Abstract
The role of specific human papillomaviruses (HPVs) in the aetiology of cancer of the cervix is firmly established. Progression of an HPV-infected cell clone to invasive growth involves consecutive modifications of a set of host cell genes. Some of these modifications suppress viral oncogene functions post-transcriptionally, and others suppress transcription via a signalling pathway stimulated by activated macrophages and possibly by additional cells. I describe a scheme that tries to unify available data by postulating the existence of two intracellular signalling pathways in the control of latent HPV infections.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
