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Sökning: WFRF:(Dimberg Jan)

  • Resultat 1-10 av 74
  • [1]234567...8Nästa
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  • Alehagen, Urban, et al. (författare)
  • Increased mortality in the A/A genotype of the SNP rs28372698 of interleukin 32
  • 2021
  • Ingår i: Experimental and Therapeutic Medicine. - : SPANDIDOS PUBL LTD. - 1792-0981 .- 1792-1015. ; 21:2
  • Tidskriftsartikel (refereegranskat)abstract
    • One of the major causes of mortality in the western hemisphere is cardiovascular disease. Therefore, a variety of markers to identify those at risk are required. Interleukin-32 (IL-32) is a cytokine that is associated with inflammation. The aim of the current study was to investigate variations in single nucleotide polymorphisms (SNPs) of IL-32 and plasma expression, and their associations with mortality. A population of 486 elderly community-living persons were evaluated. The participants were followed for 7.1 years and underwent a clinical examination and blood sampling. SNP analyses of IL-32 rs28372698 using allelic discrimination and plasma measurement of IL-32, using ELISA, were performed. During the follow-up period, 140 (28.8%) all-cause and 87 (17.9%) cardiovascular deaths were registered. No significant difference between mortality and plasma concentration of IL-32 was observed. The A/A genotype group exhibited significantly higher all-cause mortality (P=0.036), and an almost two-fold increased risk in a multivariate Cox regression model for all-cause and cardiovascular mortality. A highly significant difference in all-cause and cardiovascular mortality between the A/A and the T/T groups was demonstrated (P=0.015 resp. P=0.014). In the present study, the cytokine IL-32 was demonstrated to have prognostic information, with an increased risk of all-cause and cardiovascular mortality for those with the A/A genotype rs28372698 of IL-32. The A/A genotype could therefore be regarded as a possible biomarker for mortality risk that may be used to offer optimized cardiovascular patient handling in the future. However, the present study sample was small, and the results should be regarded as hypothesis-generating.
  • Dimberg, Jan, et al. (författare)
  • Gene polymorphism in DNA repair genes XRCC1 and XRCC6 and association with colorectal cancer in Swedish patients
  • 2016
  • Ingår i: Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS). - : WILEY-BLACKWELL. - 0903-4641 .- 1600-0463. ; 124:9, s. 736-740
  • Tidskriftsartikel (refereegranskat)abstract
    • The DNA repair genes XRCC1 and XRCC6 have been proposed to participate in the pathological process of cancer by modulating the DNA repair capacity. This study evaluated the susceptibility of the single-nucleotide polymorphisms (SNPs) XRCC1 (rs25487, G amp;gt; A) and XRCC6 (rs2267437, C amp;gt; G) to colorectal cancer (CRC) and their association with clinical parameters in Swedish patients with CRC. Using the TaqMan system, these SNPs were screened in 452 patients and 464 controls. No significant difference in genotype distribution was found between the patients and controls, or any significant association with cancer-specific or disease-free survival in patients. However, we showed that the carriers of allele A in XRCC1 (rs25487, G amp;gt; A) were connected with a higher risk of disseminated CRC (Odds Ratio = 1.64; 95% Confidence Interval = 1.12-2.41, p = 0.012).
  • Dimberg, Jan, et al. (författare)
  • Genomic Profiling of Stage II Colorectal Cancer Identifies Candidate Genes Associated with Recurrence-Free Survival, Tumor Location, and Differentiation Grade.
  • 2020
  • Ingår i: Oncology. - : S. Karger. - 0030-2414 .- 1423-0232. ; 98:8, s. 575-582
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Identification of high-risk stage II colorectal cancer (CRC) patients, potential candidates for adjuvant chemotherapy, is challenging. Current clinical guidelines rely mainly on histopathological markers with relatively weak prognostic value. This motivates further search for prognostic markers.METHODS: This explorative study aimed to identify potential candidate gene mutations to facilitate differentiation between subgroups of patients with CRC stage II. Panel-based massive parallel sequencing was used to genetically characterize tumor tissues from 85 patients radically operated for CRC stage II, of which 12 developed recurrent cancer during follow-up. Genetic data was compared between patients with or without cancer recurrence, between tumors located in colon and in rectum, and for association with tumor differentiation grade.RESULTS: Genetic variation in ATM, C11ORF65 was associated with recurrence-free survival. Previous reports regarding the association between BRAF mutation and a higher age at diagnosis, and tumor location in colon were confirmed. APC, BRAF, or KRAS mutation was associated with tumor differentiation grade. Multiple correspondence analyses revealed no obvious clustering of patients with the studied clinical characteristics, indicating that the genetic signatures observed here were unique for each individual.CONCLUSIONS: Taken together, we have demonstrated the utility of panel-based massive parallel sequencing to explore the pathogenesis of CRC stage II. We have identified promising candidate gene mutations associated with cancer recurrence, tumor location, and differentiation grade in patients with CRC stage II, which merit further investigation.
