To examine the role of gender, age at immigration and length of stay on incidence trends of common cancers, we studied risk of colorectal, lung, breast and prostate cancers in immigrants to Sweden from 1958 to 2008. The nationwide Swedish Family-Cancer Database was used to calculate standardized incidence ratios for common cancers among immigrants compared to Swedes. Immigrants were classified into "high-risk" countries when their risk was increased, into "low-risk" when their risk was decreased and into "other" when their risk was nonsignificant. Among those who immigrated at younger age (
OBJECTIVES: A family history of prostate cancer is associated with a higher risk for prostate cancer to first-degree relatives. If greater surveillance of men at familial risk is considered to be useful, population-based estimates of the differences in the age at diagnosis between familial and sporadic prostate cancer cases are needed. METHODS: The men in the nationwide Swedish Family-Cancer Database were classified according to the number and type of affected first-degree relatives (father or brother) and according to the relative's age at diagnosis. The cumulative incidence of prostate cancer and cumulative prostate cancer-specific mortality were estimated using a stratified Cox model. RESULTS: The cumulative incidence was highest for men with multiple affected first-degree relatives, and it was higher for brothers than for sons of prostate cancer patients. The age to reach the same cumulative incidence as the general population at age 55 years decreased with decreasing age at diagnosis of the relative, ranging from 48.7 years (father diagnosed before 60 years of age) to 53.7 years (father diagnosed after 82 years of age). Prostate cancer-specific mortality was also related to the number and type of affected relatives but there was no clear evidence for a dependency on the age at diagnosis of the relative. CONCLUSIONS: Men with a father or a brother affected by prostate cancer are diagnosed and die at earlier ages than men without a family history of prostate cancer. This study should encourage further analysis in order to assess the risks and benefits of screening for prostate cancer in men at higher risk.
In order to describe a novel approach for the clinical study of metastases, we provide here age-specific incidence and survival data for cancer of unknown primary (CUP). Metastases in various organs are found at CUP diagnosis, which have implications for prognosis, and we hypothesize similar prognostic implications for metastases found at diagnosis of primary cancers. We identified 33,224 CUP patients from the Swedish Cancer Registry and calculated incidence rates (IRs) for CUP development. Cox proportional hazards regression models were performed to estimate hazard ratios (HRs) for relative survival in CUP patients compared to the general population. In age-group specific analyses, a maximal IR was reached at age 85-89 years, followed by a marked decline to age 90+ (7-fold in men and 3-fold in women). The overall HR for relative survival declined systematically by age. CUP may be applied as an epidemiological age-incidence model for cancer metastases providing evidence in line with autopsy data that the metastatic potential, as shown by the incidence of CUP, appears to weaken markedly at age 85 years, depending on metastatic locations. The relative death rates were highest among young patients, which was probably entirely due to the low death rates in young background population.
BACKGROUND: Familial risks by proband status and age are useful for clinical counseling, and they can be used to calculate population-attributable fractions (PAFs), which show the proportion of disease that could be prevented if the cause could be removed. METHODS: The authors used the nationwide Swedish Family-Cancer Database on 10.2 million individuals and 182,104 fathers and 3710 sons with medically verified prostate carcinoma to calculate age specific familial standardized incidence ratios (SIRs) with 95% confidence intervals (95%CI) and familial PAFs for prostate carcinoma in sons ages 0-66 years. RESULTS: The incidence of prostate carcinoma was doubled between the years 1961 and 1998. The familial SIRs for prostate carcinoma were 2.38 (95%CI, 2.18-2.59) for men with prostate carcinoma in the father only, 3.75 (95%CI, 2.73-4.95) for men with prostate carcinoma in a brother only, and 9.44 (95%CI, 5.76-14.03) for men with prostate carcinoma in both a father and a brother. The corresponding familial PAFs were 8.86%, 1.78%, and 0.99%, respectively, yielding a total PAF of 11.63%. Age specific risks were shown for the same proband histories. The SIR was 8.05 for prostate carcinoma before age 55 if a brother had been diagnosed before that age. If, in addition, a father was diagnosed at any age, then the SIR was 33.09. CONCLUSIONS: The authors recommend that having a brother who is diagnosed with prostate carcinoma before age 55 years or having a brother and father who are diagnosed at any age are indications to screen for prostate carcinoma. The familial PAF of prostate carcinoma among a population of sons ages 0-66 years was 11.63%.
