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  • 1.
    Ahmad, Abrar
    et al.
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Askari, Shlear
    Department of Clinical Medicine, Örebro University, Örebro, Sweden.
    Befekadu, Rahel
    Region Örebro län. Department of Laboratory Medicine, Section for Transfusion Medicine.
    Hahn-Strömberg, Victoria
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Investigating the association between polymorphisms in connective tissue growth factor and susceptibility to colon carcinoma2015Ingår i: Molecular Medicine Reports, ISSN 1791-2997, E-ISSN 1791-3004, Vol. 11, nr 4, s. 2493-2503Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    There have been numerous studies on the gene expression of connective tissue growth factor (CTGF) in colorectal cancer, however very few have investigated polymorphisms in this gene. The present study aimed to determine whether single nucleotide polymorphisms (SNPs) in the CTGF gene are associated with a higher susceptibility to colon cancer and/or an invasive tumor growth pattern. The CTGF gene was genotyped for seven SNPs (rs6918698, rs1931002, rs9493150, rs12526196, rs12527705, rs9399005 and rs12527379) by pyrosequencing. Formalin-fixed paraffin-embedded tissue samples (n=112) from patients diagnosed with colon carcinoma, and an equal number of blood samples from healthy controls, were selected for genomic DNA extraction. The complexity index was measured using images of tumor samples (n=64) stained for cytokeratin-8. The images were analyzed and correlated with the identified CTGF SNPs and clinicopathological parameters of the patients, including age, gender, tumor penetration, lymph node metastasis, systemic metastasis, differentiation and localization of tumor. It was demonstrated that the frequency of the SNP rs6918698 GG genotype was significantly associated (P=0.05) with an increased risk of colon cancer, as compared with the GC and CC genotypes. The other six SNPs (rs1931002, rs9493150, rs12526196, rs12527705, rs9399005 and rs12527379) exhibited no significant difference in the genotype and allele frequencies between patients diagnosed with colon carcinoma and the normal healthy population. A trend was observed between genotype variation at rs6918698 and the complexity index (P=0.052). The complexity index and genotypes for any of the studied SNPs were not significantly correlated with clinical or pathological parameters of the patients. These results indicate that the rs6918698 GG genotype is associated with an increased risk of developing colon carcinoma, and genetic variations at the rs6918698 are associated with the growth pattern of the tumor. The present results may facilitate the identification of potential biomarkers of the disease in addition to drug targets.

  • 2.
    Farkas, Sanja A.
    et al.
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Befekadu, Rahel
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Hahn-Strömberg, Victoria
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Nilsson, Torbjörn K.
    Department of Medical Biosciences, Clinical Chemistry, Umeå University, Umeå, Sweden.
    DNA methylation and expression of the folate transporter genes in colorectal cancer2015Ingår i: Tumor Biology, ISSN 1010-4283, E-ISSN 1423-0380, Vol. 36, nr 7, s. 5581-5590Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Folate has a central role in the cell metabolism. This study aims to explore the DNA methylation pattern of the folate transporter genes FOLR1, PCFT, and RFC1 as well as the corresponding protein expressions in colorectal cancer (CRC) tissue and adjacent non-cancerous mucosa (ANCM). Our results showed statistically significant differences in the DNA-methylated fraction of all three genes at several gene regions; we identified three differentially methylated CpG sites in the FOLR1 gene, five CpG sites in the PCFT gene, and six CpG sites in the RFC1 gene. There was a pronounced expression of the FR alpha and RFC proteins in both the CRC and ANCM tissues, though the expression was attenuated in cancer compared to the paired ANCM tissues. The PCFT protein was undetectable or expressed at a very low level in both tissue types. Higher methylated fractions of the CpG sites 3-5 in the RFC1 gene were associated with a lower protein expression, suggestive of epigenetic regulation by DNA methylation of the RFC1 gene in the colorectal cancer. Our results did not show any association between the RFC and FR alpha protein expression and tumor stage, TNM classification, or tumor location. In conclusion, this is the first study to simultaneously evaluate both DNA methylation and protein expression of all three folate transporter genes, FOLR1, PCFT, and RFC1, in colorectal cancer. The results encourage further investigation into the possible prognostic implications of folate transporter expression and DNA methylation.

