Hemmerlein, Bernhard

[["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","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 prüfen"],["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"]]

[["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"]]

[["dc.bibliographiccitation.artnumber","262"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Frontiers in physiology"],["dc.bibliographiccitation.lastpage","2"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Rahat, Michal A."],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.contributor.author","Iragavarapu-Charyulu, Vijaya"],["dc.date.accessioned","2019-07-09T11:41:12Z"],["dc.date.available","2019-07-09T11:41:12Z"],["dc.date.issued","2014"],["dc.identifier.doi","10.3389/fphys.2014.00262"],["dc.identifier.pmid","25071604"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11806"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58370"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","1664-042X"],["dc.relation.issn","1664-042X"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.title","The regulation of angiogenesis by tissue cell-macrophage interactions."],["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.artnumber","144"],["dc.bibliographiccitation.journal","Frontiers in Physiology"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Rahat, Michal A."],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.date.accessioned","2018-11-07T09:30:59Z"],["dc.date.available","2018-11-07T09:30:59Z"],["dc.date.issued","2013"],["dc.description.abstract","Tumor cell-macrophage interactions change as the tumor progresses, and the generation of nitric oxide (NO) by the inducible nitric oxide synthase (iNOS) plays a major role in this interplay. In early stages, macrophages employ their killing mechanisms, particularly the generation of high concentrations of NO and its derivative reactive nitrogen species (RNS) to initiate tumor cell apoptosis and destroy emerging transformed cells. If the tumor escapes the immune system and grows, macrophages that infiltrate it are reprogramed in situ by the tumor microenvironment. Low oxygen tensions (hypoxia) and immunosuppressive cytokines inhibit iNOS activity and lead to production of low amounts of NO/RNS, which are pro-angiogenic and support tumor growth and metastasis by inducing growth factors (e.g., VEGF) and matrix metalloproteinases (MMPs). We review here the different roles of NO/RNS in tumor progression and inhibition, and the mechanisms that regulate iNOS expression and NO production, highlighting the role of different subtypes of macrophages and the microenvironment. We finally claim that some tumor cells may become resistant to macrophage-induced death by increasing their expression of microRNA-146a (miR-146a), which leads to inhibition of iNOS translation. This implies that some cooperation between tumor cells and macrophages is required to induce tumor cell death, and that tumor cells may control their fate. Thus, in order to induce susceptibility of tumors cells to macrophage-induced death, we suggest a new therapeutic approach that couples manipulation of miR-146a levels in tumors with macrophage therapy, which relies on ex vivo stimulation of macrophages and their re introduction to tumors."],["dc.identifier.doi","10.3389/fphys.2013.00144"],["dc.identifier.isi","000346774000142"],["dc.identifier.pmid","23785333"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31438"],["dc.language.iso","en"],["dc.notes.intern","DeepGreen Import"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","1664-042X"],["dc.relation.issn","1664-042X"],["dc.rights","http://creativecommons.org/licenses/by/3.0/"],["dc.title","Macrophage-tumor cell interactions regulate the function of nitric oxide"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1606"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Molecular Endocrinology"],["dc.bibliographiccitation.lastpage","1621"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Kaulfuss, Silke"],["dc.contributor.author","Grzmil, Michal"],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.contributor.author","Thelen, Paul"],["dc.contributor.author","Schweyer, Stefan"],["dc.contributor.author","Neesen, Juergen"],["dc.contributor.author","Bubendorf, Lukas"],["dc.contributor.author","Glass, Andrew G."],["dc.contributor.author","Jarry, Hubertus"],["dc.contributor.author","Auber, Bernd"],["dc.contributor.author","Burfeind, Peter"],["dc.date.accessioned","2018-11-07T11:13:42Z"],["dc.date.available","2018-11-07T11:13:42Z"],["dc.date.issued","2008"],["dc.description.abstract","In the present study, we demonstrate that leupaxin mRNA is overexpressed in prostate cancer (PCa) as compared with normal prostate tissue