• Corpus ID: 45584342

Human papillomavirus type 16 integrations in cervical tumors frequently occur in common fragile sites.

@article{Thorland2000HumanPT,
  title={Human papillomavirus type 16 integrations in cervical tumors frequently occur in common fragile sites.},
  author={Erik C. Thorland and Shannon L. Myers and David H. Persing and Gobinda Sarkar and Renee M. McGovern and Bobbie S. Gostout and D. Smith},
  journal={Cancer research},
  year={2000},
  volume={60 21},
  pages={
          5916-21
        }
}
The development of cervical cancer is highly associated with human papillomavirus (HPV) infection. HPV integration into the genome of infected cervical cells is temporally associated with the acquisition of the malignant phenotype. A relationship between the sites of HPV integration in cervical cancer and the position of the common fragile sites (CFSs) has been observed at the cytogenetic level. To explore this relationship at the molecular level, we used a PCR-based method to rapidly isolate… 

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Preferential sites for the integration and disruption of human papillomavirus 16 in cervical lesions.

  • Hui LiYi Yang B. Zhu
  • Biology, Medicine
    Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology
  • 2013

Multiplex Identification of Human Papillomavirus 16 DNA Integration Sites in Cervical Carcinomas

A novel multiplex strategy for sequence determination of HPV16 DNA integration sites worked very efficiently and will open new avenues for comprehensive mapping of HPV integration sites and for the possible use of HPV Integration sites as individualized biomarkers after cancer treatment of patients for the early diagnosis of residual and recurrent disease.

The majority of viral-cellular fusion transcripts in cervical carcinomas cotranscribe cellular sequences of known or predicted genes.

The influence of HPV integration on host gene expression may not be a rare effect and should encourage more detailed analyses, as it is tempting to speculate that as yet unknown fragile sites may be identified on the basis of HPV Integration hotspots.

Mapping and analysis of HPV16 integration sites in a head and neck cancer cell line

The results suggest that viral integration of HPV in SCCHN appears to occur nonrandomly through targeting specific chromosomal sequences prone to breakage.

Human Papillomavirus Integration Strictly Correlates with Global Genome Instability in Head and Neck Cancer

The results indicate that HPV integration in head and neck cancer correlates with extensive pangenomic structural variation, which may have prognostic implications and suggests that HPV Integration status may inform prognosis.

Human papilloma viruses and cervical tumours: mapping of integration sites and analysis of adjacent cellular sequences

Using the known locations of homologous cDNAs and the RH-mapping techniques, mapping studies showed that the INTs are distributed among different human chromosomes for each tumour sample and are located in regions with the high levels of expression.

Systematic Review of Genomic Integration Sites of Human Papillomavirus Genomes in Epithelial Dysplasia and Invasive Cancer of the Female Lower Genital Tract

It is confirmed that HPV integration sites are randomly distributed over the whole genome with a clear predilection for genomic fragile sites, and no evidence for targeted disruption or functional alteration of critical cellular genes by the integrated viral sequences could be found.
...

References

SHOWING 1-10 OF 24 REFERENCES

Integration of papillomavirus DNA near myc genes in genital carcinomas and its consequences for proto-oncogene expression

DNA sequences of specific human papillomavirus (HPV) types are found integrated in the cell genome in most invasive genital carcinomas and support the hypothesis that integration plays a part in tumor progression via an activation of cellular oncogenes.

Allelotyping of all chromosomal arms in invasive cervical cancer.

The results indicate that a significant number of invasive cervical cancers have lost specific chromsomal regions, thereby suggesting that genes involved in the cell cycle regulation or the suppression of tumor development are located in these regions.

Analysis of integrated human papillomavirus type 16 DNA in cervical cancers: amplification of viral sequences together with cellular flanking sequences

It was demonstrated that the integrated HPV-16 DNAs, with different sizes in the same specimens, shared the same cellular flanking sequences at the ends, and it was shown that the viral sequences together with cellular flanks sequences were amplified.

Detection of high-risk cervical intraepithelial neoplasia and cervical cancer by amplification of transcripts derived from integrated papillomavirus oncogenes.

A protocol for the amplification of papillomavirus oncogene transcripts (APOT) from cervical specimens is established that allows us to distinguish episome- from integrate-derived HPV mRNAs.

Molecular analysis of cellular loci disrupted by papillomavirus 16 integration in cervical cancer: Frequent viral integration in topologically destabilized and transcriptionally active chromosomal regions

It is suggested that HPV‐16 genome integrates frequently into topologically destabilized and transcriptionally active chromosomal sites and the myc oncogenes.

FRA3B extends over a broad region and contains a spontaneous HPV16 integration site: direct evidence for the coincidence of viral integration sites and fragile sites.

To the knowledge, this is the first molecular characterization of an in vivo viral integration event within a confirmed fragile site region, supporting previous cytogenetic observations linking viral integration sites and fragile sites.

Chromosomal fragile site FRA16D and DNA instability in cancer.

The FRA16D chromosomal fragile site locus has a role to play in predisposing DNA sequences within and adjacent to the fragile site to DNA instability (such as deletion or translocation), which could lead to or be associated with neoplasia.

APM‐1, a novel human gene, identified by aberrant co‐transcription with papillomavirus oncogenes in a cervical carcinoma cell line, encodes a BTB/POZ‐zinc finger protein with growth inhibitory activity

The identification of a novel human gene, named APM‐1, which is co‐transcribed with the HPV68 E6 and E7 genes and is present in the 3′‐cellular part of the ME180 viral–cellular fusion transcripts.