  • 3.
    Farkas, Sanja A.
    et al.
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Befkadu, Rahel
    Department of Laboratory Medicine; Örebro University Hospital; Örebro, Sweden.
    Hahn-Strömberg, Victoria
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Nilsson, Torbjörn K.
    Department of Medical Biosciences/Clinical Chemistry, Umeå University, Umeå, Sweden.
    DNA methylation and expression of the folate transporting genes in colorectal cancerManuskript (preprint) (Övrigt vetenskapligt)
    Abstract [en]

    This study investigated the DNA methylation pattern and protein expression of the FOLR1, PCFT, and RFC1 genes in colorectal cancer (CRC) tissue. Our results showed statistically significant differences in the DNA methylated fraction of all three genes at several gene regions, we identified 3 differentially methylated CpG sites in the FOLR1 gene, 5 CpG sites in the PCFT gene, and 6 CpG sites in the RFC1 gene. We observed a pronounced expression of the FRα and RFC proteins in both the cancer and normal tissues, though the proteins were moderately expressed in cancer compared to the high expression in the paired healthy mucosa. The PCFT protein was undetectable or expressed very low in both tissues. Higher methylated fractions of the CpG sites 3-5 in the RFC1 gene were associated with a lower protein expression. When analyzing the association between DNA methylation and tumor characteristics (differentiation, location, primary tumor stage and lymph node involvement) we detected lower methylated fraction of specific CpG sites in the RFC1 gene in CRC located in the distal colon and rectum compared to the proximal colon. In the FOLR1 gene, we found CpG sites with a lower methylated fraction of colorectal cancers with the primary tumor stage 4 (pT4) compared to the pT2 and pT3 stages. Our results did not show association between the RFC and FRα protein expression and tumor stage, TNM classification or tumor location. In conclusion, these data suggest that there is a possible epigenetic regulation by DNA methylation of the RFC1 gene in the colorectal cancer.

  • 4.
    Franzén, Lennart E.
    et al.
    Örebro universitet, Hälsoakademin.
    Hahn-Strömberg, Victoria
    Edvardsson, Henrik
    Bodin, Lennart
    Characterization of colon carcinoma growth pattern by computerized morphometry: definition of a complexity index2008Ingår i: International Journal of Molecular Medicine, ISSN 1107-3756, E-ISSN 1791-244X, Vol. 22, nr 4, s. 465-472Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The invasive front of carcinomas may vary in complexity from smooth to highly complex when the front splits up into small cell clusters or even single cancer cells. The degree of complexity is usually estimated visually and semiquantitatively by a pathologist, although more objective methods based on computer-assisted image analysis are available. In this study, we compared the visual estimation of the irregularity of the tumour invasion front of colon carcinomas to different quantitative image analytical techniques and defined a complexity index for the invasive margin. Sections from 29 archived colon carcinomas were stained immunohistochemically for cytokeratin 8. Images of the tumour invasion front were read into a computer and thresholded so that the tumour tissue became black and the background white or so that the tumour front was outlined by a single pixel line. The invasive front was visually classified into four degrees of irregularity by a pathologist. The complexity of the front was then assessed using four different image analysis techniques, i.e. the estimation of fractal dimension, tumour front length, number of tumour cell clusters and lacunarity. Fractal dimension and tumour cell clusters together gave the best correlation to visual grading using a discriminant analysis. A cluster analysis and a tree diagram analysis were then performed and were found to be superior to visual estimation. The clusters represent different degrees of complexity and the result of the tree diagram analysis can be used to assign complexity indices to colon tumours. The fractal dimension separated tumours up to a certain level (1.5-1.6) of complexity. When the tumour front split up into small cell clusters, the counting of tumour cell clusters separated the cells over and above the fractal dimension. This new technique can be used to objectively and quantitatively describe the complexity of the invasive front of tumours.

