| 1. |
- Fang, Fang, et al.
(author)
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Risk of infection-related cancers after the loss of a child : a follow-up study in Sweden
- 2011
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In: Cancer Research. - Philadelphia, USA : American Association for Cancer Research. - 0008-5472 .- 1538-7445. ; 71:1, s. 116-22
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Journal article (peer-reviewed)abstract
- It is unknown whether severe emotional stress due to loss of a child influences the risk of cancers susceptible to immune modulation such as infection-related cancers. We conducted a historic cohort study in 1990 to 2004 on the basis of the Swedish Multi-Generation Register including 4,687,073 parents. Death of a child was identified through the Causes of Death Register. Poisson regression was used to derive the relative risks (RR) and 95% confidence intervals (CI) of infection-related cancers, comparing the incidence rates of parents who lost a child with those who never lost a child. A total of 101,306 parents (2%) had lost a child during follow-up, among whom 1,608 subsequently developed infection-related cancers. After adjustment for age, sex, calendar year, educational level, and civil status, the overall RR of 14 cancers studied was 1.07 (95% CI: 1.02-1.12). Parents who lost a child were particularly at a higher risk for cancers potentially associated with human papilloma virus (HPV) infection such as cervical cancer (RR: 1.46; 95% CI: 1.17-1.80). Higher RRs for most cancers were obtained within 5 years after child loss and excess risk for liver and stomach cancers was confined to that period. No association was observed for lymphoma and nonmelanoma skin cancer at any time point after child loss. Although potential confounding by unmeasured factors cannot be ruled out, our findings lend support to the hypothesis that severe life stressors, such as child loss, may raise the risk for several, chiefly HPV-related, cancers.
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| 2. |
- Hardardottir, Hronn, et al.
(author)
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Psychobiological stress response to a lung cancer diagnosis : a prospective study of patients in Iceland and Sweden
- 2023
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In: Acta Oncologica. - : Taylor & Francis. - 0284-186X .- 1651-226X. ; 62:10, s. 1338-1347
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Journal article (peer-reviewed)abstract
- Background: A diagnostic work-up leading to a lung cancer diagnosis is a severely stressful experience that may impact tumor progression. Yet, prospective data are scarce on psychological and biological components of stress at the time of lung cancer diagnosis. The aim of this study was to assess pre-to-post diagnosis change in psychological distress and urinary excretion of catecholamines in patients with suspected lung cancer.Methods: Participants were 167 patients within the LUCASS study, recruited at referral for suspected lung cancer to University Hospitals in Iceland and Sweden. Patients completed questionnaires on perceived distress (Hospital Anxiety and Depression Scale, HADS) before and after diagnosis of lung cancer or a non-malignant origin. A subpopulation of 85 patients also provided overnight urine for catecholamine analysis before and at a median of 24 days after diagnosis but before treatment.Results: A lung cancer diagnosis was confirmed in 123 (73.7%) patients, with a mean age of 70.1 years. Patients diagnosed with lung cancer experienced a post-diagnosis increase in psychological distress (p = 0.010), while patients with non-malignant lung pathology showed a reduction in distress (p = 0.070). Both urinary epinephrine (p = 0.001) and norepinephrine (p = 0.032) levels were higher before the diagnosis among patients eventually diagnosed with lung cancer compared to those with non-malignant lung pathology. We observed indications of associations between pre-to-post diagnosis changes in perceived distress and changes in urinary catecholamine levels.Conclusion: Receiving a lung cancer diagnosis is associated with an increase in psychological distress, while elevated catecholamine levels are evident already before lung cancer diagnosis.
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| 3. |
- Vidarsdottir, Halldora, et al.
