Now showing 1 - 8 of 8
  • 2007Conference Abstract
    [["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 prĂĽfen"],["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"]]
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  • 2017Journal Article
    [["dc.bibliographiccitation.journal","Molecular and Clinical Oncology"],["dc.contributor.author","Sievers, Denise"],["dc.contributor.author","Bunzendahl, Jens"],["dc.contributor.author","Frosch, Alice"],["dc.contributor.author","Perske, Christina"],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.contributor.author","Schliephake, Henning"],["dc.contributor.author","Brockmeyer, Phillipp"],["dc.date.accessioned","2021-06-01T10:48:53Z"],["dc.date.available","2021-06-01T10:48:53Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.3892/mco.2017.1514"],["dc.identifier.eissn","2049-9469"],["dc.identifier.issn","2049-9450"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86085"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","2049-9469"],["dc.relation.issn","2049-9450"],["dc.title","Generation of highly differentiated BHY oral squamous cell carcinoma multicellular spheroids"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]
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  • 2010Journal Article
    [["dc.bibliographiccitation.firstpage","335"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","World Journal of Urology"],["dc.bibliographiccitation.lastpage","341"],["dc.bibliographiccitation.volume","28"],["dc.contributor.author","Bedke, Jens"],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.contributor.author","Perske, Christina"],["dc.contributor.author","Gross, Andreas"],["dc.contributor.author","Heuser, Markus"],["dc.date.accessioned","2018-11-07T08:43:06Z"],["dc.date.available","2018-11-07T08:43:06Z"],["dc.date.issued","2010"],["dc.description.abstract","Renal cell carcinomas (RCC) frequently express the gastrin-releasing peptide receptor (GRP-R). Gastrin-releasing peptide (GRP) stimulates tumor cell proliferation and neoangiogenesis. Tumor-associated macrophages (TAM) comprise an important cellular component of these tumors. We analyzed the GRP/GRP-R network in clear cell RCC (ccRCC) and non-clear cell RCC (non-ccRCC) with special regard to its expression by macrophages, tumor cells and microvessels. Gastrin-releasing peptide and GRP-R expression in 17 ccRCC and 9 non-ccRCC were analyzed by RT-PCR, immunohistochemistry and double immunofluorescence staining. Tumor-associated macrophages expressed GRP and GRP receptor in ccRCC. Tumor cells and microvessels showed low to intermediate GRP-R expression in nearly all cases. In 12 ccRCC tumor epithelia also expressed low levels of GRP. Microvascular GRP expression was found in nine cases of ccRCC. For non-RCC, the expression of GRP and GRP receptor expression pattern was similar. Tumor-associated macrophages are the main source of GRP in RCC. GRP receptor on TAM, tumor epithelia and microvessels might be a molecular base of a GRP/GRP receptor network, potentially acting as a paracrine/autocrine modulator of TAM recruitment, tumor growth and neoangiogenesis."],["dc.identifier.doi","10.1007/s00345-009-0492-z"],["dc.identifier.isi","000277943600014"],["dc.identifier.pmid","20012906"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/4239"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19876"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0724-4983"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Tumor-associated macrophages in clear cell renal cell carcinoma express both gastrin-releasing peptide and its receptor: a possible modulatory role of immune effectors cells"],["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"]]
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  • 2017Journal Article
    [["dc.bibliographiccitation.artnumber","14677"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Brockmeyer, Phillipp"],["dc.contributor.author","Kling, Alexander"],["dc.contributor.author","Schulz, Xenia"],["dc.contributor.author","Perske, Christina"],["dc.contributor.author","Schliephake, Henning"],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.date.accessioned","2018-06-25T07:26:32Z"],["dc.date.available","2018-06-25T07:26:32Z"],["dc.date.issued","2017"],["dc.description.abstract","This study evaluates the effects of tumour-associated mast cells on the prognosis of patients suffering from oral squamous cell carcinoma (OSCC). Tryptase-positive (MCT+) and CD117-positive (CD117+) mast cells were immunohistochemically evaluated in tissue samples of 118 OSCC patients. Besides, various clinicopathological parameters, the influence of the MCT+ and CD117+ mast cell density on overall survival and the incidence of first local recurrence was analysed by Cox regression and competing risk regression. Among all