  • 5.
    Hahn-Strömberg, Victoria
    Örebro universitet, Hälsoakademin.
    Cell adhesion proteins in different invasive patterns of colon carcinomas: a morphometric and molecular genetic study2008Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
    Abstract [en]

    Colorectal carcinoma is the second most common type of cancer in both men and women in Sweden. Cancer of the colon and rectum are often considered together and their ten year survival rate is approximately 50 – 60 % depending on sex and location. Different histopathological characteristics of such cancers, including the complexity of growth, are of importance for prognosis.

    This thesis has compared different morphometric methods in order to achieve a quantitative and objective measurement of the invasive front of colon carcinoma. Since the growth pattern is dependent on the cell adhesiveness of different proteins we studied the distribution and localization of E-cadherin, Beta-catenin, Claudin 1,2,7 and Occludin as well as screened the genes for mutations.

    We found a perturbed protein expression of E-cadherin, Beta-catenin, Claudin 1,2,7 and Occludin in tumor sections compared to normal mucosa, but no relation to tumor volume or growth pattern could be seen. The tumor volume was found to be correlated to the growth pattern but not responsible to the perturbed protein expression. In the mutation screening we found a SNP in exon 13 the E-cadherin gene in the tumor, as well as in exon 2 of Claudin 1 and exon 4 of Claudin 7 in both tumor and normal mucosa. No correlation between mutations and growth pattern or tumor volume was found.

    In conclusion, this thesis shows that the computer image analysis with estimation of fractal dimension and number of free tumor cell clusters is superior to the semi quantitative visual grading of tumor invasive complexity. The aberrant expression of cell adhesion proteins in the tumor compared to normal mucosa as well as polymorphisms in the cell adhesion genes CLDN1 and CLDN7 in both tumor and normal mucosa can suggest that these aberrations are important in the tumorigenesis of colon carcinoma.

     

    Delarbeten
    1. Characterization of colon carcinoma growth pattern by computerized morphometry: definition of a complexity index
    Öppna denna publikation i ny flik eller fönster >>Characterization of colon carcinoma growth pattern by computerized morphometry: definition of a complexity index
    2008 (Engelska)Ingår i: International Journal of Molecular Medicine, ISSN 1107-3756, E-ISSN 1791-244X, Vol. 22, nr 4, s. 465-472Artikel i tidskrift (Refereegranskat) Published
    Abstract [en]

    The invasive front of carcinomas may vary in complexity from smooth to highly complex when the front splits up into small cell clusters or even single cancer cells. The degree of complexity is usually estimated visually and semiquantitatively by a pathologist, although more objective methods based on computer-assisted image analysis are available. In this study, we compared the visual estimation of the irregularity of the tumour invasion front of colon carcinomas to different quantitative image analytical techniques and defined a complexity index for the invasive margin. Sections from 29 archived colon carcinomas were stained immunohistochemically for cytokeratin 8. Images of the tumour invasion front were read into a computer and thresholded so that the tumour tissue became black and the background white or so that the tumour front was outlined by a single pixel line. The invasive front was visually classified into four degrees of irregularity by a pathologist. The complexity of the front was then assessed using four different image analysis techniques, i.e. the estimation of fractal dimension, tumour front length, number of tumour cell clusters and lacunarity. Fractal dimension and tumour cell clusters together gave the best correlation to visual grading using a discriminant analysis. A cluster analysis and a tree diagram analysis were then performed and were found to be superior to visual estimation. The clusters represent different degrees of complexity and the result of the tree diagram analysis can be used to assign complexity indices to colon tumours. The fractal dimension separated tumours up to a certain level (1.5-1.6) of complexity. When the tumour front split up into small cell clusters, the counting of tumour cell clusters separated the cells over and above the fractal dimension. This new technique can be used to objectively and quantitatively describe the complexity of the invasive front of tumours.

