10 maart 2005: Bron: British Journal of Cancer (2005) 92, 891-894. doi:10.1038/sj.bjc.6602436 Published online 1 March 2005

Hoge virale waarden van het human papillomavirus voorspellen hoog riscio op uitgezaaide baarmoederhalskanker. Aldus een studie uitgevoerd in Zweden.Hier achtereenvolgens het abstract en daaronder de deeplink naar het volledige studieverslag en de conclusie.

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

M Moberg1, I Gustavsson1, E Wilander1 and U Gyllensten1 1Department of Genetics and Pathology, Rudbeck Laboratory, Uppsala University, Uppsala 751 85, Sweden. Correspondence to: Dr U Gyllensten, E-mail: ulf.gyllensten@genpat.uu.se

Received 28 July 2004; revised 13 December 2004; accepted 4 January 2005; published online 1 March 2005

Abstract:
High loads of human papillomavirus (HPV) 16 and HPV 18/45 increase the risk of developing invasive cervical carcinoma, revealing higher risk in percentiles of highest viral loads for HPV 16 (odds ratio (OR) 58.7, 95% confidence interval (CI) 21.9-151.4) compared to HPV 18/45 (OR 3.3, 95% CI 1.5-7.2). Thus, HPV load is a type-dependent risk marker for invasive carcinoma.

Op deze website kunt u het volledige studieverslag lezen. Hier alleen de conclusie van deze studie:

Results and discussion:

Our results indicate that increasing viral load of HPV 16 in cervical smears increases the risk of future invasive cervical cancer. For HPV 18/45, a significant OR was only seen for the highest viral-load percentile. The relationship between OR of invasive cancer and viral load of HPV 16 is similar to that previously described for CIS (Moberg et al, 2004) (Figure 1); consistent with this, CIS and invasive cervical cancer reflect the same basic aetiology. Thus, our results show that a high viral load in PAP smears is a risk factor not only for the development of CIS but also for invasive cancer. Our data support the hypothesis of Peitsaro et al (2002) that high viral loads are likely to increase the risk for events initiating dysplasia such as viral integration. Given that integration is a random event, the risk for such an event would increase with high viral loads, independent of whether a high viral load reflects widespread infection or high copy numbers per cell. 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. Longitudinal studies including both the physical state and load of the virus are needed in order to determine their relative importance for development of cervical cancer. Judging from our data, HPV load provides information about the risk for subsequent development of invasive carcinomas, but the extent correlates strongly with the HPV type.

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