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 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.
Vinokurova
Svetlana
S
Institute of Molecular Pathology, University of Heidelberg, Germany.
Wentzensen
Nicolas
N
von Knebel Doeberitz
Magnus
M
D001483:Base Sequence; D015415:Biomarkers; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000032:analysis / Q000235:genetics*; D017931:DNA Primers; D004279:DNA, Viral / Q000235:genetics / Q000302:isolation & purification; D018450:Disease Progression; D005260:Female; D006801:Humans; D027383:Papillomaviridae / Q000235:genetics*; D030361:Papillomavirus Infections / Q000175:diagnosis / Q000473:pathology; D014158:Transcription, Genetic; D016662:Virus Integration; D002578:Uterine Cervical Dysplasia / Q000473:pathology / Q000821:virology
D015415:Biomarkers; D019941:Cyclin-Dependent Kinase Inhibitor p16; D017931:DNA Primers; D004279:DNA, Viral