Publications (523)2874.2 Total impact
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Article: Genetic variants in C-type lectin genes are associated with colorectal cancer susceptibility and clinical outcome.
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ABSTRACT: Inflammatory responses play a vital role at different stages of colorectal carcinogenesis. C-type lectins mediate inflammatory/immune responses and participate in immune escape of pathogens and tumors. Our study aimed to evaluate the correlation between polymorphisms in three C-type lectin genes, CD209, MBL2 and REG4, and colorectal cancer (CRC) risk and clinical outcome. We genotyped 15 potentially functional single nucleotide polymorphisms (SNPs) and assessed their associations with CRC risk in a case-control study of 1353 CRC cases and 767 healthy controls from the Czech Republic. We also analyzed these SNPs in relation to overall and event-free survival in 414 patients. Two CD209 SNPs were associated with CRC risk after adjustment for multiple comparison. Minor allele carriers of the promoter SNP rs2287886 had an increased risk of CRC (OR 1.30, 95%CI 1.08-1.56), while minor allele carriers of the 3'UTR SNP, rs7248637, had a decreased risk (OR 0.74, 95%CI 0.60-0.91). Multivariate survival analyses, including age, gender, TNM stage and grade, showed that patients without distant metastasis at the time of diagnosis and carrying the rs2994809 T allele had a decreased overall and event-free survival (HR 2.11, 95%CI 1.20-3.72 and HR 2.00, 95%CI 1.18-3.39, respectively). We show that SNPs in CD209 may affect CRC risk, while a SNP in REG4 may be a useful marker for CRC progression. © 2013 Wiley Periodicals, Inc.International Journal of Cancer 05/2013; · 5.44 Impact Factor -
Article: Risk of thyroid cancer in first-degree relatives of patients with non-medullary thyroid cancer by histology type and age at diagnosis: a joint study from five Nordic countries.
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ABSTRACT: BACKGROUND: We aimed to estimate lifetime cumulative risk of thyroid cancer (CRTC) in first-degree relatives of patients with non-medullary thyroid cancers (NMTC), including papillary (PTC)/follicular/oxyphilic/anaplastic thyroid carcinoma, by histology and age at diagnosis in patients and their relatives. DESIGN: A population-based cohort of 63 495 first-degree relatives of 11 206 NMTC patients diagnosed in 1955-2009 in Nordic countries was followed for cancer incidence. Standardised incidence ratios (SIRs) were calculated using histology-specific, age-specific, sex-specific, period-specific and country-specific incidence rates as reference. RESULTS: The 0-84-year CRTC in female relatives of a patient with PTC was 2%, representing a threefold increase over the general population risk (SIR=2.9, 95% CI 2.4 to 3.4; Men: CRTC=1%, SIR=2.5, 95% CI 1.9 to 3.3). When there were ≥2 PTC patients diagnosed at age <60 years in a family, CRTC for female relatives was 10% (male 24%). Twins had a 23-fold increased risk of concordant PTC. Family history of follicular/oxyphilic/anaplastic carcinoma increased CRTC in relatives to about 1-2%. Although no familial case of concordant oxyphilic/anaplastic carcinoma was found, familial risks of discordant histology types of NMTC were interchangeably high for most of the types, for example, higher risk of PTC when a first-degree relative had follicular (SIR=3.0, 95%CI 1.7 to 4.9) or anaplastic (SIR=3.6, 95% CI 1.2 to 8.4) carcinoma. The earlier a patient was diagnosed with PTC in a family, the higher was the SIR in his/her younger relatives. There was a tendency towards concordant age at diagnosis of thyroid cancer among relatives of PTC patients. CONCLUSIONS: This study provides clinically relevant risk estimates for family members of NMTC patients.Journal of Medical Genetics 04/2013; · 6.36 Impact Factor -
Article: Subsequent leukaemia in autoimmune disease patients.
