The cancer registry data in combination with tumour and vital status from the Toltrazuril database were used as the observed numbers of breast cancers for the purpose of comparison.For analysis, women had all elements of hormonal, reproductive, and Epiandrosterone computerised pedigree available, and of these had cancer at initial assessment.There was a missing element to the dataset for women, which did not allow analysis in every risk package.Lifetime and year risk for developing breast cancer were estimated using each of the models.Methods for risk estimation differed between the models. These computerised models were then compared with a manual risk calculation, which was calculated in clinic.The latter of these can then used to compute year risks.This adjustment allowed for a maximum upwards or downwards change in risk based on a combination of hormonal and reproductive factors.In practice, this meant a greater reduction than increase in the higher risk categories.As it is not possible to increase lifetime risk of above, only a maximum upwards variation of the heterozygote risk is possible.Therefore her risk calculated from family history can vary upwards from to, but may drop by to, that is, a population risk of and a hereditary risk of. The outputs of all these models were used as the expected numbers of breast cancers.In order to express the predicted risk in terms of the follow up period, projections of the absolute year risk were obtained from the models.These were then converted first into an annual risk, and then into a follow up risk by multiplication by the number of years of follow up.This was carried out by first solving the CI for O, specifically the values of OL for the lower limit and OU for the upper limit, and then dividing E by the values of OL and OU to obtain the upper and lower CI for this ratio.Downo adedlfrom part, comparison based on subgroups of the study population, using the following risk factor categories.In addition to the overall accuracy in terms of the numbers of cancers predicted, the accuracy for individual cases was also evaluated, that is, the ability of the models to separate individuals who will go on to develop disease from those who will be disease free.To do this, the probability of developing cancer for the period at risk was calculated for each woman using the different models, and receiver operating characteristic curves were generated.These are plots of the true positive rate against the false positive rate for different possible cut off points.They show the trade off between sensitivity and specificity of the different models. In order to distinguish formally high risk from low risk subjects, the C statistic was calculated.The age range of diagnosed cancers was years in the overall population and years in the screening group, although one cancer was detected in a year old woman who commenced screening at years.The degree of family history is presented in table. Risk assessment using all five models was not possible in women on the database because of missing values for one or more of the criteria used by the models.