Hahn, Heidi Eva

[["dc.bibliographiccitation.firstpage","1863"],["dc.bibliographiccitation.issue","16"],["dc.bibliographiccitation.journal","Cellular and Molecular Life Sciences"],["dc.bibliographiccitation.lastpage","1870"],["dc.bibliographiccitation.volume","62"],["dc.contributor.author","Koleva, M."],["dc.contributor.author","Kappler, R."],["dc.contributor.author","Vogler, M."],["dc.contributor.author","Herwig, A."],["dc.contributor.author","Fulda, S."],["dc.contributor.author","Hahn, H."],["dc.date.accessioned","2021-06-01T10:49:01Z"],["dc.date.available","2021-06-01T10:49:01Z"],["dc.date.issued","2005"],["dc.identifier.doi","10.1007/s00018-005-5072-9"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86134"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","1420-9071"],["dc.relation.issn","1420-682X"],["dc.title","Pleiotropic effects of sonic hedgehog on muscle satellite cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","8785"],["dc.bibliographiccitation.issue","54"],["dc.bibliographiccitation.journal","Oncogene"],["dc.bibliographiccitation.lastpage","8795"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Kappler, Roland"],["dc.contributor.author","Bauer, R."],["dc.contributor.author","Calzada-Wack, J."],["dc.contributor.author","Rosemann, M."],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.contributor.author","Hahn, H."],["dc.date.accessioned","2018-11-07T10:43:46Z"],["dc.date.available","2018-11-07T10:43:46Z"],["dc.date.issued","2004"],["dc.description.abstract","Rhabdomyosarcoma (RMS) is a highly malignant tumor that is histologically related to skeletal muscle, yet genetic and molecular lesions underlying its genesis and progression remain largely unknown. In this study we have compared the molecular profiles of two different mouse models of RMS, each associated with a defined primary genetic defect known to play a role in rhabdomyosarco-magenesis in man. We report that RMS of heterozygous Patched1 (Ptch1) mice show less aggressive growth and a greater degree of differentiation than RMS of heterozygous p53 mice. By means of cDNA microarray analysis we demonstrate that RMS in Ptch1 mutants predominantly express a number of myogenic markers, including myogenic differentiation 1, myosin heavy chain, actin, troponin and tropomyosin, as well as genes associated with Hedgehog/Patched signaling like insulin-like growth factor 2, forkhead box gene Foxf1 and the growth arrest and DNA-damage-inducible gene Gadd45a. In sharp contrast, RMS in p53 mutants display higher expression levels of cell cycle-associated genes like cyclin B1, cyclin-dependent kinase 4 and the proliferation marker Ki-67. These results demonstrate that different causative mutations lead to distinct gene expression profiles in RMS, which appear to reflect their different biological characteristics. Our results provide a first step towards a molecular classification of different forms of RMS. If the described differences can be confirmed in human RMS our results will contribute to a new molecular taxonomy of this cancer, which will be critical for gene mutation- and expression-specific therapy."],["dc.identifier.doi","10.1038/sj.onc.1208133"],["dc.identifier.isi","000225165100008"],["dc.identifier.pmid","15480423"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47133"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","0950-9232"],["dc.title","Profiling the molecular difference between Patched- and p53-dependent rhabdomyosarcoma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","501"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Fetal Diagnosis and Therapy"],["dc.bibliographiccitation.lastpage","503"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Schulz, Sarah"],["dc.contributor.author","Gerloff, C."],["dc.contributor.author","Kalinski, T."],["dc.contributor.author","Mawrin, C."],["dc.contributor.author","Kanakis, D."],["dc.contributor.author","Haas, D."],["dc.contributor.author","Hahn, H."],["dc.contributor.author","Wieacker, P."],["dc.date.accessioned","2018-11-07T08:38:43Z"],["dc.date.available","2018-11-07T08:38:43Z"],["dc.date.issued","2005"],["dc.description.abstract","The