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ABSTRACT: Previous studies have shown that patients diagnosed with some autoimmune (AI) diseases are at an increased risk of leukaemia but limited data are available on survival. We systematically analysed the risks (standardized incidence ratio, SIR) and survival (hazard ratio, HR) in nine types of leukaemia among 402 462 patients hospitalized for any of 33 AI diseases and compared to persons not hospitalized for AI diseases. Risk for all leukaemia was increased after 13 AI diseases and survival was decreased after six AI diseases. SIRs were increased after all AI diseases for seven types of leukaemia, including SIR 1·69 (95% confidence interval (CI): 1·29-2·19) for acute lymphoblastic leukaemia (ALL), 1·85 (95% CI: 1·65-2·07) for acute myeloid leukaemia, 1·68 (95% CI: 1·37-2·04) for chronic myeloid leukaemia, 2·20 (95% CI: 1·69-2·81) for 'other myeloid leukaemia', 2·45 (95% 1·99-2·98) for 'other and unspecified leukaemia', 1·81 (95% CI: 1·11-2·81) for monocytic leukaemia, and 1·36 (95% CI: 1·08-1·69) for myelofibrosis. The HRs were increased for four types of leukaemia, most for myelofibrosis (1·74, 95% CI: 1·33-2·29) and ALL (1·42, 95% CI: 1·03-1·95). Some AI diseases, including rheumatoid arthritis, were associated with increased SIRs and HRs in many types of leukaemia. The present data showed increases in risk and decreases in survival for many types of leukaemia after various AI diseases. Leukaemia is a rare complication in AI disease but findings about this comorbidity at the time of leukaemia diagnosis may help to optimize the treatment and improve survival.British Journal of Haematology 04/2013; · 4.94 Impact Factor -
Article: Genetic Polymorphisms in Host Innate Immune Sensor Genes and the Risk of Nasopharyngeal Carcinoma in North Africa.
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ABSTRACT: Nasopharyngeal carcinoma (NPC) is a rare malignancy in most parts of the world. It is an Epstein-Barr virus-associated malignancy with an unusual racial and geographical distribution. The host innate immune sensor genes play an important role in infection recognition and immune response against viruses. Therefore, we examined the association between polymorphisms in genes within a group of pattern recognition receptors (including families of toll-like receptors, C-type lectin receptors, and RIG-I-like receptors) and NPC susceptibility. Twenty six single nucleotide polymorphisms (SNPs) in five pattern-recognition genes were genotyped in 492 North African NPC cases and 373 frequency-matched controls. TLR3_rs3775291 was the most significantly associated SNP (OR: 1.49; 95%CI: 1.11-2.00; P: 0.008; dominant model). The analysis showed also that CD209_rs7248637 (OR: 0.69; 95%CI: 0.52-0.93; P: 0.02; dominant model) and DDX58_rs56309110 (OR: 0.70; 95%CI: 0.51-0.98; P: 0.04) were associated with the risk of NPC. An 18% increased risk per allele was observed for the five most significantly associated SNPs, TLR3_rs3775291, CD209_rs7248637, DDX58_rs56309110, CD209_rs4804800 and MBL2_rs10824792, (ptrend 8.2x10(-4)). Our results suggest that genetic variation in pattern-recognition genes is associated with the risk of NPC. These preliminary findings require replication in larger studies.G3 (Bethesda, Md.). 04/2013; -
Article: Chromosomal damage among medical staff occupationally exposed to volatile anesthetics, antineoplastic drugs, and formaldehyde.
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ABSTRACT: OBJECTIVES: Structural chromosomal aberrations in blood lymphocytes represent a biomarker for cellular damage caused by genotoxic carcinogens and are an indicator of increased cancer risk. We evaluated the association between frequencies of total chromosomal aberrations, chromatid- and chromosome-type aberrations, and occupational exposures to volatile anesthetics, antineoplastic agents, and formaldehyde among 601 medical professionals. METHODS: Chromosomal damage among exposed individuals and unexposed controls was determined by conventional cytogenetic analysis. We used binary logistic regression to evaluate the effects of workplace exposures and major confounders on chromosomal damage. RESULTS: Significantly higher frequencies of total chromosomal, chromatid-type and chromosome-type aberrations were observed among subjects occupationally exposed to volatile anesthetics, antineoplastic agents, and formaldehyde compared to age- and sex-matched controls (P<0.0001). The risk of an increased frequency of chromosomal aberrations was associated with exposure to anesthetics [odds ratio (OR) 3.9, 95% confidence interval (95% CI) 2.7-5.8], cytostatics (OR 2.7, 95% CI 1.9-3.9), and formaldehyde (OR 1.7, 95% CI 1.1-2.7). No other covariate contributed significantly to the model. Chromatid- and chromosome-type aberrations were associated with exposure to anesthetics and cytostatics without any contribution of other variables. Stratified data analysis showed the risk of increased chromosomal aberrations among non-smoking female nurses and physicians exposed to anesthetics, cytostatics and, partially, formaldehyde. Chromatid and chromosome exchanges were significantly higher in the exposed groups than among controls. CONCLUSION: Our findings indicate that the presence of genotoxic compounds in operating rooms, oncological units, and pathological departments results in a significant increase of chromosomal damage (impair of chromosomal integrity) among medical workers employed in these facilities.Scandinavian journal of work, environment & health 03/2013; · 3.12 Impact Factor -
Article: The CCND1 c.870G>A polymorphism is a risk factor for t(11;14)(q13;q32) multiple myeloma.
