Our cells are constantly exposed to endogenous and exogenous agents that can damage our genetic material (DNA) and cause mutations (potentially leading to cancer). In addition, the normal cellular processes of DNA replication and mitosis pose a risk to genomic stability during each cell division, for example due to DNA polymerase errors and/or incorrect segregation of sister chromatids. To protect our DNA, cells have evolved complex protein signalling pathways that control DNA repair and cell cycle regulation. Our research aims to:
1) Characterise novel regulatory mechanisms that help to maintain genomic stability. Current studies involve functional characterisation of novel post translational modifications that we have identified in the microcephalin-1 (MCPH1) tumour suppressor protein
2) Investigate cellular/cytogenetic changes induced by DNA damage that could contribute to disease. Current studies focus on amplification of the c-MYC oncogene after exposure of cells to ionising radiation (X-rays).
3) Identify novel genetic factors and gene-environment interactions that might increase susceptibility to DNA damage and cancer. Current studies focus on the impact of certain environmental factors on cells carrying a mutation in the BRCA1 or BRCA2 breast cancer susceptibility genes.
Such knowledge is essential to understand normal cellular function, understand disease mechanisms and identify potential novel targets for therapeutic intervention.
PhD, Biochemistry3 Dec 2003 - 31 Dec 2099