Detailed screening data for the 40- to 49-year age group of all Swedish trials should be analyzed to specifically estimate the natural history and performance of screening in this age group.

No abstract

Summary Human papillomavirus (HPV) is the main risk factor for invasive cervical cancer. High risk ratios are found in cross-sectional data on HPV prevalence. The question raised is whether this present evidence is sufficient for making firm recommendations on HPV screening. A validated cervical cancer screening model was extended by adding HPV infection as a possible precursor of cervical intraepithelial neoplasia (CIN). Two widely different model quantifications were constructed so that both were compatible with the observed HPV risk ratios. One model assumed a much longer duration of HPV infection before progressing to CIN and a higher sensitivity of the HPV test than the other. In one version of the model, the calculated mortality reduction from HPV screening was higher and the (cost-)effectiveness was much better than for Pap smear screening. In the other version, outcomes were the opposite, although the cost-effectiveness of the combined HPV + cytology test was close to that of Pap smear screening. Although small follow-up studies and studies with limited strength of design suggest that HPV testing may well improve cervical cancer screening, only large longitudinal screening studies on the association between HPV infection and the development of neoplasias can give outcomes that would enable a firm conclusion to be made on the (cost-)effectiveness of HPV screening. Prospective studies should address women aged 30-60 years.Keywords: cervical cancer; human papilloma virus; mass screening; Pap smear; cost-effectiveness Molecular and epidemiological studies have clearly demonstrated that HPV is the main risk factor for cervical cancer (IARC working group, 1995;Zur Hausen, 1994). These epidemiological studies are case-control studies that consistently show a very highrisk ratio for HPV in women with (precursors of) cervical cancer compared with controls with negative cytology (Morrison et al, 1991; Munoz et al, 1992; Elut-Neto et al, 1994;De SanJose et al, 1994). The association between CIN and high-risk HPV infection is stronger in high-grade than in low-grade abnormalities (van den Brule et al, 1991;Bergeron et al, 1992;Lorincz et al, 1992;Gaarenstroom, 1994; Kjear et al, 1996) and is well over 90% in invasive cancers (van den Brule et al, 1991;Bosch et al, 1995). A few small follow-up studies also corroborate the crucial role of HPV infections: progression is found almost only in women with (persistent) high-risk HPV genotypes both in normal (Rozendaal et al, 1996) and in dysplastic cases Remmink et al, 1995). In a small retrospective study on archived false-negative smears from women with subsequent invasive cervical cancer, the high-risk HPV types found in the cancers were detected in nearly 100% of the preceding smears (Munoz et al, 1992;Bauer et al, 1993;Cuzick et al, 1995;Rozendaal et al, 1996). This is much higher than can be explained by the life-time risk of developing cervical cancer in these countries. For example, in the Netherlands, the rate for high-risk HPV types in woman aged 30+ with norm...

If the budget for the NHS breast screening programme were to allow for two more invitations per woman, substantial mortality reductions would follow from extending the age range screened or reducing the screening interval. The difference between the two policies is so small that either could be chosen.

Objectives-To estimate the number of breast cancer deaths induced by low dose radiation in breast cancer screening programmes compared with numbers prevented. Methods-A computer simulation model on the natural history of breast cancer was combined with a model from BEIR-V on induced breast cancer mortality from low levels of radiation.