    Nationell ämneskategori
    Medicin och hälsovetenskap
    Forskningsämne
    Medicin
    Identifikatorer
    urn:nbn:se:oru:diva-3031 (URN)10.3892/ijmm_00000044 (DOI)18813853 (PubMedID)
    Tillgänglig från: 2008-11-10 Skapad: 2008-11-10 Senast uppdaterad: 2017-12-14Bibliografiskt granskad
    2. Disturbed expression of E-cadherin, beta-catenin and tight junction proteins in colon carcinoma is unrelated to growth pattern and genetic polymorphisms
    Öppna denna publikation i ny flik eller fönster >>Disturbed expression of E-cadherin, beta-catenin and tight junction proteins in colon carcinoma is unrelated to growth pattern and genetic polymorphisms
    2008 (Engelska)Ingår i: Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), ISSN 0903-4641, E-ISSN 1600-0463, Vol. 116, nr 4, s. 253-262Artikel i tidskrift (Refereegranskat) Published
    Abstract [en]

    Adhesion proteins are responsible for the structural integrity of epithelial tissue and in tumors this integrity is often lost, resulting in a disorganization of the tissue. In the present study the complexity of the invasive front of colon carcinomas was correlated with cell adhesion protein expression and with polymorphisms in their genes. A complexity index was constructed from 32 colon carcinomas using computer-assisted morphometry estimating fractal dimension and tumor cell clusters followed by tree analysis. Immunohistochemical staining of beta-catenin, E-cadherin, occludin and claudin 2 was used for assessment of protein expression. Genetic screening of tissue from the tumor invasion front with laser microdissection was performed using SSCP and DNA sequencing. Adhesion protein distribution was significantly disturbed in most carcinomas. A single mutation in the gene of beta-catenin was found but there was no correlation between protein expression and genetic polymorphism. Nor was there any correlation between the complexity of the invasive border and protein distribution or genetic alterations. The results indicate that the complexity of colon carcinoma invasion is not dependent on genetic derangements in the genes of adhesion proteins or the protein distribution. Rather, aberrations in the function of other proteins related to the adhesive proteins could be responsible.

    Nyckelord
    patology, molecular cell biology
    Nationell ämneskategori
    Medicin och hälsovetenskap Cell- och molekylärbiologi
    Forskningsämne
    Medicin
    Identifikatorer
    urn:nbn:se:oru:diva-3032 (URN)10.1111/j.1600-0463.2008.00894.x (DOI)18397460 (PubMedID)
    Tillgänglig från: 2008-11-10 Skapad: 2008-11-10 Senast uppdaterad: 2018-01-13Bibliografiskt granskad
    3. Tumor volume of colon carcinoma is related to the invasive pattern but not to the expression of cell adhesion proteins
    Öppna denna publikation i ny flik eller fönster >>Tumor volume of colon carcinoma is related to the invasive pattern but not to the expression of cell adhesion proteins
    2009 (Engelska)Ingår i: Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), ISSN 0903-4641, E-ISSN 1600-0463, Vol. 117, nr 3, s. 205-211Artikel i tidskrift (Refereegranskat) Published
    Abstract [en]

    Tumor volume increases during growth and due to tumor progression various mutations appear that may cause phenotypic changes. The invasive pattern may thus be affected resulting in a more disorganized growth. This phenomenon might be due to mutations in the genome of the adhesion proteins, which are responsible for the structural integrity of epithelial tissue. Tumor volume was assessed in whole mount sections of 33 colon carcinomas using Cavalieri's principle. Images from the entire invasive border were captured and used for calculating the irregularity of the border (Complexity Index). The expression of the adhesion proteins E-cadherin, beta-catenin, Claudin 2 and Occludin was assessed after immunohistochemical staining of two randomly selected areas of the invasive front of the tumor. Statistical significance for differences in volume was obtained for tumor Complexity Index, tumor stage (pT) and lymph node status (pN). Expression of adhesion proteins was significantly perturbed in the tumors compared with normal mucosa but only infrequently correlated to tumor differentiation or invasive pattern. The results show that when tumor volume increases the invasive pattern becomes more irregular which is compatible with tumor progression. A direct contribution of adhesion protein derangement to this process appears to be insignificant.

