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We have 19 Pathology (blood) PhD Projects, Programmes & Scholarships

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Pathology (blood) PhD Projects, Programmes & Scholarships

We have 19 Pathology (blood) PhD Projects, Programmes & Scholarships

Identifying causal pathways to disease using DNA methylation predicted blood traits.

Project Background. Blood cell types have been implicated in pathogenesis of chronic diseases. Genome wide association studies have identified thousands of variants associated with blood trait variation. Read more

Investigation of short-term effects of colchicine on blood proteins using proteomics

The anti-inflammatory medication colchicine has been shown to significantly improve cardiovascular outcomes post heart attack and in chronic heart disease patient groups, suggesting it may be a suitable candidate for repurposing in cardiovascular diseases. Read more

Identifying secreted biomarkers in brain cancer

Stage IV brain cancer or glioblastoma (GBM) poses a major challenge with only 5 FDA approved chemotherapeutic drugs available for treatment. Read more

Identifying DNA methylation signatures of prostate cancer progression and mortality among patients with clinically confirmed, localised disease at baseline in a large prospective clinical trial

Rationale. Prostate Cancer (PCa) is a leading cause of male mortality, with 336,000 deaths worldwide each year (1). Although most PCa cases are indolent, slow-growing, and tend not to progress, a subset of PCa cases are more aggressive and will progress to metastases, treatment resistance and death. Read more

Investigating Lysosomal Dysfunction in Ageing and Neurodegeneration

Lysosomes are key cellular organelles that degrade and recycle macromolecules, act as signalling hubs and are implicated in many diseases including Parkinson’s disease (PD) and Alzheimer’s dementia (AD) where old age is a major risk factor. Read more

Harnessing the genetics of DNA methylation to understand context-specific gene regulation in disease

Project Background. Genome wide association studies (GWAS) have discovered many genetic associations with health outcomes. However, most GWAS signals reside in non-coding regions and it is likely that GWAS variants confer their effects through a regulatory mechanism. Read more

(MRC DTP CASE) Investigating the mechanisms contributing to impaired regulatory function of B cells in autoimmunity

The implementation of biological therapies has significantly advanced the management of autoimmune diseases (AIDs). However, the failure to achieve clinical remission in ‘non-responders’ remains a significant and unmet challenge. Read more

NIHR Leeds BRC: Multimodal predictive modelling of outcome in patients with gastrointestinal cancer

Worldwide, cancer of the upper (oesophagus, stomach) and lower gastrointestinal (colon and rectum) tract is newly diagnosed in 3.6 million patients every year and 2.2 million patients die from this disease every year. Read more

NIHR Leeds BRC: Force sensing mechanisms of haemostasis in heart failure and diabetes

Since the original identification of the role of PIEZO1 in vascular integrity and endothelial cell biology by our group in Leeds in 2014, there have been many publications on the role of PIEZO1 in endothelial function and its role in processes such as atherosclerosis, hypertension, cell-cell junctions, vascular permeability and leukocyte diapedesis. Read more

Translating biomarkers towards clinical trial application in osteoarthritis

Stipend. Standard Research Council London Rate + Tuition Fees (Home rate) for 3 years. A consumables budget is also provided. Applications are invited for a 3-year PhD studentship based in the Centre for Inflammatory Disease, Department of Immunology & Inflammation at Imperial College London. Read more

Investigating the neuro-stromal-immune interactions in inflammageing and osteoarthritis.

Ageing is associated with a higher risk of developing multiple chronic conditions (multimorbidity) including osteoarthritis. Age-associated chronic low-grade inflammation (inflammageing) is a hallmark of osteoarthritis. Read more

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