  • Dimberg, Jan, et al. (författare)
  • Polymorphisms of Fractalkine receptor CX3CR1 and plasma levels of its ligand CX3CL1 in colorectal cancer patients
  • 2007
  • Ingår i: International Journal of Colorectal Disease. - : Springer. - 0179-1958 .- 1432-1262. ; 22:10, s. 1195-1200
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND AND AIMS:The chemokine Fractalkine/CX3CL1, which is expressed by epithelial cells within normal colorectal mucosa and in colorectal cancer (CRC), is thought to have a crucial role in colorectal mucosal immunity by recruiting leucocytes via the receptor CX3CR1. The purpose of this study was to investigate two single-nucleotide polymorphisms of the Fractalkine receptor/CX3CR1 gene, V249I and T280M, in CRC to find out whether they occur more often in patients with CRC than in non-CRC individuals. In the search for tumour markers, we also intended to determine whether plasma levels of Fractalkine were correlated with parameters such as Dukes' stage, tumour localisation, gender and age in CRC patients.MATERIALS AND METHODS:Genomic deoxyribonucleic acid from 223 CRC patients and 229 controls was amplified by polymerase chain reaction, and the polymorphisms were detected by the restriction fragment length polymorphism analysis. Fractalkine/CX3CL1 was analysed in plasma from 62 CRC patients and 78 controls using enzyme-linked immunosorbent assay.RESULTS:The variant V249I was significantly different in genotype and allelic distribution between CRC patients and control subjects, P = 0.028 and P = 0.048, respectively. We also found that individuals with the I249 allele in homozygote state were less frequent in the CRC group (3.1%) compared with controls (9.2%; P = 0.008). No significant difference was observed regarding Fractalkine/CX3CL1 levels in plasma between patients and the control group.CONCLUSION:Our results suggest that the lack of the allele I249 of the CX3CR1 gene may play a partial or minor role in CRC and that plasma Fractalkine/CX3CL1 does not seem to be a useful tumour marker that reflects the disease outcome of CRC.
  • Dimberg, Jan, et al. (författare)
  • Protein expression and gene polymorphism of CXCL10 in patients with colorectal cancer
  • 2014
  • Ingår i: Biomedical Reports. - 2049-9442 .- 2049-9434. ; 2:3, s. 340-343
  • Tidskriftsartikel (refereegranskat)abstract
    • Chemokines (chemotactic cytokines) promote leukocyte attraction to sites of inflammation and cancer. Certain chemokines promote and regulate neoplastic progression, including metastasis and angiogenesis. One such chemokine, CXCL10, was found to be expressed in colorectal cancer (CRC) tissue. To gain insight into the prognostic significance of CXCL10, we investigated whether the levels of this chemokine were altered in the colorectal tissue or plasma of CRC patients. Using Luminex technology for protein analyses, we observed a significantly higher CXCL10 protein level in cancer tissue compared to that in paired normal tissue. Moreover, significantly higher plasma levels of CXCL10 were detected in patients compared to those in control subjects and the plasma levels of CXCL10 in disseminated disease were found to be significantly higher compared to those in localized disease. The single‑nucleotide polymorphism rs8878, which has been described in exon 4 in the 3'‑untranslated region of the CXCL10 gene, was investigated using a TaqMan system. There were significant differences in genotype distribution and allelic frequencies between CRC patients and control subjects. In conclusion, altered CXCL10 protein concentrations in CRC tissues or plasma and the rs8878 genotype variant of CXCL10 may contribute to the prediction of clinical outcome.
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