    Ort, förlag, år, upplaga, sidor
    Wiley-Blackwell Publishing Inc., 2009
    Nationell ämneskategori
    Medicin och hälsovetenskap
    Forskningsämne
    Biomedicin
    Identifikatorer
    urn:nbn:se:oru:diva-3033 (URN)10.1111/j.1600-0463.2008.00011.x (DOI)000265487600006 ()19245593 (PubMedID)2-s2.0-61349175837 (Scopus ID)
    Tillgänglig från: 2008-11-10 Skapad: 2008-11-10 Senast uppdaterad: 2017-12-14Bibliografiskt granskad
    4. Claudin 1 and Claudin 7 gene polymorphisms and protein derangement are unrelated to the growth pattern of colon carcinoma
    Öppna denna publikation i ny flik eller fönster >>Claudin 1 and Claudin 7 gene polymorphisms and protein derangement are unrelated to the growth pattern of colon carcinoma
    (Engelska)Manuskript (Övrigt vetenskapligt)
    Nationell ämneskategori
    Medicin och hälsovetenskap
    Forskningsämne
    Biomedicin
    Identifikatorer
    urn:nbn:se:oru:diva-3034 (URN)
    Tillgänglig från: 2008-11-10 Skapad: 2008-11-10 Senast uppdaterad: 2017-10-18Bibliografiskt granskad
    Ladda ner fulltext (pdf)
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    Ladda ner (pdf)
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  • 6.
    Hahn-Strömberg, Victoria
    et al.
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Department of Laboratory Medicine, Section for Pathology, Örebro University Hospital, Örebro, Sweden.
    Askari, Shlear
    Department of Laboratory Medicine, Section for Pathology, Örebro University Hospital, Örebro, Sweden.
    Befekadu, Rahel
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Department of Laboratory Medicine, Section for Pathology, Örebro University Hospital, Örebro, Sweden.
    Matthiessen, Peter
    Region Örebro län. Department of Clinical Surgery, Örebro University Hospital, Örebro, Sweden.
    Karlsson, Sune
    Örebro universitet, Handelshögskolan vid Örebro Universitet.
    Nilsson, Torbjorn K.
    Department of Medical Biosciences/Clinical Chemistry, Umeå University, Umeå, Sweden.
    Polymorphisms in the CLDN1 and CLDN7 genes are related to differentiation and tumor stage in colon carcinoma2014Ingår i: Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), ISSN 0903-4641, E-ISSN 1600-0463, Vol. 122, nr 7, s. 636-642Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Tight junction is composed of transmembrane proteins important for maintaining cell polarity and regulating ion flow. Among these proteins are the tissue-specific claudins, proteins that have recently been suggested as tumor markers for several different types of cancer. An altered claudin expression has been observed in colon, prostatic, ovarian, and breast carcinoma. The aim of this study was to analyze the allele frequencies of three common single nucleotide polymorphisms (SNPs) in the genes for claudin 1 and claudin 7 in colon cancer (CC) patients and in a control population of healthy blood donors. Pyrosequencing was used to genotype the CLDN1 SNP rs9869263 (c.369C>T), and the CLDN7 SNPs rs4562 (c.590C>T) and rs374400 (c.606T>G) in DNA from 102 formalin fixed paraffin embedded (FFPE) colon cancer tissue, and 111 blood leukocyte DNA from blood/plasma donors. These results were correlated with clinical parameters such as TNM stage, tumor localization, tumor differentiation, complexity index, sex, and age. We found that there was a significant association between the CLDN1 genotype CC in tumor samples and a higher risk of colon cancer development (OR 3.0, p < 0.001). We also found that the CLDN7 rs4562 (c.590C>T) genotype CT had a higher risk of lymph node involvement (p = 0.031) and a lower degree of tumor differentiation (p = 0.028). In the control population, the allele frequencies were very similar to those in the HapMap cohort for CLDN7. The CLDN1 rs9869263 genotype (c.369C>T) was related to increased risk of colon cancer, and the CLDN7 rs4562 genotype (c.590C>T) was related to tumor differentiation and lymph node involvement in colon carcinoma. Further studies are warranted to ascertain their potential uses as biomarkers predicting tumor development, proliferation, and outcome in this disease.

