Bristow, Robert

Biography

Bristow, Robert, Professor MD, PhD, University of Toronto.Research includes  Cells have developed a sophisticated approach to the initial sensing and subsequent repair of DNA damage to preserve genetic stability. The objective of our clinico-translational laboratory is to understand the effect of the tumour microenvironment on the ATM-p53-53BP1 DNA damage signaling pathway and DNA double-strand break (DNA-dsb) repair. Our studies suggest that hypoxic tumour cells can have decreased DNA-dsb repair (e.g. decreased homologous recombination) and an aggressive “mutator” phenotype. We are therefore tracking DNA damage responses and repair within normal and tumour tissues to develop novel diagnostics and molecular-targeted therapies. We interrogate protein-protein interactions during DNA-dsb repair and cell-cycle checkpoints using: siRNA knockdowns, DNA-rejoining assays (comet and CFGE assays), chromatin immunoprecipitation (ChIP), biochemical fractionation, fluorescently-tagged proteins and quantitative confocal microscopy with UV-microbeams  Bristow, Robert, Professor MD, PhD, University of Toronto.Research includes  Cells have developed a sophisticated approach to the initial sensing and subsequent repair of DNA damage to preserve genetic stability. The objective of our clinico-translational laboratory is to understand the effect of the tumour microenvironment on the ATM-p53-53BP1 DNA damage signaling pathway and DNA double-strand break (DNA-dsb) repair. Our studies suggest that hypoxic tumour cells can have decreased DNA-dsb repair (e.g. decreased homologous recombination) and an aggressive “mutator” phenotype. We are therefore tracking DNA damage responses and repair within normal and tumour tissues to develop novel diagnostics and molecular-targeted therapies. We interrogate protein-protein interactions during DNA-dsb repair and cell-cycle checkpoints using: siRNA knockdowns, DNA-rejoining assays (comet and CFGE assays), chromatin immunoprecipitation (ChIP), biochemical fractionation, fluorescently-tagged proteins and quantitative confocal microscopy with UV-microbeams 

Research Interest

Cells have developed a sophisticated approach to the initial sensing and subsequent repair of DNA damage to preserve genetic stability. The objective of our clinico-translational laboratory is to understand the effect of the tumour microenvironment on the ATM-p53-53BP1 DNA damage signaling pathway and DNA double-strand break (DNA-dsb) repair. Our studies suggest that hypoxic tumour cells can have decreased DNA-dsb repair (e.g. decreased homologous recombination) and an aggressive “mutator” phenotype. We are therefore tracking DNA damage responses and repair within normal and tumour tissues to develop novel diagnostics and molecular-targeted therapies. We interrogate protein-protein interactions during DNA-dsb repair and cell-cycle checkpoints using: siRNA knockdowns, DNA-rejoining assays (comet and CFGE assays), chromatin immunoprecipitation (ChIP), biochemical fractionation, fluorescently-tagged proteins and quantitative confocal microscopy with UV-microbeams