Open Access

Herpes and polyoma family viruses in thyroid cancer (Review)

  • Authors:
    • Dimitris P. Stamatiou
    • Stavros P. Derdas
    • Odysseas L. Zoras
    • Demetrios A. Spandidos
  • View Affiliations

  • Published online on: January 26, 2016     https://doi.org/10.3892/ol.2016.4144
  • Pages: 1635-1644
  • Copyright: © Stamatiou et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Thyroid cancer is considered the most common malignancy that affects the endocrine system. Generally, thyroid cancer derives from follicular epithelial cells, and thyroid cancer is divided into well‑differentiated papillary (80% of cases) and follicular (15% of cases) carcinoma. Follicular thyroid cancer is further divided into the conventional and oncocytic (Hürthle cell) type, poorly differentiated carcinoma and anaplastic carcinoma. Both poorly differentiated and anaplastic carcinoma can arise either de novo, or secondarily from papillary and follicular thyroid cancer. The incidence of thyroid cancer has significantly increased for both males and females of all ages, particularly for females between 55‑64 years of age, from 1999 through 2008. The increased rates refer to tumors of all stages, though they were mostly noted in localized disease. Recently, viruses have been implicated in the direct regulation of epithelial‑mesenchymal transition (EMT) and the development of metastases. More specifically, Epstein‑Barr virus (EBV) proteins may potentially lead to the development of metastasis through the regulation of the metastasis suppressor, Nm23, and the control of Twist expression. The significant enhancement of the metastatic potential, through the induction of angiogenesis and changes to the tumor microenvironment, subsequent to viral infection, has been documented, while EMT also contributes to cancer cell permissiveness to viruses. A number of viruses have been identified to be associated with carcinogenesis, and these include lymphotropic herpesviruses, namely EBV and Kaposi's sarcoma-associated herpesvirus [KSHV, also known as human herpesvirus type 8 (HHV8)]; two hepatitis viruses, hepatitis B virus (HBV) and hepatitis C virus (HCV); human papillomaviruses (HPVs); human T cell lymphoma virus (HTLV); and a new polyomavirus, Merkel cell polyomavirus identified in 2008. In this review, we examined the association between thyroid cancer and two oncogenic virus families, the herpes and polyoma family viruses, and we discuss their potential role as causative agents in thyroid carcinogenesis.
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March-2016
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Spandidos Publications style
Stamatiou DP, Derdas SP, Zoras OL and Spandidos DA: Herpes and polyoma family viruses in thyroid cancer (Review). Oncol Lett 11: 1635-1644, 2016.
APA
Stamatiou, D.P., Derdas, S.P., Zoras, O.L., & Spandidos, D.A. (2016). Herpes and polyoma family viruses in thyroid cancer (Review). Oncology Letters, 11, 1635-1644. https://doi.org/10.3892/ol.2016.4144
MLA
Stamatiou, D. P., Derdas, S. P., Zoras, O. L., Spandidos, D. A."Herpes and polyoma family viruses in thyroid cancer (Review)". Oncology Letters 11.3 (2016): 1635-1644.
Chicago
Stamatiou, D. P., Derdas, S. P., Zoras, O. L., Spandidos, D. A."Herpes and polyoma family viruses in thyroid cancer (Review)". Oncology Letters 11, no. 3 (2016): 1635-1644. https://doi.org/10.3892/ol.2016.4144