Emmert, Steffen

[["dc.bibliographiccitation.artnumber","e0141827"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Welz, Christian"],["dc.contributor.author","Emmert, Steffen"],["dc.contributor.author","Canis, Martin"],["dc.contributor.author","Becker, Sven"],["dc.contributor.author","Baumeister, Philipp"],["dc.contributor.author","Shimizu, Tetsuji"],["dc.contributor.author","Morfill, Gregor E."],["dc.contributor.author","Harreus, Uli"],["dc.contributor.author","Zimmermann, Julia L."],["dc.date.accessioned","2018-11-07T09:48:49Z"],["dc.date.available","2018-11-07T09:48:49Z"],["dc.date.issued","2015"],["dc.description.abstract","Head and neck squamous cell cancer (HNSCC) is the 7th most common cancer worldwide. Despite the development of new therapeutic agents such as monoclonal antibodies, prognosis did not change for the last decades. Cold atmospheric plasma (CAP) presents the most promising new technology in cancer treatment. In this study the efficacy of a surface micro discharging (SMD) plasma device against two head and neck cancer cell lines was proved. Effects on the cell viability, DNA fragmentation and apoptosis induction were evaluated with the MTT assay, alkaline microgel electrophoresis (comet assay) and Annexin-V/PI staining. MTT assay revealed that the CAP treatment markedly decreases the cell viability for all tested treatment times (30, 60, 90, 120 and 180 s). IC 50 was reached within maximal 120 seconds of CAP treatment. Comet assay analysis showed a dose dependent high DNA fragmentation being one of the key players in anti-cancer activity of CAP. Annexin-V/PI staining revealed induction of apoptosis in CAP treated HNSCC cell lines but no significant dose dependency was seen. Thus, we confirmed that SMD Plasma technology is definitely a promising new approach on cancer treatment."],["dc.description.sponsorship","Friedrich-Baur-Stiftung Munich [40/13]"],["dc.identifier.doi","10.1371/journal.pone.0141827"],["dc.identifier.isi","000365251500006"],["dc.identifier.pmid","26588072"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12554"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35387"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Cold Atmospheric Plasma: A Promising Complementary Therapy for Squamous Head and Neck Cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e1006248"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","PLOS Genetics"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Rump, Andreas"],["dc.contributor.author","Benet-Pages, Anna"],["dc.contributor.author","Schubert, Steffen"],["dc.contributor.author","Kuhlmann, Jan Dominik"],["dc.contributor.author","Janavičius, Ramūnas"],["dc.contributor.author","Macháčková, Eva"],["dc.contributor.author","Foretová, Lenka"],["dc.contributor.author","Kleibl, Zdenek"],["dc.contributor.author","Lhota, Filip"],["dc.contributor.author","Zemankova, Petra"],["dc.contributor.author","Betcheva-Krajcir, Elitza"],["dc.contributor.author","Mackenroth, Luisa"],["dc.contributor.author","Hackmann, Karl"],["dc.contributor.author","Lehmann, Janin"],["dc.contributor.author","Nissen, Anke"],["dc.contributor.author","DiDonato, Nataliya"],["dc.contributor.author","Opitz, Romy"],["dc.contributor.author","Thiele, Holger"],["dc.contributor.author","Kast, Karin"],["dc.contributor.author","Wimberger, Pauline"],["dc.contributor.author","Holinski-Feder, Elke"],["dc.contributor.author","Emmert, Steffen"],["dc.contributor.author","Schröck, Evelin"],["dc.contributor.author","Klink, Barbara"],["dc.date.accessioned","2019-07-09T11:42:49Z"],["dc.date.available","2019-07-09T11:42:49Z"],["dc.date.issued","2016"],["dc.description.abstract","The increasing application of gene panels for familial cancer susceptibility disorders will probably lead to an increased proposal of susceptibility gene candidates. Using ERCC2 DNA repair gene as an example, we show that proof of a possible role in cancer susceptibility requires a detailed dissection and characterization of the underlying mutations for genes with diverse cellular functions (in this case mainly DNA repair and basic cellular transcription). In case of ERCC2, panel sequencing of 1345 index cases from 587 German, 405 Lithuanian and 353 Czech families with breast and ovarian cancer (BC/OC) predisposition revealed 25 mutations (3 frameshift, 2 splice-affecting, 20 missense), all absent or very rare in the ExAC database. While 16 mutations were unique, 9 mutations showed up repeatedly with population-specific appearance. Ten out of eleven mutations that were tested exemplarily in cell-based functional assays exert diminished excision repair efficiency and/or decreased transcriptional activation capability. In order to provide evidence for BC/OC predisposition, we performed familial segregation analyses and screened ethnically matching controls. However, unlike the recently published RECQL example, none of our recurrent ERCC2 mutations showed convincing co-segregation with BC/OC or significant overrepresentation in the BC/OC