| 1. |
- Brandt, Andreas, et al.
(författare)
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Age at Diagnosis and Age at Death in Familial Prostate Cancer
- 2009
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Ingår i: The Oncologist. - : Oxford University Press (OUP). - 1083-7159 .- 1549-490X. ; 14:12, s. 1209-1217
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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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| 2. |
- Brendle, Annika, et al.
(författare)
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Single nucleotide polymorphisms in chromosomal instability genes and risk and clinical outcome of breast cancer : a Swedish prospective case-control study.
- 2009
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Ingår i: European journal of cancer (Oxford, England : 1990). - : Elsevier BV. - 1879-0852 .- 0959-8049. ; 45:3, s. 435-442
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Tidskriftsartikel (refereegranskat)abstract
- Chromosomal instability (CIN) is a major characteristic of many cancers. We investigated whether putatively functional single nucleotide polymorphisms (SNPs) in genes related to CIN (CENPF, ESPL1, NEK2, PTTG1, ZWILCH, ZWINT) affect breast cancer (BC) risk and clinical outcome in a Swedish cohort of 749 incident BC cases with detailed clinical data and up to 15 years of follow-up and 1493 matched controls. As a main observation, carriers of the A allele of the CENPF SNP rs438034 had a worse BC-specific survival compared to the wild type genotype GG carriers (hazard ratio (HR) 2.65, 95% confidence interval (CI) 1.19-5.90), although they were less likely to have regional lymph node metastases (odds ratio (OR) 0.71, 95% CI 0.51-1.01) and tumours of stage II-IV (OR 0.73, 95% CI 0.54-0.99). As there is increasing evidence that CENPF is associated with poor prognosis in patients with primary BC, further independent studies are needed to clarify the importance of genetic variation in the CENPF gene in the clinic.
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| 3. |
- Castro, Felipe A, et al.
(författare)
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Association of HLA-DRB1, interleukin-6 and cyclin D1 polymorphisms with cervical cancer in the Swedish population-A candidate gene approach.
- 2009
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Ingår i: International Journal of Cancer. - : John Wiley & Sons. - 0020-7136 .- 1097-0215. ; 125:8, s. 1851-1858
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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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| 4. |
- Hemminki, Kari, et al.
(författare)
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Associated cancers in parents and offspring of polycythaemia vera and myelofibrosis patients
- 2009
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Ingår i: British Journal of Haematology. - : Wiley. - 0007-1048 .- 1365-2141. ; 147:4, s. 526-530
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Tidskriftsartikel (refereegranskat)abstract
- 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).
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| 5. |
- Hemminki, Kari, et al.
(författare)
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Familial risks for hospitalized Graves' disease and goiter
- 2009
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Ingår i: European Journal of Endocrinology. - 1479-683X. ; 161:4, s. 623-629
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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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| 6. |
- Hemminki, Kari, et al.
(författare)
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Familial risks in nervous-system tumours: a histology-specific analysis from Sweden and Norway
- 2009
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Ingår i: The Lancet Oncology. - 1474-5488. ; 10:5, s. 481-488
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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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| 7. |
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| 8. |
- Hiripi, E., et al.
