Although the risk factors contributing to the etiology of
brain tumors remain largely unknown, this pilot study suggests that genetically determined sensitivity to
environmental carcinogens may play a role in the pathogenesis of these
tumors. In this study, we examined short-term lymphocyte cultures from 45 adult
malignant glioma patients and 117 age-, sex-, and ethnicity-matched healthy controls for
mutagen-induced chromatid breaks and evaluated their family history of
cancer, smoking, and demographic variables to ascertain the association between
mutagen sensitivity and risk of
brain tumors. The
mutagen selected was gamma-radiation. The mean number of induced breaks/cell was 0.72 (SD=0.45) for the cases and 0.45 (SD = 0.35) for the controls (P < 0.0001). Using the median number of induced breaks/cell in the controls as the breakpoint for defining
mutagen sensitivity, we observed an unadjusted odds ratio of 5.36 (95% confidence interval = 2.12-13.69) for
mutagen sensitivity and
brain tumor risk and an adjusted odds ratio of 5.79 (2.26-14.83), when we controlled for epidemiological risk factors including smoking, race, income, and education. Although a larger study is needed to confirm this intriguing result, these preliminary findings suggest that increased sensitivity to radiation is an independent risk factor for
gliomas.