ArticleThe American journal of pathology1998
Post-transcriptional induction of p21cip1 protein in condylomata and dysplasias is inversely related to human papillomavirus activities.
Article in The American journal of pathology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 27 citations in OpenAlex.
- Human papillomavirus infections: warts or cancer?Cold Spring Harbor perspectives in biology · 2013Review
- Conditionally activated E7 proteins of high-risk and low-risk human papillomaviruses induce S phase in postmitotic, differentiated human keratinocytes.Journal of virology · 2006Article
- Expression of p21(WAF1) and p53 and polymorphism of p21(WAF1) gene in gastric carcinoma.World journal of gastroenterology · 2004Article
- Activation of adenovirus early promoters and lytic phase in differentiated strata of organotypic cultures of human keratinocytes.Journal of virology · 2003Article
- The causal relation between human papillomavirus and cervical cancer.Journal of clinical pathology · 2002Review
- Alternative fates of keratinocytes transduced by human papillomavirus type 18 E7 during squamous differentiation.Journal of virology · 2002Article
- Patterns of p21(waf1/cip1) expression in non-papillomatous nasal mucosa, endophytic sinonasal papillomas, and associated carcinomas.Journal of clinical pathology · 2001Article
- p21cip1 Degradation in differentiated keratinocytes is abrogated by costabilization with cyclin E induced by human papillomavirus E7.Journal of virology · 2001Article
- Cyclin dependent kinase inhibitor p27Kip1 expression in normal and neoplastic cervical epithelium.Journal of clinical pathology · 1999Article
- Article
- Interaction between cyclin-dependent kinases and human papillomavirus replication-initiation protein E1 is required for efficient viral replication.Proceedings of the National Academy of Sciences of the United States of America · 1999Article
- Viral E6-E7 transcription in the basal layer of organotypic cultures without apparent p21cip1 protein precedes immortalization of human papillomavirus type 16- and 18-transfected human keratinocytes.Journal of virology · 1998Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Infections of the genital and oral epithelia by human papillomaviruses cause condylomata, papillomas, and squamous intraepithelial neoplasms, some of which can progress to invasive cancers. We describe an induction of p21cip1/WAF1/sdi1 protein in a fraction of the spinous cells in benign lesions and in cervical intraepithelial neoplasia grades I and II. The induction appears to be post-transcriptional and independent of p53. p21cip1 antigen-positive cells were sporadic in cervical intraepithelial neoplasia III and rare and focal in carcinomas. In contrast, p21cip1 protein was below or at the threshold of detection in the differentiated cells of normal squamous epithelia from different body sites despite an up-regulation of p21cip1 RNA. In cervical intraepithelial neoplasias from patients who were also positive for the human immunodeficiency virus, there was an additional increase in p21cip1 RNA in the upper spinous cells without concomitant p21cip1 protein induction. A consistent inverse relationship was observed between the p21cip1 protein induction and abundant human papillomavirus DNA and RNAs. We propose that p21cip1 protein induction is a novel host response that inhibits viral DNA replication and thus prevents elevated viral transcription. This hypothesis can partly account for the heterogeneity and the differentiation-dependent viral activities commonly observed in benign human papillomavirus lesions.
Indexed as
Identifiers
9546362PMC1858250W265187898What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.