Hahn, Heidi Eva

[["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.artnumber","e93555"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Koenig, Simone"],["dc.contributor.author","Nitzki, Frauke"],["dc.contributor.author","Uhmann, Anja"],["dc.contributor.author","Dittmann, Kai"],["dc.contributor.author","Theiss-Suennemann, Jennifer"],["dc.contributor.author","Herrmann, Markus"],["dc.contributor.author","Reichardt, Holger Michael"],["dc.contributor.author","Schwendener, Reto"],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Hahn, Heidi"],["dc.date.accessioned","2018-11-07T09:41:53Z"],["dc.date.available","2018-11-07T09:41:53Z"],["dc.date.issued","2014"],["dc.description.abstract","Basal cell carcinoma (BCC) belongs to the group of non-melanoma skin tumors and is the most common tumor in the western world. BCC arises due to mutations in the tumor suppressor gene Patched1 (Ptch). Analysis of the conditional Ptch knockout mouse model for BCC reveals that macrophages and dendritic cells (DC) of the skin play an important role in BCC growth restraining processes. This is based on the observation that a clodronate-liposome mediated depletion of these cells in the tumor-bearing skin results in significant BCC enlargement. The depletion of these cells does not modulate Ki67 or K10 expression, but is accompanied by a decrease in collagen-producing cells in the tumor stroma. Together, the data suggest that cutaneous macrophages and DC in the tumor microenvironment exert an antitumor effect on BCC."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft [FOR942 HA 2197/5-2]"],["dc.identifier.doi","10.1371/journal.pone.0093555"],["dc.identifier.isi","000334101100104"],["dc.identifier.pmid","24691432"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10067"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33833"],["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","Depletion of Cutaneous Macrophages and Dendritic Cells Promotes Growth of Basal Cell Carcinoma in Mice"],["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","341"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Genetics in Medicine"],["dc.bibliographiccitation.lastpage","351"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Schröder, Simone"],["dc.contributor.author","Li, Yun"],["dc.contributor.author","Yigit, Gökhan"],["dc.contributor.author","Altmüller, Janine"],["dc.contributor.author","Bader, Ingrid"],["dc.contributor.author","Bevot, Andrea"],["dc.contributor.author","Biskup, Saskia"],["dc.contributor.author","Dreha-Kulaczewski, Steffi"],["dc.contributor.author","Christoph Korenke, G."],["dc.contributor.author","Kottke, Raimund"],["dc.contributor.author","Mayr, Johannes A."],["dc.contributor.author","Preisel, Martin"],["dc.contributor.author","Toelle, Sandra P."],["dc.contributor.author","Wente-Schulz, Sarah"],["dc.contributor.author","Wortmann, Saskia B."],["dc.contributor.author","Hahn, Heidi"],["dc.contributor.author","Boltshauser, Eugen"],["dc.contributor.author","Uhmann, Anja"],["dc.contributor.author","Wollnik, Bernd"],["dc.contributor.author","Brockmann, Knut"],["dc.date.accessioned","2021-04-14T08:31:50Z"],["dc.date.available","2021-04-14T08:31:50Z"],["dc.date.issued","2020"],["dc.description.abstract","Purpose\r\n\r\nThis study aimed to delineate the genetic basis of congenital ocular motor apraxia (COMA) in patients not otherwise classifiable.\r\nMethods\r\n\r\nWe compiled clinical and neuroimaging data of individuals from six unrelated families with distinct clinical features of COMA who do not share common diagnostic characteristics of Joubert syndrome or other known genetic conditions associated with COMA. We used exome sequencing to identify pathogenic variants and functional studies in patient-derived fibroblasts.\r\nResults\r\n\r\nIn 15 individuals, we detected familial as well as de novo heterozygous truncating causative variants in the Suppressor of Fused (SUFU) gene, a negative regulator of the Hedgehog (HH) signaling pathway. Functional studies showed no differences in cilia occurrence, morphology, or localization of ciliary proteins, such as smoothened. However, analysis of expression of HH signaling target genes detected a significant increase in the general signaling activity in COMA patient–derived fibroblasts compared with control cells. We observed higher basal HH signaling activity resulting in increased basal expression levels of GLI1, GLI2, GLI3, and Patched1. Neuroimaging revealed subtle cerebellar changes, but no full-blown molar tooth sign.