Immortalization of oral keratinocytes by functional inactivation of the p53 and pRb pathways

@article{Smeets2011ImmortalizationOO,
  title={Immortalization of oral keratinocytes by functional inactivation of the p53 and pRb pathways},
  author={Serge J. Smeets and Marlon van der Plas and Tieneke B.M. Schaaij-Visser and Eva A M van Veen and Johan van Meerloo and Boudewijn J. M. Braakhuis and Renske D. M. Steenbergen and Ruud H. Brakenhoff},
  journal={International Journal of Cancer},
  year={2011},
  volume={128}
}
A subgroup of head and neck squamous cell carcinomas (HNSCCs) contains high‐risk human papillomavirus‐type 16 (HPV16). The viral E6 and E7 oncoproteins inactivate the p53 and pRb proteins, respectively. We examined the causative effect of HPV16 E6 and E7 expression on the immortalization of normal oral keratinocytes (OKCs) and compared the resulting phenotype with alternative ways of p53‐ and pRb‐pathway abrogation frequently found in HNSCCs without HPV. Primary OKCs were conditionally… 
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101 Citations

Human Papillomavirus (HPV)-Positive Head and Neck Cancer and the Wnt Signaling Pathway

This chapter summarizes the possible cell pathways involved in the activation of Wnt signaling in HPV-positive head and neck cancer.

Molecular genetic characterization of p53 mutated oropharyngeal squamous cell carcinoma cells transformed with human papillomavirus E6 and E7 oncogenes

The data suggest that upregulated STAT1 and interferon signals by HPV16 E6 and E7 genes may play a major role in the relatively favorable prognosis for HPV-positive oropharyngeal squamous cell carcinoma cases with non-disruptive p53 mutations.

Advances in Tumor Virology Role of HPV in Head and Neck Cancer

The experimental and epidemiological data provide robust evidence for a causal role in OPSCC, but the evidence for association of HPV with other HNSCC such as oral cavity or larynx is weak.

miR-31 is upregulated in oral premalignant epithelium and contributes to the immortalization of normal oral keratinocytes.

It can be concluded that miR-31 collaborates with hTERT to immortalize NOKs and that this may contribute to early stage oral carcinogenesis.

A Non-oncogenic HPV 16 E6/E7 Vaccine Enhances Treatment of HPV Expressing Tumors

The generation of an HPV16 E6/E7 construct is described, which contains mutations that render E6-E7 non-oncogenic, while preserving antigenicity, and which statistically enhances clearance of established HPV(+) cancer in vivo.

The role of human papillomavirus in p16‐positive oral cancers

  • Simone BelobrovA. Cornall M. McCullough
  • Biology, Medicine
    Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology
  • 2018
It is shown that the presence of transcriptionally active HPV rarely occurs inOSCC and that p16 is not an appropriate surrogate marker for HPV in OSCC cases, and it is proposed that non-viral mechanisms are responsible for the majority of IHC p16 overexpression in OS CC.

Concomitant inactivation of the p53‐ and pRB‐ functional pathways predicts resistance to DNA damaging drugs in breast cancer in vivo

Differentiation-promoting culture of competent and noncompetent keratinocytes identifies biomarkers for head and neck cancer.

Identification of High-Risk Human Papillomavirus DNA, p16, and E6/E7 Oncoproteins in Laryngeal and Hypopharyngeal Squamous Cell Carcinomas

A high prevalence of HPV16 as a primary HR-HPV type in LSCC and HPSCC is suggested and the lack of HPV E6/E7 oncoproteins in some tumor samples may suggest either the absence of viral integration or the presence of other mechanisms of tumorigenesis.

HPV DNA, E6*I-mRNA expression and p16INK4A immunohistochemistry in head and neck cancer - how valid is p16INK4A as surrogate marker?

...

References

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