cohort. Interestingly, we detected that some deleterious founder mutations had an unexpectedly high frequency of > 1% in the corresponding populations, suggesting that either homozygous carriers are not clinically recognized or homozygosity for these mutations is embryonically lethal. In conclusion, we provide a useful resource on the mutational landscape of ERCC2 mutations in hereditary BC/OC patients and, as our key finding, we demonstrate the complexity of correct interpretation for the discovery of “bonafide” breast cancer susceptibility genes."],["dc.identifier.doi","10.1371/journal.pgen.1006248"],["dc.identifier.pmid","27504877"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13771"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58754"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1553-7404"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Identification and Functional Testing of ERCC2 Mutations in a Multi-national Cohort of Patients with Familial Breast- and Ovarian Cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","UNSP e141"],["dc.bibliographiccitation.journal","Blood Cancer Journal"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Glauer, J."],["dc.contributor.author","Pletz, Nadin"],["dc.contributor.author","Schoen, M."],["dc.contributor.author","Schneider, P."],["dc.contributor.author","Liu, N."],["dc.contributor.author","Ziegelbauer, Karl"],["dc.contributor.author","Emmert, Steffen"],["dc.contributor.author","Wulf, Gerald G."],["dc.contributor.author","Schoen, Michael Peter"],["dc.date.accessioned","2018-11-07T09:20:29Z"],["dc.date.available","2018-11-07T09:20:29Z"],["dc.date.issued","2013"],["dc.description.abstract","Developing effective therapies against multiple myeloma (MM) is an unresolved challenge. Phosphatidylinositol-3-kinase (PI3K) activation may be associated with tumor progression and drug resistance, and inhibiting PI3K can induce apoptosis in MM cells. Thus, targeting of PI3K is predicted to increase the susceptibility of MM to anticancer therapy. The lead compound of a novel class of PI3K inhibitors, BAY80-6946 (IC50 = 0.5 nM against PI3K-alpha), was highly efficacious in four different MM cell lines, where it induced significant antitumoral effects in a dose-dependent manner. The compound inhibited cell cycle progression and increased apoptosis (P<0.001 compared with controls). Moreover, it abrogated the stimulation conferred by insulin-like growth-factor-1, a mechanism relevant for MM progression. These cellular effects were paralleled by decreased Akt phosphorylation, the main downstream target of PI3K. Likewise, profound antitumoral activity was observed ex vivo, as BAY80-6946 significantly inhibited proliferation of freshly isolated myeloma cells from three patients (P<0.001 compared with vehicle). In addition, BAY80-6946 showed convincing in vivo activity against the human AMO-1 and MOLP-8 myeloma cell lines in a preclinical murine xenograft model, where treatment with 6 mg/kg every other day for 2 weeks reduced the cell numbers by 87.0% and 69.3%, respectively (P<0.001 compared with vehicle), without overt toxicity in treated animals."],["dc.description.sponsorship","Deutsche Krebshilfe"],["dc.identifier.doi","10.1038/bcj.2013.37"],["dc.identifier.isi","000325280500002"],["dc.identifier.pmid","24013662"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10663"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28889"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","2044-5385"],["dc.rights","CC BY-NC-ND 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/3.0"],["dc.title","A novel selective small-molecule PI3K inhibitor is effective against human multiple myeloma in vitro and in vivo"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e5"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","New England Journal of Medicine"],["dc.bibliographiccitation.volume","373"],["dc.contributor.author","Emmert, Steffen"],["dc.contributor.author","Schoen, Michael Peter"],["dc.date.accessioned","2018-11-07T09:54:25Z"],["dc.date.available","2018-11-07T09:54:25Z"],["dc.date.issued","2015"],["dc.identifier.doi","10.1056/NEJMicm1410236"],["dc.identifier.isi","000358662200011"],["dc.identifier.pmid","26222581"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13835"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36533"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Massachusetts Medical Soc"],["dc.relation.issn","1533-4406"],["dc.relation.issn","0028-4793"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Squamous-Cell Carcinoma Resembling Pyoderma Gangrenosum"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e0160096"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Emmert, Steffen"],["dc.contributor.author","Haenssle, Holger Andreas"],["dc.contributor.author","Zibert, John R."],["dc.contributor.author","Schoen, Margarete"],["dc.contributor.author","Hald, Andreas"],["dc.contributor.author","Hansen, Maria H."],["dc.contributor.author","Litman, Thomas"],["dc.contributor.author","Schoen, Michael