune system is capable of recognising and fighting cancer much in the same way it fights off infection. However, cancer develops ways of preventing the immune system from attacking tumours. One way cancer does this is by using a molecule (TGF-β) to turn off certain immune cells, known as natural killer cells. This project will examine whether a drug already used in cancer treatment, interferon, can prevent cancer from suppressing natural killer cells. This will allow the immune system to target and kill cancer cells more efficiently, improving therapy.


  • Principle investigator: Dr Graham Cook
  • University of Leeds
  • Award amount: £131,427
  • March 2013 – June 2015



Cancer ResearchDownstream consequences of cancer-associated Ciz1 variant expression

The CIZ1 gene is often altered in breast and lung cancers. This project aims to determine which forms of CIZ1 are expressed in cancer cells, and what effects these forms have on cancer growth. One particular form, CIZ1 f-variant, has been identified in breast cancer cells. This variant will be assessed as a potential therapeutic target or as a biomarker to identify cancer cells.


  • Principle investigator: Dr Dawn Coverley
  • University of York
  • Award amount: £159,206
  • July 2013 – June 2016



Cancer ResearchA study of the incorporation and release of tissue factor as cancer-derived microparticles

Inappropriate clotting within blood vessels (thrombosis) is a main cause of morbidity and mortality in cancer patients. While it is possible to prevent thrombosis, it is difficult to predict the risk in order to inform patients. The main cause of clotting is a protein called tissue-factor which is strongly associated with aggressive cancers. This project will research how tissue-factor is released from cells, initiating a cascade of events that causes clotting, and how this process is affected in cancer. By understanding the underlying mechanisms, the team hope not only to predict the risk of thrombosis, but also to intervene to prevent tissue-factor release.


  • Principle investigator: Dr Camille Ettelaie
  • University of Hull
  • Award amount: £163,684
  • August 2014 – January 2017



Cancer ResearchAn RNA polymerase III subunit linked to cell transformation and pluripotency

A proportion of cancer cells within a tumour have similar characteristics to stem cells, and are known as cancer stem cells. One function of normal stem cells is to replicate and form different cell types to provide new cells for the repair of damaged tissue. It is thought that cancer stem cells, which are resistant to many treatments, are similarly responsible for producing new cancer cells after treatment, leading to recurrence and limiting the efficacy of cancer treatment. A protein called POLR3G is expressed in both normal stem cells and cancer stem cells. In normal stem cells, reducing the levels of POLR3G limits the ability of these cells to form different cell types. This project will explore how POLR3G works, and if reducing levels in cancer cells can prevent cancer stem cells from functioning.


  • Principle investigator: Professor Robert White
  • University of York
  • Award amount: £176,339
  • July 2014 – June 2017



Cancer ResearchEnhancing tumour immunity; development of methods for the manipulation of patient-derived immune cells

The immune system has the same capacity to fight cancer as it does to fight infections like colds and the flu. However, cancer is able to inactivate the immune system. One way it does this is to inhibit a type of immune cell, “Natural Killer cells”, from responding to and attacking cancer cells. This project aims to modify Natural Killer cells to ignore the inhibitory signals from cancer cells. This will help to restore the immune system’s capacity to fight cancer.


  • Principle investigator: Dr Graham Cook
  • University of Leeds
  • Award amount: £69,480
  • October 2014 – September 2017