A comprehensive analysis of HPV integration loci in anogenital lesions combining transcript and genome-based amplification techniques.
about
The 3' region of human papillomavirus type 16 early mRNAs decrease expression.Mate-Pair Sequencing as a Powerful Clinical Tool for the Characterization of Cancers with a DNA Viral EtiologyMatrix and backstage: cellular substrates for viral vaccinesMolecular mechanisms of HPV mediated neoplastic progressionMYC activation associated with the integration of HPV DNA at the MYC locus in genital tumorsMultiple-integrations of HPV16 genome and altered transcription of viral oncogenes and cellular genes are associated with the development of cervical cancerComparison of prevalence, viral load, physical status and expression of human papillomavirus-16, -18 and -58 in esophageal and cervical cancer: a case-control study.Microbial Signatures Associated with Oropharyngeal and Oral Squamous Cell Carcinomas.High-risk HPV E5-induced cell fusion: a critical initiating event in the early stage of HPV-associated cervical cancer.HPV genotype detection using hybrid capture sample preparation combined with whole genome amplification and multiplex detection with Luminex XMAPDiagnosis of 25 genotypes of human papillomaviruses for their physical statuses in cervical precancerous/cancerous lesions: a comparison of E2/E6E7 ratio-based vs. multiple E1-L1/E6E7 ratio-based detection techniquesNon-random integration of the HPV genome in cervical cancer.HPV genotyping and site of viral integration in cervical cancers in Indian women.Subcellular localization of the human papillomavirus 16 E7 oncoprotein in CaSki cells and its detection in cervical adenocarcinoma and adenocarcinoma in situ.Some novel insights on HPV16 related cervical cancer pathogenesis based on analyses of LCR methylation, viral load, E7 and E2/E4 expressionsTwo distinct pathways to development of squamous cell carcinoma of the vulva.Human papillomavirus type 16 (HPV-16) genomes integrated in head and neck cancers and in HPV-16-immortalized human keratinocyte clones express chimeric virus-cell mRNAs similar to those found in cervical cancers.Presence of E6 and E7 mRNA from human papillomavirus types 16, 18, 31, 33, and 45 in the majority of cervical carcinomas.Human papillomavirus type 16 integration in cervical carcinoma in situ and in invasive cervical cancer.Cidofovir selectivity is based on the different response of normal and cancer cells to DNA damage.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.Mechanisms of genomic instability in human cancer: insights from studies with human papillomavirus oncoproteins.Mechanisms of human papillomavirus-induced oncogenesis.Reconstruction of human papillomavirus type 16-mediated early-stage neoplasia implicates E6/E7 deregulation and the loss of contact inhibition in neoplastic progressionMolecular mechanisms of human papillomavirus-induced carcinogenesis.Meta-Analysis of DNA Tumor-Viral Integration Site Selection Indicates a Role for Repeats, Gene Expression and Epigenetics.HPV Population Profiling in Healthy Men by Next-Generation Deep Sequencing Coupled with HPV-QUEST.Comprehensive mapping of the human papillomavirus (HPV) DNA integration sites in cervical carcinomas by HPV capture technologyLandscape of DNA virus associations across human malignant cancers: analysis of 3,775 cases using RNA-SeqGenetic determinants in head and neck squamous cell carcinoma and their influence on global personalized medicine.Expression of betapapillomavirus oncogenes increases the number of keratinocytes with stem cell-like properties.Oncogenic activities of human papillomaviruses.Evidences suggesting involvement of viruses in oral squamous cell carcinoma.HPV16 integration probably contributes to cervical oncogenesis through interrupting tumor suppressor genes and inducing chromosome instability.Role of human papillomavirus in the pathogenesis of oral squamous cell carcinoma.Cytokeratin7 and cytokeratin19 expression in high grade cervical intraepithelial neoplasm and squamous cell carcinoma and their possible association in cervical carcinogenesis.HPV positive neuroendocrine cervical cancer cells are dependent on Myc but not E6/E7 viral oncogenes.Next-generation treatment strategies for human papillomavirus-related head and neck squamous cell carcinoma: where do we go?
P2860
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P2860
A comprehensive analysis of HPV integration loci in anogenital lesions combining transcript and genome-based amplification techniques.
description
2003 nî lūn-bûn
@nan
2003年の論文
@ja
2003年学术文章
@wuu
2003年学术文章
@zh
2003年学术文章
@zh-cn
2003年学术文章
@zh-hans
2003年学术文章
@zh-my
2003年学术文章
@zh-sg
2003年學術文章
@yue
2003年學術文章
@zh-hant
name
A comprehensive analysis of HP ...... ased amplification techniques.
@en
A comprehensive analysis of HP ...... ased amplification techniques.
@nl
type
label
A comprehensive analysis of HP ...... ased amplification techniques.
@en
A comprehensive analysis of HP ...... ased amplification techniques.
@nl
prefLabel
A comprehensive analysis of HP ...... ased amplification techniques.
@en
A comprehensive analysis of HP ...... ased amplification techniques.
@nl
P2093
P2860
P356
P1433
P1476
A comprehensive analysis of HP ...... ased amplification techniques.
@en
P2093
Corina Ziegert
Fjodor Kisseljov
Jens Einenkel
Magnus von Knebel Doeberitz
Michael Hoeckel
Svetlana Vinokurova
P2860
P2888
P304
P356
10.1038/SJ.ONC.1206629
P407
P577
2003-06-01T00:00:00Z