Rave-Fränk, Margret

[["dc.bibliographiccitation.artnumber","385"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Basic Research in Cardiology"],["dc.bibliographiccitation.volume","108"],["dc.contributor.author","Sag, Can Martin"],["dc.contributor.author","Wolff, Hendrik Andreas"],["dc.contributor.author","Neumann, Kay"],["dc.contributor.author","Opiela, Marie-Kristin"],["dc.contributor.author","Zhang, J."],["dc.contributor.author","Steuer, Felicia"],["dc.contributor.author","Sowa, Thomas"],["dc.contributor.author","Gupta, Shamindra"],["dc.contributor.author","Schirmer, Markus"],["dc.contributor.author","Huenlich, Mark"],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Hess, Clemens Friedrich"],["dc.contributor.author","Anderson, Mark E."],["dc.contributor.author","Shah, Ajay M."],["dc.contributor.author","Christiansen, Hans"],["dc.contributor.author","Maier, Lars S."],["dc.date.accessioned","2018-11-07T09:19:46Z"],["dc.date.available","2018-11-07T09:19:46Z"],["dc.date.issued","2013"],["dc.description.abstract","Ionizing radiation (IR) is an integral part of modern multimodal anti-cancer therapies. IR involves the formation of reactive oxygen species (ROS) in targeted tissues. This is associated with subsequent cardiac dysfunction when applied during chest radiotherapy. We hypothesized that IR (i.e., ROS)-dependently impaired cardiac myocytes' Ca handling might contribute to IR-dependent cardiocellular dysfunction. Isolated ventricular mouse myocytes and the mediastinal area of anaesthetized mice (that included the heart) were exposed to graded doses of irradiation (sham 4 and 20 Gy) and investigated acutely (after similar to 1 h) as well as chronically (after similar to 1 week). IR induced a dose-dependent effect on myocytes' systolic function with acutely increased, but chronically decreased Ca transient amplitudes, which was associated with an acutely unaltered but chronically decreased sarcoplasmic reticulum (SR) Ca load. Likewise, in vivo echocardiography of anaesthetized mice revealed acutely enhanced left ventricular contractility (strain analysis) that declined after 1 week. Irradiated myocytes showed persistently increased diastolic SR Ca leakage, which was acutely compensated by an increase in SR Ca reuptake. This was reversed in the chronic setting in the face of slowed relaxation kinetics. As underlying cause, acutely increased ROS levels were identified to activate Ca/calmodulin-dependent protein kinase II (CaMKII). Accordingly, CaMKII-, but not PKA-dependent phosphorylation sites of the SR Ca release channels (RyR2, at Ser-2814) and phospholamban (at Thr-17) were found to be hyperphosphorylated following IR. Conversely, ROS-scavenging as well as CaMKII-inhibition significantly attenuated CaMKII-activation, disturbed Ca handling, and subsequent cellular dysfunction upon irradiation. Targeted cardiac irradiation induces a biphasic effect on cardiac myocytes Ca handling that is associated with chronic cardiocellular dysfunction. This appears to be mediated by increased oxidative stress and persistently activated CaMKII. Our findings suggest impaired cardiac myocytes Ca handling as a so far unknown mediator of IR-dependent cardiac damage that might be of relevance for radiation-induced cardiac dysfunction."],["dc.identifier.doi","10.1007/s00395-013-0385-6"],["dc.identifier.isi","000324877000001"],["dc.identifier.pmid","24068185"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10300"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28721"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/51"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | A03: Bedeutung CaMKII-abhängiger Mechanismen für die Arrhythmogenese bei Herzinsuffizienz"],["dc.relation.issn","0300-8428"],["dc.relation.workinggroup","RG L. Maier (Experimentelle Kardiologie)"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Ionizing radiation regulates cardiac Ca handling via increased ROS and activated CaMKII"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","145"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Radiation and Environmental Biophysics"],["dc.bibliographiccitation.lastpage","154"],["dc.bibliographiccitation.volume","50"],["dc.contributor.author","Wolff, Hendrik