HPV‐mediated cervical carcinogenesis: concepts and clinical implications

@article{Snijders2006HPVmediatedCC,
  title={HPV‐mediated cervical carcinogenesis: concepts and clinical implications},
  author={Peter J. F. Snijders and Renske D. M. Steenbergen and Dani{\"e}lle A.M. Heideman and Chris J.L.M. Meijer},
  journal={The Journal of Pathology},
  year={2006},
  volume={208}
}
Persistent infection with a high‐risk human papillomavirus (hrHPV) is generally accepted as a necessary cause of cervical cancer. However, cervical cancer is a rare complication of an hrHPV infection since most such infections are transient, not even giving rise to cervical lesions. On average, it takes 12–15 years before a persistent hrHPV infection may ultimately, via consecutive premalignant stages (ie CIN lesions), lead to an overt cervical carcinoma. This argues that HPV‐induced cervical… Expand
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References

SHOWING 1-10 OF 127 REFERENCES
HPV-mediated transformation of the anogenital tract.
TLDR
Early genetic events during cervical carcinogenesis associated with immortalization, include deletions at chromosomes 3p, 6 and 10p, whereas amongst others gain of chromosome 3q, loss of chromosome 11 and epigenetic alterations such as inactivation of the TSLC1 tumor suppressor gene represent later events associated with tumor invasion. Expand
Detection of high-risk cervical intraepithelial neoplasia and cervical cancer by amplification of transcripts derived from integrated papillomavirus oncogenes.
TLDR
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. Expand
Acquisition of High-Level Chromosomal Instability Is Associated with Integration of Human Papillomavirus Type 16 in Cervical Keratinocytes
TLDR
It is demonstrated that high-level chromosomal instability develops in W12 only after integration and that the forms of instability observed correlate with the physical state of HPV16 DNA and the level of E7 protein. Expand
Host genetic control of HPV 16 titer in carcinoma in situ of the cervix uteri
TLDR
Host genetic factors, e.g., variation at the HLA class II loci studied, may affect the immune reaction to the virus and thereby indirectly increase the susceptibility to carcinoma in situ of the cervix uteri. Expand
Spontaneous Regression of High-Grade Cervical Dysplasia: Effects of Human Papillomavirus Type and HLA Phenotype
TLDR
Interactions among HPV type, HLA type, and regression rate support a role for HLA-restricted HPV-specific immune responses in determining disease outcome in women with high-grade cervical lesions. Expand
Notch1 can contribute to viral-induced transformation of primary human keratinocytes.
TLDR
Moderate levels of Notch1 can exhibit oncogenic properties that transform primary cells containing HPV16 E6 and E7 proteins, and cellular proliferation in general, is reported. Expand
Chapter 1: Human papillomavirus and cervical cancer--burden and assessment of causality.
TLDR
State-of-the-art detection techniques have unequivocally shown that HPV-DNA can be detected in 95% to 100% of adequate specimens of cervical cancer, supporting the claim that HPV is the necessary cause. Expand
Type-specific persistence of human papillomavirus DNA before the development of invasive cervical cancer.
TLDR
A single positive finding of HPV DNA in a Pap smear confers an increased risk of future invasive cervical cancer that is positive for the same type of virus as identified earlier. Expand
Human papillomavirus is a necessary cause of invasive cervical cancer worldwide
TLDR
The presence of HPV in virtually all cervical cancers implies the highest worldwide attributable fraction so far reported for a specific cause of any major human cancer, and the rationale for HPV testing in addition to, or even instead of, cervical cytology in routine cervical screening. Expand
TSLC1 gene silencing in cervical cancer cell lines and cervical neoplasia.
TLDR
TSLC1 gene silencing via promoter hypermethylation is a frequent event in the progression from high-risk HPV-containing, high-grade CIN lesions to invasive cervical cancer. Expand
...
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2
3
4
5
...