Now showing 1 - 10 of 32
  • 2003Conference Abstract
    [["dc.bibliographiccitation.firstpage","6232S"],["dc.bibliographiccitation.issue","16"],["dc.bibliographiccitation.journal","Clinical Cancer Research"],["dc.bibliographiccitation.lastpage","6233S"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Mossner, Rotraut"],["dc.contributor.author","Schulz, U."],["dc.contributor.author","Kuger, U."],["dc.contributor.author","Middel, Peter"],["dc.contributor.author","Fuzesi, Laszlo"],["dc.contributor.author","Neumann, C."],["dc.contributor.author","Reich, Kristian"],["dc.date.accessioned","2018-11-07T10:34:17Z"],["dc.date.available","2018-11-07T10:34:17Z"],["dc.date.issued","2003"],["dc.identifier.isi","000187467300668"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44829"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Cancer Research"],["dc.publisher.place","Philadelphia"],["dc.relation.conference","AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics"],["dc.relation.eventlocation","BOSTON, MASSACHUSETTS"],["dc.relation.issn","1078-0432"],["dc.title","Role of peroxisome proliferator-activated receptor (PPAR) gamma in the control of melanoma cell growth."],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2006Conference Abstract
    [["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Experimental Dermatology"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Mossner, Rotraut"],["dc.contributor.author","Anders, N."],["dc.contributor.author","Konig, I. R."],["dc.contributor.author","Kruger, Ullrich"],["dc.contributor.author","Schmidt, D."],["dc.contributor.author","Berking, Carola"],["dc.contributor.author","Ziegler, Andreas"],["dc.contributor.author","Brockmoeller, Juergen"],["dc.contributor.author","Volkenandt, Matthias"],["dc.contributor.author","Kaiser, R."],["dc.contributor.author","Westphal, G."],["dc.contributor.author","Reich, Kristian"],["dc.date.accessioned","2018-11-07T10:12:01Z"],["dc.date.available","2018-11-07T10:12:01Z"],["dc.date.issued","2006"],["dc.format.extent","198"],["dc.identifier.isi","000235370600041"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40158"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Publishing"],["dc.publisher.place","Oxford"],["dc.relation.conference","33rd Annual Meeting of the Arbeitsgemeinschaft-Dermatologische-Forschung (ADF)"],["dc.relation.eventlocation","Aachen, GERMANY"],["dc.relation.issn","0906-6705"],["dc.title","Variations of the MC1R and the GSTM1 and T1 genes in cutaneous malignant melanoma"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2022Journal Article
    [["dc.bibliographiccitation.firstpage","753"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal der Deutschen Dermatologischen Gesellschaft"],["dc.bibliographiccitation.lastpage","771"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Reich, Kristian"],["dc.contributor.author","Augustin, Matthias"],["dc.contributor.author","Gerdes, Sascha"],["dc.contributor.author","Ghoreschi, Kamran"],["dc.contributor.author","Kokolakis, Georgios"],["dc.contributor.author","Mößner, Rotraut"],["dc.contributor.author","Mrowietz, Ulrich"],["dc.contributor.author","Navarini, Alexander A."],["dc.contributor.author","Pinter, Andreas"],["dc.contributor.author","Schäkel, Knut"],["dc.contributor.author","Wilsmann‐Theis, Dagmar"],["dc.date.accessioned","2022-07-01T07:35:12Z"],["dc.date.available","2022-07-01T07:35:12Z"],["dc.date.issued","2022"],["dc.identifier.doi","10.1111/ddg.14764"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112108"],["dc.language.iso","de"],["dc.notes.intern","DOI-Import GROB-581"],["dc.relation.eissn","1610-0387"],["dc.relation.issn","1610-0379"],["dc.rights.uri","http://creativecommons.org/licenses/by-nc-nd/4.0/"],["dc.title","Generalized pustular psoriasis: overview of the status quo and results of a panel discussion"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]
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  • 2002Journal Article
    [["dc.bibliographiccitation.firstpage","576"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Investigative Dermatology"],["dc.bibliographiccitation.lastpage","582"],["dc.bibliographiccitation.volume","119"],["dc.contributor.author","Mossner, Rotraut"],["dc.contributor.author","Schulz, U."],["dc.contributor.author","Kruger, Ullrich"],["dc.contributor.author","Middel, Peter"],["dc.contributor.author","Schinner, S."],["dc.contributor.author","Fuzesi, Laszlo"],["dc.contributor.author","Neumann, C."],["dc.contributor.author","Reich, Kristian"],["dc.date.accessioned","2018-11-07T10:06:19Z"],["dc.date.available","2018-11-07T10:06:19Z"],["dc.date.issued","2002"],["dc.description.abstract","Peroxisome proliferator-activated receptor gamma is a member of the nuclear receptor superfamily involved in adipocyte differentiation and glucose homeostasis. There