Andreas"],["dc.contributor.author","Rolke, David"],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Schirmer, Markus"],["dc.contributor.author","Eicheler, Wolfgang"],["dc.contributor.author","Doerfler, Annegret"],["dc.contributor.author","Hille, Andrea"],["dc.contributor.author","Hess, Clemens Friedrich"],["dc.contributor.author","Matthias, Christoph"],["dc.contributor.author","Roedel, Ralf M. W."],["dc.contributor.author","Christiansen, Hans"],["dc.date.accessioned","2018-11-07T08:58:47Z"],["dc.date.available","2018-11-07T08:58:47Z"],["dc.date.issued","2011"],["dc.description.abstract","The purpose of this work was to analyze chemokine and chemokine receptor expression in untreated and in irradiated squamous cell carcinoma of the head and neck (SCCHN) tumor cell lines, aiming at the establishment of assays to test for the relevance of chemokine and chemokine receptor expression in the response of SCCHN to radiotherapy and radiochemotherapy. Five low passage and 10 established SCCHN lines, as well as two normal cell lines, were irradiated at 2 Gy or sham-irradiated, and harvested between 1 and 48 h after treatment. For chemokines with CC and CXC structural motifs and their receptors, transcript levels of target and reference genes were quantified relatively by real-time PCR. In addition, CXCL1 and CXCL12 protein expression was analyzed by ELISA. A substantial variation in chemokine and chemokine receptor expression between SCCHN was detected. Practically, all cell lines expressed CCL5 and CCL20, while CCL2 was expressed in normal cells and in some of the tumor cell lines. CXCL1, CXCL2, CXCL3, CXCL10, and CXCL11 were expressed in the vast majority of the cell lines, while the expression of CXCL9 and CXCL12 was restricted to fibroblasts and few tumor cell lines. None of the analyzed cell lines expressed the chemokines CCL3, CCL4, or CCL19. Of the receptors, transcript expression of CCR1, CCR2, CCR3, CCR5, CCR7, CCXR2, and CCXR3 was not detected, and CCR6, CXCR1, and CXCR4 expression was restricted to few tumor cells. Radiation caused up- and down-regulation with respect to chemokine expressions, while for chemokine receptor expressions down-regulations were prevailing. CXCL1 and CXCL12 protein expression corresponded well with the mRNA expression. We conclude that the substantial variation in chemokine and chemokine receptor expression between SCCHN offer opportunities for the establishment of assays to test for the relevance of chemokine and chemokine receptor expression in the response of SCCHN to radiotherapy and radiochemotherapy."],["dc.identifier.doi","10.1007/s00411-010-0341-x"],["dc.identifier.isi","000287512400013"],["dc.identifier.pmid","21085979"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6619"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23728"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0301-634X"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Analysis of chemokine and chemokine receptor expression in squamous cell carcinoma of the head and neck (SCCHN) cell lines"],["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.firstpage","1"],["dc.bibliographiccitation.issue","19"],["dc.bibliographiccitation.journal","Radiation Oncology"],["dc.bibliographiccitation.lastpage","12"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Hermann, Robert Michael"],["dc.contributor.author","Wolff, Hendrik Andreas"],["dc.contributor.author","Jarry, Hubertus"],["dc.contributor.author","Thelen, Paul"],["dc.contributor.author","Gruendker, Carsten"],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Schmidberger, Heinz"],["dc.contributor.author","Christiansen, Hans"],["dc.date.accessioned","2018-11-07T11:13:00Z"],["dc.date.available","2018-11-07T11:13:00Z"],["dc.date.issued","2008"],["dc.description.abstract","Background: As the majority of prostate cancers (PC) express estrogen receptors, we evaluated the combination of radiation and estrogenic stimulation (estrogen and genistein) on the radiosensitivity of PC cells in vitro. Methods: PC cells LNCaP (androgen-sensitive) and PC-3 (androgen-independent) were evaluated. Estrogen receptor (ER) expression was analyzed by means of immunostaining. Cells were incubated in FCS-free media with genistein 10 mu M and estradiol 10 mu M 24 h before