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Sökning: WFRF:(Grönberg Henrik) > (2000-2004)

  • Resultat 11-20 av 20
  • Föregående 1[2]
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  • Lindmark, Fredrik, et al. (författare)
  • Analysis of the macrophage scavenger receptor 1 gene in Swedish hereditary and sporadic prostate cancer.
  • 2004
  • Ingår i: The Prostate. - 0270-4137 .- 1097-0045. ; 59:2, s. 132-140
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>BACKGROUND: The macrophage scavenger receptor 1 (MSR1) gene on chromosome 8p22 was recently reported as a candidate gene for hereditary prostate cancer (HPC). Here, we further elucidate the role of MSR1 in both Swedish families with HPC and in a cohort of unselected prostate cancer. METHODS: DNA samples from 83 Swedish HPC families and 215 unselected population based cases of prostate cancer as well as 425 age-matched controls were genotyped. RESULTS: A total of 18 variants were identified, including 2 exonic, 7 intronic changes, and 9 changes in the 5'- or 3'-uncoding region. Of the two exonic changes, one previously reported truncation mutation was identified, a R293X nonsense mutation. This mutation was found in 2 of the 83 (2.4%) HPC families. The R293X mutation was found more frequently in men with PC (4.9%) than in unaffected men (2.7%), consistent with previous published results, however our results were not significant (P = 0.16). To additionally test for potential association of common sequence variants and increased risk for the disease, five common polymorphisms (PRO3, INDEL1, IVS5-57, P275A, INDEL7) were genotyped in the group of 215 prostate cancer cases and 425 age-matched controls. No association between any of the five common sequence variants and prostate cancer were found. CONCLUSION: Our results suggest that mutations in MSR1 gene might play a role in prostate cancer susceptibility, particularly the R293X mutation. This study warrants further investigations of the role of MSR1 in prostate cancer etiology.</p>
  • Lindmark, Fredrik, et al. (författare)
  • H6D polymorphism in macrophage-inhibitory cytokine-1 gene associated with prostate cancer
  • 2004
  • Ingår i: Journal of the National Cancer Institute. - 0027-8874 .- 1460-2105. ; 96:16, s. 1248-1254
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>BACKGROUND: Accumulating epidemiologic and molecular evidence suggest that inflammation is an important component in the etiology of prostate cancer. Macrophage-inhibitory cytokine-1 (MIC-1), a member of the transforming growth factor beta superfamily, is thought to play an important role in inflammation by regulating macrophage activity. We examined whether sequence variants in the MIC-1 gene are associated with the risk of prostate cancer. METHODS: The study population, a population-based case-control study in Sweden, consisted of 1383 prostate cancer case patients and 780 control subjects. From 94 of the control subjects, we constructed gene-specific haplotypes of MIC-1 and identified four haplotype-tagging single-nucleotide polymorphisms (SNPs): Exon1+25 (V9L), Exon1+142 (S48T), IVS1+1809, and Exon2+2423 (H6D). All study subjects were genotyped for the four SNPs, and conditional logistic regression analysis was used to estimate odds ratios (ORs) with 95% confidence intervals (CIs). RESULTS: A statistically significant difference (P =.006) in genotype frequency was observed for the nonsynonymous change H6D (histidine to aspartic acid at position 6) between prostate cancer patients and control subjects. Carriers of the GC genotype, which results in the H6D change, experienced a lower risk of sporadic prostate cancer (OR = 0.80, 95% CI = 0.66 to 0.97) and of familial prostate cancer (OR = 0.61, 95% CI = 0.42 to 0.89) than the CC genotype carriers. In the study population, the proportion of prostate cancer cases attributable to the CC genotype was 7.2% for sporadic cancer and 19.2% for familial cancer. None of the other SNPs or haplotypes was associated with prostate cancer. CONCLUSION: This study shows an association between a nonsynonymous change (H6D) in the MIC-1 gene and prostate cancer. This finding supports the hypothesis that genetic variation in the inflammatory process contributes to prostate cancer susceptibility.</p>
  • Meuller, Johan, et al. (författare)
  • Identification of genomic deletions of the APC gene in familial adenomatous polyposis by two independent quantitative techniques.
