Analysis of p16INK4a and integrated HPV genomes as progression markers

Most cervical cancers are preventable when the precursor lesions are detected in time. Human papilloma viruses (HPVs) are the main risk factors for cervical cancer development, but there is a high percentage of healthy women infected with HPV that never develop a lesion. Only a small percentage of l...

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Bibliographic Details
Published inMethods in molecular medicine Vol. 119; p. 73
Main Authors Vinokurova, Svetlana, Wentzensen, Nicolas, von Knebel Doeberitz, Magnus
Format Journal Article
LanguageEnglish
Published United States 2005
Subjects
Base Sequence
Biomarkers
Cervical Intraepithelial Neoplasia - pathology
Cervical Intraepithelial Neoplasia - virology
Cyclin-Dependent Kinase Inhibitor p16 - analysis
Cyclin-Dependent Kinase Inhibitor p16 - genetics
Disease Progression
DNA Primers
DNA, Viral - genetics
DNA, Viral - isolation & purification
Female
Humans
Papillomaviridae - genetics
Papillomavirus Infections - diagnosis
Papillomavirus Infections - pathology
Transcription, Genetic
Virus Integration
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Summary:Most cervical cancers are preventable when the precursor lesions are detected in time. Human papilloma viruses (HPVs) are the main risk factors for cervical cancer development, but there is a high percentage of healthy women infected with HPV that never develop a lesion. Only a small percentage of low-grade dysplasias finally grow out to invasive cancer. Several biomarkers can be used to identify lesions at risk for malignant progression. Overexpression of p16INK4a is induced by the viral oncoprotein E7 and distinguishes dysplastic lesions from benign changes. Integration of human papillomavirus DNA into the host genome is mainly found in high-grade dysplastic lesions and invasive cancers, and points to an increased progression potential.
ISSN:1543-1894