Expression of duox1 in papillary thyroid cancer and in normal thyroid tissues and correlation with ret/ptc rearrangements

The thyroid gland is one of the most susceptible organs to the carcinogenic effects of ionizing radiation and about 90% of these cancers are papillary, presenting a RET/PTC chromosomal rearrangement in 70% of cases. Radiations are a known factor implied in up-regulation of NADPH oxidase DUOX1 that can promote longterm persistence of oxidative stress which causes DNA damage likely related to the development of RET/PTC rearrangement. The objective of this study was to evaluate the Duox1 protein expression in RET/PTC positive and negative papillary thyroid cancer (PTC) tissues and in normal thyroid tissues (NTT) and to correlate the rate of Duox1 protein expression with the clinico-pathological features of PTC cases. We analyzed Duox1 protein expression in 28 PTC tissues (RET/ PTC positive and negative, irradiated and not irradiated) and in 28 NTT. We correlated these data with the clinical pathological features of PTC tissues. Immunohistochemistry performed on formalin-fixed, paraffinembedded thyroid tissues showed that 54% of PTC tissues had a Duox1 moderate-strong staining pattern and only 11% of NTT showed a Duox1 moderate-strong staining pattern with a statistically significant difference between the two groups (p = 0.0007). Moreover Duox1 moderate-strong expression were present in 57% of PTC cells and in only 36% of normal thyroid cells (p = 0.11). Finally, no statistically significant correlation between the Duox1 protein expression and the clinical-pathological features of the PTC tissues was foundThese data suggest that the expression of Duox1 protein is greater in PTC tissues than in normal thyroid tissues, irrespectively of the presence of RET/PTC rearrangement. Duox1 protein expression does not seem to be a poor prognostic factor in PTC. The impact of DUOX1on the endogenous oxidative and replicative stress underlying the formation of RET/PTC1 translocation in PTC is under investigation.