combination of holoprosencephaly, postaxial polydactyly, and normal karyotype has been termed pseudotrisomy 13 syndrome. Here, we report the prenatal diagnosis of pseudotrisomy 13 in three siblings suggesting autosomal recessive inheritance of this syndrome. Clinical overlap with hydrolethalus syndrome, Smith-Lemli-Opitz syndrome, Meckel syndrome, and Pallister-Hall syndrome is discussed. Copyright (c) 2005 S. Karger AG, Basel."],["dc.identifier.doi","10.1159/000088038"],["dc.identifier.isi","000232668200004"],["dc.identifier.pmid","16260883"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18825"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.relation.issn","1015-3837"],["dc.title","Pseudotrisomy 13: Clinical findings and genetic implications"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1587"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Cancer Immunology Immunotherapy"],["dc.bibliographiccitation.lastpage","1597"],["dc.bibliographiccitation.volume","62"],["dc.contributor.author","Koenig, Simone"],["dc.contributor.author","Regen, Tommy"],["dc.contributor.author","Dittmann, Kai"],["dc.contributor.author","Engelke, Michael"],["dc.contributor.author","Wienands, Juergen"],["dc.contributor.author","Schwendener, Reto"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Hahn, Heidi"],["dc.date.accessioned","2018-11-07T09:19:32Z"],["dc.date.available","2018-11-07T09:19:32Z"],["dc.date.issued","2013"],["dc.description.abstract","Liposomes are frequently used in cancer therapy to encapsulate and apply anticancer drugs. Here, we show that a systemic treatment of mice bearing skin tumors with empty phosphatidylcholine liposomes (PCL) resulted in inhibition of tumor growth, which was similar to that observed with the synthetic bacterial lipoprotein and TLR1/2 agonist Pam(3)CSK(4) (BLP). Both compounds led to a substantial decrease of macrophages in spleen and in the tumor-bearing skin. Furthermore, both treatments induced the expression of typical macrophage markers in the tumor-bearing tissue. As expected, BLP induced the expression of the M1 marker genes Cxcl10 and iNOS, whereas PCL, besides inducing iNOS, also increased the M2 marker genes Arg1 and Trem2. In vitro experiments demonstrated that neither PCL nor BLP influenced proliferation or survival of tumor cells, whereas both compounds inhibited proliferation and survival and increased the migratory capacity of bone marrow-derived macrophages (BMDM). However, in contrast to BLP, PCL did not activate cytokine secretion and induced a different BMDM phenotype. Together, the data suggest that similar to BLP, PCL induce an antitumor response by influencing the tumor microenvironment, in particular by functional alterations of macrophages, however, in a distinct manner from those induced by BLP."],["dc.description.sponsorship","DFG [FOR942 HA 2197/5-2]"],["dc.identifier.doi","10.1007/s00262-013-1444-4"],["dc.identifier.isi","000325008800005"],["dc.identifier.pmid","23917775"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28662"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0340-7004"],["dc.title","Empty liposomes induce antitumoral effects associated with macrophage responses distinct from those of the TLR1/2 agonist Pam(3)CSK(4) (BLP)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","8722"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","8735"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Graab, Ulrike"],["dc.contributor.author","Hahn, Heidi"],["dc.contributor.author","Fulda, Simone"],["dc.date.accessioned","2019-07-09T11:42:39Z"],["dc.date.available","2019-07-09T11:42:39Z"],["dc.date.issued","2015-04-20"],["dc.description.abstract","We previously reported that aberrant HH pathway activation confers a poor prognosis in rhabdomyosarcoma (RMS). Searching for new treatment strategies we therefore targeted HH signaling. Here, we identify a novel synthetic lethality of