Hemmerlein, Bernhard

[["dc.bibliographiccitation.firstpage","519"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Clinical Hemorheology and Microcirculation"],["dc.bibliographiccitation.lastpage","528"],["dc.bibliographiccitation.volume","34"],["dc.contributor.author","Penkalla, R."],["dc.contributor.author","Bedke, Jens"],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.contributor.author","Kahler, Elke"],["dc.contributor.author","Strauss, A."],["dc.contributor.author","Zoller, G. M."],["dc.contributor.author","Heuser, M."],["dc.date.accessioned","2018-11-07T10:32:26Z"],["dc.date.available","2018-11-07T10:32:26Z"],["dc.date.issued","2006"],["dc.description.abstract","Introduction: Peritubular renal microcirculation has not been directly visualized in acute ureteral obstruction. Therefore, we used epiilluminescence intravital microscopy and an animal model for the assessment of microvascular perfusion. Materials and methods: In group 1 (n = 5) the left kidney of Wistar rats was exteriorized and placed on a heatable stage for microcirculatory analysis. FITC-dextran was injected for plasma staining. Microcirculatory stability of the model was assessed by a repeated intravital microscopy at baseline, 60, and 120 minutes. In detail, the functional peritubular vessel density (FVD, total vessel length per area in cm/cm(2)), the red blood cell velocities and diameters in/of arterioles and peritubular capillaries and the perfusion index were measured. In group 2 (n = 7) the left ureter was obstructed after baseline microscopy. In a third group (n = 6) the influence of the antidiuretic and vasoconstrictive peptide gastrin releasing peptide on peritubular microcirculation of the obstructed kidney was measured. Results: Repeated intravital microscopy did not induce major microcirculatory disturbances in group 1. Acute ureteral obstruction significantly decreased the index of peritubular perfusion. Moreover, FVD was found decreased at 120 minutes after a small rise at 60 minutes. Whereas blood cell velocities were not changed, arteriolar diameters were decreased after 120 minutes. GRP infusion lowered intrapelvic pressures at 60 and at 120 minutes. The transient increase of FVD (group 2) was not observed. The calculated peritubular flow remained nearly constant compared to a decrease in group 2. Histological assessment did not reveal any microscopy induced renal damage nor any differences between the groups. Conclusions: (1) The model is stable for a time period of at least 120 minutes and allows for the direct visualization of the renal peritubular vessels. (2) Peritubular microcirculation shows a significant deterioration during ureteral obstruction. (3) Infusion of GRP may be beneficial for the microcirculation of the acutely obstructed kidney."],["dc.identifier.isi","000237367700006"],["dc.identifier.pmid","16687791"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44346"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Ios Press"],["dc.relation.issn","1386-0291"],["dc.title","Changes of microvascular perfusion during acute ureteral obstruction in the rat kidney - The influence of gastrin releasing peptide"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","543"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","American Journal Of Pathology"],["dc.bibliographiccitation.lastpage","552"],["dc.bibliographiccitation.volume","163"],["dc.contributor.author","Grzmil, M."],["dc.contributor.author","Thelen, Paul"],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.contributor.author","Schweyer, Stefan"],["dc.contributor.author","Voigt, S."],["dc.contributor.author","Mury, D."],["dc.contributor.author","Burfeind, Peter"],["dc.date.accessioned","2018-11-07T10:37:03Z"],["dc.date.available","2018-11-07T10:37:03Z"],["dc.date.issued","2003"],["dc.description.abstract","To analyze differential gene expression of putative prostate tumor markers we compared the expression levels of more than 400 cancer-related genes using the cDNA array technique in a set of capsule-invasive prostate tumor and matched normal prostate tissue. The overexpression. of Bax inhibitor-1 (BI-1) in prostate carcinoma and prostate cancer cell lines was confirmed by using Northern blot and Western blot analyses. Quantitative real-time reverse transcription-polymerase chain reaction (RT-PCR) on intact RNAs from 17 paired laser-captured microdissected epithelial tissue samples confirmed up-regulated BI-1 expression in 11 of 17 prostate tumors. In addition, it was demonstrated that BI-1 expression is down-regulated in stromal cells as. compared to matched normal epithelial cells of the prostate. In situ hybridization experiments on prostate sections also revealed that BI-1 expression is mainly restricted to epithelial cells. Furthermore, quantitative RT-PCR on RNAs derived from five benign prostate hyperplasia (BPH) samples showed no significant difference in BI-1 expression as compared to normal epithelial prostate tissue. To determine the function of BI-1 in vitro, human PC-3, LNCaP, and DU-145 prostate carcinoma cells were transfected with small interfering double-strand RNA (siRNA) oligonucleotides against the BI-1 gene leading to a specific down-regulation of BI-1 expression. Furthermore, transfection of PC-3, LNCaP, and