Nature Genetics 03/2013; · 35.53 Impact Factor -
Article: The CCND1 c.870G>A polymorphism is a risk factor for t(11;14)(q13;q32) multiple myeloma.
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ABSTRACT: A number of specific chromosomal abnormalities define the subgroups of multiple myeloma. In a meta-analysis of two genome-wide association studies of multiple myeloma including a total of 1,661 affected individuals, we investigated risk for developing a specific tumor karyotype. The t(11;14)(q13;q32) translocation in which CCND1 is placed under the control of the immunoglobulin heavy chain enhancer was strongly associated with the CCND1 c.870G>A polymorphism (P = 7.96 × 10(-11)). These results provide a model in which a constitutive genetic factor is associated with risk of a specific chromosomal translocation.Nature Genetics 03/2013; · 35.53 Impact Factor -
Article: Familial Risk of Small Intestinal Carcinoid and Adenocarcinoma.
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ABSTRACT: BACKGROUND: Small intestinal cancer (SIC) is rare and its etiology is poorly understood. We compared clusters of families with SICs of different histologic subtypes. METHODS: Using the nation-wide family-cancer datasets of Sweden and Finland, we identified a cohort of 9964 first-degree relatives of 1799 patients with SIC, diagnosed from 1961 through 2009; data were collected from time periods as long as 47 y (mean, 35.4 y) and cancer incidence was determined. Standardized incidence ratios (SIRs) were calculated and stratified by sex, age, time period, and cancer type, using the incidence rates for the entire national population as the reference. RESULTS: Among the 1799 SIC cases, 1.1% had a sibling with SIC, so the SIR was 11.8 (95% confidence interval [CI], 7.2-18.2); 1.1% had a parent or child with SIC (SIR=3.5; 95% CI, 2.0-5.6). The SIR of concordant carcinoid histology of SIC among siblings was 28.4 (95% CI, 14.7-49.6; n=12) and in parent-child pairs was 9.9 (95% CI, 5.4-16.6; n=14). The familial risk of concordant histologic subtypes increased for siblings diagnosed with adenocarcinoma, but only 2 familial cases were identified. In family members of patients with SIC of the adenocarcinoma subtype, risks of colorectal and bladder cancer were modestly but significantly increased, compared with the general population. Family members of patients with SIC of the carcinoid subtype had increased risk for kidney cancer and polycythemia vera. CONCLUSIONS: Based on data from our population-based study, first-degree relatives of patients with small intestinal carcinoid tumors have developed these tumors with high incidence. Due to rareness of this tumor, the absolute risk remains moderate even within families. Gastroenterologists could inform patients with small intestinal carcinoids about the familial risk and encourage counseling for their first-degree relatives. Studies are needed to identify genetic factors that affect susceptibility to SIC.Clinical gastroenterology and hepatology: the official clinical practice journal of the American Gastroenterological Association 03/2013; · 5.64 Impact Factor -
Article: Deciphering the 8q24.21 association for glioma.