  • 7.
    Hahn-Strömberg, Victoria
    et al.
    Örebro universitet, Hälsoakademin.
    Edvardsson, Henrik
    Bodin, Lennart
    Franzén, Lennart
    Claudin 1 and Claudin 7 gene polymorphisms and protein derangement are unrelated to the growth pattern of colon carcinomaManuskript (Övrigt vetenskapligt)
  • 8.
    Hahn-Strömberg, Victoria
    et al.
    Örebro universitet, Hälsoakademin.
    Edvardsson, Henrik
    Bodin, Lennart
    Franzén, Lennart
    Disturbed expression of E-cadherin, beta-catenin and tight junction proteins in colon carcinoma is unrelated to growth pattern and genetic polymorphisms2008Ingår i: Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), ISSN 0903-4641, E-ISSN 1600-0463, Vol. 116, nr 4, s. 253-262Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Adhesion proteins are responsible for the structural integrity of epithelial tissue and in tumors this integrity is often lost, resulting in a disorganization of the tissue. In the present study the complexity of the invasive front of colon carcinomas was correlated with cell adhesion protein expression and with polymorphisms in their genes. A complexity index was constructed from 32 colon carcinomas using computer-assisted morphometry estimating fractal dimension and tumor cell clusters followed by tree analysis. Immunohistochemical staining of beta-catenin, E-cadherin, occludin and claudin 2 was used for assessment of protein expression. Genetic screening of tissue from the tumor invasion front with laser microdissection was performed using SSCP and DNA sequencing. Adhesion protein distribution was significantly disturbed in most carcinomas. A single mutation in the gene of beta-catenin was found but there was no correlation between protein expression and genetic polymorphism. Nor was there any correlation between the complexity of the invasive border and protein distribution or genetic alterations. The results indicate that the complexity of colon carcinoma invasion is not dependent on genetic derangements in the genes of adhesion proteins or the protein distribution. Rather, aberrations in the function of other proteins related to the adhesive proteins could be responsible.

  • 9.
    Hahn-Strömberg, Victoria
    et al.
    Örebro universitet, Hälsoakademin.
    Edvardsson, Henrik
    Bodin, Lennart
    Franzén, Lennart
    Tumor volume of colon carcinoma is related to the invasive pattern but not to the expression of cell adhesion proteins2009Ingår i: Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), ISSN 0903-4641, E-ISSN 1600-0463, Vol. 117, nr 3, s. 205-211Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Tumor volume increases during growth and due to tumor progression various mutations appear that may cause phenotypic changes. The invasive pattern may thus be affected resulting in a more disorganized growth. This phenomenon might be due to mutations in the genome of the adhesion proteins, which are responsible for the structural integrity of epithelial tissue. Tumor volume was assessed in whole mount sections of 33 colon carcinomas using Cavalieri's principle. Images from the entire invasive border were captured and used for calculating the irregularity of the border (Complexity Index). The expression of the adhesion proteins E-cadherin, beta-catenin, Claudin 2 and Occludin was assessed after immunohistochemical staining of two randomly selected areas of the invasive front of the tumor. Statistical significance for differences in volume was obtained for tumor Complexity Index, tumor stage (pT) and lymph node status (pN). Expression of adhesion proteins was significantly perturbed in the tumors compared with normal mucosa but only infrequently correlated to tumor differentiation or invasive pattern. The results show that when tumor volume increases the invasive pattern becomes more irregular which is compatible with tumor progression. A direct contribution of adhesion protein derangement to this process appears to be insignificant.

  • 10.
    Kozlowski, Piotr
    et al.
    Region Örebro län. Department of Medicine, Örebro University Hospital, Örebro, Sweden.
    Montgomery, Scott
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län. Clinical Epidemiology Unit, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology and Public Health, University College London, London, UK.
    Befekadu, Rahel
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Transfusion Medicine, Faculty of Medical Sciences, Örebro University, Örebro, Sweden.
    Hahn-Strömberg, Victoria
    Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden.
    The risk of renal disease is increased in lambda myeloma with bone marrow amyloid deposits2017Ingår i: Journal of Blood Medicine, ISSN 1179-2736, Vol. 8, s. 29-34Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Light chain amyloidosis (AL) is a rare deposition disease and is present in 10-15% of patients with myeloma (MM). In contrast to symptomatic AL in MM, presence of bone marrow (BM) amyloid deposits (AD) in MM is not connected to kidney damage. Renal AD but not BM-AD occur mostly in MM with lambda paraprotein (lambda MM).