\r\nConclusion\r\n\r\nTaken together, our data imply that the clinical phenotype associated with heterozygous truncating germline variants in SUFU is a forme fruste of Joubert syndrome."],["dc.identifier.doi","10.1038/s41436-020-00979-w"],["dc.identifier.pmid","33024317"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83726"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/80"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation.eissn","1530-0366"],["dc.relation.issn","1098-3600"],["dc.relation.workinggroup","RG Wollnik"],["dc.rights","CC BY 4.0"],["dc.title","Heterozygous truncating variants in SUFU cause congenital ocular motor apraxia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","The Journal of Immunology"],["dc.bibliographiccitation.volume","183"],["dc.contributor.author","Uhmann, Anja"],["dc.contributor.author","Dittmann, Kai"],["dc.contributor.author","Wienands, Juergen"],["dc.contributor.author","Hahn, Heidi"],["dc.date.accessioned","2018-11-07T11:25:03Z"],["dc.date.available","2018-11-07T11:25:03Z"],["dc.date.issued","2009"],["dc.format.extent","2891"],["dc.identifier.doi","10.4049/jimmunol.0990063"],["dc.identifier.isi","000269391400001"],["dc.identifier.pmid","19696426"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56544"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Immunologists"],["dc.relation.issn","0022-1767"],["dc.title","Comment on \"Direct Hematological Toxicity and Illegitimate Chromosomal Recombination Caused by the Systemic Activation of CreER(T2)\""],["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"]]

[["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","European Journal of Gastroenterology & Hepatology"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","van Dop, Willemijn A."],["dc.contributor.author","Uhmann, Anja"],["dc.contributor.author","Wijgerde, Mark"],["dc.contributor.author","Offerhaus, G. Johan A."],["dc.contributor.author","Boeckxstaens, Guy E."],["dc.contributor.author","Weerman, Marius A. van den Bergh"],["dc.contributor.author","Hommes, Daan W."],["dc.contributor.author","Hardwick, J. C."],["dc.contributor.author","Hahn, H."],["dc.contributor.author","van den Brink, Gijs R."],["dc.date.accessioned","2018-11-07T11:13:23Z"],["dc.date.available","2018-11-07T11:13:23Z"],["dc.date.issued","2008"],["dc.format.extent","A73"],["dc.identifier.isi","000257620600200"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53879"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.issn","0954-691X"],["dc.title","Depletion of the colonic stem cell compartment upon conditional activation of the Hedgehog pathway"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","348"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Gut"],["dc.bibliographiccitation.lastpage","357"],["dc.bibliographiccitation.volume","62"],["dc.contributor.author","van Dop, Willemijn A."],["dc.contributor.author","Rosekrans, Sanne L."],["dc.contributor.author","Uhmann, Anja"],["dc.contributor.author","Jaks, Viljar"],["dc.contributor.author","Offerhaus, G. Johan A."],["dc.contributor.author","Weerman, Marius A. van den Bergh"],["dc.contributor.author","Kasper, Maria"],["dc.contributor.author","Heijmans, Jarom"],["dc.contributor.author","Hardwick, James C. H."],["dc.contributor.author","Verspaget, Hein W."],["dc.contributor.author","Hommes, Daan W."],["dc.contributor.author","Toftgard, Rune"],["dc.contributor.author","Hahn, Heidi"],["dc.contributor.author","van den Brink, Gijs R."],["dc.date.accessioned","2018-11-07T09:27:54Z"],["dc.date.available","2018-11-07T09:27:54Z"],["dc.date.issued","2013"],["dc.description.abstract","Objective In the intestine Hedgehog (Hh) signalling is directed from epithelium to mesenchyme and negatively regulates epithelial precursor cell fate. The role of Hh signalling in the oesophagus has not been studied in vivo. Here the authors examined the role of Hh signalling in epithelial homeostasis of oesophagus. Design The authors used transgenic mice in which the Hh receptor Patched1 (Ptch1) could be conditionally inactivated in a body-wide manner and mice in which Gli1 could be induced specifically in the epithelium of the skin and oesophagus. Effects on epithelial homeostasis of the oesophagus were examined using immunohistochemistry, in situ hybridisation, transmission electron microscopy and real-time PCR. Hh signalling was examined in patients with oesophageal squamous cell carcinoma (SCC) by quantitative real-time PCR. Results Sonic Hh is signalled in an autocrine manner in the