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ABSTRACT: We have previously identified tagSNPs at 8q24.21 influencing glioma risk. We have sought to fine-map the location of the functional basis of this association using data from four genome-wide association studies, comprising a total of 4147 glioma cases and 7435 controls. To improve marker density across the 700 kb region, we imputed genotypes using 1000 Genomes Project data and high-coverage sequencing data generated on 253 individuals. Analysis revealed an imputed low-frequency SNP rs55705857 (P = 2.24 × 10(-38)) which was sufficient to fully capture the 8q24.21 association. Analysis by glioma subtype showed the association with rs55705857 confined to non-glioblastoma multiforme (non-GBM) tumours (P = 1.07 × 10(-67)). Validation of the non-GBM association was shown in three additional datasets (625 non-GBM cases, 2412 controls; P = 1.41 × 10(-28)). In the pooled analysis, the odds ratio for low-grade glioma associated with rs55705857 was 4.3 (P = 2.31 × 10(-94)). rs55705857 maps to a highly evolutionarily conserved sequence within the long non-coding RNA CCDC26 raising the possibility of direct functionality. These data provide additional insights into the aetiological basis of glioma development.Human Molecular Genetics 02/2013; · 7.64 Impact Factor -
Dataset: 2013 SCIENCE Horn.SM
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Dataset: 2013 SCIENCE Horn.SM
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Article: Comparison of survival of patients with metastases from known versus unknown primaries: survival in metastatic cancer.
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ABSTRACT: BACKGROUND: Cancer of unknown primary site (CUP) is considered an aggressive metastatic disease but whether the prognosis differs from metastatic cancers of known primary site is not known. Such data may give insight into the biology of CUP and the metastatic process in general. METHODS: 6,745 cancer patients, with primary metastatic cancer at diagnosis, were identified from the Swedish Cancer Registry, and were compared with 2,881 patients with CUP. Patients were diagnosed and died between 2002 and 2008. The influence of the primary site, known or unknown, on survival in patients with metastases at specific locations was investigated. Hazard ratios (HRs) of death were estimated for several sites of metastasis, where patients with known primary sites were compared with CUP patients. RESULTS: Overall, patients with metastatic cancers with known primary sites had decreased hazards of death compared to CUP patients (HR = 0.69 [95% CI = 0.66--0.72]). The exceptions were cancer of the pancreas (1.71 [1.54--1.90]), liver (1.58 [1.36--1.85]), and stomach (1.16 [1.02--1.31]). For individual metastatic sites, patients with liver or bone metastases of known origin had better survival than those with CUP of the liver and bone. Patients with liver metastases of pancreatic origin had an increased risk of death compared with patients with CUP of the liver (1.25 [1.06--1.46]). The median survival time of CUP patients was three months. CONCLUSIONS: Patients with CUP have poorer survival than patients with known primaries, except those with brain and respiratory system metastases. Of CUP sites, liver metastases have the worst prognosis. Survival in CUP was comparable to that in metastatic lung cancer. The aggressive behavior of CUP may be due to initial immunosuppression and immunoediting which may allow accumulation of mutations. Upon escape from the suppressed state an unstoppable tumor spread ensues. These novel data on the epidemiology of the metastatic process at the population level demonstrated large survival differences in organ defined metastases depending on the original cancer.BMC Cancer 01/2013; 13(1):36. · 3.01 Impact Factor -
Dataset: Supplementary Materials for TERT Promoter Mutations in Familial and Sporadic Melanoma
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Article: TERT Promoter Mutations in Familial and Sporadic Melanoma
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ABSTRACT: The identification of germ line mutations that co-segregate with disease in cancer-prone families often provides genetic and mechanistic insights into the more common, sporadically arising cancers. In a study of cuta-neous melanoma, the most malignant skin cancer, we investigated a large pedigree with 14 related melanoma patients, who were not carriers of germ line mutations in CDKN2A or CDK4, two known melanoma genes (Fig. 1). Multipoint linkage analysis showed a possible 2.2Mb linkage region on chromosome 5p with maximal LOD-scores of 2.35 at rs1379917 and 2.45 at rs1968011. Target enriched high throughput se-quencing (HTS) of the region was carried out on constitutional DNA from the four affected and four unaffected members of the family with an average coverage between 55 and 108-fold (table S1) (1). The HTS data revealed a single promoter variant, three intronic variants and three non-gene variants, previously unknown and unique to the DNA se-quences of the affected individuals (table S2). The disease segregating variants, seven in total, were validated by Sanger sequencing of DNA from the individuals sequenced by HTS and of DNA from additional unaffected members of the family. The new variants were also detected in an unaffected member (754, table S3), who was 36 years old and car-ried multiple nevi. DNA from affected individuals other