is evidence that peroxisome proliferator-activated receptor gamma may also act as a tumor suppressor. Here, we demonstrate expression of peroxisome proliferator-activated receptor gamma in benign melanocytic naevi, different variants of primary cutaneous melanomas, and melanoma metastases. Peroxisome proliferator-activated receptor gamma protein and peroxisome proliferator-activated receptor gamma1 mRNA were also detected in human melanoma cell lines. The peroxisome proliferator-activated receptor gamma specific agonists 15-deoxy-Delta(12,14)-prostaglandin J(2), troglitazone, and rosiglitazone dose-dependently inhibited cell proliferation in four melanoma cell lines, whereas a specific agonist of peroxisome proliferator-activated receptor alpha had no such effect. At a concentration of 50 muM rosiglitazone, the most potent peroxisome proliferator-activated receptor gamma agonist tested suppressed cell growth by approximately 90%. Apoptosis could be induced in melanoma cell lines by incubation with tumor-necrosis-factor-related apoptosis-inducing ligand. In contrast, the growth inhibitory effect of peroxisome proliferator-activated receptor gamma activation was independent of apoptosis and seemed to occur primarily through induction of cell cycle arrest. Our data indicate that melanoma cell growth may be modulated through peroxisome proliferator-activated receptor gamma."],["dc.identifier.doi","10.1046/j.1523-1747.2002.01861.x"],["dc.identifier.isi","000177951400006"],["dc.identifier.pmid","12230498"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39070"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Publishing Inc"],["dc.relation.issn","0022-202X"],["dc.title","Agonists of peroxisome proliferator-activated receptor gamma inhibit cell growth in malignant melanoma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2005Conference Abstract
    [["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Investigative Dermatology"],["dc.bibliographiccitation.volume","125"],["dc.contributor.author","Mossner, Rotraut"],["dc.contributor.author","Wussow, M."],["dc.contributor.author","Schmidt, D."],["dc.contributor.author","Kruger, Ullrich"],["dc.contributor.author","Reich, Kristian"],["dc.date.accessioned","2018-11-07T10:56:17Z"],["dc.date.available","2018-11-07T10:56:17Z"],["dc.date.issued","2005"],["dc.format.extent","A58"],["dc.identifier.isi","000231862600339"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49977"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Publishing"],["dc.publisher.place","Oxford"],["dc.relation.conference","35th Annual Meeting of the European-Society-for-Dermatological-Research"],["dc.relation.eventlocation","Tubingen, GERMANY"],["dc.relation.issn","0022-202X"],["dc.title","Evidence for a PPARgamma agonist-induced proteasomal degradation of cyclin D1 in melanoma cell lines"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2008Journal Article
    [["dc.bibliographiccitation.firstpage","486"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Clinics in Dermatology"],["dc.bibliographiccitation.lastpage","502"],["dc.bibliographiccitation.volume","26"],["dc.contributor.author","Moessner, Rotraut"],["dc.contributor.author","Schoen, Michael Peter"],["dc.contributor.author","Reich, Kristian"],["dc.date.accessioned","2018-11-07T11:11:13Z"],["dc.date.available","2018-11-07T11:11:13Z"],["dc.date.issued","2008"],["dc.description.abstract","The identification of new pathophysiological mechanisms in chronic inflammatory diseases and the development of techniques that allow production of antibodies and fusion proteins that antagonize target molecules With high specificity has not only revolutionized the treatment of rheumatoid arthritis and chronic inflammatory bowel disease, but it also has revolutionized the treatment of psoriasis in recent years. Two different classes of so-called biological therapies (biologics) have become available to treat psoriasis: tumor necrosis factor (TNF) antagonists and T-cell modulators. TNF antagonists that have been Studied with psoriasis include the antibodies infliximab and adalimumab and the fusion protein etanercept. These treatments differ in their capacity to reduce the skin symptoms of psoriasis and other important characteristics of the drug profile. This article summarizes the important aspects of efficacy, safety, and practicability of TNF antagonists in the treatment of psoriasis. This article may be helpful for the daily routine when selecting the right therapy for a patient and managing the TNF antagonist during maintenance therapy. (c) 2008 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.clindermatol.2007.10.030"],["dc.identifier.isi","000259168400010"],["dc.identifier.pmid","18755367"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53379"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","0738-081X"],["dc.title","Tumor necrosis factor antagonists in the therapy of psoriasis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2004Journal Article