by using cDNA arrays and quantitative RT-PCR analyses. Moderate to strong expression of leupaxin protein was detected in approximately 22% of the PCa tissue sections analyzed, and leupaxin expression intensities were found to be significantly correlated with Gleason patterns/scores. In addition, different leupaxin expression levels were observed in PCa cell lines, and at the subcellular level, leupaxin was usually localized in focal adhesion sites. Furthermore, mutational analysis and transfection experiments of LNCaP cells using different green fluorescent protein-leupaxin constructs demonstrated that leupaxin contains functional nuclear export signals in its LD3 and LD4 motifs, thus shuttling between the cytoplasm and the nucleus. We could also demonstrate for the first time that leupaxin interacts with the androgen receptor in a ligand-dependent manner and serves as a transcriptional activator of this hormone receptor in PCa cells. Down-regulation of leupaxin expression using RNA interference in LNCaP cells resulted in a high rate of morphological changes, detachment, spontaneous apoptosis, and a reduction of prostate-specific antigen secretion. In contrast, knockdown of leupaxin expression in androgen-independent PC-3 and DU 145 cells induced a significant decrease of both the invasive capacity and motility. Our results therefore indicate that leupaxin could serve as a potential progression marker for a subset of PCa and may represent a novel coactivator of the androgen receptor. Leupaxin could function as a putative target for therapeutic interventions of a subset of advanced PCa."],["dc.identifier.doi","10.1210/me.2006-0546"],["dc.identifier.isi","000257144500008"],["dc.identifier.pmid","18451096"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6155"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53958"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Endocrine Soc"],["dc.relation.issn","0888-8809"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Leupaxin, a novel coactivator of the androgen receptor, is expressed in prostate cancer and plays a role in adhesion and invasion of 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.artnumber","41"],["dc.bibliographiccitation.journal","Molecular Cancer"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Hemmerlein, Bernhard"],["dc.contributor.author","Weseloh, Rüdiger M."],["dc.contributor.author","Mello de Queiroz, Fernanda"],["dc.contributor.author","Knötgen, Hendrik"],["dc.contributor.author","Sanchez, Araceli"],["dc.contributor.author","Rubio, Maria E."],["dc.contributor.author","Martin, Sabine"],["dc.contributor.author","Schliephacke, Tessa"],["dc.contributor.author","Jenke, Marc"],["dc.contributor.author","Radzun, Heinz-Joachim"],["dc.contributor.author","Stühmer, Walter"],["dc.contributor.author","Pardo, Luis A."],["dc.date.accessioned","2018-11-07T09:07:28Z"],["dc.date.available","2018-11-07T09:07:28Z"],["dc.date.issued","2006"],["dc.description.abstract","Background: Certain types of potassium channels (known as Eag1, KCNHO1, Kv10.1) are associated with the production of tumours in patients and in animals. We have now studied the expression pattern of the Eag1 channel in a large range of normal and tumour tissues from different collections utilising molecular biological and immunohistochemical techniques. Results: The use of reverse transcription real-time PCR and specifically generated monoclonal anti-Eag1 antibodies showed that expression of the channel is normally limited to specific areas of the brain and to restricted cell populations throughout the body. Tumour samples, however, showed a significant overexpression of the channel with high frequency (up to 80% depending on the tissue source) regardless of the detection method (staining with either one of the antibodies, or detection of Eag1 RNA). Conclusion: Inhibition of Eag1 expression in tumour cell lines reduced cell proliferation. Eag1 may therefore represent a promising target for the tailored treatment of human tumours. Furthermore, as normal cells expressing Eag1 are either protected by the blood-brain barrier or represent the terminal stage of normal differentiation, Eag1 based therapies could produce only minor side effects."],["dc.identifier.doi","10.1186/1476-4598-5-41"],["dc.identifier.isi","000241536800001"],["dc.identifier.pmid","17022810"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25801"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","Najko"],["dc.relation.issn","1476-4598"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Overexpression of EagI potassium channels in clinical tumours"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["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"]]