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The finding of increased risks of specific cancers in individuals with constitutional deletions of chromosomes 11p and 13q led to the discovery of cancer predisposition genes at these locations, but there have been no systematic studies of cancer risks in patients with constitutional deletions, across the chromosome complement. Therefore, we assessed cancer incidence in comparison with national cancer incidence rates in a follow-up of 2561 patients with constitutional autosomal chromosome deletions diagnosed by microscopy or fluorescence in situ hybridisation in Britain during the period 1965-2002. Thirty cancers other than non-melanoma skin cancer occurred in the cohort (standardised incidence ratio (SIR)=2.4, 95% confidence interval (CI) 1.6-3.5). There were significantly increased risks of renal cancer in persons with 11p deletions (SIR=1869, 95% CI 751-3850; P=4 x 10(-21)), eye cancer with 13q deletions (SIR=1084, 95% CI 295-2775; P=2 x 10(-11)), and anogenital cancer with 11q deletions (SIR=305, 95% CI 63-890; P=3 x 10(-7)); all the three latter cancers were in the 11 subjects with 11q24 deletions. The results strongly suggest that in addition to suppressor genes relating to Wilms' tumour risk on 11p and retinoblastoma on 13q, there are suppressor genes around 11q24 that greatly affect anogenital cancer risk.

If infections are involved in the aetiology of childhood leukaemia then seasonal variation in the birth or onset dates of the malignancy may be apparent. Previous studies that have examined seasonality of these dates have produced conflicting results. Using population-based data from the National Registry of Childhood Tumours we conducted a larger study than any to date of 15 835 cases of childhood leukaemia born and diagnosed in the UK between 1953–95. We found no evidence of seasonality in either month of birth or month of diagnosis overall or in any subgroups by age, sex, histology or immunophenotype. We did however find a significant (P= 0.01) February peak in month of birth for cases born before 1960 and a significant (P= 0.02) August peak in month of diagnosis for those diagnosed before 1962. Whilst these findings may be due to chance they are also consistent with changes over time in the seasonality of exposure, or immunological response, to a relevant infection. Changes in the seasonal variation in the fatality rate of a pre-leukaemic illness, such as pneumonia, could be another explanation. © 2001 Cancer Research Campaign http://www.bjcancer.com