than those se-quenced by HTS was not available for testing. Of the seven unique variants identified, one variant (T>G), was lo-cated in the promoter at -57bp from ATG translation start site of the TERT gene. The TERT gene encodes the catalytic reverse transcriptase subunit of telomerase, the ribonucleoprotein complex that maintains telomere length. The nucleotide change in the sequence CCTGAA>CCGGAA creates a new binding motif for Ets transcription factors, with a general recognition motif GGA(A/T). Beyond the general motif for Ets transcription factors, the familial mutation also generates a binding motif CCGGAA for the ternary complex factors (TCF) Elk1 and Elk4 (2, 3). To exclude the possibility that the detected promoter mutation in TERT is a common germ line variant, we screened germ line DNA from 140 sporadic melanoma cases and 165 healthy controls and none carried the variant. Screening of DNA from index cases from 34 Spanish melanoma fami-lies also did not show any mutations. No carriers were found in dbSNP and the 1000 Genomes database (data available for 18 individuals, ENSEMBL). The familial mutation in the TERT promoter was in complete allelic link-age with a common polymorphism rs2853669 (G>A) at -246bp upstream from the ATG start site (table S3). In previous work, this polymorphism was reported to disrupt an Ets binding site and it was associated with low te-lomerase activity in patients with non small cell lung cancer (4). In Lucifer-ase reporter gene assays, we found that the activity of constructs containing the mutation at -57bp of the TERT promot-er was increased 1.5 fold and 1.2 fold over the wild type construct in Ma-Mel-86a and HEK293T cells, respec-tively. A construct with both the TERT mutation and the variant allele of the rs2853669 polymorphism showed a 2.2 fold increase in promoter activity in Ma-Mel-86a and and 1.3 fold increase in HEK293 cells (mean from three measurements, details in Supplementary text and fig. S1).Science. 01/2013; -
Article: TERT Promoter Mutations in Familial and Sporadic Melanoma.
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ABSTRACT: Cutaneous melanoma occurs in both familial and sporadic forms. We investigated a melanoma-prone family through linkage analysis and high-throughput sequencing and identified a disease-segregating germ line mutation in the promoter of the telomerase reverse transcriptase (TERT) gene, which encodes the catalytic subunit of telomerase. The mutation creates a new binding motif for Ets/TCF transcription factors near the transcription start and in reporter gene assays, caused up to 2-fold increase in transcription. We then screened the TERT promoter in sporadic melanoma and observed recurrent UV signature somatic mutations in 125/168 (74%) of human cell lines derived from metastatic melanomas, corresponding metastatic tumor tissues (45/53, 85%) and in 25/77 (33%) primary melanomas. The majority of those mutations occurred at two positions in the TERT promoter and also generated binding motifs for ETS/TCF transcription factors.Science 01/2013; · 31.20 Impact Factor -
Article: Ethnic differences in breast cancer risk and survival: A study on immigrants in Sweden.
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ABSTRACT: Background. There are large geographic differences in breast cancer risk but whether survival differs between low- and high-risk groups is less well-established. As the survival of cancer depends on the level of healthcare and awareness of disease risks, subtle differences in cancer biology cannot be revealed in international comparisons. Instead, comparison of diverse immigrant groups in a country of uniformly accessible healthcare system should enable conclusions to be made about ethnic determinants of cancer risk and survival. Material and methods. The Swedish Family-Cancer Database was used to calculate standardized incidence (SIRs) and hazard ratios (HRs) of death from female breast cancer in 12 505 and 137 547 patients diagnosed with breast cancer among immigrants and Swedes, respectively. The ratios were adjusted for age, period, region, parity, and age at first childbirth. Ordinal logistic regression analysis was used to estimate odds ratios (ORs) for the clinical TNM classes. The analyses were stratified by menopausal status and histology. Results. Turks, Southeast Asians, and Chileans had the lowest breast cancer risk (SIR = 0.44; 95% CI 0.37-0.51) and Iraqis the highest risk (1.19; 1.05-1.35), mainly due to premenopausal cancer (1.51; 1.27-1.78). The HRs for all breast cancers were between 0.98 (0.81-1.18) (low-risk Europeans) and 1.24 (0.94-1.63) (lowest-risk non-Europeans), but were not significant. No differences in survival of ductal carcinoma between immigrants and Swedes were found, while low-risk non-Europeans had a HR of 2.88 (1.37-6.08) for lobular carcinoma. Low-risk non-Europeans were diagnosed in a higher T-class (OR = 1.87; 1.21-2.87) than Swedes. Conclusion. We did not find any evidence that ethnic differences in breast cancer risk substantially affect the survival. The observed poor survival of some low-risk immigrants in lobular carcinoma may be related to treatment. The tendency of low-risk immigrants to present with higher T-class compared to Swedes may depend on their lower participation in the mammography screening program.Acta oncologica (Stockholm, Sweden) 01/2013; · 2.27 Impact Factor -
Article: Prostate cancer incidence and survival in immigrants to Sweden.