  • 2004
  • Ingår i: Genetic testing. - 1090-6576. ; 8:3, s. 248-56
  • Tidskriftsartikel (refereegranskat)abstract
    • Large deletions in the APC (adenomatous polyposis coli) gene, causing familial adenomatous polyposis (FAP), cannot easily be detected by conventional mutation-detection techniques. Therefore, we have developed two independent quantitative methods for the detection of large deletions, encompassing one or more exons, of APC. Multiplex ligation-dependent probe amplification (MLPA) is performed in one reaction for the initial quantification of all APC exon copy numbers. Subsequently, quantitative real-time PCR (QRT-PCR) is used to verify the results obtained in the MLPA reaction. The identification of a deletion of the whole APC gene in a patient with classical FAP is described. The mutation was detected with the two quantitative methods and further verified on chromosomal level by the use of FISH (fluorescence in situ hybridization) on metaphase spreads. Furthermore, a large deletion covering exons 11-13 of the APC gene was detected in two apparently unrelated families. This deletion was further verified and characterized with long-range PCR. The MLPA test ensures a sensitive high-throughput screening for large deletions of the APC gene and can easily be implemented in the diagnostic testing for FAP.
  • Nilbert, Mef, et al. (författare)
  • Viktigt att upptäcka ärftliga fall av kolorektal- och endometriecancer. Mutationer hos »HNPCC-individer» kan orsaka flera tumörsjukdomar
  • 2002
  • Ingår i: Läkartidningen. - Swedish Medical Association. - 0023-7205. ; 99:34, s. 300-3296
  • Tidskriftsartikel (refereegranskat)abstract
    • Hereditary Nonpolyposis Colorectal Cancer (HNPCC) is one of our most common hereditary cancer syndromes and confers an increased risk for several tumor types, with the greatest lifetime risks being for colorectal cancer and endometrial cancer. Hereditary mutations in one of several mismatch-repair (MMR) genes cause the syndrome, and 39 such mutations, involving the genes MLH1, MSH2 and MSH6, have been been characterized in Sweden. Screening programs for HNPCC have been shown to be cost-effective and to prevent cancer. Identification of HNPCC individuals thus allows prevention of additional tumors in the patient as well as in the family.
  • Wiklund, Fredrik, 1963- (författare)
  • Genetic epidemiology of prostate cancer
  • 2004
  • Doktorsavhandling (övrigt vetenskapligt)abstract
    • <p>Prostate cancer is a major health burden throughout the world, yet the etiology of prostate cancer is poorly understood. Evidence has accumulated supporting the existence of a hereditary form of this disease. Improved understanding of the genetic mechanisms underlying the development and progression of prostate cancer would be a major advance for improved prevention, detection and treatment strategies. This thesis evaluates different aspects of the genetic epidemiology of prostate cancer.</p> <p>In a genomic scan two chromosomal regions with evidence for linkage was observed. The strongest support was found on chromosome 19p with an allele sharing LOD score of 2.91 (genome-wide P = 0.032). The second region, showing suggestive evidence of linkage, was observed in the centromeric region of chromosome 5. Linkage analyses of densely spaced markers on chromosome 8p22-23 confirmed (P = 0.03) previously reported linkage to this region. A systematic evaluation of the possible impact that the RNASEL gene have on prostate cancer was performed. Overall, limited evidence for association with prostate cancer risk was found. The results provide strong evidence against a role of RNASEL in prostate cancer etiology in Sweden. In a comprehensive evaluation of occurrence of other malignancies in HPC families, previously reported association between gastric and prostate carcinoma was confirmed. The increased risk was of the same magnitude in early and late onset HPC families and confined to only male relatives. A genome-wide linkage analysis, stratified by occurrence of gastric carcinoma, identified a novel susceptibility locus on chromosome Xp21.</p> <p>In summary, chromosome 5q and 19p represents the regions most likely to harbor susceptibility genes predisposing to prostate cancer in the Swedish population. A common genetic basis for both gastric and prostate cancer has been confirmed and a novel susceptibility locus on chromosome Xp21 has been identified.</p>
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