Details
- Close date
- Friday, 8 December 2023
- Academic background
- Health Sciences, Sciences
- Host campus
- Dunedin
- Qualification
- PhD
- Department
- Physiology
- Supervisor
- Dr Andrew Bahn
Overview
We have previously established that elevated serum uric acid (SUA, hyperuricemia), a metabolic product known to cause gout, contributes to proliferation of prostate cancer cells facilitated by uric acid transporter GLUT9. Furthermore, we have detected a change in intracellular uric acid homeostasis in prostate cancer cells leading to changes in activin A sensitivity and possibly aggressiveness and drug resistance of cancer cells. We are now interested to further decipher uric acid-dependent mechanisms responsible for the onset and further development of cancer. We seek to determine if our findings are a general concept for the onset or development of cancer and would like to test our hypothesis for other cancers such as breast, ovarian and colon cancer. Several projects are available, which will involve mouse models and cell model studies combining different animal, molecular biological, cell culture and hormone assay techniques. Students who are interested in the topic and keen to meet a challenge to perform state of the art research on causes for the onset of cancer are encouraged to apply.
Useful information
Similar research opportunities
- Central regulation of pregnancy
- Dysregulated ghrelin signalling in pancreatic β-cells under hyperuricemic conditions – the cause for the onset of type 2 diabetes mellitus?
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