MSc by Research projects

You can start the process by contacting an individual principal investigator relevant to your research interests, or find out more about our research in the School of Cellular and Molecular Medicine.

You may wish to start your search with our pre-defined research projects available, listed below. 

Dr Borko Amulic (Lecturer in Immunology)

Mechanism and function of neutrophil extracellular traps (NETs):

Neutrophils are essential immune cells with important roles in defence against pathogens. They can trap microbes by producing neutrophil extracellular traps (NETs), consisting of the neutrophil’s own DNA that is extruded from the cell in a type of altruistic cell death. NETs are sticky and contain toxic antimicrobial proteins that prevent bacteria from spreading. The project investigate the molecular mechanism of NETs and their role in innate immunity.  

Dr Andrew Davidson (Reader in Virology)

Identification of biomarkers for the prediction of dengue disease severity using high-throughput proteomics:

The project will use clinical proteomic data from dengue patients with different disease outcomes to identify potential protein biomarkers for the disease severity. The protein biomarkers will be validated using clinical samples and the mechanisms behind the alterations in protein biomarkers investigated using cell based models.

Dr Stephanie Diezmann (Senior Lecturer)

Molecular chaperones in fungal biology and virulence:

Each year as many people die of fungal infections as of malaria or tuberculosis. This much-underappreciated problem is exacerbated by the lack of efficacious antifungals and evolution of resistance against existing drugs. To mitigate this, we study molecular chaperones in the leading fungal pathogen of humans, Candida albicans, aiming to identify novel drug targets and pathways essential in causing disease. 

Dr Abdelkader Essafi (Senior Lecturer)

The paradox of obesity-induced cancer:

One of the major cofactors in developing many epithelial cancers is obesity but although obese patients are at higher risk of developing these neoplasms, the progression of the diseases in these patients to the fatal stage is slower when compared to leaner patients. This conflicting finding is termed the obesity paradox and our understanding of its molecular mechanism remain vague. In this project the student(s) will use our cell models of pancreatic and breast cancer progression with the  main aim of delineating the molecular mechanisms underlying this paradox using basic molecular and cellular biology techniques alongside non-biased global approaches: RNA-seq, ATAC seq and mass spectroscopy for analysing the changes in RNA, DNA and protein changes, respectively.

Dr Bethan Lloyd-Lewis (Vice-Chancellor's Fellow)

Epithelial cell interactions in the mammary gland:

Communication between different mammary epithelial cell types is important for normal breast development, maintenance and remodelling. If normal cell-cell communication is perturbed, mammary epithelial cells may begin to divide and grow in an abnormal way, leading to the development of pre-cancerous lesions. This project will contribute to deciphering the mechanisms underpinning this process, using a 3D mammary organoid culture system combined with live-cell imaging and histological techniques.

Dr Gareth Jones (Senior Research Fellow)

Exploiting cytokine action to treat chronic inflammation: 

We have identified a key role for the cytokine interleukin-27 in suppressing chronic joint inflammation in arthritis. The project will now investigate mechanisms underpinning this suppression, with a particular focus on how interleukin-27 alters the behaviour of pathogenic CD4+ T helper cells.

Dr Wa'el Kafienah (Senior Lecturer in Stem Cell Biology)

Cellular reprogramming for cell-based therapy of osteoarthritis:

Osteoarthritis is a disease that affects the joints leading to disability. Treating this disease using regenerative medicine and tissue engineering approaches requires ample number of functional chondrocytes - the cells that make up cartilage. This project aims to employ a bioinformatics approach to predict critical transcription factors necessary for reprogramming any cell into chondrocytes thereby providing an unlimited source of these cells for cell-based therapies. The project can investigate mechanisms of the reprogramming process, tissue engineering using the converted cells and the evaluation of converted cells stability. 

Dr Karim Malik (Reader in Epigenetics)

Two projects available

The roles of aberrant alternative splicing in childhood cancers:

It is becoming increasingly evident that the cancer cell proteome (and therefore phenotype) can be altered due to alternative splicing of mRNAs. However, the pathways and mechanisms by which alternative splicing contributes to tumorigenesis remain largely obscure. We therefore propose to characterize aberrant alternative splicing in childhood cancer models, particularly those driven by Myc oncogenes.

Overcoming drug resistance in poor prognosis neuroblastoma:

Neuroblastoma is a childhood cancer accounting for ~15% of all paediatric cancer deaths. Drug-resistance is a major factor influencing poor survival rates with about 50% of high-risk patients succumbing to resistant disease. This project will seek to identify and validate target genes, proteins and pathways that act as mediators of drug resistance in relapsing neuroblastoma in order to improve future therapies.

