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Cullman, Inger
Publications (4 of 4) Show all publications
Strand, M., Carlsson, M., Uvell, H., Islam, K., Edlund, K., Cullman, I., . . . Almqvist, F. (2014). Isolation and characterization of anti-adenoviral secondary metabolites from marine actinobacteria. Marine Drugs, 12(2), 799-821
Open this publication in new window or tab >>Isolation and characterization of anti-adenoviral secondary metabolites from marine actinobacteria
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2014 (English)In: Marine Drugs, ISSN 1660-3397, E-ISSN 1660-3397, Vol. 12, no 2, p. 799-821Article in journal (Refereed) Published
Abstract [en]

Adenovirus infections in immunocompromised patients are associated with high mortality rates. Currently, there are no effective anti-adenoviral therapies available. It is well known that actinobacteria can produce secondary metabolites that are attractive in drug discovery due to their structural diversity and their evolved interaction with biomolecules. Here, we have established an extract library derived from actinobacteria isolated from Vestfjorden, Norway, and performed a screening campaign to discover anti-adenoviral compounds. One extract with anti-adenoviral activity was found to contain a diastereomeric 1:1 mixture of the butenolide secondary alcohols 1a and 1b. By further cultivation and analysis, we could isolate 1a and 1b in different diastereomeric ratio. In addition, three more anti-adenoviral butenolides 2, 3 and 4 with differences in their side-chains were isolated. In this study, the anti-adenoviral activity of these compounds was characterized and substantial differences in the cytotoxic potential between the butenolide analogs were observed. The most potent butenolide analog 3 displayed an EC50 value of 91 μM and no prominent cytotoxicity at 2 mM. Furthermore, we propose a biosynthetic pathway for these compounds based on their relative time of appearance and structure.

Place, publisher, year, edition, pages
MDPI, 2014
Keywords
adenovirus; antiviral; natural products; secondary metabolites; marine actinobacteria; extract screening; butenolides
National Category
Basic Medicine
Identifiers
urn:nbn:se:umu:diva-86525 (URN)10.3390/md12020799 (DOI)000335745100011 ()24477283 (PubMedID)
Available from: 2014-03-03 Created: 2014-02-28 Last updated: 2018-06-08Bibliographically approved
Borssen, M., Cullman, I., Norén-Nyström, U., Sundstrom, C., Porwit, A., Forestier, E. & Roos, G. (2011). hTERT promoter methylation and telomere length in childhood acute lymphoblastic leukemia-associations with immunophenotype and cytogenetic subgroup. Experimental Hematology, 39(12), 1144-1151
Open this publication in new window or tab >>hTERT promoter methylation and telomere length in childhood acute lymphoblastic leukemia-associations with immunophenotype and cytogenetic subgroup
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2011 (English)In: Experimental Hematology, ISSN 0301-472X, E-ISSN 1873-2399, Vol. 39, no 12, p. 1144-1151Article in journal (Refereed) Published
Abstract [en]

Telomere maintenance, important for long-term cell survival and malignant transformation, is directed by a multitude of factors, including epigenetic mechanisms, and has been implicated in outcomes for patients with leukemia. In the present study, the objective was to investigate the biological and clinical significance of telomere length and promoter methylation of the human telomerase reverse transcriptase gene in childhood acute lymphoblastic leukemia. A cohort of 169 childhood acute lymphoblastic leukemias was investigated for telomere length, human telomerase reverse transcriptase gene promoter methylation status, genomic aberrations, immunophenotype, and clinical outcomes. Methylation of the core promoter of the human telomerase reverse transcriptase (hTERT) gene was demonstrated in 24% of diagnostic samples, with a significant difference between B-cell precursor (n = 130) and T-cell acute lymphoblastic leukemia (ALL) (n = 17) cases (18% and 72%, respectively; p < 0.001). No remission sample demonstrated hTERT promoter methylation (n = 40). Within the B-cell precursor group, t(12;21)(p13;q22) [ETV6/RUNX1] cases (n = 19) showed a much higher frequency of hTERT methylation than high-hyperdiploid (51 61 chromosomes) ALL (n = 44) (63% and 7%, respectively; p < 0.001). hTERT messenger RNA levels were negatively associated with methylation status and, in the t(12;21) group, methylated cases had shorter telomeres (p = 0.017). In low-risk B-cell precursor patients (n = 101), long telomeres indicated a worse prognosis. The collected data from the present study indicate that the telomere biology in childhood ALL has clinical implications and reflects molecular differences between diverse ALL subgroups. (C) 2011 ISEH - Society for Hematology and Stem Cells. Published by Elsevier Inc.