(författare)
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Familial association of pancreatic cancer with other malignancies in Swedish families
- 2009
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Ingår i: British Journal of Cancer. - : Springer Science and Business Media LLC. - 1532-1827 .- 0007-0920. ; 101:10, s. 1792-1797
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The aim of this study was to characterise the familial association of pancreatic cancer with other malignancies. METHODS: Relative risks (RRs) of pancreatic cancer according to family history of cancer were calculated using the updated Swedish Family-Cancer Database, which includes over 11.5 million individuals. Estimates were based on Poisson regression. RRs of tumours for individuals with a parental history of pancreatic cancer were also estimated. RESULTS: The risk of pancreatic cancer was elevated in individuals with a parental history of cancers of the liver (RR 1.41; 95% CI 1.10-1.81), kidney (RR 1.37; 95% CI 1.06-1.76), lung (RR 1.50; 95% CI 1.27-1.79) and larynx (RR 1.98; 95% CI 1.19-3.28). Associations were also found between parental history of pancreatic cancer and cancers of the small intestine, colon, breast, lung, testis and cervix in offspring. There was an increased risk of pancreatic cancer associated with early-onset breast cancer in siblings. CONCLUSION: Pancreatic cancer aggregates in families with several types of cancer. Smoking may contribute to the familial aggregation of pancreatic and lung tumours, and the familial clustering of pancreatic and breast cancer could be partially explained by inherited mutations in the BRCA2 gene. British Journal of Cancer (2009) 101, 1792-1797. doi: 10.1038/sj.bjc.6605363 www.bjcancer.com Published online 13 October 2009 (C) 2009 Cancer Research UK
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| 9. |
- Hussain, Shehnaz K., et al.
(författare)
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The Effect of Having an Affected Parent or Sibling on Invasive and In Situ Skin Cancer Risk in Sweden
- 2009
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Ingår i: Journal of Investigative Dermatology. - : Elsevier BV. - 1523-1747 .- 0022-202X. ; 129:9, s. 2142-2147
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Tidskriftsartikel (refereegranskat)abstract
- Studies suggest that skin cancer aggregates within families; however, the risk of skin cancer associated with having an affected sibling or parent by subtype, tumor site, and age at diagnosis has not been established. The 2006 update of the Swedish Family-Cancer Database was used to calculate standardized incidence ratios (SIRs), representing the ratio of cancer risk among individuals with affected parents or siblings to the general population. Risk of invasive squamous cell skin cancer for individuals with an affected sibling or parent was increased between two-and three-fold compared with that in the general population. For in situ skin tumors, increased SIRs of 1.95-4.30 for squamous cell, Bowen's disease, and actinic keratosis were observed for individuals with affected siblings or parents, and SIRs were generally higher for tumors at sun-exposed versus covered sites. Finally, SIRs for in situ and invasive squamous cell skin cancer increased by increasing number of parental tumors (P <= 0.01). In conclusion, having an affected sibling or parent was associated with an increased risk of skin cancer of varied subtypes compared with that in the general population, and for some subtypes, these familial risks were increased for tumors at sun-exposed sites or by an increasing number of parental tumors.
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| 10. |
- Ji, Jianguang, et al.
(författare)
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Survival in non-Hodgkin's lymphoma by histology and family history.
- 2009
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Ingår i: Journal of Cancer Research and Clinical Oncology. - : Springer Science and Business Media LLC. - 1432-1335 .- 0171-5216. ; 135, s. 1711-1716
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Tidskriftsartikel (refereegranskat)abstract
- PURPOSE: Although survival has been studied for various subtypes of non-Hodgkin's lymphoma (NHL), there have been few comprehensive studies to quantify the prognosis, including all specific histologies. The effect of family history on survival in NHL has not been examined. METHODS: We used the Swedish Family-Cancer Database to estimate hazard ratios in NHL by histology and family history. RESULTS: Using diffuse centroblastic lymphoma as reference (HR 1.0), patients with Waldenström's macroglobulinemia and hairy-cell leukemia had the best survival. Survival advantage was also noted among patients with lymphoplasmacytic lymphoma and different kinds of follicular lymphomas. For T-cell lymphoma, mycosis fungoides showed a favorable prognosis. As for survival by family history, a total of 98 familial cases were noted in our Database with a similar prognosis compared to sporadic cases in both parental and offspring generations. A non-significant familial concordance of either good or poor survival was noted among family members when probands' prognosis was stratified by survival time. CONCLUSIONS: Our results provide quantitative prognosis data for patients with NHL according to specific histologies. Patients with a familial NHL had a similar prognosis compared to patients with sporadic disease. The data suggest familial concordance in either good or poor survival among family members.
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