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Fully-funded PhD studentships

Fully-funded PhD studentships October 2019 entry 

All applications should be made online via the University’s Applicant Portal for a PhD in Pathology (BLPA22). In the Studentship section of your application please enter the projects that you are applying for in order of preference. You are allowed to select up to 3. A completed application must be submitted by the closing date below. An application is only complete when all supporting documents, including the 2 academic references, are submitted. It is the applicants responsibility to ensure their referees submit their references before the closing date.

The list of available projects is shown below. Applicants can select up to a maximum of three supervisors/projects, although this is not a requirement.  Additionally, the Department requires that by the time of interview all potential students must have fulfilled the Language Requirements for admission.

Application information

Funding* will cover the student’s stipend at the current Research Council rate and University Fees. The studentships will be funded for three years in the first instance subject to eligibility**, with the possibility of additional funding in the fourth year depending on circumstances.

**The studentships are available to students who qualify for Home/EU fees

Applications from ineligible candidates will not be considered. 


The University values diversity and is committed to equality of opportunity. 

The University has a responsibility to ensure that all employees are eligible to live and work in the UK.

How do malaria parasites sense and respond to DNA damage? - Dr Catherine Merrick

Closing date for applications: 2 May 2019

Interviews will be held between 7th and 10th May 2019. 

The malaria parasite Plasmodium has a complex lifecycle involving several highly unusual cell cycles.  Rather than conventional binary fission, it grows via syncytial modes of replication, producing multinucleate syncytia prior to budding and cytokinesis.  This presumably requires unusual, sophisticated regulators of DNA replication, DNA repair and cell-cycle checkpoints, yet these are very poorly understood.   The current first-line antimalarial drug, artemisinin, can cause DNA damage and drug-resistant parasites have recently arisen.  Their resistance apparently involves parasite ‘dormancy’ - possibly via a cell-cycle checkpoint.  This project will investigate how Plasmodium responds to DNA damage and how this may be linked to artemisinin resistance.

Read the full proposal

Role of influenza virus mini viral RNAs in human morbidity and mortality – Dr AJ te Velthuis

Closing date for applications: 17 May 2019

Interviews will be held from 23rd May 2019 onwards. 

RNA viruses pose a significant threat to our wellbeing and economy. One of the most threatening is the influenza A virus, which infects an estimated 13 million and kills about half a million people every winter. To infect humans, the influenza virus must replicate its genome faithfully in our cells. However, recent research has shown that viral replication can go wrong and produce small molecules, called mini viral RNAs, which affect the immune response. This project will investigate how such molecules interact with components of the innate immune response and whether they affect disease in human patients.

Read the full proposal 

MicroRNA dysregulation in malignant germ cell tumours: more than a biomarker? – Professor Nicholas Coleman

Closing date for applications: 17 May 2019

Interviews will be held from 23rd May 2019 onwards. 

Malignant germ cell tumours (mGCTs) are the most common cause of cancer deaths in young adult males. Our group discovered that all mGCTs, despite being clinically and pathologically variable, are characterised by specific abnormalities in microRNA levels. This important finding has led to the development of widely-adopted blood tests for mGCT diagnosis and monitoring. The current project will investigate whether the microRNA changes can also be targeted as new biological therapies for mGCTs. Initial work will involve the generation of inducible lentivirus constructs for replenishment of tumour suppressor microRNAs and depletion of oncogenic microRNAs in established tumours. The effects of rectified microRNA expression will then be investigated using multiple in vivo model systems. The ultimate aim is to progress the work to first-in-man clinical trials. 

Read the full proposal