Hemmerlein, Bernhard

[["dc.bibliographiccitation.firstpage","384"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Archives of Dermatological Research"],["dc.bibliographiccitation.lastpage","390"],["dc.bibliographiccitation.volume","292"],["dc.contributor.author","Fayyazi, Afshin"],["dc.contributor.author","Schweyer, Stefan"],["dc.contributor.author","Eichmeyer, B."],["dc.contributor.author","Herms, J."],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.contributor.author","Radzun, H.-J."],["dc.contributor.author","Berger, H."],["dc.date.accessioned","2018-11-07T10:34:41Z"],["dc.date.available","2018-11-07T10:34:41Z"],["dc.date.issued","2000"],["dc.description.abstract","Granuloma annulare, a prototype noninfectious granulomatous dermatitis, is morphologically characterized by a necrobiotic core surrounded by a cellular infiltrate, Because of many morphological similarities to tuberculosis, granuloma annulare has been suggested to represent a delayed-type hypersensitivity (Th1) reaction in the course of which inflammatory cells elicit matrix degradation, In the present study we (1) investigated the expression of interferon-gamma as the most important Th1-associated cytokine, (2) sought in situ evidence for the coexpression of the proinflammatory cytokine tumor necrosis factor-a and cytokine-regulated matrix metalloproteinases 2 (gelatinase A) and 9 (gelatinase B), and (3) sought to determine whether shrunken cells seen within necrobiotic areas of granuloma annulare are apoptotic cells, In situ hybridization combined with immunofluorescence showed that large numbers of infiltrating CD3(+) lymphocytes express interferon-gamma, Application of catalyzed signal amplification in immunodetection revealed that the vast majority of CD3(+) lymphocytes and CD68(+) macrophages contained tumor necrosis factor-alpha. Immunohistochemistry demonstrated that macrophages producing tumor necrosis factor-ct coexpress matrix metalloproteinases 2 and 9, In situ end-labeling combined with immunofluorescence detected few apoptotic T cells in perivascular regions and numerous apoptotic macrophages within necrobiotic areas, These results suggest that in granuloma annulare interferon-gamma(+) Th-1 lymphocytes may cause a delayed-type hypersensitivity reaction whereby macrophages are differentiated to aggressive effector cells expressing tumor necrosis factor-alpha and matrix metalloproteinases, In parallel, activation-induced apoptosis in lymphocytes and macrophages may serve to restrict the destructive potential of the inflammatory cells."],["dc.identifier.doi","10.1007/s004030000150"],["dc.identifier.isi","000088939700003"],["dc.identifier.pmid","10994772"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44932"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0340-3696"],["dc.title","Expression of IFN gamma, coexpression of TNF alpha and matrix metalloproteinases and apoptosis of T lymphocytes and macrophages in granuloma annulare"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","485"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Cancer Immunology Immunotherapy"],["dc.bibliographiccitation.lastpage","492"],["dc.bibliographiccitation.volume","49"],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.contributor.author","Markus, A."],["dc.contributor.author","Wehner, M."],["dc.contributor.author","Kugler, A."],["dc.contributor.author","Zschunke, F."],["dc.contributor.author","Radzun, H.-J."],["dc.date.accessioned","2018-11-07T11:11:26Z"],["dc.date.available","2018-11-07T11:11:26Z"],["dc.date.issued","2000"],["dc.description.abstract","Purpose: Tumor cells influence the differentiation of infiltrating macrophages. In the present study, the differentiation of macrophages in renal cell carcinomas was investigated with special regard to their possible role ill tumor growth and spread. Methods: Macrophages were characterized by means of immunohistochemistry of the Ki-M1P, 25F9, MRP8, MRP14, and MRP8/14 antigens and by means of in situ hybridization of CSF-1, its c-fins-coded corresponding receptor, and human monocytic serine esterase-1 (HMSE-1) mRNA. Macrophage subgroups were quantified within central tumor tissue, the corresponding turner host interface, and tumor-free tissue and correlated with tumor necrosis, fibrosis, and tumor stage and grade. Results: Macrophage density was much higher within tumor tissue and the tumor/host interface than in tumor-free tissue. Well-differentiated carcinomas showed a lower degree of macrophage density than less-differentiated carcinomas. Tumor-associated macrophages could be divided into an active inflammatory typo (MR14(+), MRP8/14(+)) and into a late-phase inflammatory type (25F9(+), MRP8(+)). Necrosis was seen in less-differentiated carcinomas and associated with a significantly increased density of MRP14(+) macrophages, which, however, did not correlate with the extent of necrosis. The density of 25F9(+) macrophages was correlated with an extensive connective tissue formation and an advanced tumor stage. c-fms, CSF-I, and HMSE-1 mRNA expression did not discriminate between the macrophage subgroups. Conclusions: Tumor-associated macrophages of the late-stage inflammatory type potentially support the spread of renal cell cancer. CSF-1 derived from tumor cells and macrophages acts as a monocyte attractant and induces macrophage differentiation able to modulate the extracellular matrix rather than to exert cytotoxicity. CSF-1 