investigated parameters, multiple Cox regression revealed a significant influence of the MCT+ (cut-off at 14.87 mast cells/mm2 stroma; p = 0.0027) and CD117+ mast cell density (cut-off at 33.19 mast cells/mm2 stroma; p = 0.004), the age at primary diagnosis, and the T and N stage (all p-values < 0.05) on overall survival. Patients with a low mast cell density showed a significantly poorer overall survival rate compared to those with a high mast cell density in the tumour-associated stroma. Competing risk regression revealed a significant influence of the resection status (R) on the incidence of first local recurrence (p = 0.0023). A high mast cell density in the tumour-associated stroma of oral squamous cell carcinoma indicates a longer patient survival."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2017"],["dc.identifier.doi","10.1038/s41598-017-15406-5"],["dc.identifier.pmid","29116177"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14831"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/15131"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.eissn","2045-2322"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","High mast cell density indicates a longer overall survival in oral squamous cell carcinoma"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]
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  • 2007Conference Abstract
    [["dc.bibliographiccitation.firstpage","395"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Pathology - Research and Practice"],["dc.bibliographiccitation.lastpage","396"],["dc.bibliographiccitation.volume","203"],["dc.contributor.author","Perske, Christina"],["dc.contributor.author","Huemmer, T."],["dc.contributor.author","Kroesel, J."],["dc.contributor.author","Rahat, Michal A."],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.date.accessioned","2018-11-07T11:07:23Z"],["dc.date.available","2018-11-07T11:07:23Z"],["dc.date.issued","2007"],["dc.identifier.isi","000247312300358"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52548"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Gmbh, Urban & Fischer Verlag"],["dc.publisher.place","Jena"],["dc.relation.issn","0344-0338"],["dc.title","Characterisation of hypoxia and NOS activity in the subcutaneous RENCA (renal carcinoma) mouse model"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2009Conference Abstract
    [["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Cytokine"],["dc.bibliographiccitation.volume","48"],["dc.contributor.author","Rahat, Michal A."],["dc.contributor.author","Perske, Christina"],["dc.contributor.author","Sheffy, Sharon"],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.contributor.author","Lahat, Nitza"],["dc.date.accessioned","2018-11-07T11:23:27Z"],["dc.date.available","2018-11-07T11:23:27Z"],["dc.date.issued","2009"],["dc.format.extent","48"],["dc.identifier.doi","10.1016/j.cyto.2009.07.133"],["dc.identifier.isi","000270855100144"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56201"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Academic Press Ltd- Elsevier Science Ltd"],["dc.publisher.place","London"],["dc.relation.conference","Tri-Society Annual Conference of the International-Cytokine-Society/International-Society-of-Interferon-and-C ytokine-Research/Society-of-Leukocyte-Biology"],["dc.relation.eventlocation","Lisbon, PORTUGAL"],["dc.relation.issn","1043-4666"],["dc.title","Loss of iNOS expression in the mouse renal cell carcinoma RENCA cell line is mediated by miR-146a and confers resistance to macrophage-induced apoptosis"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2014Journal Article
    [["dc.bibliographiccitation.firstpage","273"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","International Journal of Oncology"],["dc.bibliographiccitation.lastpage","281"],["dc.bibliographiccitation.volume","45"],["dc.contributor.author","Brockmeyer, Phillipp"],["dc.contributor.author","Jung, Klaus"],["dc.contributor.author","Perske, Christina"],["dc.contributor.author","Schliephake, Henning"],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.date.accessioned","2018-11-07T09:38:40Z"],["dc.date.available","2018-11-07T09:38:40Z"],["dc.date.issued","2014"],["dc.description.abstract","The aim of the present study was to evaluate the expression and localization of connexin (Cx) 26, -43 and -45 in a group of 35 patients with primary oral squamous cell carcinoma (OSCC) with the objective of making a more accurate disease prognosis. We analysed the expression of connexins in tissue samples of primary OSCC, matching oral mucosa free of dysplasia, and its associated lymph node metastases (LNM) by semi-quantitative immunohistochemistry of membrane, cytoplasmic and nuclear connexin expression. The levels of expression were correlated with the overall survival time (OS). Cx43 was overexpressed