irradiation and up to 24 h after irradiation. Clonogenic survival, cell cycle changes, and expression of p21 were assessed. Results: LNCaP expressed both ER-alpha and ER-beta, PC-3 did not. Incubation of LNCaP and PC-3 with genistein resulted in a significant reduction of clonogenic survival. Incubation with estradiol exhibited in low concentrations (0.01 mu M) stimulatory effects, while higher concentrations did not influence survival. Both genistein 10 mu M and estradiol 10 mu M increased low-dose hyper-radiosensitivity [HRS] in LNCaP, while hormonal incubation abolished HRS in PC-3. In LNCaP cells hormonal stimulation inhibited p21 induction after irradiation with 4 Gy. In PC-3 cells, the proportion of cells in G2/M was increased after irradiation with 4 Gy. Conclusion: We found an increased HRS to low irradiation doses after incubation with estradiol or genistein in ER-a and ER-beta positive LNCaP cells. This is of high clinical interest, as this tumor model reflects a locally advanced, androgen dependent PC. In contrast, in ER-alpha and ER-beta negative PC-3 cells we observed an abolishing of the HRS to low irradiation doses by hormonal stimulation. The effects of both tested compounds on survival were ER and p53 independent. Since genistein and estradiol effects in both cell lines were comparable, neither ER- nor p53-expression seemed to play a role in the linked signalling. Nevertheless both compounds targeted the same molecular switch. To identify the underlying molecular mechanisms, further studies are needed."],["dc.description.sponsorship","University of Goettingen"],["dc.format.mimetype","application/pdf"],["dc.identifier.doi","10.1186/1748-717X-3-19"],["dc.identifier.fs","285846"],["dc.identifier.isi","000260416200001"],["dc.identifier.pmid","18625043"],["dc.identifier.ppn","575599979"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/4341"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53792"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1748-717X"],["dc.rights","Goescholar"],["dc.rights.access","openAccess"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","616"],["dc.title","In vitro studies on the modification of low-dose hyper-radiosensitivity in prostate cancer cells by incubation with genistein and estradiol"],["dc.title.subtitle","Research"],["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","637"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","International Journal of Molecular Sciences"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Sultan, Sadaf"],["dc.contributor.author","Ahmad, Shakil"],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Malik, Ihtzaz Ahmed"],["dc.contributor.author","Hess, Clemens Friedrich"],["dc.contributor.author","Christiansen, Hans"],["dc.contributor.author","Cameron, Silke"],["dc.date.accessioned","2018-11-07T10:14:35Z"],["dc.date.available","2018-11-07T10:14:35Z"],["dc.date.issued","2016"],["dc.description.abstract","Previously, we showed that lipocalin2 (LCN2) serum levels increased after liver irradiation and during acute-phase conditions. Here, we evaluate LCN2 expression and serum levels after single-dose lung irradiation with 25 Gy, percutaneously administered to the lung of randomly-paired male Wistar rats. Due to the concave anatomy of the lung recesses, the irradiation field included the upper part of the liver. No rat died due to irradiation. In control tissue, lung immunohistochemistry showed a high constitutive expression of LCN2+ granulocytes. LCN2 mRNA levels in lung tissue increased up to 24 h (9 +/- 2.3-fold) after irradiation. However, serum LCN2 levels remained undetectable after lung irradiation. LCN2 expression in the upper part of the liver increased up to 4.2-fold after lung irradiation, but the lower liver showed an early decrease. Acute-phase cytokines (IL-1 beta and TNF-beta) showed a significant increase on transcript level in both lung and upper liver, whilst the lower liver did not show any considerable increase. In conclusion, constitutive expression of LCN2 in local immune cells demonstrates its local role during stress conditions in the lung. The absence of LCN2 in the serum strengthens our previous findings that the liver is the key player in secreting LCN2 during stress conditions