DU-145 cells with BI-1 sequence-specific siRNAs caused a significant increase in spontaneous apoptosis in all cell lines. Taken together, our results indicate that the human BI-1 gene contains the potential to serve as a prostate cancer expression marker and as a potential target for developing therapeutic strategies for prostate cancer."],["dc.identifier.doi","10.1016/S0002-9440(10)63682-6"],["dc.identifier.isi","000184366400016"],["dc.identifier.pmid","12875974"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45473"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Investigative Pathology, Inc"],["dc.relation.issn","0002-9440"],["dc.title","Bax inhibitor-1 is overexpressed in prostate cancer and its specific down-regulation by RNA interference leads to cell death in human prostate carcinoma cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","332"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Nature Medicine"],["dc.bibliographiccitation.lastpage","336"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Kugler, A."],["dc.contributor.author","Stuhler, Gernot"],["dc.contributor.author","Walden, P."],["dc.contributor.author","Zoller, G."],["dc.contributor.author","Zobywalski, A."],["dc.contributor.author","Brossart, Peter"],["dc.contributor.author","Trefzer, U."],["dc.contributor.author","Ullrich, S."],["dc.contributor.author","Mueller, C. A."],["dc.contributor.author","Becker, V."],["dc.contributor.author","Gross, A. J."],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.contributor.author","Kanz, Lothar"],["dc.contributor.author","Mueller, Gerhard A."],["dc.contributor.author","Ringert, Rolf-Hermann"],["dc.date.accessioned","2018-11-07T09:31:01Z"],["dc.date.available","2018-11-07T09:31:01Z"],["dc.date.issued","2000"],["dc.identifier.isi","000085580500045"],["dc.identifier.pmid","10700237"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31446"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1078-8956"],["dc.title","Regression of human metastatic renal cell carcinoma after vaccination with tumor cell-dendritic cell hybrids (Retracted article. See vol. 9, p. 1221, 2003)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["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","172"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Microvascular Research"],["dc.bibliographiccitation.lastpage","178"],["dc.bibliographiccitation.volume","62"],["dc.contributor.author","Heuser, M."],["dc.contributor.author","Seseke, Florian"],["dc.contributor.author","Zoller, G."],["dc.contributor.author","Gross, A. J."],["dc.contributor.author","Kugler, A."],["dc.contributor.author","Stojanovic, Tomislav"],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.contributor.author","Ringert, Rolf-Hermann"],["dc.date.accessioned","2018-11-07T08:43:42Z"],["dc.date.available","2018-11-07T08:43:42Z"],["dc.date.issued","2001"],["dc.description.abstract","The surgically induced split hydronephrotic kidney has been generally accepted as a valid model for the assessment of renal microcirculation by means of intravital microscopy. Whereas nearly all previous work on this issue has been done with a transillumination technique, we used an epiillumination model that is suitable for investigation of microvascular perfusion in both normal and hydronephrotic kidneys without surgical manipulation of the ureter. By means of the congenital unilaterally hydronephrotic Tauchi rat, microcirculation of the hydronephrotic and that of the nonhydronephrotic kidney were compared. For that purpose both the hydronephrotic and the nonhydronephrotic kidneys of Tauchi rats were exteriorized on a specially designed microscopy stage. After injection of FITC-dextran and rhodamine 6G, microvascular perfusion was assessed in both kidneys. The new model allowed visualization of arterioles, capillaries, and postcapillary venules in both the hydronephrotic and the nonhydronephrotic kidneys. Glomeruli could only be regularly seen in the hydronephrotic kidney, but also in some normal kidneys. Capillary blood cell velocity was significantly higher in the hydronephrotic kidneys (0.67 +/-0.03 mm/s) compared to the normal kidney (0.32 +/-0.05 mm/s; P<0.05), whereas capillary diameters were smaller (4.20.02 mum vs. 5.7 +/-0.2 mum; P<0.05). In addition, the hydronephrotic kidney showed a significantly lower density of perfused microvessels compared to the normal controls. Epiillumination intravital microscopy allows assessment of the cortical microcirculation in both the hydronephrotic and the nonhydronephrotic kidneys without surgical inductin of hydronephrosis. The hydronephrotic kidney shows significant microcirculatory differences compared to normal kidneys that should be taken into account when using a hydronephrotic model for pharmacological testing. (C) 2001 Academic Press."],["dc.identifier.doi","10.1006/mvre.2001.2331"],["dc.identifier.isi","000170740600009"],["dc.identifier.pmid","11516246"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20033"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Academic Press Inc"],["dc.relation.issn","0026-2862"],["dc.title","Differences in cortical microcirculation in the kidneys of unilaterally congenital hydronephrotic rats"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

