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- Goldin, LR, et al.
(author)
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Familial risk of lymphoproliferative tumors in families of patients with chronic lymphocytic leukemia: results from the Swedish Family-Cancer Database
- 2004
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In: Blood. - : American Society of Hematology. - 0006-4971 .- 1528-0020. ; 104:6, s. 1850-1854
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Journal article (peer-reviewed)abstract
- The importance of genetic factors in etiology of chronic lymphocytic leukemia (CLL) is suggested by family and population studies. However, the spectrum of malignancies sharing common genetic factors with CLL and the effects of sex and age on familial risk are unknown. We used the Swedish Family-Cancer Database to test for increased familial risks of CLL and other lymphoproliferative tumors. Cancer diagnoses from 1958 to 1998 were assessed in 14 336 first-degree relatives of 5918 CLL cases and in 28 876 first-degree relatives of 11 778 controls. Cancer risks in relatives of cases were compared with those in relatives of controls using marginal survival models. Relatives of cases were at significantly increased risk for CLL (relative risk [RR] = 7.52; 95% confidence interval [CI], 3.63-15.56), for non-Hodgkin lymphoma (RR = 1.45; 95% CI, 0.98-2.16), and for Hodgkin lymphoma (RR = 2.35; 95% CI, 1.08-5.08). CLL risks were similar in parents, siblings, and offspring of cases, in male and female relatives, and were not affected by the case's age at diagnosis. Anticipation was not significant when analyzed using life table methods. We conclude that the familial component of CLL is shared with other lymphoproliferative malignances, suggesting common genetic pathways. However, because clinically diagnosed CLL is uncommon, absolute excess risk to relatives is small.
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- Hemminki, K, et al.
(author)
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A population-based study of familial central nervous system hemangioblastomas
- 2001
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In: Neuroepidemiology. - : S. Karger AG. - 0251-5350 .- 1423-0208. ; 20:4, s. 257-261
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Journal article (peer-reviewed)abstract
- We used the nationwide Swedish Family-Cancer Database to analyze the risk for central nervous system hemangioblastoma (HB) in offspring (0–61 years) of parents with cancer. Eighty-three offspring were identified, and the age at onset showed a bimodal distribution. The early-onset component peaked at 25–29 years, was associated with von Hippel-Lindau (VHL) disease and presented with HBs, renal cell carcinomas, pheochromocytomas and insulomas in the proband or other family members. Standardized incidence ratios (SIRs) were 600 for offspring HB by parental HB, and they were even high for the other VHL-related tumors. Second tumors were common in this early-onset group, and the types were as expected in VHL. The late-onset component peaked at 40–44 years, and it was twice as prevalent as the early-onset component. Because there was no evidence of familial risks, this is suggested to be a sporadic form of HB.
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