    Methods: We investigated amyloid presence in BM clots taken at diagnosis in 84 patients with symptomatic MM and compared disease characteristics in MM with kappa paraprotein (kappa MM)/lambda MM with and without BM-AD.

    Results: Lambda MM with BM-AD was compared with kappa MM without BM-AD, kappa MM with BM-AD, and lambda MM without BM-AD: lambda MM with BM-AD patients had a significantly higher mean creatinine level (4.23 mg/dL vs 1.69, 1.14, and 1.28 mg/dL, respectively) and a higher proportion presented with severe kidney failure (6/11 [55%] vs 6/32 [19%], 1/22 [5%], and 3/19 [16%], respectively). Proteinuria was more common in lambda MM with BM-AD patients compared with kappa MM without BM-AD patients (8/11 [73%] vs 5/32 [16%], respectively).

    Conclusion: Kidney damage was more common in lambda MM with BM-AD indicating presence of renal AD.

  • 11. Zhulina, Yaroslava
    et al.
    Hahn Strömberg, V.
    Shamikh, A.
    Gustavsson, A.
    Bohr, J.
    Nyhlin, N.
    Wickbom, Anna
    Bodin, L.
    Tysk, Curt
    Örebro universitet, Hälsoakademin.
    Carlson, M.
    Halfvarson, Jonas
    NFkB is activated in colonic mucosa of healthy co-twins to twins with inflammatory bowel disease2011Ingår i: Gut, ISSN 0017-5749, E-ISSN 1468-3288, Vol. 60, nr Suppl 3, s. A290-A290Artikel i tidskrift (Refereegranskat)
  • 12. Zhulina, Yaroslava
    et al.
    Hahn Strömberg, Victoria
    Shamikh, A.
    Gustavsson, A.
    Bohr, J.
    Nyhlin, Nils
    Wickbom, A.
    Bodin, L.
    Tysk, Curt
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Carlson, M.
    Halfvarson, Jonas
    Aktiverad NFkB i colonbiopsier hos tvillingar med inflammatorisk tarmsjukdom2012Ingår i: Gastrokuriren, ISSN 1651-0453, Vol. 17, nr 37, s. PO-27-PO-27Artikel i tidskrift (Övrigt vetenskapligt)
  • 13.
    Zhulina, Yaroslava
    et al.
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Department of Internal Medicine, Division of Gastroenterology, Örebro University Hospital, Region Örebro County, Örebro, Sweden.
    Hahn-Strömberg, Victoria
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Department of Pathology, Örebro University Hospital, Örebro, Sweden; Department of Clinical Medicine, Örebro University, Örebro, Sweden.
    Shamikh, Alia
    Department of Pathology, Örebro University Hospital, Örebro, Sweden; Department of Clinical Medicine, Örebro University, Örebro, Sweden.
    Peterson, Christer G. B.
    Department of Medical Sciences, Clinical Chemistry, Uppsala University, Uppsala, Sweden.
    Gustavsson, Anders
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Department of Internal Medicine, Division of Gastroenterology, Örebro University Hospital, Örebro, Sweden.
    Nyhlin, Nils
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Department of Internal Medicine, Division of Gastroenterology, Örebro University Hospital, Region Örebro County, Örebro, Sweden.
    Wickbom, Anna
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Department of Internal Medicine, Division of Gastroenterology, Örebro University Hospital, Örebro, Sweden.
    Bohr, Johan
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Department of Internal Medicine, Division of Gastroenterology, Örebro University Hospital, Region Örebro County, Örebro, Sweden.
    Bodin, Lennart
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Institute of Environmental Medicine, Unit of Intervention and Implementation Research, Karolinska Institute, Stockholm, Sweden.
    Tysk, Curt
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Department of Internal Medicine, Division of Gastroenterology, Örebro University Hospital, Region Örebro County, Örebro, Sweden.
    Carlson, Marie
    Department of Medical Sciences, Gastroenterology Research Group, Uppsala University, Uppsala, Sweden.
    Halfvarson, Jonas
    Örebro universitet, Institutionen för läkarutbildning. Department of Internal Medicine, Division of Gastroenterology, Örebro University Hospital, Region Örebro County, Örebro, Sweden.
    Subclinical Inflammation with Increased Neutrophil Activity in Healthy Twin Siblings Reflect Environmental Influence in the Pathogenesis of Inflammatory Bowel Disease2013Ingår i: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 19, nr 8, s. 1725-1731Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: The mechanisms behind increased fecal calprotectin (FC) in healthy relatives of patients with inflammatory bowel disease (IBD) are unknown. Our aims were to explore if there is a subclinical inflammation with increased neutrophil activity in healthy twin siblings in discordant twin pairs with IBD and to assess the influence of genetics in this context.