(author)
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Spousal loss and cognitive function in later life : a 25-year follow-up in the AGES-Reykjavik study
- 2014
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In: American Journal of Epidemiology. - Cary, USA : Oxford University Press. - 0002-9262 .- 1476-6256. ; 179:6, s. 674-83
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Journal article (peer-reviewed)abstract
- The aim of this study was to investigate the associations between loss of a life partner and the development of dementia and decline in cognitive function in later life. We used an Icelandic cohort of 4,370 participants in the Age, Gene/Environment Susceptibility-Reykjavik Study who were living as married in 1978 (born in 1907-1935) and were either still married (unexposed cohort) or widowed (exposed cohort) at follow-up (in 2002-2006). We ascertained history of marital status and spouse's death by record linkage to the Registry of the Total Population, Statistics Iceland. The outcome measures were as follows: 1) dementia and mild cognitive impairment; and 2) memory, speed of processing, and executive function. During the observation period, 3,007 individuals remained married and 1,363 lost a spouse through death. We did not find any significant associations between loss of a spouse and our outcome variables, except that widowed women had poorer executive function (mean = -0.08) during the first 2 years after their husbands' deaths compared with still-married women (mean = 0.09). Our findings do not support the notion that the risk of dementia is increased following the loss of a spouse, yet women demonstrate a seemingly temporary decline in executive function following the death of a partner.
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| 4. |
- Xu, Jianfeng, et al.
(author)
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Estimation of absolute risk for prostate cancer using genetic markers and family history
- 2009
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In: The Prostate. - : Wiley. - 0270-4137 .- 1097-0045. ; 69:14, s. 1565-1572
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Journal article (peer-reviewed)abstract
- BACKGROUND: Multiple DNA sequence variants in the form of single-nucleotide polymorphisms (SNPs) have been found to be reproducibly associated with prostate cancer (PCa) risk. METHODS: Absolute risk for PCa among men with various numbers of inherited risk alleles and family history of PCa was estimated in a population-based case-control study in Sweden (2,893 cases and 1,781 controls), and a nested case-control study from the Prostate, Lung, Colon and Ovarian (PLCO) Cancer Screening Trial in the U.S. (1,172 cases and 1,157 controls). RESULTS: Increased number of risk alleles and positive family history were independently associated with PCa risk. Considering men with 11 risk alleles (mode) and negative family history as having baseline risk, men who had >or=14 risk alleles and positive family history had an odds ratio (OR) of 4.92 [95% confidence interval (CI): 3.64-6.64] in the Swedish study. These associations were confirmed in the U.S. population. Once a man's SNP genotypes and family history are known, his absolute risk for PCa can be readily calculated and easily interpreted. For example, 55-year-old men with a family history and >or=14 risk alleles have a 52% and 41% risk of being diagnosed with PCa in the next 20 years in the Swedish and U.S. populations, respectively. In comparison, without knowledge of genotype and family history, these men had an average population absolute risk of 13%. CONCLUSION: This risk prediction model may be used to identify men at considerably elevated PCa risk who may be selected for chemoprevention.
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| 5. |
- Jendle, Johan, 1963-, et al.
(author)
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Effects on repetitive 24-hour ambulatory blood pressure in type 2 diabetic subjects randomized to liraglutide or glimepiride treatment both in combination with metformin : A randomized open parallel-group study
- 2018
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In: Journal of the American Society of Hypertension. - : Elsevier. - 1933-1711 .- 1878-7436. ; 12:5, s. 346-355
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Journal article (peer-reviewed)abstract
- In this post hoc study, we aimed to investigate liraglutide treatment on repetitive 24-hour blood pressure (BP) in patients with type II diabetes. Sixty-two individuals with type II diabetes (45 males) were randomized to 1.8 mg liraglutide once daily or 4 mg glimepiride together with 1 g metformin twice daily. Ambulatory 24-hour systolic and diastolic blood pressure (sBP/dBP) was repetitively measured at baseline, 2 weeks, and 18 weeks. Outcomes were evaluated as treatment change from baseline, 2 weeks, and 18 weeks. Baseline clinical characteristics of liraglutide (n = 33) and glimepiride (n = 29) groups were well matched. No statistically significant difference in 24-hour sBP/dBP between three time periods and groups was observed. There was no treatment change for 24-hour sBP at week 2 or after week 18. There was a transient treatment change in 24-hour dBP in the liraglutide group at week 2 (3.2 ± 5.4 vs. -1.2 ± 4.5 mm Hg, P < .01). A treatment change in 24-hour heart rate at week 2 (4.9 ± 6.8 vs. 1.0 ± 6.0 bpm, P = .03) and at week 18 (5.9 ± 7.8 vs. 0.2 ± 6.3 bpm, P < .01) was observed in the liraglutide group. In conclusion, liraglutide treatment did not lower BP. However, a small diurnal variation in dBP without affecting BP variability or nocturnal BP dipping was observed.
