Abstract
BackgroundHuman cytomegalovirus (CMV) has been detected in the thyroid gland and thyroid tumors. CMV infection may activate the mitogen-activated protein kinase pathway, of which aberrant activation is frequently associated with BRAF mutation in papillary thyroid cancer.MethodsA total of 45 paired tumorous and adjacent non-neoplastic tissue samples, including 5 follicular adenoma and 40 papillary thyroid cancer, were obtained during thyroidectomy. BRAF mutational status was determined using direct sequencing. The presence of CMV DNA was determined using conventional PCR and quantitative real-time PCR. CMV protein in the tissue samples were evaluated with Western blot analysis.ResultsBRAF mutation was identified in the cancerous part of 31 (78%) papillary thyroid cancers. Papillary cancer with BRAF mutation was significantly associated with a larger tumor size (P = 0.045), extrathyroidal invasion (P = 0.012), lymph node metastasis (P = 0.008), and a higher TNM stage (P = 0.044). CMV DNA and protein were not detected in any studied samples.ConclusionsOur results suggest no association between CMV infection and papillary thyroid cancer.
Highlights
Human cytomegalovirus (CMV) has been detected in the thyroid gland and thyroid tumors
In another study examining herpes virus tissue distribution, CMV was detected in the thyroid gland in three of the eight autopsies [13]. These findings indicate that the thyroid gland is one of the reservoirs of latent human CMV infection
Patient characteristics Tissue samples from 5 follicular adenoma and 40 papillary thyroid cancer were used in this study after confirmation of the tissue diagnosis (Table 1)
Summary
Human cytomegalovirus (CMV) has been detected in the thyroid gland and thyroid tumors. CMV infection may activate the mitogen-activated protein kinase pathway, of which aberrant activation is frequently associated with BRAF mutation in papillary thyroid cancer. Given the fact that the prevalence of familial non-medullary thyroid cancer is only about 5% [2], differentiated thyroid cancer is mostly sporadic. The only established epidemiological factors in association with thyroid cancer are ionizing radiation and iodine deficiency [3]. Most patients diagnosed to have thyroid cancer do not have these predisposing factors. The mechanisms underlying thyroid cancer development are still poorly defined. Many genetic and epigenetic alterations have been implicated in the pathogenesis of thyroid cancer.
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