EBV seroprevalence is extremely high worldwide. This member of the Herpesvirus family is considered a human carcinogen, implicated in lymphoid and epithelial malignancies. Because of its characteristics, EBV has been investigated in thyroid specimens, especially in autoimmune and neoplastic lesions. However, the role of EBV in thyroid diseases is still unclear. Reports on its presence in thyroid cancer vary drastically according to population and methodology applied. This review presents the history of EBV and thyroid cancer aiming to better understand the role of this oncogenic virus in thyroid tumorigenesis. We hope to assist researchers and discuss new possible approaches to better understand the role of EBV in thyroid cancer.

Although stressful events are known to trigger Graves’ disease (GD), the mechanisms involved in this process are not well understood. The NR3C1 gene, encoding for the glucocorticoid receptor (GR), presents single nucleotide polymorphisms (SNPs) that are associated with stress-related diseases. To investigate the relationship between NR3C1 SNPs, GD susceptibility, and clinical features, we studied 792 individuals, including 384 patients, among which 209 presented with Graves’ orbitopathy (GO), and 408 paired healthy controls. Stressful life events were evaluated in a subset of 59 patients and 66 controls using the IES-R self-report questionnaire. SNPs rs104893913, rs104893909, and rs104893911 appeared at low frequencies and presented similar profiles in patients and controls. However, variant forms of rs6198 were rarer in GD patients, suggesting a protective effect. Stressful events were more common in patients than controls, and were reported to have clearly occurred immediately before the onset of GD symptoms in 23 cases. However, no association was found between these events and rs6198 genotypes or GD/GO characteristics. We suggest that the NR3C1 rs6198 polymorphism may be an important protective factor against GD, but its relationship with stressful events needs further investigation.

Bisphenol A (BPA), a ubiquitous environmental endocrine disruptor, has been implicated in carcinogenesis; however, its effects on thyroid cells remain unclear. This study investigated BPA‐induced cytotoxicity and genotoxicity in thyroid cell lines, including normal follicular (Nthy‐ori 3‐1), papillary carcinoma (TPC‐1 and BCPAP) and anaplastic carcinoma (8505C) cells, including exposure to the specific migration limit (SML) established by Brazilian regulations (1 μg/mL). Cells were exposed for 24 and 48 h, and membrane integrity, metabolic activity, and DNA damage were assessed using trypan blue exclusion, CCK‐8, and comet assays, respectively. Nthy‐ori 3‐1 exhibited non‐monotonic cytotoxicity, with 60% mortality at the SML (24 h). The 8505C line displayed notable resistance to membrane damage at high concentrations but was highly sensitive to genotoxicity, which intensified after BPA exposure and may be related to TP53 mutations. The SML dose caused significant DNA damage in normal cells, whereas papillary lines were less affected. These findings demonstrate cell‐context‐dependent BPA effects and suggest that current regulatory thresholds may not adequately protect thyroid health, particularly in individuals with pre‐existing thyroid conditions. BPA's impact involves both metabolic disruption and impaired DNA repair pathways, supporting its potential carcinogenicity.