oru.sePublications
Change search
Link to record
Permanent link

Direct link
BETA
Hahn-Strömberg, Victoria
Alternative names
Publications (10 of 14) Show all publications
Kozlowski, P., Montgomery, S., Befekadu, R. & Hahn-Strömberg, V. (2017). The risk of renal disease is increased in lambda myeloma with bone marrow amyloid deposits. Journal of Blood Medicine, 8, 29-34
Open this publication in new window or tab >>The risk of renal disease is increased in lambda myeloma with bone marrow amyloid deposits
2017 (English)In: Journal of Blood Medicine, ISSN 1179-2736, Vol. 8, p. 29-34Article in journal (Refereed) Published
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.

Place, publisher, year, edition, pages
DOVE Medical Press Ltd., 2017
Keywords
plasma cells, neoplasms, amyloidosis, renal insufficiency, proteinuria
National Category
Hematology
Identifiers
urn:nbn:se:oru:diva-56847 (URN)10.2147/JBM.S129516 (DOI)000395472700001 ()28293126 (PubMedID)2-s2.0-85016315664 (Scopus ID)
Available from: 2017-03-28 Created: 2017-03-28 Last updated: 2018-07-30Bibliographically approved
Farkas, S. A., Befekadu, R., Hahn-Strömberg, V. & Nilsson, T. K. (2015). DNA methylation and expression of the folate transporter genes in colorectal cancer. Tumor Biology, 36(7), 5581-5590
Open this publication in new window or tab >>DNA methylation and expression of the folate transporter genes in colorectal cancer
2015 (English)In: Tumor Biology, ISSN 1010-4283, E-ISSN 1423-0380, Vol. 36, no 7, p. 5581-5590Article in journal (Refereed) Published
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.

Place, publisher, year, edition, pages
S. Karger, 2015
Keywords
CpG, T-DMR, Reduced folate carrier, CRC, Immunohistochemistry
National Category
Cancer and Oncology
Research subject
Oncology
Identifiers
urn:nbn:se:oru:diva-45755 (URN)10.1007/s13277-015-3228-2 (DOI)000359569000086 ()25697897 (PubMedID)2-s2.0-84938198358 (Scopus ID)
Note

Funding Agencies:

Lions Cancer Foundation, Nyckelfonden

Research committee of Örebro county council

Available from: 2015-09-09 Created: 2015-09-09 Last updated: 2019-06-14Bibliographically approved
Ahmad, A., Askari, S., Befekadu, R. & Hahn-Strömberg, V. (2015). Investigating the association between polymorphisms in connective tissue growth factor and susceptibility to colon carcinoma. Molecular Medicine Reports, 11(4), 2493-2503
Open this publication in new window or tab >>Investigating the association between polymorphisms in connective tissue growth factor and susceptibility to colon carcinoma
2015 (English)In: Molecular Medicine Reports, ISSN 1791-2997, E-ISSN 1791-3004, Vol. 11, no 4, p. 2493-2503Article in journal (Refereed) Published
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.

Place, publisher, year, edition, pages
Spandidos Publications, 2015
Keywords
Clinicopathological parameters; Genotyping; Pyrosequencing
National Category
Cancer and Oncology
Research subject
Oncology
Identifiers
urn:nbn:se:oru:diva-44430 (URN)10.3892/mmr.2014.3083 (DOI)000351711100018 ()25502877 (PubMedID)2-s2.0-84921364673 (Scopus ID)
Note

Funding Agencies:

Lions Cancer Research Foundation (Uppsala, Sweden)

Örebro University Hospital Research Council

Nyckelfonden, Örebro University Hospital (Örebro, Sweden)

Available from: 2015-04-24 Created: 2015-04-24 Last updated: 2017-12-04Bibliographically approved
Åström, M., Hahn-Strömberg, V., Zetterberg, E., Vedin, I., Merup, M. & Palmblad, J. (2015). X-linked thrombocytopenia with thalassemia displays bone marrow reticulin fibrosis and enhanced angiogenesis: comparisons with primary myelofibrosis. American Journal of Hematology, 90(3), E44-E48
Open this publication in new window or tab >>X-linked thrombocytopenia with thalassemia displays bone marrow reticulin fibrosis and enhanced angiogenesis: comparisons with primary myelofibrosis
Show others...
2015 (English)In: American Journal of Hematology, ISSN 0361-8609, E-ISSN 1096-8652, Vol. 90, no 3, p. E44-E48Article in journal (Refereed) Published
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.

