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Träfflista för sökning "WFRF:(Hemminki Kari) srt2:(2005-2009)"

Sökning: WFRF:(Hemminki Kari) > (2005-2009)

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1.
  • Castro, Felipe A, et al. (författare)
  • Association of HLA-DRB1, interleukin-6 and cyclin D1 polymorphisms with cervical cancer in the Swedish population-A candidate gene approach.
  • 2009
  • Ingår i: International Journal of Cancer. - : John Wiley & Sons. - 0020-7136 .- 1097-0215. ; 125:8, s. 1851-1858
  • Tidskriftsartikel (refereegranskat)abstract
    • High-risk human papillomavirus (hrHPV) infection is the major risk factor for cervical cancer (CxCa). The role of genetic susceptibility in the disease has been suggested, but the existing data lack consistency. We conducted a nested case-control study on 973 CxCa cases and 1,763 matched controls, from two Swedish population-based cohorts to examine the association of common genetic variants with CxCa risk. Human leukocyte antigen (HLA) alleles and 24 other polymorphisms in 14 genes were selected on the basis of reported association or mechanistic plausibility with an HPV infection or cervical cancer development. Genotyping was conducted using multiplex PCR and Luminex technology. A significant association of CxCa with various polymorphisms was observed: rs1800797 in the IL-6 gene (odds ratio [OR] = 0.88, 95% confidence intervals [CI]: 0.79-0.99); rs1041981 in the LTA gene (OR = 0.87, 95% CI: 0.78-0.98), and rs9344 in the CCND1 gene (OR = 1.14, 95% CI: 1.02-1.27), for those individuals carrying the rare allele. Additionally, the alleles 0401 and 1501 of the HLA class II DRB1 locus were associated with an increased risk (OR = 1.23, 95% CI: 1.04-1.45 and OR = 1.29, 95% CI: 1.11-1.50, respectively), and allele 1301 was associated with decreased risk (OR = 0.59, 95% CI: 0.47-0.73). The effects of CCND1 and the HLA*DRB1 alleles were independent of the effect of smoking. We did not find any association of risk with polymorphisms in genes related to the innate immune system. In conclusion, our study provides evidence for genetic susceptibility to CxCa due to variations in genes involved in the immune system and in cell cycle. (c) 2009 UICC.
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2.
  • Hemminki, Kari, et al. (författare)
  • Familial risks for epilepsy among siblings based on hospitalizations in Sweden
  • 2006
  • Ingår i: Neuroepidemiology. - : Karger. - 0251-5350. ; 27:2, s. 67-73
  • Tidskriftsartikel (refereegranskat)abstract
    • PURPOSE: Epilepsy is a common disabling condition, with high heritability according to twin studies. Characterization of familial risks for common subtypes of epilepsy will advance the search for the heritable causes of these conditions and their underlying mechanisms. We aim at defining familial risks for siblings to be hospitalized because of epilepsy.METHODS: A nationwide ad hoc epilepsy database was constructed by linking the Multigeneration Register on 0- to 69-year-old siblings to the Hospital Discharge Register for data on epilepsies covering the years 1987-2001. Standardized risk ratios (SIRs) were calculated for affected sibling pairs by comparing them to those whose siblings had no epilepsy.RESULTS: Among a total of 26,799 hospitalized cases, 598 affected siblings were identified with a familial SIR of 2.35; the SIR was highest at ages 0-4 years (6.82). Infantile spasms showed the highest risk for any subtype (10.45), when a co-sibling was diagnosed with any epilepsy. When both siblings were diagnosed with a concordant (same) subtype of epilepsy, the SIRs were high, i.e. 8.43 for generalized idiopathic epilepsy, 2.56 for partial epilepsy, 24.72 for status epilepticus and 24.39 for other epilepsies. Generalized idiopathic epilepsy was also associated with grand mal (4.06) and other epilepsies (7.61). The numbers of cases were small but concordant diagnoses always showing higher SIRs compared with discordant diagnoses.CONCLUSIONS: Within the limits of the present sample size, our results suggest high familial aggregation for certain subtypes of epilepsy for which distinct genetic mechanisms may underlie.
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3.