concomitant inhibition of HH and PI3K/AKT/mTOR pathways in RMS by GLI1/2 inhibitor GANT61 and PI3K/mTOR inhibitor PI103. Synergistic drug interaction is confirmed by calculation of combination index (CI < 0.2). Similarly, genetic silencing of GLI1/2 significantly increases PI103-induced apoptosis. GANT61 and PI103 also synergize to induce apoptosis in cultured primary RMS cells emphasizing the clinical relevance of this combination. Importantly, GANT61/PI103 cotreatment suppresses clonogenic survival, three-dimensional sphere formation and tumor growth in an in vivo model of RMS. Mechanistic studies reveal that GANT61 and PI103 cooperate to trigger caspase-dependent apoptosis via the mitochondrial pathway, as demonstrated by several lines of evidence. First, GANT61/PI103 cotreatment increases mRNA and protein expression of NOXA and BMF, which is required for apoptosis, since knockdown of NOXA or BMF significantly reduces GANT61/PI103-induced apoptosis. Second, GANT61/PI103 cotreatment triggers BAK/BAX activation, which contributes to GANT61/PI103-mediated apoptosis, since knockdown of BAK provides protection. Third, ectopic expression of BCL-2 or non-degradable phospho-mutant MCL-1 significantly rescue GANT61/PI103-triggered apoptosis. Fourth, GANT61/PI103 cotreatment initiate activation of the caspase cascade via apoptosome-mediated cleavage of the initiator caspase-9, as indicated by changes in the cleavage pattern of caspases (e.g. accumulation of the caspase-9 p35 cleavage fragment) upon addition of the caspase inhibitor zVAD.fmk. Thus, combined GLI1/2 and PI3K/mTOR inhibition represents a promising novel approach for synergistic apoptosis induction and tumor growth reduction with implications for new treatment strategies in RMS."],["dc.identifier.doi","10.18632/oncotarget.2726"],["dc.identifier.fs","613066"],["dc.identifier.pmid","25749378"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13615"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58714"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1949-2553"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.subject.mesh","Amino Acid Chloromethyl Ketones"],["dc.subject.mesh","Animals"],["dc.subject.mesh","Apoptosis"],["dc.subject.mesh","Apoptosis Regulatory Proteins"],["dc.subject.mesh","Caspases"],["dc.subject.mesh","Cell Line, Tumor"],["dc.subject.mesh","Chick Embryo"],["dc.subject.mesh","Drug Screening Assays, Antitumor"],["dc.subject.mesh","Drug Synergism"],["dc.subject.mesh","Furans"],["dc.subject.mesh","Gene Expression Regulation, Neoplastic"],["dc.subject.mesh","Hedgehog Proteins"],["dc.subject.mesh","Humans"],["dc.subject.mesh","Kruppel-Like Transcription Factors"],["dc.subject.mesh","Molecular Targeted Therapy"],["dc.subject.mesh","Neoplasm Proteins"],["dc.subject.mesh","Nuclear Proteins"],["dc.subject.mesh","Phosphatidylinositol 3-Kinases"],["dc.subject.mesh","Protein Kinase Inhibitors"],["dc.subject.mesh","Proto-Oncogene Proteins c-akt"],["dc.subject.mesh","Pyridines"],["dc.subject.mesh","Pyrimidines"],["dc.subject.mesh","Rhabdomyosarcoma, Alveolar"],["dc.subject.mesh","Rhabdomyosarcoma, Embryonal"],["dc.subject.mesh","Signal Transduction"],["dc.subject.mesh","TOR Serine-Threonine Kinases"],["dc.subject.mesh","Transcription Factors"],["dc.title","Identification of a novel synthetic lethality of combined inhibition of hedgehog and PI3K signaling in rhabdomyosarcoma."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Pediatrics"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Ragab, Nada"],["dc.contributor.author","Viehweger, Florian"],["dc.contributor.author","Bauer, Julia"],["dc.contributor.author","Geyer, Natalie"],["dc.contributor.author","Yang, Mingya"],["dc.contributor.author","Seils, Anna"],["dc.contributor.author","Belharazem, Djeda"],["dc.contributor.author","Brembeck, Felix