| 1. |
- Axelsson, Gösta, 1950, et al.
(författare)
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Lung cancer risk from radon exposure in dwellings in Sweden: how many cases can be prevented if radon levels are lowered?
- 2015
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Ingår i: Cancer Causes and Control. - : Springer Science and Business Media LLC. - 0957-5243 .- 1573-7225. ; 26:4, s. 541-547
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Tidskriftsartikel (refereegranskat)abstract
- Residential exposure to radon is considered to be the second cause of lung cancer after smoking. The purpose of this study was to estimate the number of lung cancer cases prevented from reducing radon exposure in Swedish dwellings. METHODS: Measurements of indoor radon are available from national studies in 1990 and 2008 with 8992 and 1819 dwellings, considered representative of all Swedish dwellings. These data were used to estimate the distribution of radon in Swedish dwellings. Lung cancer risk was assumed to increase by 16 % per 100 becquerels per cubic meter (Bq/m(3)) indoor air radon. Estimates of future and saved cases of lung cancer were performed at both constant and changed lung cancer incidence rates over time. RESULTS: The arithmetic mean concentration of radon was 113 Bq/m(3) in 1990 and 90 Bq/m(3) in 2008. Approximately 8 % of the population lived in houses with >200 Bq/m(3). The estimated current number of lung cancer cases attributable to previous indoor radon exposure was 591 per year, and the number of future cases attributable to current exposure was 473. If radon levels above 100 Bq/m(3) are lowered to 100 Bq/m(3), 183 cases will be prevented. If levels >200 Bq/m(3) are lowered to 140 Bq/m(3) (mean in the present stratum 100-200 Bq/m(3)), 131 cases per year will be prevented. CONCLUSIONS: Although estimates are somewhat uncertain, 35-40 % of the radon attributed lung cancer cases can be prevented if radon levels >100 Bq/m(3) are lowered to 100 Bq/m(3).
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| 2. |
- Barregård, Lars, 1948, et al.
(författare)
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Response to Fornalski et al
- 2015
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Ingår i: Cancer Causes and Control. - : Springer Science and Business Media LLC. - 0957-5243 .- 1573-7225. ; 26
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 3. |
- Bentmar Holgersson, Magdalena, et al.
(författare)
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Lower prostate cancer risk in Swedish men with the androgen receptor E213 A-allele
- 2017
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Ingår i: Cancer Causes & Control. - : Springer Science and Business Media LLC. - 0957-5243 .- 1573-7225. ; 28:3, s. 227-233
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Tidskriftsartikel (refereegranskat)abstract
- In a previous population-based study on 3369 European men with self-reported prostate cancer (PCa), it was shown that androgen receptor (AR) haplotype designated H2 was associated with high levels of serum PSA (prostate-specific antigen) concentration, and, at the same time, with low risk for PCa. The aim of this study was to replicate this finding in other cohorts, with registry-based cancer diagnosis. Using data from two population-based cohorts; the Malmo Diet and Cancer Study (MDCS, n = 12,121) and the Swedish Osteoporotic fractures in men study (MrOS, n = 1,120), 628 men with PCa and 1,374 controls were identified and genotyped. PCa data were collected from the Swedish national cancer registry. PCa odds ratios (ORs) and 95% confidence intervals (CIs) were calculated for carriers of the particular AR haplotype, tagged by the rs6624304 T-allele. The 15% of men who were carriers of the AR haplotype H2 had approximately one-third lower risk for PCa diagnosis compared to those with the most common H1 variant (OR 0.65; 95% CI 0.45-0.94; p = 0.021). The same trend, although not statistically significant (OR 0.75; 95% CI 0.47-1.24; p = 0.275), was observed in MrOS Sweden. When both cohorts were merged, an even more significant result was observed (OR 0.68; 95% CI 0.51-0.90; p = 0.008). Swedish men with the variant AR haplotype H2, tagged by rs6624304, have significantly lower risk of PCa compared to those with the more common variant.
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| 4. |
- Bonn, Stephanie E., et al.
(författare)
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Body mass index and weight change in men with prostate cancer : progression and mortality
- 2014
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Ingår i: Cancer Causes and Control. - : Springer Netherlands. - 0957-5243 .- 1573-7225. ; 25:8, s. 933-943
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Tidskriftsartikel (refereegranskat)abstract
- Body mass index (BMI) is a modifiable lifestyle factor that has been associated with an increased risk of fatal prostate cancer and biochemical recurrence. The main purpose of the present study was to investigate the association between the exposure BMI at the time of a prostate cancer diagnosis and weight change after diagnosis, and the outcomes of prostate cancer progression and mortality in a large cohort study. Data from 4,376 men diagnosed with clinically localized prostate cancer between 1997 and 2002 were analyzed. BMI and weight change were self-reported in 2007. Hazard ratios (HRs) with 95 % confidence intervals (CIs) were estimated in complete-case analysis (n = 3,214) using Cox proportional hazards models. Progression was experienced among 639 (14.6 %) of the study participants, and in total, 450 (10.3 %) deaths of any cause and 134 (3.1 %) prostate cancer-specific deaths were recorded during follow-up. Obese men had a 47 % increased rate of overall mortality compared to normal weight men (HR 1.47, 95 % CI 1.03-2.10). No statistically significant associations were found for BMI and prostate cancer progression or prostate cancer-specific mortality. A weight loss > 5 % after diagnosis almost doubled the rate of overall mortality compared to maintaining a stable weight (HR 1.94, 95 % CI 1.41-2.66), while a weight gain > 5 % was associated with an almost doubled increased rate of prostate cancer-specific mortality (HR 1.93, 95 % CI 1.18-3.16). Being obese was associated with an increased rate of overall mortality, and gaining weight after a prostate cancer diagnosis was associated with an increased rate of prostate cancer-specific mortality.