derived from tumor cells and macrophages acts as a monocyte attractant and induces macrophage differentiation able to modulate the extracellular matrix rather than to exert cytotoxicity."],["dc.identifier.doi","10.1007/s002620000139"],["dc.identifier.isi","000165111500004"],["dc.identifier.pmid","11092615"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53437"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0340-7004"],["dc.title","Expression of acute and late-stage inflammatory antigens, c-fms, CSF-1, and human monocytic serine esterase 1, in tumor-associated macrophages of renal cell carcinomas"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Pathology - Research and Practice"],["dc.bibliographiccitation.volume","203"],["dc.contributor.author","Perske, Christina"],["dc.contributor.author","Kosz, L."],["dc.contributor.author","Radzun, H.-J."],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.date.accessioned","2018-11-07T11:07:22Z"],["dc.date.available","2018-11-07T11:07:22Z"],["dc.date.issued","2007"],["dc.format.extent","323"],["dc.identifier.isi","000247312300178"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52543"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Gmbh, Urban & Fischer Verlag"],["dc.publisher.place","Jena"],["dc.relation.issn","0344-0338"],["dc.title","Epigenetic effects on the mRNA-Expression of MMPs, EMMPRIN, and TIMPs in urothelial carcinoma cell lines"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","976"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Apmis"],["dc.bibliographiccitation.lastpage","981"],["dc.bibliographiccitation.volume","121"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Schweyer, Stefan"],["dc.contributor.author","Martin-Ortega, M."],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.contributor.author","Strauss, A."],["dc.contributor.author","Radzun, H.-J."],["dc.contributor.author","Behnes, Carl Ludwig"],["dc.date.accessioned","2018-11-07T09:19:27Z"],["dc.date.available","2018-11-07T09:19:27Z"],["dc.date.issued","2013"],["dc.description.abstract","Leydig cell tumours comprise about 3% of all testicular tumours. The pathogenesis of Leydig cell tumours is still poorly understood. We investigated testis with Leydig cell hyperplasia and Leydig cell tumours for their expression pattern of P- and N-cadherin. We could show a switch of expression of P- and N-cadherin in Leydig cell hyperplasia and Leydig cell tumours in comparison with normal Leydig cells. Cadherins could be established as a new immunohistochemical marker for this testicular tumour entity; their possible role in tumour genesis will be discussed."],["dc.identifier.doi","10.1111/apm.12053"],["dc.identifier.isi","000325026100009"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28638"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","0903-4641"],["dc.title","Switch of cadherin expression as a diagnostic tool for Leydig cell tumours"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","645"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Virchows Archiv"],["dc.bibliographiccitation.lastpage","652"],["dc.bibliographiccitation.volume","439"],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.contributor.author","Kugler, Alexander"],["dc.contributor.author","Özisik, Rehyan"],["dc.contributor.author","Ringert, Rolf-Hermann"],["dc.contributor.author","Radzun, Heinz-Joachim"],["dc.contributor.author","Thelen, Paul"],["dc.date.accessioned","2021-06-01T10:49:14Z"],["dc.date.available","2021-06-01T10:49:14Z"],["dc.date.issued","2001"],["dc.description.abstract","Rapidly growing tumors often develop necrosis. In the present study the expression of vascular endothelial growth factor (VEGF) was investigated and compared to microvessel density and necrosis of renal cell carcinomas. In the tumor-host interface the microvessel density was significantly increased compared to central tumor areas. Tumor necrosis was associated with a decrease of microvessel density and an increase of the VEGF protein expression within the perinecrotic rim. VEGF protein was focally upregulated in vital tumor tissue. An increase of the apoptotic rate of endothelia and vital tumor tissue in tumors with necrosis could not be detected. VEGF((121,165)) mRNA was decreased in proliferatively active carcinomas compared to less proliferative tumors. Multicellular renal cell cancer spheroids as a model of chronic hypoxia developed central apoptosis but no necrosis. VEGF was upregulated in the spheroid. Tumor microvessels expressed matrix metalloproteinase -2 and -9 and an incomplete pericyte covering in comparison to tumor-free tissue indicating immature active angiogenesis. We conclude that highly proliferative renal cell carcinomas outgrow their vascular supply and develop chronic hypoxia inducing a decrease of proliferation and an increase of VEGF expression. However, chronic hypoxia does not cause significant necrosis or apoptosis. Tumor necrosis is more likely induced by acute hypoxia due to immature microvessels. Furthermore, VEGF expression associated with concomitant tumor necrosis may help identify renal cell carcinomas susceptible to antiangiogenic therapy."],["dc.identifier.doi","10.1007/s004280100464"],["dc.identifier.isi","000172511300009"],["dc.identifier.pmid","11764385"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86212"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.eissn","1432-2307"],["dc.relation.issn","0945-6317"],["dc.title","Vascular