Strauß, Arne

[["dc.bibliographiccitation.firstpage","339"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","International Journal of Molecular Medicine"],["dc.bibliographiccitation.lastpage","346"],["dc.bibliographiccitation.volume","31"],["dc.contributor.author","Thelen, Paul"],["dc.contributor.author","Krahn, Lisa"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Strauss, Arne"],["dc.contributor.author","Brehm, Ralph"],["dc.contributor.author","Loertzer, Hagen"],["dc.date.accessioned","2018-11-07T09:28:47Z"],["dc.date.available","2018-11-07T09:28:47Z"],["dc.date.issued","2013"],["dc.description.abstract","The aim of this study was to elucidate whether the treatment of a prostate carcinoma cell line (LNCaP) and LNCaP-derived tumors with the histone deacetylase (HDAC) inhibitor valproate in combination with the mammalian target of rapamycin (mTOR) inhibitor temsirolimus resulted in synergistic effects on cell proliferation and tumor growth. LNCaP cells were treated with valproate, temsirolimus or a combination of both. The proliferation rates and the expression of key markers of tumorigenesis were evaluated. In in vivo experiments, LNCaP cells were implanted into immune-suppressed male nude mice. Mice were treated with valproate (per os), temsirolimus (intravenously) or with a combination of both. Tumor volumes were calculated and mRNA expression was quantified. The incubation of LNCaP cells with the combination of valproate and temsirolimus resulted in a decrease of cell proliferation with an additive effect of both drugs in comparison to the single treatment. In particular, the combined application of valproate and temsirolimus led to a significant upregulation of insulin-like growth factor-binding protein-3 (IGFBP-3), which mediates apoptosis and inhibits tumor cell proliferation. In the mouse model, we found no significant differences in tumor growth between the different treatment arms but immunohistological analyses showed that tumors treated with a combination of valproate and temsirolimus, but not with the single drugs alone, exhibited a significant lower proliferation capacity."],["dc.identifier.doi","10.3892/ijmm.2012.1221"],["dc.identifier.isi","000313858500009"],["dc.identifier.pmid","23292124"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30859"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Spandidos Publ Ltd"],["dc.relation.issn","1107-3756"],["dc.title","Synergistic effects of histone deacetylase inhibitor in combination with mTOR inhibitor in the treatment of prostate carcinoma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal of Clinical Oncology"],["dc.bibliographiccitation.volume","31"],["dc.contributor.author","Thelen, Paul"],["dc.contributor.author","Walleck, Eiko"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Trojan, Lutz"],["dc.contributor.author","Strauss, Arne"],["dc.date.accessioned","2018-11-07T09:28:04Z"],["dc.date.available","2018-11-07T09:28:04Z"],["dc.date.issued","2013"],["dc.identifier.isi","000333679600131"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30688"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Clinical Oncology"],["dc.publisher.place","Alexandria"],["dc.relation.conference","Genitourinary Cancers Symposium of the Conquer-Cancer-Foundation of American-Society-of-Clinical-Oncology (ASCO)"],["dc.relation.eventlocation","Orlando, FL"],["dc.relation.issn","1527-7755"],["dc.relation.issn","0732-183X"],["dc.title","Analysis of putative resistance mechanisms in recent treatments targeting the androgen receptor in castration-resistant prostate cancer (CRPC)"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","574"],["dc.bibliographiccitation.journal","SpringerPlus"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Jarry, Hubertus"],["dc.contributor.author","Strauss, Arne"],["dc.contributor.author","Behnes, Carl Ludwig"],["dc.contributor.author","Trojan, Lutz"],["dc.contributor.author","Thelen, Paul"],["dc.date.accessioned","2018-11-07T09:33:49Z"],["dc.date.available","2018-11-07T09:33:49Z"],["dc.date.issued","2014"],["dc.description.abstract","Recent breakthrough therapies targeting androgen receptor signalling in castration resistant prostate cancer (CRPC) involve multifunctional androgen receptor (AR) blockade and exhaustive androgen deprivation. Nevertheless, limitations to an enduring effectiveness of new drugs are anticipated in resistance mechanisms occurring under such treatments. In this study we used CRPC cell models VCaP and LNCaP as well as AR-negative PC-3- and non-neoplastic epithelial BPH-1-cells treated with 5, 10 or 25 mu mol/L abiraterone hydrolyzed from abiraterone acetate (AA). The origin of CYP17A1 up-regulation under AA treatment was investigated in CRPC cell models by qRT-PCR and western-blot procedures. AA treatments of AR positive CRPC cell models led to decreased expression of androgen regulated genes such as PSA. In these cells diminished expression of androgen regulated genes was accompanied by an up-regulation of CYP17A1 expression within short-term treatments. No such effects became evident in AR-negative PC-3 cells. AR directed siRNA (siAR) used in VCaP cells significantly reduced mRNA expression and AR protein abundance. Such interference with AR signalling in the absence of abiraterone acetate also caused a marked up-regulation of CYP17A1 expression. Down-regulation of androgen regulated genes occurs in spite of an elevated expression of CYP17A1, the very target enzyme for this drug. CYP17A1 up-regulation already takes place within such short treatments with AA and does not require adaptation events over several cell cycles. CYP17A1 is also up-regulated in the absence of AA when AR signalling is physically eliminated by siAR. These results reveal an immediate counter-regulation of CYP17A1 expression whenever AR-signalling is inhibited adequately but not a persisting adaptation yielding drug resistance."