    [["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Archives of Dermatological Research"],["dc.bibliographiccitation.lastpage","5"],["dc.bibliographiccitation.volume","296"],["dc.contributor.author","Mossner, Rotraut"],["dc.contributor.author","Kaiser, R."],["dc.contributor.author","Matern, P."],["dc.contributor.author","Kruger, Ullrich"],["dc.contributor.author","Westphal, Goetz Alexander"],["dc.contributor.author","Brockmoeller, Juergen"],["dc.contributor.author","Ziegler, Andreas"],["dc.contributor.author","Neumann, C."],["dc.contributor.author","Konig, I. R."],["dc.contributor.author","Reich, Kristian"],["dc.date.accessioned","2018-11-07T10:48:15Z"],["dc.date.available","2018-11-07T10:48:15Z"],["dc.date.issued","2004"],["dc.description.abstract","The three peroxisome proliferator-activated receptor (PPAR) subtypes alpha, delta (beta), and gamma belong to the group of nuclear receptors that act as ligand-activated transcription factors. Recently, expression of PPARalpha and gamma in keratinocytes has been demonstrated, and ligands of PPARalpha and gamma have been found to enhance epidermal maturation and protect against cutaneous inflammation. There is evidence for a possible role of PPARs in psoriasis, as the expression of PPARalpha and gamma is decreased in lesional skin and treatment with PPARgamma agonists improves psoriatic keratinocyte pathology in vitro and in vivo. We performed a case-control study to search for possible associations between variations in the genes encoding PPARalpha and gamma and psoriasis. Seven variations in these genes were analyzed in 192 patients with chronic plaque-type psoriasis and 330 healthy controls by PCR-based methods. No association between any of the investigated PPAR variants and psoriasis was found. Our findings argue against a significant contribution of the investigated PPAR variations to the genetic basis of psoriasis."],["dc.identifier.doi","10.1007/s00403-004-0463-6"],["dc.identifier.isi","000222059400001"],["dc.identifier.pmid","15083308"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48146"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0340-3696"],["dc.title","Variations in the genes encoding the peroxisome proliferator-activated receptors alpha and gamma in psoriasis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2010Journal Article Discussion
    [["dc.bibliographiccitation.firstpage","71"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Dermatological Science"],["dc.bibliographiccitation.lastpage","73"],["dc.bibliographiccitation.volume","57"],["dc.contributor.author","Kingo, Kuelli"],["dc.contributor.author","Moessner, Rotraut"],["dc.contributor.author","Traks, Tanel"],["dc.contributor.author","Raetsep, Ranno"],["dc.contributor.author","Raud, Kristi"],["dc.contributor.author","Reimann, Ene"],["dc.contributor.author","Krueger, Ullrich"],["dc.contributor.author","Silm, Helgi"],["dc.contributor.author","Vasar, Eero"],["dc.contributor.author","Reich, Kristian"],["dc.contributor.author","Koks, Sulev"],["dc.date.accessioned","2018-11-07T08:47:55Z"],["dc.date.available","2018-11-07T08:47:55Z"],["dc.date.issued","2010"],["dc.identifier.doi","10.1016/j.jdermsci.2009.10.007"],["dc.identifier.isi","000273667200015"],["dc.identifier.pmid","19926456"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21078"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Ireland Ltd"],["dc.relation.issn","0923-1811"],["dc.title","Further association analysis of chr 6q22-24 suggests a role of IL-20RA polymorphisms in psoriasis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]
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  • 2009Journal Article
    [["dc.bibliographiccitation.firstpage","355"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Investigative Dermatology"],["dc.bibliographiccitation.lastpage","358"],["dc.bibliographiccitation.volume","129"],["dc.contributor.author","Hueffmeier, Ulrike"],["dc.contributor.author","Lascorz, Jesus"],["dc.contributor.author","Boehm, Beate"],["dc.contributor.author","Lohmann, Joerg"],["dc.contributor.author","Wendler, Joerg"],["dc.contributor.author","Moessner, Rotraut"],["dc.contributor.author","Reich, Kristian"],["dc.contributor.author","Traupe, Heiko"],["dc.contributor.author","Kurrat, Werner"],["dc.contributor.author","Burkhardt, Harald"],["dc.contributor.author","Reis, Andre"],["dc.date.accessioned","2018-11-07T08:33:09Z"],["dc.date.available","2018-11-07T08:33:09Z"],["dc.date.issued","2009"],["dc.description.abstract","Variants in two genes of the IL-23 receptor (R) pathway have recently been shown to be associated with psoriasis vulgaris (PV). We were interested