in tumour cells compared to epithelia in dysplasia-free mucosa. High membrane expression of Cx43 on tumour cells was the only statistically significant and independent prognostic factor of short OS (P=0.0088). Membrane expression of Cx43 in matching dysplasia-free mucosa acted similarly, but did not reach statistical significance (P=0.059). No correlation was found between the Cx26, Cx45 expression and OS. We conclude that Cx43 expression in dysplasia-free mucosa may indicate a very early stage of tumour promotion. Although overexpression of Cx43 is found in invasive tumours we only found membrane Cx43 expression to correlate with OS. This observation suggests that cytoplasmic Cx43 serves as storage and only membrane translocation may promote the formation of gap junctions and gap junctional intercellular communication (GJIC) with prognostic relevance."],["dc.identifier.doi","10.3892/ijo.2014.2394"],["dc.identifier.isi","000336881600030"],["dc.identifier.pmid","24788723"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33114"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Spandidos Publ Ltd"],["dc.relation.issn","1791-2423"],["dc.relation.issn","1019-6439"],["dc.title","Membrane connexin 43 acts as an independent prognostic marker in oral squamous cell carcinoma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2010Journal Article
    [["dc.bibliographiccitation.firstpage","2046"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","The American journal of pathology"],["dc.bibliographiccitation.lastpage","2054"],["dc.bibliographiccitation.volume","177"],["dc.contributor.author","Perske, Christina"],["dc.contributor.author","Lahat, Nitza"],["dc.contributor.author","Sheffy Levin, Sharon"],["dc.contributor.author","Bitterman, Haim"],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.contributor.author","Rahat, Michal Amit"],["dc.date.accessioned","2019-07-09T11:53:00Z"],["dc.date.available","2019-07-09T11:53:00Z"],["dc.date.issued","2010"],["dc.description.abstract","Tumor-associated macrophages can potentially kill tumor cells via the high concentrations of nitric oxide (NO) produced by inducible nitric oxide synthase (iNOS); however, tumor-associated macrophages actually support tumor growth, as they are skewed toward M2 activation, which is characterized by low amounts of NO production and is proangiogenic. We show that the mouse renal cell carcinoma cell line, RENCA, which, on stimulation, expresses high levels of iNOS mRNA, loses its ability to express the iNOS protein. This effect is mediated by the microRNA miR-146a, as inhibition of RENCA cells with anti-miR- 146a restores iNOS expression and NO production (4.8 ± 0.4 versus 0.3 ± 0.1 μmol/L in uninhibited cells, P < 0.001). In vivo, RENCA tumor cells do not stain for iNOS, while infiltrating tumor-associated macrophages showed intense staining, and both cell types expressed iNOS mRNA. Restoring iNOS protein expression in RENCA cells using anti-miR-146a increases macrophage-induced death of RENCA cells by 73% (P < 0.01) in vitro and prevents tumor growth in vivo. These results suggest that, in addition to NO production by macrophages, tumor cells must produce NO to induce their own deaths, and some tumor cells may use miR-146a to reduce or abolish endogenous NO production to escape macrophage-mediated cell death. Thus, inhibiting miR-146a may render these tumor cells susceptible to therapeutic strategies, such as adoptive transfer of M1-activated macrophages."],["dc.identifier.doi","10.2353/ajpath.2010.091111"],["dc.identifier.fs","576544"],["dc.identifier.pmid","20709800"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6304"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60317"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1525-2191"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.subject.mesh","Animals"],["dc.subject.mesh","Apoptosis"],["dc.subject.mesh","Blotting, Western"],["dc.subject.mesh","Carcinoma, Renal Cell"],["dc.subject.mesh","Cell Movement"],["dc.subject.mesh","Cell Proliferation"],["dc.subject.mesh","Female"],["dc.subject.mesh","In Situ Hybridization"],["dc.subject.mesh","Kidney Neoplasms"],["dc.subject.mesh","Macrophages"],["dc.subject.mesh","Mice"],["dc.subject.mesh","Mice, Inbred BALB C"],["dc.subject.mesh","MicroRNAs"],["dc.subject.mesh","Neovascularization, Pathologic"],["dc.subject.mesh","Nitric Oxide"],["dc.subject.mesh","Nitric Oxide Synthase Type II"],["dc.subject.mesh","Protein Biosynthesis"],["dc.subject.mesh","RNA, Messenger"],["dc.subject.mesh","Reverse Transcriptase Polymerase Chain Reaction"],["dc.title","Loss of inducible nitric oxide synthase expression in the mouse renal cell carcinoma cell line RENCA is mediated by microRNA miR-146a."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]
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