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Reliable data on familial risks are important for clinical counseling and cancer genetics. We wanted to study incidence trends and familial risks for pituitary adenomas and associated tumors through parental and sibling probands, using the nation-wide Swedish Family-Cancer Database on 10.5 million individuals, containing families with parents and offspring. Cancer data were retrieved from the Swedish Cancer Registry from years 1958 to 2002, including 3239 pituitary tumor patients. Familial risk for offspring was defined through standardized incidence ratio (SIR), adjusted for many variables. The incidence of pituitary adenoma has increased moderately from 1958 to the 1990s and declined thereafter. There were only three offspring–parent pairs with a concordant pituitary tumor, the SIR was not significant. Parental skin cancer (SIR 1.60) and leukemia (1.90, chronic lymphatic leukemia 2.59) were associated with offspring pituitary adenoma diagnosed at any age up to 70 years. There was a strong association of pituitary adenomas with nervous system hemangiopericytomas, SIR 182. The only significant association among siblings was between pituitary tumors and breast cancer (1.46). The risk of pituitary adenoma was marginally increased in individuals whose siblings were diagnosed with colorectal cancer. The results suggest an association of pituitary adenomas with nervous system hemangiopericytomas and breast and colorectal cancers, in addition to some other tumor types. Whether these associations can be explained by the recently identified pituitary adenoma predisposing gene, AIP, remains to be established.

The concentrations of endogenous hormones differ between women with twin and singleton births, with a possible influence on the risk of cancer. We used the nationwide Swedish Family-Cancer Database, including 30 409 women with a twin birth, to examine the subsequent risks of breast, endometrial, and ovarian cancers. Relative risks (RRs) were calculated in a log-linear Poisson regression model of person-years as offset. Cancer data were retrieved from the Swedish Cancer Registry; a total of 1010, 210, and 174 women were diagnosed with breast, endometrial, and ovarian cancers respectively, after a twin birth. A significant decrease in the risk of breast cancer was noted among women with a twin birth compared with women with a singleton birth (RR 0.85, 95% confidence interval (CI) 0.74–0.98). The protective effects were observed throughout the intervals after last pregnancy and they were strongest shortly after the last pregnancy in women who delivered a twin birth before 30 years of age. Twin birth did not change the risk of endometrial cancer (1.08, 95% CI 0.79–1.47) but the RR was increased for women with the number of pregnancies ≥4 (1.39, 95% CI 1.11–1.76). The RR for ovarian cancer was 0.95 (95% CI 0.79–1.15). Our study showed that twin births significantly reduced the subsequent risk of breast cancer. However, the associations of twin births with endometrial and ovarian cancers were not substantial.

The changes of cancer incidence upon immigration have been used as an estimator of environmental influence on cancer risk. The previous immigrant studies have indicated that the origins of testicular cancer are at an early age in life, probably in the intrauterine period. We wanted to reexamine the critical periods on histology-specific testicular cancer in sons of immigrants to Sweden. We used the nationwide Swedish Family-Cancer Database to calculate standardized incidence ratios (SIRs) for testicular cancer in sons of parents immigrating to Sweden from low- and high-risk countries compared with the native Swedes. Among the large immigrant groups, the SIRs for sons of two Finnish and Asian parents were decreased if the sons were born outside Sweden. The sons of a Danish immigrant couple showed an increased risk of testicular cancer. The changes in SIR were most systematic for seminoma. The present patterns of testicular cancer risk among sons of immigrants point to the early environmental risk factors, which influence the risk probably after the intrauterine period. These factors appear to influence seminoma risk in a more enduring way than they influence non-seminoma.