Kaulfuß, Silke

[["dc.bibliographiccitation.firstpage","593"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Histopathology"],["dc.bibliographiccitation.lastpage","606"],["dc.bibliographiccitation.volume","78"],["dc.contributor.author","Fichtner, Alexander"],["dc.contributor.author","Richter, Annika"],["dc.contributor.author","Filmar, Simon"],["dc.contributor.author","Gaisa, Nadine T"],["dc.contributor.author","Schweyer, Stefan"],["dc.contributor.author","Reis, Henning"],["dc.contributor.author","Nettersheim, Daniel"],["dc.contributor.author","Oing, Christoph"],["dc.contributor.author","Gayer, Fabian A"],["dc.contributor.author","Leha, Andreas"],["dc.contributor.author","Küffer, Stefan"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Kaulfuß, Silke"],["dc.contributor.author","Bremmer, Felix"],["dc.date.accessioned","2021-04-14T08:23:39Z"],["dc.date.available","2021-04-14T08:23:39Z"],["dc.date.issued","2020"],["dc.description.abstract","Aims Malignant germ cell tumours (GCTs) of the testis are rare neoplasms, but the most common solid malignancies in young men. World Health Organization guidelines divide GCTs into five types, for which numerous immunohistochemical markers allow exact histological subtyping in the majority of cases. In contrast, a germ cell origin is often hard to prove in metastatic GCTs that have developed so‐called somatic malignant transformation. A high percentage, up to 89%, of GCTs are characterised by the appearance of isochromosome 12p [i(12p)]. Fluorescence in‐situ hybridisation has been the most common diagnostic method for the detection of i(12p) so far, but has the disadvantages of being time‐consuming, demanding, and not being a stand‐alone method. The aim of the present study was to establish a quantitative real‐time polymerase chain reaction assay as an independent method for detecting i(12p) and regional amplifications of the short arm of chromosome 12 by using DNA extracted from formalin‐fixed paraffin‐embedded tissue. Methods and results A cut‐off value to distinguish between the presence and absence of i(12p) was established in a control set consisting of 36 tumour‐free samples. In a training set of 149 GCT samples, i(12p) was detectable in 133 tumours (89%), but not in 16 tumours (11%). In a test set containing 27 primary and metastatic GCTs, all 16 tumours with metastatic spread and/or somatic malignant transformation were successfully identified by the detection of i(12p). Conclusion In summary, the qPCR assay presented here can help to identify, further characterise and assign a large proportion of histologically inconclusive malignancies to a GCT origin."],["dc.description.sponsorship","Wilhelm Sander‐Stiftung http://dx.doi.org/10.13039/100008672"],["dc.identifier.doi","10.1111/his.14258"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81003"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1365-2559"],["dc.relation.issn","0309-0167"],["dc.rights","This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited."],["dc.title","The detection of isochromosome i(12p) in malignant germ cell tumours and tumours with somatic malignant transformation by the use of quantitative real‐time polymerase chain reaction"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","34971"],["dc.bibliographiccitation.issue","21"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","34979"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Gehrig, Julia"],["dc.contributor.author","Kaulfuss, Silke"],["dc.contributor.author","Jarry, Hubertus"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Stettner, Mark"],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","Thelen, Paul"],["dc.date.accessioned","2018-11-07T10:23:41Z"],["dc.date.available","2018-11-07T10:23:41Z"],["dc.date.issued","2017"],["dc.description.abstract","Advanced prostate cancer can develop into castration-resistant prostate cancer (CRPC). This process is mediated either by intratumoral ligand synthesis or by mutations or aberrations of the androgen receptor (AR) or its cofactors. To date, no curative therapy for CRPC is available, as AR-targeted therapies eventually result in the development of resistance. The human prostate cancer cell line VCaP (vertebral cancer of the prostate) overexpresses AR and its splice variants (ARVs) as a mechanism of resistance to androgen-deprivation therapy (ADT) of external and intratumoral origin. In the present study, we demonstrate that stimulating estrogen receptor beta activity with the specific agonist 8 beta-VE2 in VCaP cells in successive stages of ADT induced a time-and dose-dependent decrease in cell survival and an increase in apoptosis. Furthermore, 8 beta-VE2 treatment reduced the overexpression of the AR as well as ARVs in VCaP cells under maximum ADT. Our results indicate that decreased survival of the androgen-dependent CRPC cells employing apoptosis together with the regulative effect on AR expression could have beneficial effects over current AR-targeting therapies."