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft (DFG)"],["dc.identifier.doi","10.1186/2193-1801-3-574"],["dc.identifier.isi","000359105300002"],["dc.identifier.pmid","25332874"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11151"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32049"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","2193-1801"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Increased expression of CYP17A1 indicates an effective targeting of the androgen receptor axis in castration resistant prostate cancer (CRPC)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","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.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","1"],["dc.bibliographiccitation.journal","Disease Markers"],["dc.bibliographiccitation.lastpage","14"],["dc.bibliographiccitation.volume","2019"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Küffer, Stefan"],["dc.contributor.author","Oellerich, Thomas"],["dc.contributor.author","Serve, Hubert"],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Strauß, Arne"],["dc.contributor.author","Maatoug, Yasmine"],["dc.contributor.author","Behnes, Carl Ludwig"],["dc.contributor.author","Oing, Christoph"],["dc.contributor.author","Radzun, Heinz Joachim"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Balabanov, Stefan"],["dc.contributor.author","Honecker, Friedemann"],["dc.date.accessioned","2019-09-24T07:40:13Z"],["dc.date.available","2019-09-24T07:40:13Z"],["dc.date.issued","2019"],["dc.description.abstract","Malignant germ cell tumors (GCT) are the most common malignant tumors in young men between 18 and 40 years. The correct identification of histological subtypes, in difficult cases supported by immunohistochemistry, is essential for therapeutic management. Furthermore, biomarkers may help to understand pathophysiological processes in these tumor types. Two GCT cell lines, TCam-2 with seminoma-like characteristics, and NTERA-2, an embryonal carcinoma-like cell line, were compared by a quantitative proteomic approach using high-resolution mass spectrometry (MS) in combination with stable isotope labelling by amino acid in cell culture (SILAC). We were able to identify 4856 proteins and quantify the expression of 3936. 347 were significantly differentially expressed between the two cell lines. For further validation, CD81, CBX-3, PHF6, and ENSA were analyzed by western blot analysis. The results confirmed the MS results. Immunohistochemical analysis on 59 formalin-fixed and paraffin-embedded (FFPE) normal and GCT tissue samples (normal testis, GCNIS, seminomas, and embryonal carcinomas) of these proteins demonstrated the ability to distinguish different GCT subtypes, especially seminomas and embryonal carcinomas. In addition, siRNA-mediated knockdown of these proteins resulted in an antiproliferative effect in TCam-2, NTERA-2, and an additional embryonal carcinoma-like cell line, NCCIT. In summary, this study represents a proteomic resource for the discrimination of malignant germ cell tumor subtypes and the observed antiproliferative effect after knockdown of selected proteins paves the way for the identification of new potential drug targets."],["dc.identifier.doi","10.1155/2019/8298524"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16378"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/62439"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","0278-0240"],["dc.relation.issn","1875-8630"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Proteomic Comparison of Malignant Human Germ Cell Tumor Cell Lines"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","165"],["dc.bibliographiccitation.journal","Diagnostic Pathology"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Kluemper, Niklas"],["dc.contributor.author","Syring, Isabella"],["dc.contributor.author","Offermann, Anne"],["dc.contributor.author","Shaikhibrahim, Zaki"],["dc.contributor.author","Vogel, Wenzel"],["dc.contributor.author","Mueller, Stefan C."],["dc.contributor.author","Ellinger, Joerg"],["dc.contributor.author","Strauss, Arne"],["dc.contributor.author","Radzun, Heinz Joachim"],["dc.contributor.author","Stroebel, Philipp"],["dc.contributor.author","Braegelmann, Johannes"],["dc.contributor.author","Perner, Sven"],["dc.contributor.author","Bremmer, Felix"],["dc.date.accessioned","2018-11-07T09:51:35Z"],["dc.date.available","2018-11-07T09:51:35Z"],["dc.date.issued","2015"],["dc.description.abstract","Background: Testicular germ cell tumors (TGCT) are the most common cancer entities in young men with increasing incidence observed