basal layer of the oesophagus. Activation of Hh signalling resulted in an expansion of the epithelial precursor cell compartment and failure of epithelial maturation and migration. Levels of Hh targets GLI1, HHIP and PTCH1 were increased in SCC compared with normal tissue from the same patients. Conclusion Here the authors find that Hh signalling positively regulates the precursor cell compartment in the oesophageal epithelium in an autocrine manner. Since Hh signalling targets precursor cells in the oesophageal epithelium and signalling is increased in SCCs, Hh signalling may be involved in oesophageal SCC formation."],["dc.identifier.doi","10.1136/gutjnl-2011-301141"],["dc.identifier.isi","000314631900004"],["dc.identifier.pmid","22504664"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30651"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Bmj Publishing Group"],["dc.relation.issn","0017-5749"],["dc.title","Hedgehog signalling stimulates precursor cell accumulation and impairs epithelial maturation in the murine oesophagus"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","19614"],["dc.bibliographiccitation.issue","32"],["dc.bibliographiccitation.journal","Journal of Biological Chemistry"],["dc.bibliographiccitation.lastpage","19628"],["dc.bibliographiccitation.volume","290"],["dc.contributor.author","Linder, Benedikt"],["dc.contributor.author","Weber, Susanne"],["dc.contributor.author","Dittmann, Kai"],["dc.contributor.author","Adamski, Jerzy"],["dc.contributor.author","Hahn, Heidi"],["dc.contributor.author","Uhmann, Anja"],["dc.date.accessioned","2018-11-07T09:53:20Z"],["dc.date.available","2018-11-07T09:53:20Z"],["dc.date.issued","2015"],["dc.description.abstract","The Patched1 (Ptch)-mediated inhibition of Smoothened (Smo) is still an open question. However, a direct Ptch/Smo interaction has been excluded, Smo modulators were identified, but the endogenous signal transmitting molecule remains undiscovered. Here, we demonstrate that calcitriol, the hormonally active form of vitamin D-3, is an excellent candidate for transmission of Ptch/Smo interaction. Our study reveals that Ptch expression is sufficient to release calcitriol from the cell and that calcitriol inhibits Smo action and ciliary translocation by acting on a site distinct from the 7-transmembrane domain or the cysteine-rich domain. Moreover calcitriol strongly synergizes with itraconazole (ITZ) in Smo inhibition, which did not result from elevated calcitriol bioavailability due to ITZ-mediated 24-hydroxylase inhibition but rather from a direct interaction of the compounds at the level of Smo. Together, we suggest that calcitriol represents a possible endogenous transmitter of Ptch/Smo interaction. Moreover calcitriol or calcitriol derivatives combined with ITZ might be a treatment option of Hedgehog-associated cancers."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft [UH 228/2-1, UH228/2-2]"],["dc.identifier.doi","10.1074/jbc.M115.646141"],["dc.identifier.isi","000359364600023"],["dc.identifier.pmid","26126827"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36311"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Biochemistry Molecular Biology Inc"],["dc.relation.issn","1083-351X"],["dc.relation.issn","0021-9258"],["dc.title","A Functional and Putative Physiological Role of Calcitriol in Patched1/Smoothened Interaction"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","47"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Klinische Pädiatrie"],["dc.bibliographiccitation.lastpage","48"],["dc.bibliographiccitation.volume","223"],["dc.contributor.author","Hahn, H."],["dc.contributor.author","Nitzki, F."],["dc.contributor.author","Zibat, Arne"],["dc.contributor.author","Uhmann, Anja"],["dc.contributor.author","Ecke, I."],["dc.contributor.author","Rosenberger, Albert"],["dc.contributor.author","Witt, Olaf"],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.date.accessioned","2018-11-07T09:00:30Z"],["dc.date.available","2018-11-07T09:00:30Z"],["dc.date.issued","2011"],["dc.identifier.doi","10.1055/s-0030-1270305"],["dc.identifier.isi","000287627100024"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24177"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Georg Thieme Verlag Kg"],["dc.publisher.place","Stuttgart"],["dc.relation.issn","0300-8630"],["dc.title","Hedgehog Signaling: A Therapeutic Target in Embryonal Rhabdomyosarcoma?"