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2017"],["dc.identifier.doi","10.18632/oncotarget.16496"],["dc.identifier.isi","000402051700085"],["dc.identifier.pmid","28380417"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14426"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42509"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Impact Journals Llc"],["dc.relation.issn","1949-2553"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.title","Prospects of estrogen receptor beta activation in the treatment of castration-resistant prostate 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.firstpage","93"],["dc.bibliographiccitation.journal","Cancer Letters"],["dc.bibliographiccitation.lastpage","105"],["dc.bibliographiccitation.volume","407"],["dc.contributor.author","Oberthür, Rabea"],["dc.contributor.author","Seemann, Henning"],["dc.contributor.author","Gehrig, Julia"],["dc.contributor.author","Rave-Fränk, Margret"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Halpape, Rovena"],["dc.contributor.author","Conradi, Lena-Christin"],["dc.contributor.author","Scharf, Jens-Gerd"],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","Kaulfuß, Silke"],["dc.date.accessioned","2020-12-10T14:22:49Z"],["dc.date.available","2020-12-10T14:22:49Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1016/j.canlet.2017.08.009"],["dc.identifier.issn","0304-3835"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/71746"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Simultaneous inhibition of IGF1R and EGFR enhances the efficacy of standard treatment for colorectal cancer by the impairment of DNA repair and the induction of cell death"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1115"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Carcinogenesis"],["dc.bibliographiccitation.lastpage","1124"],["dc.bibliographiccitation.volume","34"],["dc.contributor.author","Witt, Daria"],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","von Hardenberg, Sandra"],["dc.contributor.author","Opitz, Lennart"],["dc.contributor.author","Salinas-Riester, Gabriela"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Schweyer, Stefan"],["dc.contributor.author","Thelen, Paul"],["dc.contributor.author","Neesen, Juergen"],["dc.contributor.author","Kaulfuss, Silke"],["dc.date.accessioned","2018-11-07T09:25:10Z"],["dc.date.available","2018-11-07T09:25:10Z"],["dc.date.issued","2013"],["dc.description.abstract","In this study, primary murine prostate cancer (PCa) cells were derived using the well-established TRAMP model. These PCa cells were treated with the histone deacetylase inhibitor, valproic acid (VPA), and we demonstrated that VPA treatment has an antimigrative, antiinvasive and antiproliferative effect on PCa cells. Using microarray analyses, we discovered several candidate genes that could contribute to the cellular effects we observed. In this study, we could demonstrate that VPA treatment of PCa cells causes the re-expression of cyclin D2, a known regulator that is frequently lost in PCa as we could show using immunohistochemical analyses on PCa specimens. We demonstrate that VPA specifically induces the re-expression of cyclin D2, one of the highly conserved D-type cyclin family members, in several cancer cell lines with weak or no cyclin D2 expression. Interestingly, VPA treatment had no effect in fibroblasts, which typically have high basal levels of cyclin D2 expression. The re-expression of cyclin D2 observed in PCa cells is activated by increased histone acetylation in the promoter region of the Ccnd2 gene and represents one underlying molecular mechanism of VPA treatment that inhibits the proliferation of cancer cells. Altogether, our results confirm that VPA is an anticancer