H."],["dc.contributor.author","Schildhaus, Hans-Ulrich"],["dc.contributor.author","Marx, Alexander"],["dc.contributor.author","Hahn, Heidi"],["dc.contributor.author","Simon-Keller, Katja"],["dc.date.accessioned","2020-12-10T18:44:36Z"],["dc.date.available","2020-12-10T18:44:36Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.3389/fped.2018.00378"],["dc.identifier.eissn","2296-2360"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78522"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Canonical WNT/β-Catenin Signaling Plays a Subordinate Role in Rhabdomyosarcomas"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1567"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","International Journal of Oncology"],["dc.bibliographiccitation.lastpage","1575"],["dc.bibliographiccitation.volume","27"],["dc.contributor.author","Uhmann, Anja"],["dc.contributor.author","Ferch, U."],["dc.contributor.author","Bauer, R."],["dc.contributor.author","Tauber, S."],["dc.contributor.author","Arziman, Z."],["dc.contributor.author","Chen, C."],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.contributor.author","Wojnowski, Leszek"],["dc.contributor.author","Hahn, H."],["dc.date.accessioned","2018-11-07T10:53:52Z"],["dc.date.available","2018-11-07T10:53:52Z"],["dc.date.issued","2005"],["dc.description.abstract","Mutations of the Sonic hedgehog (SHH) receptor, Patched I (PITCH I), have been identified in a variety of tumors. PTCH1 is usually considered to be a tumor suppressor gene. However, one normal allele is retained in many tumors. We investigated the mechanism of tumorigenesis in murine heterozygous Ptch1 knock-out mice. Here we show that Ptch1 transcripts, which are consistently overexpressed in tumors in these mice, are derived predominantly from the mutated allele. These transcripts give rise to a mutant protein incapable of pathway inhibition. In contrast, the expression of wild-type transcripts in the tumor is reduced. The transcriptional activity of a Ptch1 promoter is sensitive to methylation. Based on these results, we propose a model, in which tumorigenesis begins with the transcriptional silencing of one PTCH1/Ptch1 allele. This alone has no functional consequences. Upon mutational inactivation of the other allele, the resulting loss of PTCH1/Ptch1 function activates PTCH1/Ptch1 transcription from the non-silenced, i.e. the mutant, allele. These events can occur in an opposite order. This model is consistent with the expression of PTCH1/Ptch1-derived transcripts and proteins found in tumors, with the sensitivity of the murine Ptch1 promoter to methylation, and with the recently reported effect of demethylating agents on Ptch1 expression. These latter agents could be effective in treatment of, at least, some tumors associated with loss of PTCH1 function."],["dc.identifier.isi","000233575100014"],["dc.identifier.pmid","16273213"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49440"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Professor D A Spandidos"],["dc.relation.issn","1019-6439"],["dc.title","A model for PTCH1/Ptch1-associated tumors comprising mutational inactivation and gene silencing"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","7580"],["dc.bibliographiccitation.issue","49"],["dc.bibliographiccitation.journal","Oncogene"],["dc.bibliographiccitation.lastpage","7584"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Pazzaglia, S."],["dc.contributor.author","Mancuso, M."],["dc.contributor.author","Atkinson, M. J."],["dc.contributor.author","Tanori, M."],["dc.contributor.author","Rebessi, S."],["dc.contributor.author","Di Majo, V."],["dc.contributor.author","Covelli, V."],["dc.contributor.author","Hahn, H."],["dc.contributor.author","Saran, A."],["dc.date.accessioned","2018-11-07T09:55:05Z"],["dc.date.available","2018-11-07T09:55:05Z"],["dc.date.issued","2002"],["dc.description.abstract","Individuals affected with the Gorlin syndrome inherit a germ-line mutation of the patched (Ptc1) developmental gene and, analogously to Ptc1 heterozygous mice, show an increased susceptibility to spontaneous tumor development. Human and mouse Ptc1 heterozygotes (Ptc1(+/-)) are also hypersensitive to ionizing radiation (IR)-induced tumorigenesis in terms of basal