Fixed-term

Research positions in Understanding how p53 isoforms drive intestinal inflammation

Overview Inflammatory bowel disease (IBD) is a chronic, relapsing condition with no cure, driven by persistent intestinal inflammation. Our research has identified a p53 isoform, Δ133p53, with pro-inflammatory and immunomodulatory properties that is associated with disease progression and colorectal cancer in patients with ulcerative colitis. Using a Δ122p53 transgenic mouse model (the murine homologue of human Δ133p53), this project aims to define how aberrant p53 isoform expression promotes chronic gut inflammation. Students will work with established mouse models of colitis to examine intestinal pathology and immune responses using histology and flow cytometry. This project provides strong training in translational immunology, inflammation, and cancer-associated disease mechanisms. Student requirements We are seeking highly motivated postgraduate students with a background in biomedical science, immunology, pathology, or a related discipline A one-year Master’s by thesis student is strongly preferred, but suitable Honours candidates are also encouraged to apply Prior experience in mouse handling and monitoring, tissue dissection/digestion, or histology is highly desirable, but full training will be provided Funding A stipend is available for a qualified, full-time Master’s by thesis student. How to apply Please send the following to Dr Kunyu Li: Curriculum vitae (CV) Academic transcript A brief statement outlining your research interests and motivation Applications will be assessed on a rolling basis until the position is filled. Contact Contact name Dr Kunyu LiMob+64 21 155 9148Emai lkunyu.li@otago.ac.nz

Research positions in Understanding spinal cord circuits in scoliosis using genetics and exercise

Overview Cancer immunotherapy can induce potent anti-tumour immune responses; however, disease relapse remains a major clinical challenge, often driven by tumour immune escape. Defining the mechanisms that underlie tumour remission and subsequent relapse is essential for improving the long-term effectiveness of immunotherapeutic strategies. Our preliminary studies using a mouse melanoma model have identified distinct transcriptomic changes during tumour regression and relapse. These findings reveal a shift from immune activation during remission to tissue remodelling and immune suppression at relapse. The overall aim of this project is to characterise the immune and structural alterations that accompany tumour remission and relapse following immunotherapy. By experimentally validating transcriptomic findings, this research will provide new insights into mechanisms of immune escape and may inform strategies to prevent tumour relapse after treatment. The successful student will undertake a combination of in vivo and tissue-based analyses, including: Performing adoptive cell transfer (ACT) in tumour-bearing mice and collecting tumours at defined time points Immunohistochemistry and immunofluorescence staining of tumour tissues at early remission, stable remission, and relapse Analysis of tumour structural changes, including extracellular matrix deposition and cytoskeletal organisation Integration of phenotypic and histological data with existing transcriptomic datasets to explore mechanisms driving tumour relapse Student requirements Highly motivated postgraduate students with a background in biomedical science, immunology, pathology, or a related discipline A one-year master’s by thesis student is strongly preferred, although suitable honours candidates are also encouraged to apply Prior experience in mouse handling and monitoring, tissue dissection/digestion, or histology is highly desirable; however, full training will be provided How to apply Please send the following to Dr Kunyu Li at kunyu.li@otago.ac.nz: Curriculum vitae (CV) Academic transcript A brief statement outlining your research interests and motivation Applications will be assessed on a rolling basis until the position is filled. Contact Contact nameKunyu LiTel+64 21 155 9148

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