National Category
Hematology
Identifiers
urn:nbn:se:oru:diva-43473 (URN)10.1002/ajh.23907 (DOI)000349889300003 ()25421114 (PubMedID)2-s2.0-84923092920 (Scopus ID)
Note

Funding Agencies:

Örebro County Council Research Committee OLL-158661  OLL-164431  OLL-239301  OLL-268261

Lions Cancer Research Foundation

Swedish Society of Hematology

Alexion

Available from: 2015-03-10 Created: 2015-03-10 Last updated: 2017-12-04Bibliographically approved
Hahn-Strömberg, V., Askari, S., Befekadu, R., Matthiessen, P., Karlsson, S. & Nilsson, T. K. (2014). Polymorphisms in the CLDN1 and CLDN7 genes are related to differentiation and tumor stage in colon carcinoma. Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), 122(7), 636-642
Open this publication in new window or tab >>Polymorphisms in the CLDN1 and CLDN7 genes are related to differentiation and tumor stage in colon carcinoma
Show others...
2014 (English)In: Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), ISSN 0903-4641, E-ISSN 1600-0463, Vol. 122, no 7, p. 636-642Article in journal (Refereed) Published
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.

Place, publisher, year, edition, pages
Wiley-Blackwell, 2014
Keywords
Tight junction, SNP, colon cancer, claudin
National Category
Immunology in the medical area Microbiology in the medical area
Identifiers
urn:nbn:se:oru:diva-35806 (URN)10.1111/apm.12211 (DOI)000338030400009 ()24479816 (PubMedID)2-s2.0-84902835219 (Scopus ID)
Note

Funding Agencies:

Nyckelfonden, Örebro University Hospital, Örebro, Sweden

Lions cancer research foundation, Uppsala, Sweden

Available from: 2014-08-28 Created: 2014-07-30 Last updated: 2018-06-09Bibliographically approved
Zhulina, Y., Hahn-Strömberg, V., Shamikh, A., Peterson, C. G. B., Gustavsson, A., Nyhlin, N., . . . Halfvarson, J. (2013). Subclinical Inflammation with Increased Neutrophil Activity in Healthy Twin Siblings Reflect Environmental Influence in the Pathogenesis of Inflammatory Bowel Disease. Inflammatory Bowel Diseases, 19(8), 1725-1731
Open this publication in new window or tab >>Subclinical Inflammation with Increased Neutrophil Activity in Healthy Twin Siblings Reflect Environmental Influence in the Pathogenesis of Inflammatory Bowel Disease
Show others...
2013 (English)In: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 19, no 8, p. 1725-1731Article in journal (Refereed) Published
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.

Place, publisher, year, edition, pages
Philadelphia, USA: Lippincott Williams & Wilkins, 2013
Keywords
Inflammatory bowel disease, twins, genetics, subclinical activity, nuclear factor-kappa B, myeloperoxidase, F-calprotectin
National Category
Medical and Health Sciences Gastroenterology and Hepatology
Research subject
Medicine
Identifiers
urn:nbn:se:oru:diva-33716 (URN)10.1097/MIB.0b013e318281f2d3 (DOI)000329363800019 ()23669399 (PubMedID)2-s2.0-84884574092 (Scopus ID)
Funder
Swedish Research Council
Note

Funding Agencies:

