Iodine nutritional status is not a direct factor in the prevalence of the BRAFV600E mutation in papillary thyroid cancer

Abstract

Objectives: Papillary thyroid carcinoma (PTC) accounts for approximately 85%-90% of all thyroid cancers. Of the iodine-metabolizing genes, BRAFV600E is a highly specific target for PTC and may have a reciprocal causative relationship with iodide-metabolizing genes. Materials and methods: In this study, we performed a data analysis of selected quantitative studies to determine the relationship between iodine nutritional status and the prevalence of the BRAF600E mutation in patients with PTC. Five studies were selected for meta-analysis based on the selection criteria. Results: A total of 2,068 patients were divided into three groups: low (urinary iodine concentration [UIC] < 100 μg/L), adequate (UIC 100-200 μg/L), and high (UIC ≥ 200 μg/L). The results were obtained using RevMan software, and the pooled odds ratios (ORs) were calculated using Mantel-Haenszel statistics with a 95% confidence interval (CI). The OR for the prevalence of the BRAFV600E mutation between the high and adequate groups was 1.25 (95% CI 0.64-2.43, p = 0.51), and the OR between the low and adequate groups was 0.98 (95% CI 0.42-2.31, p = 0.96). The BRAFV600E mutation risk did not change significantly at different levels of iodine nutrition (p = 0.33) in statistical analyses. Conclusion: We conducted preliminary research on dietary iodine intake and the BRAFV600E mutation in PTC. The results suggested that abnormal iodine intake might not directly influence the prevalence of the BRAFV600E mutation in these patients. Further research into the associations between dietary iodine intake and the BRAFV600E mutation in PTC, including the underlying mechanisms, is required.

Circ_0004851 regulates the molecular mechanism of miR-296-3p/FGF11 in the influence of high iodine on PTC

“…A Korean study found that both relatively excessive iodine intake and low iodine intake appear to be important risk factors for BRAF mutations in PTC patients [ 24 ]. A recent Meta-Analysis study found that the incidence of BRAF V600E mutations in PTC patients with high iodine intake was 77.6%, which was higher than 64.61% in patients with low iodine intake and 60.15% in patients with normal iodine intake [ 7 ]. Despite a considerable body of research on the impact of iodine on thyroid cancer tumorigenesis and progression, the association involving high iodine intake and TC risk remains contentious, and the mechanisms behind iodine excess in the development of PTC are still unclear [ 25 – 34 ].…”

“…Iodine intake may induce BRAF V600E gene mutations in PTC patients through various indirect pathways [ 7 ]. However, the effect of BRAF V600E gene mutation on the circ-0004851/miR-296-3p/FGF11 pathway is unknown.…”

“…The above findings suggest that miR-296-3p may indirectly regulate the level of HIF1α by targeting and regulating its downstream genes. Iodine intake may induce BRAF V600E gene mutations in PTC patients through various indirect pathways [7]. However, the effect of BRAF V600E gene mutation on the circ-0004851/miR-296-3p/FGF11 pathway is unknown.…”

“…Furthermore, the BRAF V600E gene mutation is the most common genetic mutation in PTC, with an average incidence of about 45% [ 6 ]. Interestingly, previous studies have concluded that among the iodine metabolism genes, BRAF V600E is a highly specific target for PTC [ 7 ]. Nonetheless, the impact of high iodine levels on existing thyroid cancer and its underlying mechanisms warrant further investigation.…”