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- A new regulator of stemness to create dendritic cell factories for immunotherapy
- Advanced methods for genomic rearrangement detection
- Control of cytokine signaling by SOCS1
- Defining the protein modifications associated with respiratory disease
- Delineating the pathways driving cancer development and therapy resistance
- Developing a new drug that targets plasmacytoid dendritic cells for the treatment of lupus
- Development and mechanism of action of novel antimalarials
- Development of a novel particle-based malaria vaccine
- Development of tau-specific therapeutic and diagnostic antibodies
- Discovering novel therapies for major human pathogens
- Dissecting host cell invasion by the diarrhoeal pathogen Cryptosporidium
- Epigenetic biomarkers of tuberculosis infection
- Essential role of glycobiology in malaria parasites
- Evolution of haematopoiesis in vertebrates
- Human lung protective immunity to tuberculosis
- Identifying novel treatment options for ovarian carcinosarcoma
- Interaction with Toxoplasma parasites and the brain
- Interactions between tumour cells and their microenvironment in non-small cell lung cancer
- Investigating the role of mutant p53 in cancer
- Microbiome strain-level analysis using long read sequencing
- Minimising rheumatic adverse events of checkpoint inhibitor cancer therapy
- Modelling spatial and demographic heterogeneity of malaria transmission risk
- Naturally acquired immune response to malaria parasites
- Predicting the effect of non-coding structural variants in cancer
- Structural basis of catenin-independent Wnt signalling
- Structure and biology of proteins essential for Toxoplasma parasite invasion
- T lymphocytes: how memories are made
- TICKER: A cell history recorder for longitudinal patient monitoring
- Targeting host pathways to develop new broad-spectrum antiviral drugs
- Targeting post-translational modifications to disrupting the function of secreted proteins
- Targeting the epigenome to rewire pro-allergic T cells
- Targeting the immune microenvironment to treat KRAS-mutant adenocarcinoma
- The E3 ubiquitin ligase Parkin and mitophagy in Parkinson’s disease
- The molecular controls on dendritic cell development
- Understanding malaria infection dynamics
- Understanding the genetics of neutrophil maturation
- Understanding the neuroimmune regulation of innate immunity
- Understanding the proteins that regulate programmed cell death at the molecular level
- Using cutting-edge single cell tools to understand the origins of cancer
- When healthy cells turn bad: how immune responses can transition to lymphoma
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Kate Sutherland-Projects
Researcher:
Exploiting KEAP1 vulnerabilities to treat aggressive lung cancer
Alternations in the KEAP1-NRF2 pathway are found in a high percentage of non-small cell lung cancers and led to enhanced NRF2 activity. Critically, increased expression of NRF2 is associated with poor prognosis, highlighting the urgent need for new therapeutic strategies for this subgroup of patients.
To understand the effect of KEAP1-NRF2 pathway alternations on lung cancer, we have engineered in vivo models that faithfully mimic KEAP1-mutant human lung cancers.
Current work is focused on identifying effective treatments that target KEAP1-mutant lung cancer. To achieve this, we will utilise CRISPR/Cas9 technologies and perform high-throughput drug screening in collaboration with the National Drug Discovery Centre (NDDC).
Immune regulation in lung cancer
Immunotherapeutic approaches, such as monoclonal antibodies targeting PD-1/PD-L1 and CTLA-4 unleash the T cell response to eliminate tumour cells. While this approach has shown considerable promise in lung cancer patients, not all patients will respond to conventional T cell-based immunotherapies.
In response to this, we aim to harness the anti-tumour activity of other immune cell populations, such as Natural Killer cells and macrophages.
Identifying drivers of small cell lung cancer metastasis
Small cell lung cancer (SCLC) is the most aggressive subtype of lung cancer, with a five-year survival rate of less than 7 per cent. Critically, SCLC has a high propensity for early spread, with 50-80 per cent of patients harbouring metastatic lesions in multiple organs at the time of diagnosis.
To understand underlying mechanisms controlling metastatic dissemination, we have developed in vivo SCLC models to augment metastatic activity.
We aim to identify novel therapeutic approaches to restrict primary and metastatic disease in SCLC.
Unravelling small cell lung cancer heterogeneity
Emerging evidence suggests that small cell lung cancer (SCLC) is a heterogeneous disease that can be classified into four distinct subtypes based on the differential expression of the transcription factors ASCL1, NEUROD1, POU2F3 and YAP1. This raises interesting biological questions that could directly inform the therapeutic treatment of SCLC patients.
We aim to develop sophisticated CRISPR/Cas9 in vivo models to explore the genetic and cellular drivers of heterogeneity.