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06:57
Chromogenic In Situ Hybridization as a Tool for HPV-Related Head and Neck Cancer Diagnosis
Published on: June 14, 2019
HPV: from infection to cancer
M A Stanley1, M R Pett, N Coleman
1Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QP, U.K. mas@mole.bio.cam.ac.uk
Biochemical Society Transactions
|November 23, 2007
Summary
Human papillomavirus (HPV) 16 infection can lead to cervical cancer. Interferon (IFN) treatment can select for HPV16-integrated cells, driving cancer progression by altering viral gene expression.
Area of Science:
- Oncology
- Virology
- Immunology
Background:
- Human papillomavirus (HPV) 16 causes over 50% of cervical cancers.
- Most HPV infections are cleared by the immune system, but persistent infections carry cancer risk.
- HPV evades innate immunity by avoiding inflammation during viral replication and disrupting interferon (IFN) signaling via E6 and E7 oncoproteins.
Purpose of the Study:
- To investigate IFN-related interactions in cervical carcinogenesis using the W12 model.
- To understand the selection of cells with integrated HPV16 DNA during cancer progression.
- To examine the effects of exogenous IFN-beta on HPV16-infected keratinocytes.
Main Methods:
- Utilized the W12 model of cervical carcinogenesis.
- Investigated the impact of exogenous IFN-beta treatment on W12 keratinocytes.
- Analyzed changes in viral DNA (episomal vs. integrated), gene expression (E2, E6, E7), and cellular response to IFN.
Main Results:
- Episome loss and induction of antiviral genes precede the selection of cervical keratinocytes with integrated HPV16.
- IFN-beta treatment rapidly selects for IFN-resistant cells, leading to the loss of episome-containing cells.
- Selected cells with integrated HPV16 showed down-regulated E2 expression and up-regulated E6 and E7 oncoprotein expression.
Conclusions:
- Antiviral responses and episome loss are critical events in selecting for integrated HPV16 in cervical cancer progression.
- IFN-beta treatment can inadvertently promote the selection of cells with integrated HPV16, potentially exacerbating cancer development.
- The observed up-regulation of E6 and E7 in integrated HPV16 cells suggests a mechanism for immune evasion and oncogenesis.
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