with liver involvement."],["dc.description.sponsorship","Open-Access Publikationsfonds 2016"],["dc.identifier.doi","10.3390/ijms17050637"],["dc.identifier.isi","000378791400031"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13241"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40644"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Mdpi Ag"],["dc.relation.issn","1422-0067"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Induction of Lipocalin2 in a Rat Model of Lung Irradiation"],["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","85"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Radiation and Environmental Biophysics"],["dc.bibliographiccitation.lastpage","94"],["dc.bibliographiccitation.volume","48"],["dc.contributor.author","Guerleyen, Hakan"],["dc.contributor.author","Christiansen, Hans"],["dc.contributor.author","Tello, Khodr"],["dc.contributor.author","Dudas, Joszef"],["dc.contributor.author","Hermann, Robert Michael"],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Hess, Clemens Friedrich"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Saile, Bernhard"],["dc.date.accessioned","2018-11-07T08:33:19Z"],["dc.date.available","2018-11-07T08:33:19Z"],["dc.date.issued","2009"],["dc.description.abstract","This study aimed to reveal the pathophysiological signalling responsible for radiation-induced sensitization of hepatocytes to TNF-alpha-mediated apoptosis. I kappa B was upregulated in irradiated hepatocytes. Administration of I kappa B antisense oligonucleotides prior to irradiation inhibited occurrence of apoptosis after TNF-alpha administration. Caspases-8, -9 and -3 activities were increased in irradiated hepatocytes and downregulation of apoptosis by I kappa B antisense oligonucleotides was mediated by suppression of caspases-9 and -3 activation but not of caspase-8 activation, suggesting that radiation-induced sensitization of hepatocytes to TNF-alpha-mediated apoptosis additionally requires changes upstream of caspase-8 activation. Herein, upregulation of FLIP may play a crucial role. Cleavage of bid, upregulation of bax, downregulation of bcl-2 and release of cytochrome c after TNF-alpha-administration depend on radiation-induced upregulation of I kappa B, thus demonstrating an apoptosis permitting effect of I kappa B."],["dc.description.sponsorship","Deutsche Krebshilfe [106760]"],["dc.identifier.doi","10.1007/s00411-008-0200-1"],["dc.identifier.isi","000262316300009"],["dc.identifier.pmid","18956207"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?goescholar/3523"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17548"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","1432-2099"],["dc.relation.issn","0301-634X"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Irradiation leads to sensitization of hepatocytes to TNF-alpha-mediated apoptosis by upregulation of I kappa B expression"],["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","31"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","31"],["dc.bibliographiccitation.journal","Radiation Oncology"],["dc.bibliographiccitation.lastpage","10"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Hermann, Robert Michael"],["dc.contributor.author","Schwarten, Dag"],["dc.contributor.author","Fister, Stefanie"],["dc.contributor.author","Grundker, Carsten"],["dc.contributor.author","Rave-Frank, Margret"],["dc.contributor.author","Nitsche, Mirko"],["dc.contributor.author","Hille, Andrea"],["dc.contributor.author","Thelen, Paul"],["dc.contributor.author","Schmidberger, Heinz"],["dc.contributor.author","Christiansen, Hans"],["dc.date.accessioned","2018-11-07T10:59:33Z"],["dc.date.available","2018-11-07T10:59:33Z"],["dc.date.issued","2007"],["dc.description.abstract","Background: Oncological results of radiotherapy for locally advanced prostate cancer (PC) are significantly improved by simultaneous application of LHRH analoga (e. g. goserelin). As 85% of PC express LHRH receptors, we investigated the interaction of goserelin incubation with radiotherapy under androgen-deprived conditions in vitro. Methods: LNCaP and PC-3 cells were stained for LHRH receptors. Downstream the LHRH receptor, changes in protein expression of c-fos, phosphorylated p38 and phosphorylated ERK1/2 were analyzed by means of Western blotting after incubation with goserelin and irradiation with 4 Gy. Both cell lines were incubated with different concentrations of goserelin in hormone-free medium. 