Abstract
OBJECTIVE: Thyroid nodules are a common occurrence in adults. Although the majority of thyroid nodules are benign, a small percentage are cancerous. The combined phosphorylated histone H2AX (γ-H2AX) and p53-binding protein 1 (53BP1) assay was utilized to detect deoxyribonucleic acid (DNA) damage and DNA repair as biomarkers of the cellular stress response. Using the combined γ-H2AX and 53BP1 assay, we evaluated DNA damage, DNA repair capacity, and malignancy risk in peripheral blood mononuclear cells (PBMCs) of euthyroid individuals with nodular goiter. MATERIALS AND METHODS: Peripheral blood samples were collected from 33 euthyroid patients with newly diagnosed nodular goiter and 30 healthy control participants. A fully automatic image analysis system was used for analyzing DNA damage (γ-H2AX), including DNA double-strand breaks (DSBs), and DNA repair (53BP1). RESULTS: Euthyroid patients with nodular goiter exhibited a higher mean number of γ-H2AX foci per cell and a higher percentage of apoptotic cells compared to the control subjects (p=0.022 and p=0.005, respectively). CONCLUSION: This study found considerably higher DNA damage in euthyroid patients with nodular goiter than in control individuals. The increase in DNA damage occurs in the early stages of carcinogenesis. These patients were expected to exhibit compromised DNA repair along with enhanced DNA damage, increasing the risk of carcinogenesis. However, euthyroid patients with nodular goiter might be at a high risk of thyroid malignancy due to the high level of DNA damage. A long-term follow-up of these patients would provide better evidence of the relationship between DNA damage and the malignancy risk of thyroid.