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| 6. |
- Ludvigsson, Jonas F., 1969-, et al.
(author)
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No association between biopsy-verified celiac disease and subsequent amyotrophic lateral sclerosis : a population-based cohort study
- 2014
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In: European Journal of Neurology. - : Wiley-Blackwell. - 1351-5101 .- 1468-1331. ; 21:7, s. 976-982
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Journal article (peer-reviewed)abstract
- Background and purpose: Earlier data suggest an association between amyotrophic lateral sclerosis (ALS) and autoimmune disease, but data on its association with celiac disease (CD) are limited.Methods: The risk of ALS in 29093 individuals with CD, according to small intestine biopsy (villous atrophy, Marsh 3) carried out at Sweden's 28 pathology departments in 1969-2008, was compared with that in 144515 age- and sex-matched reference individuals from the general population. ALS was defined as a hospitalization or outpatient visit with ALS according to the Swedish Patient Register. We used Cox regression to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for ALS.Results: During follow-up 12 (3.7/100000 person-years) individuals with CD and 56 (3.5/100000 person-years) reference individuals had a diagnosis of ALS. This corresponded to an HR of 1.0 (95% CI0.5-1.8). HRs were significantly higher in the first year of follow-up (4.1; 1.2-13.4) than 1-5years after first CD diagnosis (0.8; 0.2-2.7) or after more than 5years of follow-up (0.5; 0.2-1.5). Relative risk estimates were similar in men and women but were higher at the end of the study period [HR for ALS in patients diagnosed with CD in year 2000 or later was 2.1 (95% CI0.9-4.8)].Conclusions: This study found no association between CD and ALS. Earlier reports of a positive association may be due to surveillance bias just after CD diagnosis or expedited diagnostic work-up of ALS.
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| 7. |
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| 8. |
- Sun, Jielin, et al.
(author)
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Evidence for two independent prostate cancer risk-associated loci in the HNF1B gene at 17q12
- 2008
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In: Nature Genetics. - London : Nature Publishing Group. - 1061-4036 .- 1546-1718. ; 40:10, s. 1153-1155
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Journal article (other academic/artistic)abstract
- We carried out a fine-mapping study in the HNF1B gene at 17q12 in two study populations and identified a second locus associated with prostate cancer risk, 26 kb centromeric to the first known locus (rs4430796); these loci are separated by a recombination hot spot. We confirmed the association with a SNP in the second locus (rs11649743) in five additional populations, with P = 1.7 10-9 for an allelic test of the seven studies combined. The association at each SNP remained significant after adjustment for the other SNP.
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| 9. |
- Zheng, S. Lilly, et al.
(author)
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Genetic variants and family history predict prostate cancer similar to prostate-specific antigen
- 2009
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In: Clinical Cancer Research. - 1078-0432 .- 1557-3265. ; 15:3, s. 1105-1111
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Journal article (peer-reviewed)abstract
- PURPOSE: Although prostate-specific antigen (PSA) is the best biomarker for predicting prostate cancer, its predictive performance needs to be improved. Results from the Prostate Cancer Prevention Trial revealed the overall performance measured by the areas under curve of the receiver operating characteristic at 0.68. The goal of the present study is to assess the ability of genetic variants as a PSA-independent method to predict prostate cancer risk. EXPERIMENTAL DESIGN: We systematically evaluated all prostate cancer risk variants that were identified from genome-wide association studies during the past year in a large population-based prostate cancer case-control study population in Sweden, including 2,893 prostate cancer patients and 1,781 men without prostate cancer. RESULTS: Twelve single nucleotide polymorphisms were independently associated with prostate cancer risk in this Swedish study population. Using a cutoff of any 11 risk alleles or family history, the sensitivity and specificity for predicting prostate cancer were 0.25 and 0.86, respectively. The overall predictive performance of prostate cancer using genetic variants, family history, and age, measured by areas under curve was 0.65 (95% confidence interval, 0.63-0.66), significantly improved over that of family history and age (0.61%; 95% confidence interval, 0.59-0.62; P = 2.3 x 10(-10)). CONCLUSION: The predictive performance for prostate cancer using genetic variants and family history is similar to that of PSA. The utility of genetic testing, alone and in combination with PSA levels, should be evaluated in large studies such as the European Randomized Study for Prostate Cancer trial and Prostate Cancer Prevention Trial.
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