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In everyday life we are continuously exposed to radiation from a wide variety of sources, both natural and artificial. Radiation is known to cause damage to our cells, the most obvious and well reported is damage to DNA which is held in the nucleus. However we now understand the target for radiation is much wider and crosses traditional spatiotemporal boundaries. For example we now know that radiation can instigate a process termed genomic instability; the cell is unable to maintain and accurately copy its genetic information the result of which is the gradual accumulation of genomic damage. This usually appears many cell generations after the initial insult despite the cell appearing normal for much of that time. We also know ionizing radiation can induce bystander effects; whereby irradiated cells communicate with unirradiated cells, this communication results in damage to the unirradiated cell. These are collectively known as non-targeted effects and have many influencing factors including the radiation type, radiation dose and dose rate and even genetic background.
My research group investigates some of the questions regarding induction of genomic instability and bystander effect. We are particularly interested in molecular communication between cells and the functional effects on a population of cells. One mechanism of communication is through is through extracellular vesicles, specifically exosomes. These are small vesicles released by all cell types under normal and stressed conditions. It appears that following radiation exposure cells release a qualitatively different type of exosome that can induce bystander effects in unirradiated cells. This fact has profound implications for radiation exposure particularly those undergoing radiotherapy as well as those exposed to radiation in an occupational setting.
We hope by investigating and understanding these processes we will one day can enhance our therapeutic use of radiation as well as better protect those who are occupationally exposed to it, even astronauts.