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| 5. |
- Christensen, J. S., et al.
(författare)
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Brain tumors in children and adolescents and exposure to animals and farm life: a multicenter case-control study (CEFALO)
- 2012
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Ingår i: Cancer Causes & Control. - : Springer Science and Business Media LLC. - 0957-5243 .- 1573-7225. ; 23:9, s. 1463-1473
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Tidskriftsartikel (refereegranskat)abstract
- The etiology of brain tumors in children and adolescents is largely unknown, and very few environmental risk factors have been identified. The aim of this study was to examine the relationship between pre- or postnatal animal contacts or farm exposures and the risk of childhood brain tumors (CBTs), since infectious agents may pose a risk factor and a proposed mechanism is transferral of infectious agents from animals to humans. The case-control study conducted in Denmark, Norway, Sweden, and Switzerland included brain tumor cases diagnosed from 2004 to 2008 aged 7-19 years at diagnosis. Three hundred and fifty-two cases (83 % participation rate) were matched to 646 population-based controls (71 % participation rate). Conditional logistic regression was used to estimate odds ratios. Maternal farm residence during pregnancy was inversely related to all CBTs combined (adjusted odds ratio (aOR) = 0.40, 95 % confidence interval (CI) = 0.19-0.88), as was the child's farm residence but not statistically significantly so (aOR = 0.57, 95 % CI = 0.28-1.17). Exposure to animals was in general not related to CBT risk except postnatal contact with birds showing reduced aORs of all CBTs (0.67, 95 % CI = 0.46-0.97) and primitive neuroectodermal tumor (0.28, 95 % CI = 0.10-0.83). Sensitivity analyses focusing on early exposure of the child did not change the associations observed for the entire exposure period with the exception of exposure to goats and sheep which was associated with reduced risks of both all CBTs (aOR = 0.48, 95 % CI = 0.24-0.97) and astrocytomas (aOR = 0.29, 95 % CI = 0.10-0.87). Altogether, our data indicate an inverse association between the mother during pregnancy or the child living on a farm and CBT risk, which contrasts with the existing literature and merits further attention. With respect to exposure to animals, we did not observe any systematic pattern. This suggests that a potential protective effect of farm residence is mediated by some other factor than animal contact.
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| 6. |
- Holmberg, Erik, 1951, et al.
(författare)
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The impact of reproductive factors on breast cancer risk--the feasibility of using Swedish population-based registers to account for the effect of confounding in cohort studies.
- 2005
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Ingår i: Cancer causes & control : CCC. - : Springer Science and Business Media LLC. - 0957-5243 .- 1573-7225. ; 16:3, s. 235-43
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: The aim of this study was to analyze the impact of reproductive factors on breast cancer risk among Swedish women by using nationwide population registers. METHODS: A cohort including all Swedish women born between 1920 and 1959 was followed up to 1997 by record linkage to different population-based registers. More than 4 million children were linked to the women in the cohort and 60,328 women were diagnosed with breast cancer. Poisson regression was used to model the breast cancer incidence by risk groups. In a sub-cohort of 18,164 women irradiated for skin hemangioma in infancy, the breast cancer risk was analyzed in relation to radiation dose and accounting for reproductive factors. RESULTS: The relative breast cancer risk (RR) for the reproductive factors was 0.35 [ 95% confidence interval (CI) 0.30--0.42] for women with 6 or more children and the first child before the age of 20 years, and RR was 1.11 (95% CI 1.06--1.18) for uniparous women with the first child at age 35 years or older, compared to nulliparous women. The discrepancies of reproductive factors in the hemangioma cohort compared to Swedish women had a minor effect on RR, with a reduction from 1.13 (95%CI 1.00--1.26) to 1.11 (95% CI 0.99--1.25). CONCLUSIONS: This study shows the feasibility of using population-based registers to retrieve reliable information on reproductive factors to eliminate its confounding effect when analyzing other risk factors.
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| 7. |
- Lindkvist, Björn, et al.