    Methods: Nuclear factor kappa B (NF-B) and neutrophil activity, based on myeloperoxidase (MPO) and FC, were analyzed in healthy twin siblings in discordant twin pairs with IBD and compared with healthy controls. NF-B and MPO were assessed by immunohistochemistry and FC by enzyme-linked immunosorbent assay.

    Results: In total, 33 of 34 healthy twin siblings were histologically normal. Increased NF-B was more often observed in healthy twin siblings in discordant twin pairs with Crohn's disease (13/18 [73%]) and with ulcerative colitis (12/16 [75%]) than in healthy controls (8/45 [18%]). MPO was more often increased in healthy twin siblings in discordant pairs with Crohn's disease (12/18 [67%]) than in healthy controls (11/45 [24%]) and FC more often in healthy twin siblings in discordant pairs with ulcerative colitis (14/21 [67%]) than in healthy controls (6/31 [19%]). Interestingly, the observed differences remained when healthy monozygotic and dizygotic twin siblings were analyzed separately.

    Conclusions:We observed increased NF-B, MPO, and FC in healthy twins in both monozygotic and dizygotic discordant pairs with IBD. These novel findings speak for an ongoing subclinical inflammation with increased neutrophil activity in healthy first-degree relatives.

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  • 14.
    Åström, Maria
    et al.
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Hahn-Strömberg, Victoria
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Zetterberg, Eva
    Departments of Medicine and Hematology, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden .
    Vedin, Inger
    Departments of Medicine and Hematology, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden .
    Merup, Mats
    Departments of Medicine and Hematology, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden .
    Palmblad, Jan
    Departments of Medicine and Hematology, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden .
    X-linked thrombocytopenia with thalassemia displays bone marrow reticulin fibrosis and enhanced angiogenesis: comparisons with primary myelofibrosis2015Ingår i: American Journal of Hematology, ISSN 0361-8609, E-ISSN 1096-8652, Vol. 90, nr 3, s. E44-E48Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    X-linked thrombocytopenia with thalassemia (XLTT) is caused by the mutation 216R > Q in exon 4 of the GATA1 gene. Male hemizygous patients display macrothrombocytopenia, splenomegaly, and a β-thalassemia trait. We describe two XLTT families where three males were initially misdiagnosed as having primary myelofibrosis (PMF) and all five investigated males showed mild-moderate bone marrow (BM) reticulin fibrosis. Comparative investigations were performed on blood samples and BM biopsies from males with XLTT, PMF patients and healthy controls. Like PMF, XLTT presented with high BM microvessel density, low GATA1 protein levels in megakaryocytes, and elevated blood CD34+ cell counts. But unlike PMF, the BM microvessel pericyte coverage was low in XLTT, and no collagen fibrosis was found. Further, as evaluated by immunohistochemistry, expressions of the growth factors VEGF, AGGF1, and CTGF were low in XLTT megakaryocytes and microvessels but high in PMF. Thus, although the reticulin fibrosis in XLTT might simulate PMF, opposing stromal and megakaryocyte features may facilitate differential diagnosis. Additional comparisons between these disorders may increase the understanding of mechanisms behind BM fibrosis in relation to pathological megakaryopoiesis.

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