Sameh ElBadry

Characterisation of the mechanism of HIF mediated genoprotection in zebrafish

About me

Understanding the intrinsic mechanisms behind how cancerous cells grow and thrive can help answer one of science’s toughest questions: how can we cure cancer? Having completed my BSc in Biomedical Science and MSc in Translational Neuroscience, both in Sheffield, I knew I wanted to stay and continue utilizing zebrafish as a model for human disease. I can contribute to an exciting field, which has recently been recognised in the media due to the Nobel prize, and further our understanding of what makes cancer such a difficult disease to treat.

My project

Radiotherapy and chemotherapy are ineffective against renal cell carcinoma (RCC). This cancer is caused by mutations in the von Hippel-Lindau protein (VHL), which helps to maintain hypoxia-inducible factor (HIF) at low levels during normal oxygen levels. However, when VHL is mutated, HIF is constantly activated in both normoxia and hypoxia – stimulating genes downstream that promote cell survival, such as angiogenesis and cellular proliferation. High levels of HIF in RCC patients seems to protect them from traditional anti-cancer treatments. Therefore, I shall be identifying methods to downregulate HIF, allowing for cells to be resensitised to radiotherapy and/or chemotherapy.

One potential target is the glucocorticoid/mineralocorticoid (GC/MC) pathway, which is activated during hypoxia – upregulating HIF in response. We have identified compounds that inhibit the GC/MC pathway, with the intention of downregulating HIF.  Zebrafish models and human RCC cells will be used to establish whether resensitisation is successful. Overall, I hope to contribute to the wider understanding of how high levels of HIF protect the genome from destruction, and identifying compounds that can be used for clinical trials.

Connect

Twitter: @samehkelbadry

LinkedIn: https://www.linkedin.com/in/samehkelbadry/