  • Hemminki, Kari, et al. (författare)
  • Familial risks for hospitalized Graves' disease and goiter
  • 2009
  • Ingår i: European Journal of Endocrinology. - : Society of the European Journal of Endocrinology. - 1479-683X. ; 161:4, s. 623-629
  • Tidskriftsartikel (refereegranskat)abstract
    • Objectives: Familial Clustering of a disease is an indicator of a possible heritable Cause. provided that environmental sharing can be excluded. Thus. data on familial risks are important For genetic Studies and for clinical genetic counseling. Design: We carried Out a nationwide family study on nontoxic and toxic nodular goiters, and Graves' disease in order to search for familial clustering of these diseases at the population level. Methods: The Swedish Multigeneration Register on 0-75 year old Subjects was linked to the Hospital Discharge Register from years 1987 to 2007. Standardized incidence ratios (SIRs) were calculated for offspring of affected parents and for siblings by comparing to those whose relatives had no hospitalization for thyroid disease. Results: The number of hospitalized patients in the offspring generations was 11 659 for nontoxic goiter, 9514 for Graves' disease, and 1728 For toxic nodular goiter. Familial Cases accounted for 8.2, 5.2, and 2.1% of all patients respectively The highest familial risk for offspring of affected parents was noted for Graves' disease (SIR 3.87), followed by toxic nodular goiter (3.37) and nontoxic goiter (3.15). Familial risks were higher for affected siblings: toxic nodular goiter (11.66). Graves' disease (5.51). and nontoxic goiter (5.40). Weaker familial associations were observed between the three diseases. Conclusions: To Our knowledge this is it first population-based family study On these thyroid diseases. The observed high familial aggregation for defined thyroid diseases cannot be explained by the known genetic basis, calling for further Studies into genetic and environmental etiology of thyroid diseases.
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4.
  • Hemminki, Kari, et al. (författare)
  • Familial risks in nervous-system tumours: a histology-specific analysis from Sweden and Norway
  • 2009
  • Ingår i: The Lancet Oncology. - : Elsevier. - 1474-5488. ; 10:5, s. 481-488
  • Tidskriftsartikel (refereegranskat)abstract
    • Background There are limited data available on tumour subtype-specific familial risks for nervous-system tumours. We aimed to provide such data at the population level. Methods We used data from the nationwide Swedish and Norwegian databases on familial cancer to calculate standardised incidence ratios (SIRS) for the familial risk of developing a nervous-system tumour in offspring born after 1931 (Sweden) or 1900 (Norway) whose parents or siblings were probands. Findings 54195 patients had nervous-system tumours, 22331 of whom belonged to the offspring generation aged 0-72 years in Sweden and 0-51 years in Norway. Of 709 familial patients in the offspring generation, 438 (61.8%) had a parent affected by a nervous-system tumour (SIR 1.66; 95% CI 1.51-1.82), 236 (33.3%) had a sibling affected by a nervous-system tumour (SIR 2.01; 95% CI 1.76-2.28), and 35 (4.9%) belonged to families with a parent and at least two siblings affected by a nervous-system tumour (multiplex families; SIR 13.40; 95% CI 9.33-18.66). The SIR for glioma was 1.8 (1.5-2.0) when a parent was a proband, but increased to 11.2 (5.7-19.5) in multiplex families. Early-onset neurinoma and haemangioma showed high familial risks; with an SIR for neurinoma of 1.7 (1.4-2.2) for offspring of affected parents, 2.7 (2.0-3.5) for siblings, and 27.2 (13.5-48.8) for multiplex families, and an SIR for haemangioma of 2.4 (1.4-3.8) for offspring of affected parents. Histology-specific population-based familial risks were shown for meningioma (1.6 for offspring of affected parents; 95% CI 1.3-2.0), ependymoma (2.7 for young offspring <20 years; 1.1-5.5), medulloblastoma (4.1 for siblings; 1.7-8.1), and neuroblastoma (3.2 for siblings; 1.1-6.9). Interpretation Our results suggest a complex genetic background for nervous-system tumours, which differs depending on the age of onset and histological subtype of the tumour. High sibling risks might suggest recessive inheritance. As the high-penetrant multiplex families only accounted for about 5% of familial nervous-system tumours, most familial cases are probably caused by low-penetrance genes.
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6.
  • Hemminki, Kari, et al. (författare)
  • Survival in breast cancer is familial
  • 2008
  • Ingår i: ; 110:1, s. 177-182
  • Tidskriftsartikel (refereegranskat)abstract
    • Several earlier studies have assessed survival in breast cancer based on familial risk of this disease. The results have been conflicting and suggest that the risk and prognostic factors of cancer are largely distinct. As a novel concept, we searched for familial clustering of survival, i.e., concordance of survival among family members. We used the nation-wide Swedish Family-Cancer Database to estimate hazard ratios (HRs) for cause-specific and overall survival in invasive breast cancer. HR shows the probability of death in the study group compared the reference group. The study covered 1277 mother-daughter pairs with familial breast cancer. Their median follow-up times for survival ranged from 96 to 122 months. When the survival in daughters was analyzed according to the mothers' length of survival, there was a concordance of prognosis. The HR was 0.65 in daughters whose mothers had survived > or = 120 months compared to daughters whose mothers had survived less than 36 months (P-value for trend 0.02). When the analysis was reversed and HRs were derived for mothers, the results were essentially similar (P-value for trend 0.02). The survival did not differ between patients with familial or sporadic breast cancer. The results are consistent in showing that both good and poor survival in breast cancer aggregates in families, which is a novel population-level finding for any cancer. The consistency of the results suggests that the prognosis in breast cancer is in part heritable which is likely to be explained by yet unknown genetic mechanisms.