cell carcinoma (BCC) induction. We have analysed the involvement of Ptc1 in the tumorigenic response to a single dose of 3 Gy X-rays in neonatal and adult Ptc1 heterozygous and wild type mice. We report that irradiation dramatically increased the incidence of medulloblastoma development (51%) over the spontaneous rate (7%) in neonatal but not adult Ptc1 heterozygotes, indicating that medulloblastoma induction by IR is subjected to temporal restriction. Analysis of Ptc1 allele status in the tumors revealed loss of the wild type allele in 17 of 18 medulloblastomas from irradiated mice and in two of three spontaneous medulloblastomas. To our knowledge, irradiated newborn Ptc1(+/-) heterozygous mice constitute the first mouse model of IR-induced medulloblastoma tumorigenesis, providing a useful tool to elucidate the molecular basis of medulloblastoma development."],["dc.identifier.doi","10.1038/sj.onc.1205973"],["dc.identifier.isi","000178618200013"],["dc.identifier.pmid","12386820"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36675"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","0950-9232"],["dc.title","High incidence of medulloblastoma following X-ray-irradiation of newborn Ptc1 heterozygous mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","218"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Laboratory Animals"],["dc.bibliographiccitation.lastpage","228"],["dc.bibliographiccitation.volume","41"],["dc.contributor.author","Nitzki, F."],["dc.contributor.author","Kruger, A."],["dc.contributor.author","Reifenberg, Kurt"],["dc.contributor.author","Wojnowski, Leszek"],["dc.contributor.author","Hahn, H."],["dc.date.accessioned","2018-11-07T11:03:44Z"],["dc.date.available","2018-11-07T11:03:44Z"],["dc.date.issued","2007"],["dc.description.abstract","Rapid detection of genetic contamination is critical in mouse studies involving inbred strains. During a Quantitative Trait Locus (QTL) study using simple sequence length polymorphism (SSLP) markers, we noticed heterozygosity at some loci of a commercially available inbred C57BL/6N mouse strain, suggesting a contamination by another mouse strain. A panel of 100 single-nucleotide polymorphism (SNP) markers was used to confirm and specify the genetic contamination suspected. Retrospective analyses demonstrated that the contamination took place as early as autumn 2003 and has persisted ever since at a fairly constant level. Contaminating alleles most probably originated from a DBA strain. Our data demonstrate the suitability of SNP markers for rapid detection and identification of the source of genetic contamination. Further, our results show the importance of a state-of-the art genetic monitoring of the authenticity of murine inbred strains."],["dc.identifier.doi","10.1258/002367707780378104"],["dc.identifier.isi","000246017100007"],["dc.identifier.pmid","17430621"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51677"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Royal Soc Medicine Press Ltd"],["dc.relation.issn","0023-6772"],["dc.title","Identification of a genetic contamination in a commercial mouse strain using two panels of polymorphic markers"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Pediatric Blood & Cancer"],["dc.bibliographiccitation.volume","63"],["dc.contributor.author","Kofler, B."],["dc.contributor.author","Feichtinger, R. G."],["dc.contributor.author","Vidali, S."],["dc.contributor.author","Hauser-Kronberger, C."],["dc.contributor.author","Ridzewski, Rosalie"],["dc.contributor.author","Hahn, H."],["dc.date.accessioned","2018-11-07T10:06:09Z"],["dc.date.available","2018-11-07T10:06:09Z"],["dc.date.issued","2016"],["dc.format.extent","S261"],["dc.identifier.isi","000384818801540"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39034"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.issn","1545-5017"],["dc.relation.issn","1545-5009"],["dc.title","Alterations of the Oxidative Phosphorylation Complexes in Rhabdomyosarcomas"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]