Physical state and expression of HPV DNA in benign and dysplastic cervical tissue: different levels of viral integration are correlated with lesion grade

Hudelist, Gernot; Manavi, M.; Pischinger, K.; Watkins-Riedel, Thomas; Singer, Christian F.; Kubista, E.; Czerwenka, K.

doi:10.1016/j.ygyno.2003.11.035

Cited by 171 publications

(162 citation statements)

References 29 publications

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“…HPV 16 displays a generally higher risk for invasive cervical cancer development over viral load categories than HPV 18 and HPV 31. Interestingly, HPV 16 appears to be able to induce malignant transformation without integration (Pirami et al, 1997;Badaracco et al, 2002;Hudelist et al, 2004). This indicates that additional factors to integration may be important for malignant transformation.…”

Section: Discussionmentioning

confidence: 99%

High viral loads of human papillomavirus predict risk of invasive cervical carcinoma

et al. 2005

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Section: Discussionmentioning

confidence: 99%

High viral loads of human papillomavirus predict risk of invasive cervical carcinoma

et al. 2005

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“…The RTPCR probes were modified at the 5 0 terminus with the reporter dye 6-carboxy-fluorescein (FAM), and at the 3 0 terminus with the non-fluorescent quencher Black Hole TM -1. The primers and probe sequences for HPV16 and HPV18 were from Tucker et al 29 The nucleotide sequences of the selected HPV types (16,18,31,39,45, 51, 52 and 58) primers and probes sequences are described elsewhere. 28 The standard curves for absolute quantification of HPV type specific target transcripts were generated as previously reported 28 using the E6-E7 region of HPV16, HPV18, HPV45 and HPV51 and the complete sequence for HPV31, HPV39, HPV52 and HPV58, that had been cloned into plasmid vectors.…”

Section: Hpv Viral Load Assessmentmentioning

confidence: 99%

“…A cross-sectional study of 2,319 women was conducted between 1997 and 1998. Viral load of oncogenic HPV types (16,18,31,39, 45, 51, 52, and 58) was measured among 173 HPV (1) women using quantitative real-time PCR. Overall, HPV 16, 31, 52 and 58 showed the highest viral load.…”

mentioning

confidence: 99%

Cross‐sectional analysis of oncogenic HPV viral load and cervical intraepithelial neoplasia

Flores

Papenfuss

Klimecki

et al. 2005

Intl Journal of Cancer

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In human papillomavirus (HPV)-associated carcinogenesis, HPV infection characteristics such as viral load may play an important role in lesion development. The purpose of this study was to determine the association between quantitative assessment of oncogenic HPV viral load, and abnormal cytology among women residing along the United States-Mexico border. A cross-sectional study of 2,319 women was conducted between 1997 and 1998. Viral load of oncogenic HPV types (16,18,31,39, 45, 51, 52, and 58) was measured among 173 HPV (1) women using quantitative real-time PCR. Overall, HPV 16, 31, 52 and 58 showed the highest viral load. Single type infection had higher viral loads compared to multiple type infections. HPV viral load declined significantly (p 5 0.04) with age. No significant association was observed with other known HPV risk factors such as oral contraceptive use, parity, sexual and STD history. Viral load was independently associated with degree of cervical lesions. An adjusted odds ratio (AOR) of 4.7 for the association between increasing total viral load and Atypical Squamous Cells of Undetermined Significance (ASCUS)/ Atypical Glandular Cells of Undetermined Significance (AGUS) was observed (p for trend <0.01). Increased risk of low-grade SIL was observed with higher viral load compared with HPV negative women (AOR 5 47.7 for total viral load; AOR 5 37.1 for HPV viral load not including HPV16, and AOR 5 25.9 for HPV16 viral load). Likewise, increased risk of high-grade SIL with higher viral loads was observed (AOR 5 58.4 for high total viral load compared with HPV negative women, AOR 5 58.1 for HPV viral load not including HPV16, and AOR 5 69.8 for HPV16 high viral load). Results from this study suggest a dose-response relationship between increasing oncogenic HPV viral load and risk of LSIL and HSIL. ' 2005 Wiley-Liss, Inc.Key words: human papillomavirus; viral load; cervical lesions Squamous intraepithelial lesions (SIL) are the precursor lesions for the development of cervical cancer and are caused primarily by infection with human papillomavirus (HPV). Cervical cancer, however, does not occur without the persistent presence of HPV in the squamo-columnar junction. 1 Since the majority of cervical lesions regress to normal cytology after a period of 12 months from presumed first infection, it is thought that the remaining cervical lesions persist due to environmental, host and viral cofactors that have a pleiotropic effect on HPV viral replication, the immune system and tissue microenvironment. [2][3][4][5][6][7][8][9][10] Recent studies suggest that HPV16 viral load may be a possible molecular biomarker in the natural history of HPV infection. Using a semi-quantitative measure of HPV16 DNA levels, several observational studies have found a high correlation between high viral load and high-grade intra-epithelial lesions. Although a possible role for HPV16 viral load has emerged, only a few studies have used quantitative measures of viral load to study the association of distinct oncogenic HPV types a...

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“…Oncogenic transformation is believed to be triggered in part by the integration of the viral genome into a host chromosome, leading to unregulated expression of the oncogenes E6 and E7 (Hudelist et al, 2004). E6 degrades p53, whereas E7 is involved in deregulation of the Rb/E2F pathway (reviewed by Doorbar, 2006).…”

mentioning

confidence: 99%

The E7 protein from human papillomavirus type 16 enhances keratinocyte migration in an Akt-dependent manner

Charette

McCance

2007

Oncogene

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Physical state and expression of HPV DNA in benign and dysplastic cervical tissue: different levels of viral integration are correlated with lesion grade

Cited by 171 publications

References 29 publications

High viral loads of human papillomavirus predict risk of invasive cervical carcinoma

High viral loads of human papillomavirus predict risk of invasive cervical carcinoma

Cross‐sectional analysis of oncogenic HPV viral load and cervical intraepithelial neoplasia

The E7 protein from human papillomavirus type 16 enhances keratinocyte migration in an Akt-dependent manner

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