therapeutic drug for the treatment of tumors with epigenetically repressed cyclin D2 expression."],["dc.identifier.doi","10.1093/carcin/bgt019"],["dc.identifier.isi","000318646000021"],["dc.identifier.pmid","23349020"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30001"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0143-3334"],["dc.title","Valproic acid inhibits the proliferation of cancer cells by re-expressing cyclin D2"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","13591"],["dc.bibliographiccitation.issue","15"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","13606"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Dierks, Sascha"],["dc.contributor.author","von Hardenberg, Sandra"],["dc.contributor.author","Schmidt, Thomas"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","Kaulfuß, Silke"],["dc.date.accessioned","2021-11-22T14:31:34Z"],["dc.date.available","2021-11-22T14:31:34Z"],["dc.date.issued","2015-05-30"],["dc.description.abstract","The focal adhesion protein leupaxin (LPXN) is overexpressed in a subset of prostate cancers (PCa) and is involved in the progression of PCa. In the present study, we analyzed the LPXN-mediated adhesive and cytoskeletal changes during PCa progression. We identified an interaction between the actin-binding protein caldesmon (CaD) and LPXN and this interaction is increased during PCa cell migration. Furthermore, knockdown of LPXN did not affect CaD expression but reduced CaD phosphorylation. This is known to destabilize the affinity of CaD to F-actin, leading to dynamic cell structures that enable cell motility. Thus, downregulation of CaD increased migration and invasion of PCa cells. To identify the kinase responsible for the LPXN-mediated phosphorylation of CaD, we used data from an antibody array, which showed decreased expression of TGF-beta-activated kinase 1 (TAK1) after LPXN knockdown in PC-3 PCa cells. Subsequent analyses of the downstream kinases revealed the extracellular signal-regulated kinase (ERK) as an interaction partner of LPXN that facilitates CaD phosphorylation during LPXN-mediated PCa cell migration. In conclusion, we demonstrate that LPXN directly influences cytoskeletal dynamics via interaction with the actin-binding protein CaD and regulates CaD phosphorylation by recruiting ERK to highly dynamic structures within PCa cells."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft [KA2946/1-1, KA2946/1-2]"],["dc.identifier.doi","10.18632/oncotarget.3792"],["dc.identifier.fs","613073"],["dc.identifier.isi","000359009400054"],["dc.identifier.pmid","26079947"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13616"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/93389"],["dc.language","eng"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Impact Journals Llc"],["dc.relation.issn","1949-2553"],["dc.rights","CC BY 3.0"],["dc.rights.access","openAccess"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.subject","prostate cancer, leupaxin, caldesmon, migration"],["dc.subject.mesh","Actins"],["dc.subject.mesh","Calmodulin-Binding Proteins"],["dc.subject.mesh","Cell Adhesion"],["dc.subject.mesh","Cell Adhesion Molecules"],["dc.subject.mesh","Cell Line, Tumor"],["dc.subject.mesh","Cell Movement"],["dc.subject.mesh","Disease Progression"],["dc.subject.mesh","Gene Knockdown Techniques"],["dc.subject.mesh","Humans"],["dc.subject.mesh","Male"],["dc.subject.mesh","Mitogen-Activated Protein Kinase 1"],["dc.subject.mesh","Mitogen-Activated Protein Kinase 3"],["dc.subject.mesh","Phosphoproteins"],["dc.subject.mesh","Phosphorylation"],["dc.subject.mesh","Prostatic Neoplasms"],["dc.subject.mesh","Signal Transduction"],["dc.subject.mesh","Transfection"],["dc.title","Leupaxin stimulates adhesion and migration of prostate cancer cells through modulation of the phosphorylation status of the actin-binding protein caldesmon."],["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","16951"],["dc.bibliographiccitation.issue","24"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","16961"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Jarry, Hubertus"],["dc.contributor.author","Unterkircher, Valerie"],["dc.contributor.author","Kaulfuss, Silke"],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","Radzun, Heinz-Joachim"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Thelen, Paul"],["dc.date.accessioned","2019-07-09T11:45:18Z"],["dc.date.available","2019-07-09T11:45:18Z"],["dc.date.issued","2018"],["dc.description.abstract","Novel