Peter"],["dc.date.accessioned","2018-11-07T10:08:37Z"],["dc.date.available","2018-11-07T10:08:37Z"],["dc.date.issued","2016"],["dc.description.abstract","The rapid and strong clinical efficacy of the first-in-class, ingenol mebutate, against actinic keratosis (AK) has resulted in its recent approval. We conducted the first comprehensive analysis of the cellular and molecular mode of action of topical ingenol mebutate 0.05% gel in both AK and uninvolved skin of 26 patients in a phase I, single-center, open-label, within-patient comparison. As early as 1 day after application, ingenol mebutate induced profound epidermal cell death, along with a strong infiltrate of CD4(+) and CD8(+) T-cells, neutrophils, and macrophages. Endothelial ICAM-1 activation became evident after 2 days. The reaction pattern was significantly more pronounced in AK compared with uninvolved skin, suggesting a tumor-preferential mode of action. Extensive molecular analyses and transcriptomic profiling of mRNAs and microRNAs demonstrated alterations in gene clusters functionally associated with epidermal development, inflammation, innate immunity, and response to wounding. Ingenol mebutate reveals a unique mode of action linking directly to anti-tumoral effects."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2016"],["dc.identifier.doi","10.1371/journal.pone.0160096"],["dc.identifier.isi","000383255900002"],["dc.identifier.pmid","27612149"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13695"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39498"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights.access","openAccess"],["dc.title","Tumor-Preferential Induction of Immune Responses and Epidermal Cell Death in Actinic Keratoses by Ingenol Mebutate"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","115025"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","New Journal of Physics"],["dc.bibliographiccitation.volume","11"],["dc.contributor.affiliation","Helmke, A;"],["dc.contributor.affiliation","Hoffmeister, D;"],["dc.contributor.affiliation","Mertens, N;"],["dc.contributor.affiliation","Emmert, S;"],["dc.contributor.affiliation","Schuette, J;"],["dc.contributor.affiliation","Vioel, W;"],["dc.contributor.author","Helmke, Andreas"],["dc.contributor.author","Hoffmeister, D."],["dc.contributor.author","Mertens, Nina"],["dc.contributor.author","Emmert, Steffen"],["dc.contributor.author","Schuette, J."],["dc.contributor.author","Vioel, Wolfgang"],["dc.date.accessioned","2018-11-07T11:21:51Z"],["dc.date.available","2018-11-07T11:21:51Z"],["dc.date.issued","2009"],["dc.date.updated","2022-02-09T16:00:27Z"],["dc.description.abstract","We studied the acidifying efficiency of a cold atmospheric pressure plasma treatment and ambient air as a working gas on lipid films. Acidification of a thin water film could be observed on plasma-treated surfaces of wool wax, pork sebum and human lipids. This pH shift was partly attributable to NOx species and to the formation of nitric acid in the upper layers of the substrates. The acidic compounds on the lipid surfaces resulted in pH shifts for up to 2 h after plasma exposure, which might be beneficial for pH-targeted therapies in dermatology."],["dc.description.sponsorship","German Government BMBF [13N9089]"],["dc.identifier.doi","10.1088/1367-2630/11/11/115025"],["dc.identifier.eissn","1367-2630"],["dc.identifier.fs","541448"],["dc.identifier.isi","000272153600015"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?goescholar/4059"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55877"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Iop Publishing Ltd"],["dc.relation.issn","1367-2630"],["dc.relation.orgunit","Fakultät für Physik"],["dc.rights","Goescholar"],["dc.rights.access","openAccess"],["dc.rights.uri","https://goedoc.uni-goettingen.de/licenses"],["dc.subject.ddc","530"],["dc.title","The acidification of lipid film surfaces by non-thermal DBD at atmospheric pressure in air"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","353"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Archives of Dermatological Research"],["dc.bibliographiccitation.lastpage","361"],["dc.bibliographiccitation.volume","304"],["dc.contributor.author","Schaefer, Annika"],["dc.contributor.author","Emmert, Steffen"],["dc.contributor.author","Kruppa, Jochen"],["dc.contributor.author","Schubert, Steffen"],["dc.contributor.author","Tzvetkov, Mladen"],["dc.contributor.author","Moessner, Rotraut"],["dc.contributor.author","Reich, Kristian"],["dc.contributor.author","Berking, Carola"],["dc.contributor.author","Volkenandt, Matthias"],["dc.contributor.author","Pfoehler, Claudia"],["dc.contributor.author","Schoen, Michael Peter"],["dc.contributor.author","Vogt, Thomas"],["dc.contributor.author","Koenig, Inke R."],["dc.contributor.author","Reichrath, Joerg"],["dc.date.accessioned","2018-11-07T09:08:44Z"],["dc.date.available","2018-11-07T09:08:44Z"],["dc.date.issued","2012"],["dc.description.abstract","Melanoma