in the last decades. For therapeutic management it is important, that TGCT are divided into several histological subtypes. MED15 is part of the multiprotein Mediator complex which presents an integrative hub for transcriptional regulation and is known to be deregulated in several malignancies, such as prostate cancer and bladder cancer role, whereas the role of the Mediator complex in TGCT has not been investigated so far. Aim of the study was to investigate the implication of MED15 in TGCT development and its stratification into histological subtypes. Methods: Immunohistochemical staining (IHC) against Mediator complex subunit MED15 was conducted on a TGCT cohort containing tumor-free testis (n = 35), intratubular germ cell neoplasia unclassified (IGCNU, n = 14), seminomas (SEM, n = 107) and non-seminomatous germ cell tumors (NSGCT, n = 42), further subdivided into embryonic carcinomas (EC, n = 30), yolk sac tumors (YST, n = 5), chorionic carcinomas (CC, n = 5) and teratomas (TER, n = 2). Quantification of MED15 protein expression was performed through IHC followed by semi-quantitative image analysis using the Definiens software. Results: In tumor-free seminiferous tubules, MED15 protein expression was absent or only low expressed in spermatogonia. Interestingly, the precursor lesions IGCNU exhibited heterogeneous but partly very strong MED15 expression. SEM weakly express the Mediator complex subunit MED15, whereas NSGCT and especially EC show significantly enhanced expression compared to tumor-free testis. Conclusions: In conclusion, MED15 is differentially expressed in tumor-free testis and TGCT. While MED15 is absent or low in tumor-free testis and SEM, NSGCT highly express MED15, hinting at the diagnostic potential of this marker to distinguish between SEM and NSGCT. Further, the precursor lesion IGCNU showed increased nuclear MED15 expression in the preinvasive precursor cells, which may provide diagnostic value to distinguish between benign and pre-malignant testicular specimen, and may indicate a role for MED15 in carcinogenesis in TGCT."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2015"],["dc.identifier.doi","10.1186/s13000-015-0398-6"],["dc.identifier.isi","000361281600004"],["dc.identifier.pmid","26377566"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13462"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35945"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1746-1596"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Differential expression of Mediator complex subunit MED15 in testicular germ cell tumors"],["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","1699"],["dc.bibliographiccitation.issue","15"],["dc.bibliographiccitation.journal","The Prostate"],["dc.bibliographiccitation.lastpage","1709"],["dc.bibliographiccitation.volume","73"],["dc.contributor.author","Thelen, Paul"],["dc.contributor.author","Heinrich, Elmar"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Trojan, Lutz"],["dc.contributor.author","Strauss, Arne"],["dc.date.accessioned","2018-11-07T09:18:22Z"],["dc.date.available","2018-11-07T09:18:22Z"],["dc.date.issued","2013"],["dc.description.abstract","BACKGROUNDThe primary therapeutic target for non-organ-confined prostate cancer is the androgen receptor (AR). Main strategies to ablate AR function are androgen depletion and direct receptor blockade by AR antagonists. However, incurable castration resistant prostate cancer (CRPC) develops resistance mechanisms to cope with trace amounts of androgen including AR overexpression and mutation in the AR ligand binding domain. METHODSThe CRPC cell model VCaP derivative of a prostate cancer bone metastasis was used in vitro and in nude mice in vivo to examine the effects of immediate testosterone boost on CRPC cells. In addition, a testosterone tolerant cell model was established by incremental acclimatization of VCaP cells to 1nM testosterone. The effects of androgen withdrawal and testosterone boosts on gene expression were assessed by quantitative real-time polymerase chain reaction, ELISA, and Western blots. Tumor cell proliferation was evaluated with a BrdU test. RESULTSTestosterone boosts on CRPC VCaP cells eliminate tumor cells to a higher extent than androgen withdrawal in androgen tolerant cells. The pronounced decrease of tumor cell proliferation was accompanied by a marked downregulation of AR expression regarding full-length AR and splice variant AR V7. CONCLUSIONSAcquiring castration resistance of prostate cancer cells by AR overexpression and amplification obviously sensitizes such cells to testosterone concentrations as low as physiological values. This introduces novel therapeutic means to treat CRPC with non-toxic measures and may find clinical implementation in intermittent androgen deprivation regimens. Prostate 73: 1699-1709, 2013. (c) 2013 Wiley Periodicals, Inc."],["dc.description.sponsorship","Deutsche Krebshilfe"],["dc.identifier.doi","10.1002/pros.22711"],["dc.identifier.isi","000324923400010"],["dc.identifier.pmid","23868789"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28396"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1097-0045"],["dc.relation.issn","0270-4137"],["dc.title","Testosterone Boosts for Treatment of Castration Resistant