Loss of gene function as a consequence of human papillomavirus DNA integration.
about
Identification of episomal human papillomavirus and other DNA viruses in cytological anal samples of HIV-uninfected men who have sex with men.Reduction in the copy number and expression level of the recurrent human papillomavirus integration gene fragile histidine triad (FHIT) predicts the transition of cervical lesions.Mobile elements and viral integrations prompt considerations for bacterial DNA integration as a novel carcinogenNon-random integration of the HPV genome in cervical cancer.Characterization of HPV and host genome interactions in primary head and neck cancers.Multiplex Identification of Human Papillomavirus 16 DNA Integration Sites in Cervical Carcinomas.Comprehensive analysis of HPV16 integration in OSCC reveals no significant impact of physical status on viral oncogene and virally disrupted human gene expression.Transcriptionally active regions are the preferred targets for chromosomal HPV integration in cervical carcinogenesis.Chromosomal copy number alterations and HPV integration in cervical precancer and invasive cancerEvidence of disrupted high-risk human papillomavirus DNA in morphologically normal cervices of older women.CASZ1 inhibits cell cycle progression in neuroblastoma by restoring pRb activityDysregulation of host cellular genes targeted by human papillomavirus (HPV) integration contributes to HPV-related cervical carcinogenesis.HPV16 integration probably contributes to cervical oncogenesis through interrupting tumor suppressor genes and inducing chromosome instability.Identification of CASZ1 NES reveals potential mechanisms for loss of CASZ1 tumor suppressor activity in neuroblastoma.Genome-wide analysis of HPV integration in human cancers reveals recurrent, focal genomic instabilityRUNX3 and CAMK2N1 hypermethylation as prognostic marker for epithelial ovarian cancer.Genomic characterization of viral integration sites in HPV-related cancers.Genome-wide profiling of HPV integration in cervical cancer identifies clustered genomic hot spots and a potential microhomology-mediated integration mechanism.Induction of dormancy in hypoxic human papillomavirus-positive cancer cells.Viral-Cellular DNA Junctions as Molecular Markers for Assessing Intra-Tumor Heterogeneity in Cervical Cancer and for the Detection of Circulating Tumor DNA.Development of safer gene delivery systems to minimize the risk of insertional mutagenesis-related malignancies: a critical issue for the field of gene therapy.The precision prevention and therapy of HPV-related cervical cancer: new concepts and clinical implications
P2860
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P2860
Loss of gene function as a consequence of human papillomavirus DNA integration.
description
2012 nî lūn-bûn
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2012年の論文
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2012年学术文章
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2012年学术文章
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2012年学术文章
@zh-cn
2012年学术文章
@zh-hans
2012年学术文章
@zh-my
2012年学术文章
@zh-sg
2012年學術文章
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2012年學術文章
@zh-hant
name
Loss of gene function as a consequence of human papillomavirus DNA integration.
@en
Loss of gene function as a consequence of human papillomavirus DNA integration.
@nl
type
label
Loss of gene function as a consequence of human papillomavirus DNA integration.
@en
Loss of gene function as a consequence of human papillomavirus DNA integration.
@nl
prefLabel
Loss of gene function as a consequence of human papillomavirus DNA integration.
@en
Loss of gene function as a consequence of human papillomavirus DNA integration.
@nl
P2093
P2860
P356
P1476
Loss of gene function as a consequence of human papillomavirus DNA integration.
@en
P2093
Corina Driesch
Ingo B Runnebaum
Katrin Beer-Grondke
Lars Jansen
Martina Schmitz
Matthias Dürst
P2860
P304
P356
10.1002/IJC.27433
P577
2012-02-22T00:00:00Z