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ABSTRACT: PURPOSE: The large international variation in the incidence of prostate cancer (PC) is well known but the underlying reasons are not understood. We want to compare PC incidence and survival among immigrants to Sweden in order to explain the international differences. METHODS: Cancer data were obtained from the Swedish Cancer Registry. Standardized incidence ratios (SIRs) were calculated for PC in first-degree immigrants by country of birth. The immigrants were classified into four groups by SIR and area of origin. Survival in PC was assessed by hazard ratio (HR) in the four groups. In some analyses, clinical stage of PC was assessed by the tumor, node, and metastasis classification. RESULTS: The SIR was 0.47 (95 % confidence interval 0.43-0.51) for immigrants with the lowest risk, constituting men from Turkey, Middle East, Asia, and Chile. The HR was 0.60 (0.45-0.81) for these men and it was 0.49 if they had stayed 20+ years in Sweden. The SIR in screening detected PC, T1c, was 0.55. Among these men, screening detected PC constituted 34.5 % of all PC, compared to 29.0 % among Swedes (p = 0.10). CONCLUSIONS: The results showed that the non-European immigrants, of mainly Middle East, Asian, and Chilean origin, with the lowest risk of PC, also had the most favorable survival in PC. As the available clinical features of PC at diagnosis or the distribution of known risk factors could not explain the differences, a likely biological mechanism through a favorable androgenic hormonal host environment is suggested as an explanation of the observed effects.World Journal of Urology 01/2013; · 2.41 Impact Factor -
Dataset: 1471-2350-13-94
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Article: Somatic mutations in exocrine pancreatic tumors: association with patient survival.
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ABSTRACT: KRAS mutations are major factors involved in initiation and maintenance of pancreatic tumors. The impact of different mutations on patient survival has not been clearly defined. We screened tumors from 171 pancreatic cancer patients for mutations in KRAS and CDKN2A genes. Mutations in KRAS were detected in 134 tumors, with 131 in codon 12 and only 3 in codon 61. The GGT>GAT (G12D) was the most frequent mutation and was present in 60% (80/134). Deletions and mutations in CDKN2A were detected in 43 tumors. Analysis showed that KRAS mutations were associated with reduced patient survival in both malignant exocrine and ductal adenocarcinomas (PDAC). Patients with PDACs that had KRAS mutations showed a median survival of 17 months compared to 30 months for those without mutations (log-rank P = 0.07) with a multivariate hazard ratio (HR) of 2.19 (95%CI 1.09-4.42). The patients with G12D mutation showed a median survival of 16 months (log-rank-test P = 0.03) and an associated multivariate HR 2.42 (95%CI 1.14-2.67). Although, the association of survival in PDAC patients with CDKN2A aberrations in tumors was not statistically significant, the sub-group of patients with concomitant KRAS mutations and CDKN2A alterations in tumors were associated with a median survival of 13.5 months compared to 22 months without mutation (log-rank-test P = 0.02) and a corresponding HR of 3.07 (95%CI 1.33-7.10). Our results are indicative of an association between mutational status and survival in PDAC patients, which if confirmed in subsequent studies can have potential clinical application.PLoS ONE 01/2013; 8(4):e60870. · 4.09 Impact Factor -
Article: Autoimmune diseases and subsequent urological cancers.