Prostate Cancer: An Experimental Implementation of Intermittent Androgen Deprivation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","191"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Virchows Archiv"],["dc.bibliographiccitation.lastpage","196"],["dc.bibliographiccitation.volume","464"],["dc.contributor.author","Behnes, Carl Ludwig"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.contributor.author","Strauss, Arne"],["dc.contributor.author","Stroebel, Philipp"],["dc.contributor.author","Radzun, Heinz-Joachim"],["dc.date.accessioned","2018-11-07T09:44:21Z"],["dc.date.available","2018-11-07T09:44:21Z"],["dc.date.issued","2014"],["dc.description.abstract","Tumor-associated macrophages (TAMs) play a key role in cancer development. Especially, the immunosuppressive M2 phenotype is associated with increased tumor growth, invasiveness and metastasis. The differentiation of macrophages to the alternative phenotype M2 is mediated, inter alia, by macrophage colony-stimulating factor (M-CSF). Papillary renal cell carcinoma (RCC) represents a rare tumor type which, based upon histological criteria, can be subdivided into two subtypes (I and II), of which type II is associated with poor prognosis. In both subtypes, typically, a dense infiltrate of macrophages is found. In the present study, the expression of CD68, CD163, M-CSF, Ki-67, and CD31 was examined in 30 type I and 30 type II papillary RCCs (n = 60). Both types of papillary RCCs contained an equally dense infiltrate of CD68-positive macrophages. Nearly all macrophages in papillary RCC type II expressed CD163, a characteristic for M2 macrophages. In type I papillary RCC, less than 30 % of macrophages expressed CD163. Furthermore, tumor cells in type II papillary RCC expressed significantly more M-CSF and showed increased (Ki-67 expression defined) proliferative activity in comparison with type I papillary RCC. In addition, the (CD31 defined) capillary density was higher in type II than in type I papillary RCC. A dense infiltrate of M2 phenotype TAM and high M-CSF expression in tumor cells are key features of type II papillary RCC. These findings might explain why the prognosis of papillary RCC type II is worse than that of type I."],["dc.identifier.doi","10.1007/s00428-013-1523-0"],["dc.identifier.isi","000331642700007"],["dc.identifier.pmid","24327306"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34374"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","1432-2307"],["dc.relation.issn","0945-6317"],["dc.title","Tumor-associated macrophages are involved in tumor progression in papillary 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","UNSP 7"],["dc.bibliographiccitation.journal","Diagnostic Pathology"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Stroebel, Philipp"],["dc.contributor.author","Jarry, Hubertus"],["dc.contributor.author","Strecker, Jasmin"],["dc.contributor.author","Gaisa, Nadine"],["dc.contributor.author","Strauss, Arne"],["dc.contributor.author","Schweyer, Stefan"],["dc.contributor.author","Radzun, Heinz-Joachim"],["dc.contributor.author","Behnes, Carl-Ludwig"],["dc.date.accessioned","2018-11-07T09:59:28Z"],["dc.date.available","2018-11-07T09:59:28Z"],["dc.date.issued","2015"],["dc.description.abstract","Background: Malignant germ cell tumours are the most common malignant tumours in young men. They are histologically divided into seminomas and non-seminomas. Non-seminomas are further subdivided into embryonic carcinomas, yolk sac tumours, chorionic carcinomas, and teratomas. For the therapeutic management it is essential to differentiate between these histological subtypes. Methods: Investigated cases included normal testis (n = 50), intratubular germ cell neoplasia (n = 25), seminomas (n = 67), embryonic carcinomas (n = 56), yolk sac tumours (n = 29), chorionic carcinomas (n = 2), teratomas (n = 7) and four metastases of YST's for their CK19 expression. In addition Leydig cell-(n = 10) and Sertoli cell-tumours (n = 4) were included in this study. Results: All investigated seminomas, embryonic carcinomas as well as normal testis and intratubular germ cell neoplasias did not express CK19. In contrast, all investigated yolk sac tumours strongly expressed CK19 protein. These findings became also evident in mixed germ cell tumours consisting of embryonic carcinomas and yolk sac tumours, although CK19-expression could also be observed in analysed chorionic carcinomas and epithelial components of teratomas. Conclusion: CK19 proved to be a sensitive marker to identify yolk sac tumours of the testis and to distinguish them from other germ cell tumours, especially seminomas and embryonic carcinomas."],["dc.description.sponsorship","research program, faculty of medicine, Georg-August-University Gottingen"],["dc.identifier.doi","10.1186/s13000-015-0243-y"],["dc.identifier.isi","000352070000001"],["dc.identifier.pmid","25889715"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12289"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37594"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1746-1596"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","CK19 is a sensitive marker for yolk sac tumours of the testis"],["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"]]