whether the risk conferred by these variants differs between psoriatic skin and joint disease. Four variants of the IL12B and IL23R genes were analyzed in 1,114 PV patients, 748 patients with psoriatic arthritis (PA) and 937 healthy controls before and after stratification for the major psoriasis risk allele at psoriasis susceptibility locus 1 (PSORS1). For both PA and PV, we detected the strongest association with two IL12B single-nucleotide polymorphisms and the corresponding haplotype as reflected by minimal P-values of 10(-7) and highest odds ratios of 1.50 (1.28-1.75) for rs6887695 in PA patients and 1.50 (1.27-1.76) for rs3212227 in the PV cohort, respectively. For IL23R, only rs11209026 showed an association. The results remained significant after correction for multiple testing. No difference was observed after stratification for the PSORS1 risk allele. While confirming recent reports on variants of the IL-23R pathway as susceptibility factors for PV, our study is the first to extend analysis of both genes to PA. However, our results indicate that these variants are not specific risk factors for arthritis, but relevant for susceptibility to psoriasis in general."],["dc.description.sponsorship","University of Erlangen-Nuremberg [IZKF B32/A8]"],["dc.identifier.doi","10.1038/jid.2008.233"],["dc.identifier.isi","000262655600015"],["dc.identifier.pmid","18800148"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17510"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","0022-202X"],["dc.title","Genetic Variants of the IL-23R Pathway: Association with Psoriatic Arthritis and Psoriasis Vulgaris, but No Specific Risk Factor for Arthritis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2004Journal Article
    [["dc.bibliographiccitation.firstpage","340"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Experimental Dermatology"],["dc.bibliographiccitation.lastpage","346"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Mossner, Rotraut"],["dc.contributor.author","Beckmann, I."],["dc.contributor.author","Hallermann, Christian"],["dc.contributor.author","Neumann, C."],["dc.contributor.author","Reich, Kristian"],["dc.date.accessioned","2018-11-07T10:48:24Z"],["dc.date.available","2018-11-07T10:48:24Z"],["dc.date.issued","2004"],["dc.description.abstract","Psoriasis is a chronic inflammatory skin disorder characterized by accumulation of Th1-type T cells and neutrophils, regenerative keratinocyte proliferation and differentiation, and enhanced epidermal production of antimicrobial peptides. The underlying cause is unknown, but there are some similarities with the immunologic defense program against bacteria. Development of psoriasiform skin lesions has been reported after administration of granulocyte colony-stimulating factor (G-CSF), a cytokine induced in monocytes by bacterial antigens. To further investigate the relation between this type of cytokine-induced dermatitis and psoriasis, we analyzed the cutaneous cytokine profile [tumor necrosis factor-alpha (TNF-alpha), interferon-gamma, transforming growth factor-beta1 (TGF-beta1), interleukin-10 (IL-10), IL-12p35 and p40, and IL-8] and expression of markers of epidermal activation [Ki-67, cytokeratin-16, major histocompatibility complex (MHC) class II, intercellular adhesion molecule-1 (ICAM-1)] in a patient who developed G-CSF-induced psoriasiform dermatitis by using quantitative real-time reverse transcriptase-polymerase chain reaction and immunohistology. The histologic picture resembled psoriasis with regard to epidermal hyperparakeratosis and the accumulation of lymphocytes in the upper corium. CD8(+) T cells were found to infiltrate the epidermis which was associated with an aberrant expression of Ki-67, cytokeratin-16, MHC class II, and ICAM-1 on adjacent keratinocytes. As compared to normal skin (n = 7), there was an increased expression of TNF-alpha, IL-12p40, and IL-8, a decreased expression of TGF-beta1, and a lack of IL-10, similar to the findings in active psoriasis (n = 8). Therefore, G-CSF may cause a lymphocytic dermatitis that, similar to psoriasis, is characterized by a pro-inflammatory Th1-type cytokine milieu and an epidermal phenotype indicative of aberrant maturation and acquisition of non-professional immune functions."],["dc.identifier.doi","10.1111/j.0906-6705.2004.00190.x"],["dc.identifier.isi","000221790100002"],["dc.identifier.pmid","15186319"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48182"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Munksgaard"],["dc.relation.issn","0906-6705"],["dc.title","Granulocyte colony-stimulating-factor-induced psoriasiform dermatitis resembles psoriasis with regard to abnormal cytokine expression and epidermal activation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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