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ABSTRACT: PURPOSE: To examine the subsequent risk and prognosis of urological cancers among individuals diagnosed with autoimmune(AI) diseases. MATERIALS AND METHODS: We analyzed systematically the risk and prognosis of prostate, kidney and bladder cancers among individuals diagnosed with any of 33 different AI diseases based on nation-wide Swedish database covering years 1964 through 2008. Standardized incidence ratios (SIRs) and hazard ratios (HRs) were calculated for subsequent urological cancers between 1964 and 2008 in individuals hospitalized for an AI disease. RESULTS: Increased SIRs for urological cancers were recorded after 26 AI diseases; increased HRs for cancer-specific survival were noted after 4 AI diseases and for overall survival after 18 AI diseases. The highest SIRs were seen for kidney cancer after polyarteritis nodosa (2.85), and polymyositis/dermatomyositis (2.68), and for bladder cancer after polymyositis/dermatomyositis (2.45). For prostate cancer, the highest risk (1.70) was observed after polyarteritis nodosa; the SIRs were lower in follow-up period 1990 to 2008 compared to the previous period. Individuals diagnosed with prostate and kidney cancers showed an improved cancer-specific prognosis, in contrast to the poorer overall prognosis for all 3 urological cancers. CONCLUSIONS: The risks for urological cancers were increased after all AI diseases and most significant changes after individual AI diseases were towards higher risks. The data on survival were reassuring that AI diseases influenced the prognosis of cancer-specific mortality marginally. However, the overall survival was decreased for the three cancers.The Journal of urology 12/2012; · 4.02 Impact Factor
Top co-authors
Top Journals
Institutions
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2009–2013
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Universität Heidelberg
- • Institute of Transfusion Medicine and Immunology
- • Institute of Medical Biometry and Informatics
Heidelberg, Baden-Wuerttemberg, Germany -
Lund University
- Center for Primary Health Care Research
Lund, Skane, Sweden -
University of Texas MD Anderson Cancer Center
- Department of Epidemiology
Houston, TX, USA -
Erasmus MC
Rotterdam, South Holland, Netherlands
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2003–2013
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Deutsches Krebsforschungszentrum
- Division of Molecular Genetic Epidemiology
Heidelberg, Baden-Wuerttemberg, Germany
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2002–2013
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Academy of Sciences of the Czech Republic
- • Oddělení molekulární biologie nádorů
- • Ústav experimentální medicíny
- • Laboratoř vývojové genetiky
Praha, Hlavni mesto Praha, Czech Republic
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2011
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Istituto di Ricerche Farmacologiche Mario Negri
Milano, Lombardy, Italy
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2009–2011
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deCODE genetics, Inc.
Reykjavík, Capital Region, Iceland
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2008–2011
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Università di Pisa
- Department of Biology
Pisa, Tuscany, Italy -
Institute of Cancer Research
London, ENG, United Kingdom -
London Research Institute
London, ENG, United Kingdom -
Comenius University in Bratislava
- Jessenius Faculty of Medicine
Bratislava, Bratislavsky Kraj, Slovakia
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2007–2011
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Università degli Studi di Torino
Torino, Piedmont, Italy -
University of Tampere
- Medical School
Tampere, Western Finland, Finland -
Helsinki University Central Hospital
- Department of Obstetrics and Gynaecology
Helsinki, Province of Southern Finland, Finland -
International Agency for Research on Cancer
Lyon, Rhone-Alpes, France
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2010
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Tehran University of Medical Sciences
- Cancer Research Center
Tehrān, Ostan-e Tehran, Iran -
University of California, Los Angeles
- Department of Epidemiology
Los Angeles, CA, USA
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2005–2010
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University of Bologna
Bologna, Emilia-Romagna, Italy -
University of Bergen
- The Gade Institute
Bergen, Hordaland Fylke, Norway
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1998–2010
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Karolinska Institute
Stockholm, Stockholm, Sweden
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2001–2009
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Karolinska Institutet
- Institutionen för medicinsk epidemiologi och biostatistik
Solna, Stockholm, Sweden
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2006–2008
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Danish Cancer Society
Copenhagen, Capital Region, Denmark -
Karolinska University Hospital
Stockholm, Stockholm, Sweden
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2004–2008
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National Cancer Institute (USA)
- • Division of Cancer Epidemiology and Genetics
- • Genetic Epidemiology
Bethesda, MD, USA -
Päijät-Hämeen Central Hospital
Lahti, Province of Southern Finland, Finland
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2003–2008
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National Institutes of Health
- • Division of Cancer Epidemiology and Genetics
- • Branch of Genetic Epidemiology
- • Laboratory of Human Carcinogenesis
Bethesda, MD, USA
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2000
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Uppsala University
- Department of Mathematics
Uppsala, Uppsala, Sweden
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