treatments for castration-resistant prostate cancer (CRPC) such as abiraterone acetate (AA) or enzalutamide effectively target the androgen pathway to arrest aberrant signalling and cell proliferation. Testosterone is able to inhibit tumour cell growth in CRPC. Estrogen receptor-beta (ERβ) binds the testosteronemetabolites 3β-androstanediol and 3α-androstanediol in parallel to the canonical estradiol. In the prostate it is widely accepted that ERβ regulates estrogen signalling, mediating anti-proliferative effects. We used the prostate cancer cell lines LNCaP, PC-3, VCaP, and the non-neoplastic BPH-1. VCaP cells were treated with 1 nmol/L testosterone over 20 passages, yielding the cell line VCaPrev, sensitive to hormone therapies. In contrast, LNCaP cells were grown for more than 100 passages yielding a high passage therapy resistant cell line (hiPLNCaP). VCaP and hiPLNCaP cell lines were treated with 5 μmol/L AA for more than 20 passages, respectively, generating the AAtolerant- subtypes VCaPAA and hiPLNCaPAA. Cell lines were treated with testosterone, dihydrotestosterone (DHT), R1881, and the androgen-metabolites 3β-androstanediol and 3α-androstanediol. 3β-androstanediol or 3α-androstanediol significantly reduced proliferation in all cell lines except the BPH-1 and androgen receptor-negative PC-3 and markedly downregulated AR and estrogen receptor alpha (ERα). Whereas ERβ expression was increased in all cell lines except BPH-1 or PC-3. In summary, 3β-adiol or 3α-adiol, as well as DHT and R1881, significantly reduced tumour cell growth in CRPC cells. Thus, these compounds represent novel potential therapeutic approaches to overcome drug-resistance in CRPC, especially with regard to AR-V7 function in therapy resistance. Furthermore, these data confirm the tumour suppressor properties of ERβ in CRPC."],["dc.identifier.doi","10.18632/oncotarget.24763"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15104"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59207"],["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.ddc","610"],["dc.title","Testosterone metabolites inhibit proliferation of castration- and therapy-resistant prostate cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","cge.14174"],["dc.bibliographiccitation.firstpage","239"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Clinical Genetics"],["dc.bibliographiccitation.lastpage","241"],["dc.bibliographiccitation.volume","102"],["dc.contributor.affiliation","Bremmer, Felix; 2\r\nInstitute of Pathology\r\nUniversity Medical Center Göttingen\r\nGöttingen Germany"],["dc.contributor.affiliation","Brockmann, Knut; 3\r\nInterdisciplinary Pediatric Center for Children With Developmental Disabilities and Severe Chronic Disorders\r\nUniversity Medical Center Göttingen\r\nGöttingen Germany"],["dc.contributor.affiliation","Kaulfuß, Silke; 1\r\nInstitute of Human Genetics\r\nUniversity Medical Center Göttingen\r\nGöttingen Germany"],["dc.contributor.affiliation","Wollnik, Bernd; 1\r\nInstitute of Human Genetics\r\nUniversity Medical Center Göttingen\r\nGöttingen Germany"],["dc.contributor.author","Schmidt, Julia"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Brockmann, Knut"],["dc.contributor.author","Kaulfuß, Silke"],["dc.contributor.author","Wollnik, Bernd"],["dc.date.accessioned","2022-07-01T07:35:10Z"],["dc.date.available","2022-07-01T07:35:10Z"],["dc.date.issued","2022"],["dc.date.updated","2022-11-11T13:13:44Z"],["dc.description.abstract","Proteus syndrome is a very rare disorder with progressive, asymmetrical, and disproportionate overgrowth of body parts with a highly variable phenotype. It is associated with mosaicism for the recurrent heterozygous somatic gain-of-function variant c.49G>A (p.Glu17Lys) in the protein kinase AKT1. We report on a girl with a progressive intraosseous lipoma of the frontal bone and additional, nonspecific features including mild developmental delay, strabism, and a limbal dermoid of the left eye. She did not fulfill the criteria for a clinical diagnosis of Proteus syndrome. However, mutation analysis of AKT1 in a lipoma biopsy revealed this specific activating variant. Several cases of progressive intraosseous lipoma of the frontal bone have been reported in the literature. Only in two of