endothelial growth factor expression, angiogenesis, and necrosis in renal cell carcinomas"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","19"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","BMC Clinical Pathology"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.contributor.author","Strauss, Arne"],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","Thelen, Paul"],["dc.contributor.author","Radzun, Heinz-Joachim"],["dc.contributor.author","Behnes, Carl Ludwig"],["dc.date.accessioned","2019-07-09T11:54:07Z"],["dc.date.available","2019-07-09T11:54:07Z"],["dc.date.issued","2012"],["dc.description.abstract","Background Testicular germ cell tumours (TGCTs) are the most common malignancy in young men aged 18–35 years. They are clinically and histologically subdivided into seminomas and non-seminomas. Cadherins are calcium-dependent transmembrane proteins of the group of adhesion proteins. They play a role in the stabilization of cell-cell contacts, the embryonic morphogenesis, in the maintenance of cell polarity and signal transduction. N-cadherin (CDH2), the neuronal cadherin, stimulates cell-cell contacts during migration and invasion of cells and is able to suppress tumour cell growth. Methods Tumour tissues were acquired from 113 male patients and investigated by immunohistochemistry, as were the three TGCT cell lines NCCIT, NTERA-2 and Tcam2. A monoclonal antibody against N-cadherin was used. Results Tumour-free testis and intratubular germ cell neoplasias (unclassified) (IGCNU) strongly expressed N-cadherin within the cytoplasm. In all seminomas investigated, N-cadherin expression displayed a membrane-bound location. In addition, the teratomas and yolk sac tumours investigated also differentially expressed N-cadherin. In contrast, no N-cadherin could be detected in any of the embryonal carcinomas and chorionic carcinomas examined. This expression pattern was also seen in the investigated mixed tumours consisting of seminomas, teratomas, and embryonal carcinoma. Conclusions N-cadherin expression can be used to differentiate embryonal carcinomas and chorionic carcinomas from other histological subtypes of TGCT."],["dc.identifier.doi","10.1186/1472-6890-12-19"],["dc.identifier.fs","593171"],["dc.identifier.pmid","23066729"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8499"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60578"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","N-cadherin expression in malignant germ cell tumours of the testis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","795"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Gut"],["dc.bibliographiccitation.lastpage","803"],["dc.bibliographiccitation.volume","49"],["dc.contributor.author","Middel, Peter"],["dc.contributor.author","Reich, Kristian"],["dc.contributor.author","Polzien, F."],["dc.contributor.author","Blaschke, V."],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.contributor.author","Herms, J."],["dc.contributor.author","Korabiowska, M."],["dc.contributor.author","Radzun, H.-J."],["dc.date.accessioned","2018-11-07T11:21:05Z"],["dc.date.available","2018-11-07T11:21:05Z"],["dc.date.issued","2001"],["dc.description.abstract","Background-The mechanisms involved in the initiation and maintenance of Crohn's disease are poorly understood. Previous studies have demonstrated an increased number of infiltrating CD4+ T cells within the inflammatory affected bowel wall in Crohn's disease. Novel therapy approaches using anti-CD4 antibodies are thought to be effective in Crohn's disease. Aims-Interleukin 16 (IL-16) has been characterised as a chemokine with selective chemoattraction for CD4+ inflammatory T cells. In this study, cellular expression of IL-16 in Crohn's disease and ulcerative colitis was investigated. Methods-Expression of IL-16 was analysed in tissue samples of Crohn's disease, ulcerative colitis, and normal controls by applying reverse transcription-polymerase chain reaction, non-radioactive in situ hybridisation, and immunohistochemistry. Double staining methods were used to characterise cells expressing IL-16. The amount of infiltrating CD4+ cells was determined by immunohistochemistry and correlated with the corresponding IL-16+ cell number by step sections. Results-An increased number of IL-16+ cells in Crohn's disease in comparison with ulcerative colitis and control probes was demonstrated. IL-16 was expressed by CD4 and CD8 positive T cells. In addition, in active Crohn's disease there was a substantial number of IL-16 positive mast cells. The increased number of CD4+ lymphocytes correlated positively with the increased number of IL- 16 positive cells in Crohn's disease. Conclusion-Our results demonstrate that increased expression of IL-16 in T cells and mast cells in active Crohn's disease is associated with increased numbers of CD4+ lymphocytes. Local expression of IL-16 seems to play a significant role in the initiation and persistence of the inflammatory process in Crohn's disease, presumably by IL-16 mediated recruitment of CD4+ cells, mostly lymphocytes, into the bowel wall."],["dc.identifier.doi","10.1136/gut.49.6.795"],["dc.identifier.isi","000172340900015"],["dc.identifier.pmid","11709514"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55689"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","British Med Journal Publ Group"],["dc.relation.issn","0017-5749"],["dc.title","Interleukin 16 expression and phenotype of interleukin 16 producing cells in Crohn's disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","78"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Histopathology"],["dc.bibliographiccitation.lastpage","83"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.contributor.author","Scherbening, J."],["dc.contributor.author","Kugler, A."],["dc.contributor.author","Radzun, H.