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7.
  • Ji, Jianguang, et al. (författare)
  • Survival in Familial Pancreatic Cancer
  • 2008
  • Ingår i: Pancreatology (Print). - : S. Karger. - 1424-3903 .- 1424-3911. ; 8:3, s. 252-256
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Family history has been reported to be associated with an increased risk of pancreatic cancer. However, its possible influence on pancreatic cancer survival has rarely been studied, probably because of the rareness of cases in the same family.METHODS: We used the nationwide Swedish Family-Cancer Database to examine the survival differences between familial and sporadic pancreatic cancers. Hazard ratios (HRs) for cause-specific and overall survival in pancreatic cancer were examined. HRs show the probability of death in the study group compared to the reference group.RESULTS: A total of 75 familial pancreatic cancers were noted. HRs were significantly higher among offspring with an affected parent compared to those without an affected parent; for cause-specific and overall survival, the HRs were 1.44 and 1.37, respectively. Reversing the analysis and deriving HRs for parents (offspring as probands) showed that familial pancreatic cancer had a worse prognosis than sporadic cases (HR 1.37 for cause-specific and 1.28 for overall survival). The HRs were close to unity among spouses with concordant pancreatic cancer.CONCLUSION: The data show that survival in familial pancreatic cancer is worse than that in sporadic disease, which could be explained by genetic factors, if other confounding factors can be excluded. and IAP.
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8.
  • Shete, Sanjay, et al. (författare)
  • Genome-wide association study identifies five susceptibility loci for glioma.
  • 2009
  • Ingår i: Nature Genetics. - 1061-4036 .- 1546-1718. ; 41:8, s. 899-904
  • Tidskriftsartikel (refereegranskat)abstract
    • To identify risk variants for glioma, we conducted a meta-analysis of two genome-wide association studies by genotyping 550K tagging SNPs in a total of 1,878 cases and 3,670 controls, with validation in three additional independent series totaling 2,545 cases and 2,953 controls. We identified five risk loci for glioma at 5p15.33 (rs2736100, TERT; P = 1.50 x 10(-17)), 8q24.21 (rs4295627, CCDC26; P = 2.34 x 10(-18)), 9p21.3 (rs4977756, CDKN2A-CDKN2B; P = 7.24 x 10(-15)), 20q13.33 (rs6010620, RTEL1; P = 2.52 x 10(-12)) and 11q23.3 (rs498872, PHLDB1; P = 1.07 x 10(-8)). These data show that common low-penetrance susceptibility alleles contribute to the risk of developing glioma and provide insight into disease causation of this primary brain tumor.
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9.
  • Sundquist, Jan, et al. (författare)
  • Risks of subarachnoid hemorrhage in siblings : a nationwide epidemiological study from Sweden
  • 2007
  • Ingår i: Neuroepidemiology. - : Karger. - 1423-0208. ; 29:3-4, s. 84-178
  • Tidskriftsartikel (refereegranskat)abstract
    • This nationwide study aimed to enhance available data by determining sibling risks of subarachnoid hemorrhage in a total population. The MigMed database at the Karolinska Institute, Stockholm, was used to identify all cases of subarachnoid hemorrhage diagnosed in Sweden between 1987 and 2001. Incidence ratios standardized for age, region, and socioeconomic status (SIRs) were calculated for persons with at least 1 sibling with subarachnoid hemorrhage. The reference group consisted of persons whose siblings had no subarachnoid hemorrhage. A total of 90 affected siblings were identified; their SIR of subarachnoid hemorrhage was 2.75. The risk decreased with increasing age in both men and women. Within the limits of the sample size, no sex differences could be observed. The relatively high sibling risks are likely to be due to heritable causes and shared environmental factors. Genetic causes possibly weigh more in early- than late-onset cases. This study shows the feasibility of carrying out nationwide family studies on subarachnoid hemorrhage.
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10.
  • Brandt, Andreas, et al. (författare)
  • Age at Diagnosis and Age at Death in Familial Prostate Cancer
  • 2009
  • Ingår i: Oncologist. - : AlphaMed Press. - 1083-7159. ; 14:12, s. 1209-1217
  • Tidskriftsartikel (refereegranskat)abstract
    • 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. The Oncologist 2009; 14: 1209-1217
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