these observations, a tentative diagnosis of Proteus syndrome was made, based on additional clinical features, although without molecular-genetic verification. We conclude that oligosymptomatic Proteus syndrome should be considered in progressive intraosseous lipoma, as recognition of this diagnosis has relevant implications for genetic counseling and opens novel treatment options with AKT1 inhibitors rather than surgical procedures."],["dc.description.abstract","We report a case of progressive frontal intraosseous lipoma associated with the specific mosaic AKT1 variant c.49G>A (p.Glu17Lys) and expand the complex phenotypic spectrum of Proteus syndrome.\r\n\r\nimage"],["dc.description.sponsorship"," Deutsche Forschungsgemeinschaft https://doi.org/10.13039/501100001659"],["dc.identifier.doi","10.1111/cge.14174"],["dc.identifier.pmid","35670639"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112102"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/500"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-581"],["dc.publisher","Blackwell Publishing Ltd"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation.eissn","1399-0004"],["dc.relation.issn","0009-9163"],["dc.relation.workinggroup","RG Wollnik"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","http://creativecommons.org/licenses/by-nc-nd/4.0/"],["dc.title","Progressive frontal intraosseous lipoma: Detection of the mosaic AKT1 variant discloses Proteus syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","33426"],["dc.bibliographiccitation.issue","32"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","33437"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Schallenberg, Simon"],["dc.contributor.author","Jarry, Hubertus"],["dc.contributor.author","Kueffer, Stefan"],["dc.contributor.author","Kaulfuss, Silke"],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","Strauss, Arne"],["dc.contributor.author","Thelen, Paul"],["dc.contributor.author","Radzun, Heinz Joachim"],["dc.contributor.author","Stroebel, Philipp"],["dc.contributor.author","Honecker, Friedemann"],["dc.contributor.author","Behnes, Carl Ludwig"],["dc.date.accessioned","2018-11-07T09:50:04Z"],["dc.date.available","2018-11-07T09:50:04Z"],["dc.date.issued","2015"],["dc.description.abstract","Germ cell tumors (GCTs) are the most common malignancies in young men. Most patients with GCT can be cured with cisplatin-based combination chemotherapy, even in metastatic disease. In case of therapy resistance, prognosis is usually poor. We investigated the potential of N-cadherin inhibition as a therapeutic strategy. We analyzed the GCT cell lines NCCIT, NTERA-2, TCam-2, and the cisplatin-resistant sublines NCCIT-R and NTERA-2R. Effects of a blocking antibody or siRNA against N-cadherin on proliferation, migration, and invasion were investigated. Mouse xenografts of GCT cell lines were analyzed by immunohistochemistry for N-cadherin expression. All investigated GCT cell lines were found to express N-cadherin protein in vitro and in vivo. Downregulation of N-cadherin in vitro leads to a significant inhibition of proliferation, migration, and invasion. N-cadherin-downregulation leads to a significantly higher level of pERK. N-cadherin-inhibition resulted in significantly higher rates of apoptotic cells in caspase-3 staining. Expression of N-cadherin is preserved in cisplatin-resistant GCT cells, pointing to an important physiological role in cell survival. N-cadherin-downregulation results in a significant decrease of proliferation, migration, and invasion and stimulates apoptosis in cisplatin-naive and resistant GCT cell lines. Therefore, targeting N-cadherin may be a promising therapeutic approach, particularly in cisplatin-resistant, therapy refractory and metastatic GCT."],["dc.description.sponsorship","Open-Access Publikationsfonds 2015"],["dc.identifier.doi","10.18632/oncotarget.5288"],["dc.identifier.isi","000363186600100"],["dc.identifier.pmid","26451610"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12456"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35638"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Impact Journals Llc"],["dc.relation.issn","1949-2553"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.title","Role of N-cadherin in proliferation, migration, and invasion of germ cell tumours"],["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"]]