-J."],["dc.date.accessioned","2018-11-07T10:41:12Z"],["dc.date.available","2018-11-07T10:41:12Z"],["dc.date.issued","2000"],["dc.description.abstract","Aims: Neoangiogenesis is accompanied by an increase in endothelial surface, which can support infiltration by immune cells depending on adhesion molecule expression. Therefore, the expression of cell adhesion molecules on microvessels and epithelial cells was analysed in renal cell carcinomas as compared to tumour-free tissue. Methods and results: PECAM-1, CD34, ICAM-1, VCAM-1, VLA-4. P- and E-selectin, the macrophage antigens Ki-M1P and Mac-1, and lymphocyte function antigen LFA-1 were identified immunohistochemically. VCAM-1, ICAM-1, and E-selectin were equally or less expressed, whereas P-selectin was increased on microvessels in tumour tissue. The density of VCAM-1-positive tumour microvessels correlated positively with an advanced tumour stage and E- and P-selectin-positive tumour microvessels with the amount of associated macrophages. The expression of ICAM-1 and VCAM-1 on neoplastic epithelia correlated with an increased density of macrophages and a minor degree of tumour differentiation. Conclusions: The positive correlation of macrophage infiltration and expression of cell adhesion molecules on tumour microvessels and epithelia with minor tumour differentiation and an advanced stage indicates that adhesion molecule expression is not associated with an effective antitumour function of macrophages."],["dc.identifier.doi","10.1046/j.1365-2559.2000.00933.x"],["dc.identifier.isi","000088938200011"],["dc.identifier.pmid","10931222"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/46482"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Science Ltd"],["dc.relation.issn","0309-0167"],["dc.title","Expression of VCAM-1, ICAM-1, E- and P-selectin and tumour-associated macrophages in renal cell carcinoma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","95"],["dc.bibliographiccitation.journal","Diagnostic Pathology"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Behnes, Carl Ludwig"],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.contributor.author","Strauss, Arne"],["dc.contributor.author","Radzun, Heinz-Joachim"],["dc.contributor.author","Bremmer, Felix"],["dc.date.accessioned","2018-11-07T09:07:12Z"],["dc.date.available","2018-11-07T09:07:12Z"],["dc.date.issued","2012"],["dc.description.abstract","Background: Papillary renal cell carcinoma (RCC) represents a rare tumor, which is divided, based on histological criteria, into two subtypes. In contrast to type I papillary RCC type II papillary RCC shows a worse prognosis. So far, reliable immunohistochemical markers for the distinction of these subtypes are not available. Methods: In the present study the expression of N(neural)-, E(epithelial)-, P(placental)-, und KSP(kidney specific)cadherin was examined in 22 papillary RCC of histological type I and 18 papillary RCC of histological type II (n = 40). Results: All papillary RCC type II displayed a membranous expression for N-cadherin, whereas type I did not show any membranous positivity for N-cadherin. E-cadherin exhibited a stronger, but not significant, membranous as well as cytoplasmic expression in type II than in type I papillary RCC. A diagnostic relevant expression of P- and KSP-cadherin could not be demonstrated in both tumor entities. Conclusion: Thus N-cadherin represents the first immunhistochemical marker for a clear cut differentiation between papillary RCC type I and type II and could be a target for therapy and diagnostic in the future."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2012"],["dc.identifier.doi","10.1186/1746-1596-7-95"],["dc.identifier.isi","000313263100001"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8476"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25739"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","Najko"],["dc.relation.issn","1746-1596"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","N-cadherin is differentially expressed in histological subtypes of papillary renal cell carcinoma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","311"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Pathology - Research and Practice"],["dc.bibliographiccitation.lastpage","312"],["dc.bibliographiccitation.volume","203"],["dc.contributor.author","Spohr, H."],["dc.contributor.author","Radzun, H.-J."],["dc.contributor.author","Stuhmer, Walter"],["dc.contributor.author","Pardo, L."],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.date.accessioned","2018-11-07T11:07:22Z"],["dc.date.available","2018-11-07T11:07:22Z"],["dc.date.issued","2007"],["dc.identifier.isi","000247312300148"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52539"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Gmbh, Urban & Fischer Verlag"],["dc.publisher.place","Jena"],["dc.relation.issn","0344-0338"],["dc.title","Expression of Eag1 potassium channels in renal cell carcinomas"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]