Abstract
Background:
Papillary thyroid carcinoma (PTC) represents the most frequent thyroid neoplasia and is associated with radiation exposure. A consistent proportion of PTC is characterized by chromosome rearrangements producing RET and TRK oncogenes, but the mechanisms underlying the thyrocyte propensity to such alterations are poorly understood. Diminished capacity of thyrocytes to repair radiation-induced DNA double strand breaks (DSBs) might play a role in chromosome rearrangements; however, this question has not been fully addressed due to the lack of physiologically relevant experimental models.
Methods:
Several normal human thyroid primary cultures were produced and characterized for their capacity to repair the DNA DSBs induced by ionizing radiation. For comparison, normal human bronchial epithelial cells were used. We employed the γH2AX foci assay; counts were determined at different time points after irradiation.
Results:
All the thyrocyte samples analyzed showed similar DNA DSBs induction. The rate of γH2AX foci clearance was homogenous, showing only small differences among samples.
Conclusion:
This work reports the first characterization of DNA DSB repair in human primary thyrocytes, a relevant clinical model for thyroid carcinogenesis, and represents an important step toward dissection of the link between DNA DSB repair and thyroid-specific oncogenic rearrangements.