is one of the most aggressive human cancers. The vitamin D system contributes to the pathogenesis and prognosis of malignancies including cutaneous melanoma. An expression of the vitamin D receptor (VDR) and an anti-proliferative effect of vitamin D in melanocytes and melanoma cells have been shown in vitro. Studies examining associations of polymorphisms in genes coding for vitamin D metabolism-related proteins (1 alpha-hydroxylase [CYP27B1], 1,25(OH)(2)D-24hydroxylase [CYP24A1], vitamin D-binding protein [VDBP]) and cancer risk are scarce, especially with respect to melanoma. Mainly VDR polymorphisms regarding melanoma risk and prognosis were examined although other vitamin D metabolism-related genes may also be crucial. In our hospital-based case-control study including 305 melanoma patients and 370 healthy controls single nucleotide polymorphisms in the genes CYP27B1 (rs4646536), CYP24A1 (rs927650), VDBP (rs1155563, rs7041), and VDR (rs757343, rs731236, rs2107301, rs7975232) were analyzed for their association with melanoma risk and prognosis. Except VDR rs731236 and VDR rs2107301, the other six polymorphisms have not been analyzed regarding melanoma before. To further improve the prevention as well as the treatment of melanoma, it is important to identify further genetic markers for melanoma risk as well as prognosis in addition to the crude phenotypic, demographic, and environmental markers used in the clinic today. A panel of genetic risk markers could help to better identify individuals at risk for melanoma development or worse prognosis. We, however, found that none of the polymorphisms tested was associated with melanoma risk as well as prognosis in logistic and linear regression models in our study population."],["dc.identifier.doi","10.1007/s00403-012-1243-3"],["dc.identifier.isi","000305680200003"],["dc.identifier.pmid","22576141"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8093"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26096"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0340-3696"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","No association of vitamin D metabolism-related polymorphisms and melanoma risk as well as melanoma prognosis: a case-control study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1443"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Nucleic Acids Research"],["dc.bibliographiccitation.lastpage","1452"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Emmert, Steffen"],["dc.contributor.author","Schneider, Thomas D."],["dc.contributor.author","Kraemer, Kenneth H."],["dc.contributor.author","Khan, Sikandar G."],["dc.date.accessioned","2018-11-07T09:14:51Z"],["dc.date.available","2018-11-07T09:14:51Z"],["dc.date.issued","2001"],["dc.description.abstract","Defects in the XPG DNA repair endonuclease gene can result in the cancer-prone disorders xeroderma pigmentosum (XP) or the XP-Cockayne syndrome complex. While the XPG cDNA sequence was known, determination of the genomic sequence was required to understand its different functions. In cells from normal donors, we found that the genomic sequence of the human XPG gene spans 30 kb, contains 15 exons that range from 61 to 1074 bp and 14 introns that range from 250 to 5763 bp, Analysis of the splice donor and acceptor sites using an information theory-based approach revealed three splice sites with low information content, which are components of the minor (U12) spliceosome, We identified six alternatively spliced XPG mRNA isoforms in cells from normal donors and from XPG patients: partial deletion of exon 8, partial retention of intron 8, two with alternative exons tin introns 1 and 6) and two that retained complete introns (introns 3 and 9), The amount of alternatively spliced XPG mRNA isoforms varied in different tissues. Most alternative splice donor and acceptor sites had a relatively high information content, but one has the U12 spliceosome sequence. A single nucleotide polymorphism has allele frequencies of 0.74 for 3507G and 0.26 for 3507C in 91 donors. The human XPG gene contains multiple splice sites with low information content in association with multiple alternatively spliced isoforms of XPG mRNA."],["dc.description.sponsorship","Intramural NIH HHS [Z01 BC004517-31]"],["dc.format.mimetype","application/pdf"],["dc.identifier.doi","10.1093/nar/29.7.1443"],["dc.identifier.fs","10209"],["dc.identifier.isi","000167970300006"],["dc.identifier.pmid","11266544"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?goescholar/4101"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27524"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0305-1048"],["dc.relation.issn","1362-4962"],["dc.rights","Goescholar"],["dc.rights.access","openAccess"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject","nucleic acids"],["dc.subject.ddc","610"],["dc.title","The human XPG gene: gene architecture, alternative splicing and single nucleotide polymorphisms"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]