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Analysis of p16(CDKN2A) methylation and HPV-16 infection in oral mucosal dysplasia

Thiago Fonseca-Silva1, Lucyana Conceição Farias, Claudio Marcelo Cardoso

  • 1Department of Dentistry, Universidade Estadual de Montes Claros, Montes Claros, Brazil.

Pathobiology : Journal of Immunopathology, Molecular and Cellular Biology
|January 31, 2012
PubMed
Abstract

Insights

p16(CDKN2A) methylation and HPV-16 presence are linked to epithelial dysplasia (ED) development. These factors may play a role in oral cancer progression, warranting further investigation.

Area of Science:

  • Oncology
  • Molecular Biology
  • Virology

Background:

  • Epithelial dysplasia (ED) is a precancerous condition.
  • p16(CDKN2A) gene methylation is implicated in various cancers.
  • Human Papillomavirus (HPV) infection is a known risk factor for dysplasia and cancer.

Purpose of the Study:

  • To investigate the association between p16(CDKN2A) methylation and epithelial dysplasia (ED).
  • To evaluate the expression of methylation-related proteins (DNMT3B and DNMT1).
  • To determine if HPV-16/18 or the dmt3b polymorphism correlates with p16(CDKN2A) methylation status.

Main Methods:

  • A case-control study involving 72 tissue samples (24 control, 48 ED).
  • Methylation-specific PCR to assess p16(CDKN2A) methylation.
  • RFLP for dmt3b (C46359T) genotyping and immunohistochemistry for protein levels.

Main Results:

  • p16(CDKN2A) methylation and HPV-16 presence were significantly associated with ED gradation (p=0.001 and p=0.002).
  • 77.8% of HPV-16-positive samples showed p16(CDKN2A) methylation.
  • No significant changes in DNMT3B or DNMT1 protein levels were observed in HPV-positive samples; HPV-18 and dmt3b polymorphism were not linked to p16(CDKN2A) methylation.

Conclusions:

  • An association exists between HPV-16, p16(CDKN2A) methylation, and ED.
  • Both HPV-16 and p16(CDKN2A) methylation are linked to ED development.
  • Further research is needed to clarify their independent roles and impact on oral cancer progression.

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