Bengt Ihre's foundation  

Nanna Svartz' foundation  

Orebro University Hospital Research Foundation  

Orebro County Research Foundation  

Swedish Foundation for Gastrointestinal research

Available from: 2014-02-12 Created: 2014-02-12 Last updated: 2018-09-11Bibliographically approved
Zhulina, Y., Hahn Strömberg, V., Shamikh, A., Gustavsson, A., Bohr, J., Nyhlin, N., . . . Halfvarson, J. (2012). Aktiverad NFkB i colonbiopsier hos tvillingar med inflammatorisk tarmsjukdom. Gastrokuriren, 17(37), PO-27-PO-27
Open this publication in new window or tab >>Aktiverad NFkB i colonbiopsier hos tvillingar med inflammatorisk tarmsjukdom
Show others...
2012 (Swedish)In: Gastrokuriren, ISSN 1651-0453, Vol. 17, no 37, p. PO-27-PO-27Article in journal, Meeting abstract (Other academic) Published
Place, publisher, year, edition, pages
Svensk Gastroenterologisk Förening, 2012
National Category
Gastroenterology and Hepatology
Research subject
Medicine
Identifiers
urn:nbn:se:oru:diva-25524 (URN)
Available from: 2012-08-29 Created: 2012-08-29 Last updated: 2017-10-18Bibliographically approved
Zhulina, Y., Hahn Strömberg, V., Shamikh, A., Gustavsson, A., Bohr, J., Nyhlin, N., . . . Halfvarson, J. (2011). NFkB is activated in colonic mucosa of healthy co-twins to twins with inflammatory bowel disease. Gut, 60(Suppl 3), A290-A290
Open this publication in new window or tab >>NFkB is activated in colonic mucosa of healthy co-twins to twins with inflammatory bowel disease
Show others...
2011 (English)In: Gut, ISSN 0017-5749, E-ISSN 1468-3288, Vol. 60, no Suppl 3, p. A290-A290Article in journal, Meeting abstract (Refereed) Published
Place, publisher, year, edition, pages
BMJ Publishing Group Ltd, 2011
National Category
Gastroenterology and Hepatology
Research subject
Medicine
Identifiers
urn:nbn:se:oru:diva-25519 (URN)
Available from: 2012-08-29 Created: 2012-08-29 Last updated: 2019-03-06Bibliographically approved
Hahn-Strömberg, V., Edvardsson, H., Bodin, L. & Franzén, L. (2009). Tumor volume of colon carcinoma is related to the invasive pattern but not to the expression of cell adhesion proteins. Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), 117(3), 205-211
Open this publication in new window or tab >>Tumor volume of colon carcinoma is related to the invasive pattern but not to the expression of cell adhesion proteins
2009 (English)In: Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), ISSN 0903-4641, E-ISSN 1600-0463, Vol. 117, no 3, p. 205-211Article in journal (Refereed) 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.

Place, publisher, year, edition, pages
Wiley-Blackwell Publishing Inc., 2009
National Category
Medical and Health Sciences
Research subject
Biomedicine
Identifiers
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)
Available from: 2008-11-10 Created: 2008-11-10 Last updated: 2017-12-14Bibliographically approved
Hahn-Strömberg, V. (2008). Cell adhesion proteins in different invasive patterns of colon carcinomas: a morphometric and molecular genetic study. (Doctoral dissertation). Örebro: Örebro universitet
Open this publication in new window or tab >>Cell adhesion proteins in different invasive patterns of colon carcinomas: a morphometric and molecular genetic study
2008 (English)Doctoral thesis, comprehensive summary (Other academic)
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.

 

Place, publisher, year, edition, pages
Örebro: Örebro universitet, 2008. p. 61
Series
Örebro Studies in Medicine, ISSN 1652-4063 ; 24
Keywords
colon carcinoma, growth pattern, tight junction, Complexity Index, cell adhesion, E-cadherin, Beta-catenin, Occludin, Claudin.
National Category
Clinical Science
Research subject
Biomedicine
Identifiers
urn:nbn:se:oru:diva-2603 (URN)978-91-7668-640-9 (ISBN)
Public defence
2008-11-28, Wilandersalen, USÖ, Universitetsjukhuset, Örebro, 09:00 (English)
Opponent
Supervisors
Available from: 2008-11-10 Created: 2008-11-10 Last updated: 2017-10-18Bibliographically approved
Organisations

Search in DiVA

Show all publications