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","International Journal of Oncology"],["dc.bibliographiccitation.volume","61"],["dc.contributor.author","Ragab, Nada"],["dc.contributor.author","Bauer, Julia"],["dc.contributor.author","Uhmann, Anja"],["dc.contributor.author","Marx, Alexander"],["dc.contributor.author","Hahn, Heidi"],["dc.contributor.author","Simon-Keller, Katja"],["dc.date.accessioned","2022-09-01T09:51:17Z"],["dc.date.available","2022-09-01T09:51:17Z"],["dc.date.issued","2022"],["dc.identifier.doi","10.3892/ijo.2022.5392"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/113925"],["dc.notes.intern","DOI-Import GROB-597"],["dc.relation.eissn","1791-2423"],["dc.relation.issn","1019-6439"],["dc.title","Tumor suppressive functions of WNT5A in rhabdomyosarcoma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","9295"],["dc.bibliographiccitation.issue","23"],["dc.bibliographiccitation.journal","International Journal of Molecular Sciences"],["dc.bibliographiccitation.volume","21"],["dc.contributor.affiliation","Brandes, Nadine; \t\t \r\n\t\t Tumor Genetics Group, Institute of Human Genetics, University Medical Center Göttingen, Heinrich-Düker-Weg 12, 37079 Göttingen, Germany, nadine.brandes@med.uni-goettingen.de"],["dc.contributor.affiliation","Mitkovska, Slavica Hristomanova; \t\t \r\n\t\t Tumor Genetics Group, Institute of Human Genetics, University Medical Center Göttingen, Heinrich-Düker-Weg 12, 37079 Göttingen, Germany, s.hristomanovamitk@stud.uni-goettingen.de"],["dc.contributor.affiliation","Botermann, Dominik Simon; \t\t \r\n\t\t Tumor Genetics Group, Institute of Human Genetics, University Medical Center Göttingen, Heinrich-Düker-Weg 12, 37079 Göttingen, Germany, dominik.botermann@med.uni-goettingen.de"],["dc.contributor.affiliation","Maurer, Wiebke; \t\t \r\n\t\t Tumor Genetics Group, Institute of Human Genetics, University Medical Center Göttingen, Heinrich-Düker-Weg 12, 37079 Göttingen, Germany, wiebke.maurer@stud.uni-goettingen.de"],["dc.contributor.affiliation","Müllen, Anna; \t\t \r\n\t\t Tumor Genetics Group, Institute of Human Genetics, University Medical Center Göttingen, Heinrich-Düker-Weg 12, 37079 Göttingen, Germany, anna.muellen@stud.uni-goettingen.de"],["dc.contributor.affiliation","Scheile, Hanna; \t\t \r\n\t\t Tumor Genetics Group, Institute of Human Genetics, University Medical Center Göttingen, Heinrich-Düker-Weg 12, 37079 Göttingen, Germany, hannarabe@gmx.de"],["dc.contributor.affiliation","Zabel, Sebastian; \t\t \r\n\t\t Tumor Genetics Group, Institute of Human Genetics, University Medical Center Göttingen, Heinrich-Düker-Weg 12, 37079 Göttingen, Germany, sebastian.zabel@live.de"],["dc.contributor.affiliation","Frommhold, Anke; \t\t \r\n\t\t Tumor Genetics Group, Institute of Human Genetics, University Medical Center Göttingen, Heinrich-Düker-Weg 12, 37079 Göttingen, Germany, anke.frommhold@med.uni-goettingen.de"],["dc.contributor.affiliation","Heß, Ina; \t\t \r\n\t\t Tumor Genetics Group, Institute of Human Genetics, University Medical Center Göttingen, Heinrich-Düker-Weg 12, 37079 Göttingen, Germany, ihess@gwdg.de"],["dc.contributor.affiliation","Hahn, Heidi; \t\t \r\n\t\t Tumor Genetics Group, Institute of Human Genetics, University Medical Center Göttingen, Heinrich-Düker-Weg 12, 37079 Göttingen, Germany, hhahn@gwdg.de"],["dc.contributor.affiliation","Uhmann, Anja; \t\t \r\n\t\t Tumor Genetics Group, Institute of Human Genetics, University Medical Center Göttingen, Heinrich-Düker-Weg 12, 37079 Göttingen, Germany, auhmann@gwdg.de"],["dc.contributor.author","Brandes, Nadine"],["dc.contributor.author","Mitkovska, Slavica Hristomanova"],["dc.contributor.author","Botermann, Dominik Simon"],["dc.contributor.author","Maurer, Wiebke"],["dc.contributor.author","Müllen, Anna"],["dc.contributor.author","Scheile, Hanna"],["dc.contributor.author","Zabel, Sebastian"],["dc.contributor.author","Frommhold, Anke"],["dc.contributor.author","Heß, Ina"],["dc.contributor.author","Hahn, Heidi"],["dc.contributor.author","Uhmann, Anja"],["dc.date.accessioned","2021-04-14T08:24:51Z"],["dc.date.available","2021-04-14T08:24:51Z"],["dc.date.issued","2020"],["dc.date.updated","2022-09-06T08:37:10Z"],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft"],["dc.identifier.doi","10.3390/ijms21239295"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81445"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1422-0067"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Spreading of Isolated Ptch Mutant Basal Cell Carcinoma Precursors Is Physiologically Suppressed and Counteracts Tumor Formation in Mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]