Radiation therapy is becoming more and more common and as with many things that we have discussed here, the person to person variation in response to radiation exposure can be large. So what drives this difference in response to radiation dose. An answer is emerging from a series of studies that were undertaken using cells from xeroderma pigmentosum patients. You can read more about xeroderma pigmentosum here, but briefly these patients suffer from a dysfunction in the molecular system that repairs DNA double strand breaks.
In a 2010 Journal of Medical Genetics paper by Abbaszadeh et al. The authors piece together the role that a specific protein, DNA-dependent protein kinase catalytic subunit (DNA-PKcs) plays double strand break repair induced by ionizing radiation. Ultimately specific alleles of the DNA-PK protein are identified that predispose these individuals to an extreme radiation sensitivity.
The authors leave us with an interesting statement:
“Finally, these data show how seemingly ‘mild’ or undiagnosed defects in DNA repair factors, while consistent with viability, can have catastrophic consequences should such an individual require cytotoxic anticancer RT. Simple pretreatment screening protocols such as measuring the induction of repair of nuclear gamma-H2AX foci in patient cells, to identify individuals at risk, would increase the safety of RT for such patients.”
I am asking the Tox1401 students to look into exactly what “pretreatment screening protocols such as measuring the induction of repair of nuclear gamma-H2AX foci in patient cells” is, so if you would like to know more, head on over to the comments section where they will provide a brief description of the procedure.