(författare)
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Prospective cohort study of metabolic risk factors and gastric adenocarcinoma risk in the Metabolic Syndrome and Cancer Project (Me-Can)
- 2013
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Ingår i: Cancer Causes and Control. - : Springer Science and Business Media LLC. - 1573-7225 .- 0957-5243. ; 24:1, s. 107-116
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Tidskriftsartikel (refereegranskat)abstract
- Little is known about the association between the metabolic syndrome (MetS) and the risk of gastric adenocarcinoma. The aim of this study was to investigate whether metabolic risk factors, together or combined, were associated with the risk of gastric adenocarcinoma. The Metabolic Syndrome and Cancer Project (Me-Can) is a pooling of prospective cohorts in Austria, Norway, and Sweden with information on blood pressure, lipids, glucose, and BMI available in 578,700 individuals. Cox proportional hazards analysis was used to calculate hazard ratio (HR) of gastric adenocarcinoma using metabolic risk factors categorized into quintiles and transformed into z-scores (with mean = 0 and SD = 1). The standardized sum of all z-scores created a composite MetS score. In total, 1,210 incident cases of gastric adenocarcinoma were identified. Glucose was significantly associated with the risk of gastric adenocarcinoma [calibrated HR 1.58 (1.14-2.20) per one unit increment in z-score] in women. There was a statistically significant association between triglycerides and risk of gastric adenocarcinoma per mmol increment in triglycerides [HR 1.20 (1.06-1.36) per mmol] but not for the adjusted z-score in women. There were no significant association between any metabolic factors and gastric cancer among men. The composite MetS score was associated with the risk of gastric adenocarcinoma in women [HR 1.18 (1.00-1.38) per one unit increment in z-score] but not in men. Glucose and high levels of the composite MetS score were associated with an increased risk of gastric adenocarcinoma in women but not in men.
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| 8. |
- Loeb, Stacy, et al.
(författare)
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Risk of localized and advanced prostate cancer among immigrants versus native-born Swedish men: a nation-wide population-based study.
- 2013
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Ingår i: Cancer causes & control : CCC. - : Springer Science and Business Media LLC. - 1573-7225 .- 0957-5243. ; 24:2, s. 383-390
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Tidskriftsartikel (refereegranskat)abstract
- PURPOSE: Prostate cancer (PCa) incidence and prognosis vary geographically. We examined possible differences in PCa risk by clinical risk category between native-born and immigrant populations in Sweden. Our hypothesis was that lower PSA-testing uptake among foreign-born men would result in lower rates of localized disease, and similar or higher risk of metastatic disease. METHODS: Using the Prostate Cancer database Sweden, we identified 117,328 men with PCa diagnosed from 1991 to 2008, of which 8,332 were foreign born. For each case, 5 cancer-free matched controls were randomly selected from the population register. Conditional logistic regression was used to compare low risk, intermediate risk, high risk, regionally metastatic, and distant metastatic PCa based upon region of origin. RESULTS: Across all risk categories, immigrants had significantly lower PCa risk than native-born Swedish men, except North Americans and Northern Europeans. The lowest PCa risk was observed in men from the Middle East, Southern Europe, and Asia. Multivariable adjustment for socioeconomic factors and comorbidities did not materially change risk estimates. Older age at immigration and more recent arrival in Sweden were associated with lower PCa risk. Non-native men were less likely to be diagnosed with PCa through PSA testing during a health checkup. CONCLUSIONS: The risk for all stages of PCa was lower among first-generation immigrants to Sweden compared with native-born men. Older age at immigration and more recent immigration were associated with particularly low risks. Patterns of PSA testing appeared to only partly explain the differences in PCa risk, since immigrant men also had a lower risk of metastatic disease.
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| 9. |
- Yu, E. Y. W., et al.
(författare)
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The association between coffee consumption and bladder cancer in the bladder cancer epidemiology and nutritional determinants (BLEND) international pooled study
- 2019
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Ingår i: Cancer Causes & Control. - : Springer Science and Business Media LLC. - 0957-5243 .- 1573-7225. ; 30:8, s. 859-870
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Tidskriftsartikel (refereegranskat)abstract
- BackgroundInconsistent results for coffee consumption and bladder cancer (BC) risk have been shown in epidemiological studies. This research aims to increase the understanding of the association between coffee consumption and BC risk by bringing together worldwide case-control studies on this topic.MethodsData were collected from 13 case-control comprising of 5,911 cases and 16,172 controls. Pooled multivariate odds ratios (ORs), with corresponding 95% confidence intervals (CIs), were obtained using multilevel logistic regression models. Furthermore, linear dose-response relationships were examined using fractional polynomial models.ResultsNo association of BC risk was observed with coffee consumption among smokers. However, after adjustment for age, gender, and smoking, the risk was significantly increased for never smokers (ever vs. never coffee consumers: ORmodel2 1.30, 95% CI 1.06-1.59; heavy (>4 cups/day) coffee consumers vs. never coffee consumers: ORmodel2 1.52, 95% CI 1.18-1.97, p trend=0.23). In addition, dose-response analyses, in both the overall population and among never smokers, also showed a significant increased BC risk for coffee consumption of more than four cups per day. Among smokers, a significant increased BC risk was shown only after consumption of more than six cups per day.ConclusionThis research suggests that positive associations between coffee consumption and BC among never smokers but not smokers.
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