Place, publisher, year, edition, pages
New York: Elsevier, 2011
National Category
Hematology
Identifiers
urn:nbn:se:umu:diva-50932 (URN)10.1016/j.exphem.2011.08.014 (DOI)000297566500005 ()
Available from: 2012-01-05 Created: 2012-01-02 Last updated: 2018-06-08Bibliographically approved
Van Guelpen, B., Dahlin, A. M., Hultdin, J., Eklöf, V., Johansson, I., Henriksson, M. L., . . . Palmqvist, R. (2010). One-carbon metabolism and CpG island methylator phenotype status in incident colorectal cancer: a nested case-referent study. Cancer Causes and Control, 21(4), 557-566
Open this publication in new window or tab >>One-carbon metabolism and CpG island methylator phenotype status in incident colorectal cancer: a nested case-referent study
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2010 (English)In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 21, no 4, p. 557-566Article in journal (Refereed) Published
Abstract [en]

OBJECTIVE: We related prediagnostic plasma folate, vitamin B12, and total homocysteine concentrations, and the MTHFR 677C>T and 1298A>C polymorphisms, to the risk of colorectal cancer with and without the CpG island methylator phenotype (CIMP).

METHODS: This was a nested case-referent study of 190 cases and double, matched referents from the large, population-based Northern Sweden Health and Disease Study. Using archival tumor tissue, promoter methylation in an eight-gene panel was analyzed by MethyLight.

RESULTS: A reduced risk of CIMP-low/CIMP-high CRC (>/=1 gene methylated) was observed in subjects with very low plasma folate concentrations [multivariate odds ratio 2.96 (95% CI 1.24-7.08) for quintiles two to five versus one (lowest)]. With the exception of a reduced risk in MTHFR 677 TT-homozygotes, none of the other one-carbon variables were associated with the risk of CIMP-low/CIMP-high CRC. For CIMP-negative CRC, only the MTHFR polymorphisms were statistically significantly related to risk, inversely for 677C>T and positively for 1298A>C, but a tendency toward a reduced risk was observed in subjects with an adequate methyl availability, combining the plasma variables [multivariate odds ratio 0.61 (95% CI 0.32-1.15)].

CONCLUSION: Though limited by low power, these findings suggest the possibility of different roles for one-carbon metabolism in different pathways of colorectal tumorigenesis.

Identifiers
urn:nbn:se:umu:diva-31577 (URN)10.1007/s10552-009-9484-y (DOI)000275631900006 ()20012180 (PubMedID)
Available from: 2010-02-11 Created: 2010-02-11 Last updated: 2018-06-08Bibliographically approved
Gu, X., Bäckman, B., Coates, P. J., Cullman, I., Hellman, U., Lind, L. & Nylander, K. (2006). Exclusion of p63 as a candidate gene for autosomal-dominant amelogenesis imperfecta.. Acta Odontologica Scandinavica, 64(2), 111-114
Open this publication in new window or tab >>Exclusion of p63 as a candidate gene for autosomal-dominant amelogenesis imperfecta.
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2006 (English)In: Acta Odontologica Scandinavica, ISSN 0001-6357, E-ISSN 1502-3850, Vol. 64, no 2, p. 111-114Article in journal (Refereed) Published
Keywords
Amelogenesis Imperfecta/*genetics, Case-Control Studies, Chromatography; High Pressure Liquid, DNA Mutational Analysis, Female, Genes; Dominant, Humans, Male, Membrane Proteins/*genetics, Pedigree, Polymerase Chain Reaction
Identifiers
urn:nbn:se:umu:diva-15332 (URN)10.1080/00016350500443206 (DOI)16546853 (PubMedID)
Available from: 2008-01-12 Created: 2008-01-12 Last updated: 2018-06-09Bibliographically approved
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