Dr Parthive Patel (Sir Henry Dale Research Fellow)

Three projects available

Regulation of tissue regeneration by stress signalling:

Reactive oxygen species (ROS) promote regeneration in many contexts. In the adult Drosophila (fruit fly) intestine, ROS are produced by damaged intestinal epithelial cells (IECs). This promotes intestinal stem cell (ISC)-mediated regeneration, partly via stress-activated p38 MAPK signalling in enterocytes (Patel et al., 2019). You will further determine the molecular mechanism underpinning ROS-mediated fly intestinal regeneration.

Circadian regulation of tissue renewal:

Many of our tissues are rhythmically exposed to environmental stress, due to our circadian-regulated behaviour (e.g. eating). However, the impact of the rhythmic stress exposure on tissue renewal is not well understood. You will determine if maintenance and regenerative signals have circadian activity in the adult fly intestine and determine the cause of their activation.

Identifying adaptive mechanisms of epithelial cell lifespan extension:

When the production of new adult fly intestinal epithelial cells (IECs) from ISCs is inhibited, IECs increase their lifespan to ensure tissue maintenance (Jin et al., 2017). This indicates that IEC resilience and lifespan are adaptive and respond to local cues. You will determine the molecular mechanism controlling this process. 

These studies will use Drosophila genetics, dissection and immunostaining of Drosophila tissues, fluorescent microscopy, Western blotting and enzymatic assays. For more info, please visit

Professor Adam Perriman (Professor of Bioengineering) and Dr Asme Boussahel 

A 3D bioprinted model of the human subcutaneous tissue for drug bioavailability testing:

Subcutaneous delivery is the preferred route for administering therapeutic peptides and proteins, such as beta interferons and monoclonal antibodies (mAbs) for the treatment of multiple sclerosis and cancers respectively. However, determining the bioavailability of these macromolecules relies on animal testing. This approach is limited, often very costly and inefficient. In order to develop a biomimetic model of the human subcutaneous tissue, the complex composition of the subcutaneous tissue needs to be replicated in-vitro. The project will aim to develop a bioprinted subcutaneous tissue composition that captures the complex mechanisms of drug absorption. The composition will be tested with a range if biopharmaceuticals formulations to determine its ability to predict bioavailability.

Professor Anne Ridley FRS (Professor of Cell Biology and Head of School)

Rho GTPase signalling in cancer migration and invasion:

Once cancers have spread from their site of origin to other sites in the body they are difficult to treat.  This project will investigate the first step of cancer spreading: migration and invasion.  We have identified several Rho GTPases that are important for this step, and the project will use RNAi, timelapse microscopy and biochemical analysis to test how they affect cancer cell migration and invasion.

Dr Laura Rivino (Senior Lecturer)

Human T cell immunity to dengue virus:

Virus-specific T cells constitute an essential line of defence during viral infection, however the role of these cells in the context of dengue virus infection remains unclear, with evidence suggesting that they can mediate pathogenesis and/or immune protection. Our work aims to define the features of the T cell response to dengue virus that associate with differential disease outcomes, particularly in patient groups with higher risk of severe disease, such as those that are overweight/obese. This project will use multi-parameter flow cytometry and the Seahorse XF platform to study the phenotypic, functional and metabolic features of T cells.

Professor Stefan Roberts (Professor of Cancer Biology)

Transcriptional regulation by the WT1-BASP1 complex:

WT1 and BASP1 play a central role in regulating the transcription programmes involved in development and cancer. This project will explore the mechanisms that are involved in the modulation of the chromatin environment by WT1-BASP1 that leads to transcriptional repression.

Professor Christoph Wuelfing (Professor of Immunology)

Two projects available

Rebuilding tumour-mediated immune suppression in vitro:

Tumours suppress the immune response directed against them. Using three-dimensional tissue culture models you will rebuild the interactions of tumours with immune cells from defined components to elucidate mechanisms of tumour-mediated immune suppression. 

Vesicular trafficking of inhibitory receptors:

Inhibitory receptors attenuate T cell activation with a critical role in tumour-mediated immune suppression. Curiously, they are largely located inside the cell in vesicles rather than on the cell surface where they can engage their ligands. You will use imaging, biochemical and functional approaches to learn what the vesicles are that harbour the inhibitory receptors and how they travel to control T cell activation.

Edit this page