BACKGROUND: Systematic comparisons of mode of inheritance for renal cell carcinoma (RCC) have not been carried out. The occurrence of cancer in parents and offspring may be due to dominant causes, whereas cancer affecting only siblings may indicate a recessive causation. Environmental effects need to be excluded. METHODS: The Swedish Family-Cancer Database includes all Swedes born after 1931 with their biologic parents, totaling 10.2 million persons. Cancer data were retrieved from the Swedish Cancer Registry from years 1961 to 2000, included 2415 cases of RCC in offspring and 18531 in parents. Standardized incidence ratios (SIRs) and 95% CI limits were calculated for offspring whose parents or sibling were diagnosed with RCC. RESULTS: The SIRs for siblings for RCC depended on their age difference. SIR was 7.63 (95% CI 3.63-14.08) when the age difference was less than 3 years and compared to 3.43 (95% CI 1.77-6.02) for large age difference. SIRs for familial risk of RCC were 1.73 (95% CI 1.31-2.26) when a parent and 4.58 (95% CI 2.87-6.94) when a sibling had RCC. Age-specific analysis of familial RCC among siblings revealed maxima at ages 40 to 49 and 60 to 68 years. CONCLUSION: The findings in the present study offer evidence on recessive effects in early onset RCC.
Survival after non-Hodgkin lymphoma (NHL) has increased thanks to improved treatment but NHL survivors have an increased risk of second neoplasms. The assessment of cancer risk patterns after NHL may help to quantify the late side-effects of therapy. Poisson regression was used to estimate relative risks (RRs) and absolute incidence rates for nine solid tumours based on a nationwide cohort of 60 901 NHL survivors from Finland, Norway and Sweden. Patients were diagnosed between 1980 and 2006 and developed 6815 s neoplasms. NHL patients showed an increased risk of each of the nine investigated cancer sites: prostate and pancreas (both RRs 1·28), breast (1·37), colorectum (1·48), urinary bladder (1·52), stomach and lung (both RRs 1·87), skin (melanoma 2·27) and kidney (2·56). The RRs showed a U-shaped relationship with time after NHL for all nine-second cancer types. NHL diagnosis early in life was a risk factor for the development of second cancers with the exception of melanoma, but a risk excess was even observed in patients diagnosed with NHL at age 80+ years. The present study provides accurate estimates on the adverse late effects of NHL therapy, which should guide the establishment of cancer prevention strategies in NHL survivors.
Estimating familial cancer risks is clinically important in being able to discriminate between individuals in the population at differing risk for malignancy. To gain insight into the familial risk for the different hematological malignancies and their possible inter-relationship, we analyzed data on more than 16 million individuals from the Swedish Family-Cancer Database. After identifying 153?115 patients diagnosed with a primary hematological malignancy, we quantified familial relative risks (FRRs) by calculating standardized incident ratios (SIRs) in 391?131 of their first-degree relatives. The majority of hematological malignancies showed increased FRRs for the same tumor type, with the highest FRRs being observed for mixed cellularity Hodgkin lymphoma (SIR, 16.7), lymphoplasmacytic lymphoma (SIR, 15.8), and mantle cell lymphoma (SIR, 13.3). There was evidence for pleiotropic relationships; notably, chronic lymphocytic leukemia was associated with an elevated familial risk for other B-cell tumors and myeloproliferative neoplasms. Collectively, these data provide evidence for shared etiological factors for many hematological malignancies and provide information for identifying individuals at increased risk, as well as informing future gene discovery initiatives.
A few twin studies on cancer have addressed questions on the possible carcinogenic or protective effects of twining by comparing the occurrence of cancer in twins and singletons. The nationwide Swedish Family-Cancer Database of 10.2 million individuals and 69,654 0- to 70-year-old twin pairs were used to calculate standardized incidence ratios (SIRs) and 95% confidence intervals (CIs) for all main cancers compared to singletons. The overall risk of cancer in same- or different-sex twins was at the same level as the risk for singletons. Testicular cancer, particularly seminoma, was increased among same-sex twins (1.54) and all twins to an SIR of 1.38. Among other tumors, neurinomas and non-thyroid endocrine gland tumors were increased. Colorectal cancers and leukemia were decreased among all twins. Melanoma and squamous cell skin cancer were decreased in male same-sex twins. The data on this unselected population of twins suggest that twinning per se is not a risk factor of cancer. In utero hormonal exposures or postnatal growth stimulation may be related to the risk of testicular cancer and pituitary tumors. Protective effects against colorectal cancer may be related to a beneficial diet, and in melanoma and skin cancer, to socioeconomic factors. The study involved multiple comparisons, and internal consistency between the results was one of the main factors considered for their plausibility. The results should encourage others working on twin and singleton populations to examine the specific associations and emerging hypotheses.
Polycythaemia vera (PV) and primary myelofibrosis (MF) show concordant familial clustering but limited population level data are available on the aggregation of other discordant neoplasms in these families. We used the Swedish Family-Cancer Database to assess risks for VP and MF in families of cancer patients. A total of 3530 first PV and 1606 MF patients were identified, with high concordant familial risks. Several discordant familial associations were found for PV (acute myeloid leukaemia, Hodgkin disease, prostate and bladder cancers) or for MF (chronic lymphatic leukaemia, colorectal, kidney and cervical cancers) or for both (nervous system, eye and endocrine tumours).