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HPV E2, E4, E5 drive alternative carcinogenic pathways in HPV positive cancers.

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A novel pathway in human papillomavirus (HPV) carcinogenesis involves episomal E2/E4/E5 expression, not genome integration. This subtype of HPV-positive cancers shows p53-dependent proliferation and FGFR pathway activation, suggesting new therapeutic targets.

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Area of Science:

  • Oncology
  • Virology
  • Molecular Biology

Background:

  • The established model of human papillomavirus (HPV) carcinogenesis involves viral DNA integration into the host genome, leading to the expression of E6 and E7 oncoproteins.
  • This integration is thought to disrupt host cell cycle regulation, driving malignant transformation.

Purpose of the Study:

  • To investigate an alternative pathway of HPV-driven carcinogenesis characterized by the expression of episomal E2, E4, and E5 proteins.
  • To identify and characterize HPV-positive cancer subtypes associated with this alternative pathway and explore their molecular drivers and therapeutic vulnerabilities.

Main Methods:

  • Analysis of HPV integration status and viral gene expression in patient-derived cervical and pharyngeal cancer samples.
  • In vitro and in vivo modeling to assess the oncogenic potential of episomal E2/E4/E5 expression.
  • Whole-genome expression profiling of identified cancer subtypes.

Main Results:

  • Approximately half of HPV-positive cervical and pharyngeal cancers exhibited a subtype characterized by increased expression of episomal E2/E4/E5 and a lack of viral DNA integration.
  • In vitro and in vivo models demonstrated that E2/E4/E5 expression promotes p53-dependent cellular proliferation and enhances cancer induction.
  • Whole-genome analysis revealed that the E2/E4/E5 pharyngeal cancer subtype is defined by activation of the fibroblast growth factor receptor (FGFR) pathway.

Conclusions:

  • An alternative HPV carcinogenic pathway exists, driven by episomal E2/E4/E5 expression, which is prevalent in a significant subset of HPV-positive cancers.
  • This pathway confers distinct molecular characteristics, including FGFR pathway activation, offering potential for targeted therapeutic strategies.
  • Combination inhibition of FGFR and mTOR pathways shows promise as a targeted therapy for this specific cancer subtype.