Viral interaction: a possible contributing factor in head and neck cancer progression

  title={Viral interaction: a possible contributing factor in head and neck cancer progression},
  author={Michael P Underbrink and Stephen L. Hoskins and Anna Maria Pou and Thomas Albrecht},
  journal={Acta Oto-Laryngologica},
  pages={1361 - 1369}
Conclusion. Human herpesvirus-8 could potentiate the effects of human papillomavirus (HPV)-16 on cell cycle dysregulation by up-regulating the transcription of HPV-16 E7, which can lead to malignant transformation of normal epithelial cells. Objectives. High-risk HPV-16 is known for its association with development of head and neck carcinoma, leading to considerable morbidity and mortality worldwide. HPV-16 produces two early proteins, E6 and E7, that can disrupt the cell cycle and transform… 

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The recent finding from clinic and bench indicating KSHV co-infection may represent a co-factor for the development of HPV-related carcinogenesis is summarized.

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    Clinical journal of oncology nursing
  • 2011
High-risk strains of the human papillomavirus (HPV) already are associated with cervical, oral, and anal cancers; however, HPV DNA has been detected in about a third of head and neck malignancies.

Acetylcholinesterase and HHV-8 in squamous cell carcinoma and retinoblastoma.

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The oncogenic role of human papillomavirus proteins.

  • M. Barbosa
  • Biology
    Critical reviews in oncogenesis
  • 1996
The evidence, molecular and biological, in vitro and in vivo, supporting a direct role for the "high-risk" HPV type encoded E6 and E7 proteins in cervical carcinogenesis is discussed.

Effect of herpes simplex virus on the DNA of human papillomavirus 18

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Viruses in human cancers

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Rta of the human herpesvirus 8/Kaposi sarcoma-associated herpesvirus up-regulates human interleukin-6 gene expression.

Evidence is presented that the human IL-6 (hIL-6) gene is up-regulated by Rta, a transcriptional activator encoded by HHV-8/KSHV that activates the viral lytic cycle leading to the expression of several viral genes implicated in viral pathogenesis.

The role of Kaposi's sarcoma-associated herpesvirus/human herpesvirus-8 regulator of transcription activation (RTA) in control of gene expression

Modulation of transactivation, through alternate RTA-protein, or Rta-promoter interactions, is hypothesisized to participate in the selective tissue tropism and differential pathogenesis observed in KS.

Human herpesvirus-8 (Kaposi's sarcoma-associated herpesvirus) ORF50 interacts synergistically with the tat gene product in transactivating the human immunodeficiency virus type 1 LTR.

It is suggested that ORF57 can modulate ORF50 activity and that OrF50 may render biologically active small amounts of tat, which is likely mediated by the induction of other viral functions.

The E6 and E7 genes of the human papillomavirus type 16 together are necessary and sufficient for transformation of primary human keratinocytes

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DNA Binding by Kaposi's Sarcoma-Associated Herpesvirus Lytic Switch Protein Is Necessary for Transcriptional Activation of Two Viral Delayed Early Promoters

A DNA binding site for the ORF50 protein is identified that is shared by the promoters of two delayed early genes (ORF57 and K-bZIP) and transfer of this element to heterologous promoters confers on them high-level responsiveness to OrF50, indicating that the element is both necessary and sufficient for activation.

Kaposi’s sarcoma-associated herpesvirus/human herpesvirus-8 ORF50 gene product contains a potent C-terminal activation domain which activates gene expression via a specific target sequence

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