Risk of induced abortions in childhood cancer survivors.

BACKGROUND: The relative probability of pregnancy and parenthood in cancer survivors is reduced. Studies have shown that cancer survivors are concerned about the health of their offspring and the recurrence of their own cancer. This could lead to an increased risk of induced abortion. The aim of this study was to examine whether pregnancies of childhood cancer survivors (CCSs) who were 0 to 14 years old at diagnosis in 1971-2012 were more likely to result in induced abortions in comparison with population controls. METHODS: Data from Finnish registries for cancer, births, and induced abortions were merged to identify 420 first pregnancies of CCSs and 2508 first pregnancies of age-matched population controls in 1987-2013. Poisson regression and logistic regression modeling were used to estimate incidence rates and relative risks (RRs) with 95% confidence intervals (CIs) of first pregnancies and induced abortions in CCSs in comparison with population controls. RESULTS: The risk of first pregnancy was reduced in CCSs in comparison with population controls (RR, 0.72; 95% CI, 0.64-0.80), whereas the risk of a first pregnancy resulting in an induced abortion was similar in CCSs and population controls (RR, 1.01; 95% CI, 0.77-1.33). In subanalyses stratifying by decade of diagnosis and cancer treatment, the risk of induced abortion was similar in CCSs and population controls. CONCLUSIONS: Female CCSs do not have an overall increased risk of induced abortions. The reduced probability of pregnancy among CCSs highlights the continued need for interventions to preserve fertility at the time of a cancer diagnosis.

Risk for congenital anomalies in offspring of childhood, adolescent and young adult cancer survivors.

Offspring of cancer survivors (CS) may be at risk for congenital anomalies due to the mutagenic therapies received by their parents. Our population-based cohort study aimed to investigate the risk for congenital anomalies in offspring of CS compared to offspring of their siblings. Using the Finnish Cancer Registry, Central Population Register, and Hospital Discharge Register, we identified hospital contacts due to congenital anomalies in 6,862 offspring of CS (early-onset cancer between 1953 and 2004) and 35,690 offspring of siblings. Associations between congenital anomalies and cancer were evaluated using generalized linear regression modelling. The ratio of congenital anomalies in offspring of CS (3.2%) was slightly, but non-significantly, elevated compared to that in offspring of siblings (2.7%) [prevalence ratio (PR) 1.07, 95% confidence interval (CI) 0.91-1.25]. When offspring of childhood and adolescent survivors (0-19 years at cancer diagnosis) were compared to siblings' offspring, the risk for congenital anomalies was non-significantly increased (PR 1.17, 95% CI 0.92-1.49). No such increase existed for offspring of young adult survivors (20-34 years at cancer diagnosis) (PR 1.01, 95% CI 0.83-1.23). The risks for congenital anomalies were elevated among offspring of CS diagnosed with cancer in the earlier decades (1955-1964: PR 2.77, 95% C I 1.26-6.11; and 1965-1974: PR 1.55, 95% C I 0.94-2.56). In our study, we did not detect an overall elevated risk for congenital anomalies in offspring of survivors diagnosed in young adulthood. An association between cancer exposure of the parent and congenital anomalies in the offspring appeared only for those CS who were diagnosed in the earlier decades.