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

[["dc.bibliographiccitation.firstpage","43"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","British Journal of Cancer"],["dc.bibliographiccitation.lastpage","51"],["dc.bibliographiccitation.volume","103"],["dc.contributor.author","Eichenmueller, M."],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.contributor.author","von Schweinitz, Dietrich"],["dc.contributor.author","Kappler, Roland"],["dc.date.accessioned","2018-11-07T08:42:08Z"],["dc.date.available","2018-11-07T08:42:08Z"],["dc.date.issued","2010"],["dc.description.abstract","BACKGROUND: Rhabdomyosarcoma (RMS) is the most common soft-tissue sarcoma in childhood with the ability to resist apoptosis by the activation of survival promoting and anti-apoptotic proteins. METHODS: Efficacy of the apoptosis-inducing agent betulinic acid (BA) was determined in RMS cell cultures and in vivo by measuring cell viability, survival, apoptosis, hedgehog signalling activity, and neovascularisation. RESULTS: Betulinic acid had a strong cytotoxic effect on RMS cells in a dose-dependent manner. The BA treatment caused a massive induction of apoptosis mediated by the intrinsic mitochondrial pathway, which could be inhibited by the broad-range caspase inhibitor zVAD.fmk. Exposure of hedgehog-activated RMS-13 cells to BA resulted in a strong decrease in GLI1, GLI2, PTCH1, and IGF2 expression as well as hedgehog-responsive luciferase activity. Intraperitoneal injection of 20 mg BA per kg per day significantly retarded growth of RMS-13 xenografts in association with markedly higher counts of apoptotic cells and down-regulation of GLI1 expression compared with control tumours, while leaving microvascular density, cell proliferation, and myogenic differentiation unaffected. CONCLUSION: Our data show that induction of apoptosis and inhibition of hedgehog signalling are important features of the anti-tumourigenic effect of BA in RMS and advices this compound for the use in a multimodal therapy of this highly aggressive paediatric tumour. British Journal of Cancer (2010) 103, 43-51. doi:10.1038/sj.bjc.6605715 www.bjcancer.com Published online 1 June 2010 (C) 2010 Cancer Research UK"],["dc.identifier.doi","10.1038/sj.bjc.6605715"],["dc.identifier.isi","000279374800007"],["dc.identifier.pmid","20517313"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19638"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","0007-0920"],["dc.title","Betulinic acid induces apoptosis and inhibits hedgehog signalling in rhabdomyosarcoma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

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

[["dc.bibliographiccitation.firstpage","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"]]