12 h later cells were irradiated (0 - 4 Gy) and after 12 h goserelin was withdrawn. Endpoints were clonogenic survival and cell viability (12 h, 36 h and 60 h after irradiation). Results: Both tested cell lines expressed LHRH-receptors. Changes in protein expression demonstrated the functional activity of goserelin in the tested cell lines. Neither in LNCaP nor in PC-3 any significant effects of additional goserelin incubation on clonogenic survival or cell viability for all tested concentrations in comparison to radiation alone were seen. Conclusion: The clinically observed increase in tumor control after combination of goserelin with radiotherapy in PC cannot be attributed to an increase in radiosensitivity of PC cells by goserelin in vitro."],["dc.description.sponsorship","Deutsche Krebshilfe [106240]"],["dc.format.mimetype","application/pdf"],["dc.identifier.doi","10.1186/1748-717X-2-31"],["dc.identifier.fs","119077"],["dc.identifier.isi","000260343200001"],["dc.identifier.pmid","17718927"],["dc.identifier.ppn","559810636"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/4370"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50728"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1748-717X"],["dc.rights","Goescholar"],["dc.rights.access","openAccess"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","616"],["dc.title","No supra-additive effects of goserelin and radiotherapy on clonogenic survival of prostate carcinoma cells in vitro"],["dc.title.subtitle","Research"],["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","545"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Breast Cancer Research and Treatment"],["dc.bibliographiccitation.lastpage","550"],["dc.bibliographiccitation.volume","126"],["dc.contributor.author","Bogdanova, Natalia"],["dc.contributor.author","Sokolenko, Anna P."],["dc.contributor.author","Iyevleva, Aglaya G."],["dc.contributor.author","Abysheva, Svetlana N."],["dc.contributor.author","Blaut, Magda"],["dc.contributor.author","Bremer, Michael"],["dc.contributor.author","Christiansen, Hans"],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Doerk, Thilo"],["dc.contributor.author","Imyanitov, Evgeny N."],["dc.date.accessioned","2018-11-07T08:57:52Z"],["dc.date.available","2018-11-07T08:57:52Z"],["dc.date.issued","2011"],["dc.description.abstract","Since germline mutations in the PALB2 (Partner and Localizer of BRCA2) gene have been identified as breast cancer (BC) susceptibility alleles, the geographical spread and risks associated with PALB2 mutations are subject of intense investigation. Patients with bilateral breast cancer constitute a valuable group for genetic studies. We have thus scanned the whole coding region of PALB2 in a total of 203 German or Russian bilateral breast cancer patients using an approach based on high-resolution melting analysis and direct sequencing of genomic DNA samples. Truncating PALB2 mutations were identified in 4/203 (2%) breast cancer patients with bilateral disease. The two nonsense mutations, p.E545X and p.Q921X, have not been previously described whereas the two other mutations, p.R414X and c.509_510delGA, are recurrent. Our results indicate that PALB2 germline mutations account for a small, but not negligible, proportion of bilateral breast carcinomas in German and Russian populations."],["dc.identifier.doi","10.1007/s10549-010-1290-4"],["dc.identifier.isi","000288251000028"],["dc.identifier.pmid","21165770"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7349"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23508"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0167-6806"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","PALB2 mutations in German and Russian patients with bilateral breast cancer"],["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","1801"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","American Journal Of Pathology"],["dc.bibliographiccitation.lastpage","1815"],["dc.bibliographiccitation.volume","176"],["dc.contributor.author","Malik, Ihtzaz Ahmed"],["dc.contributor.author","Moriconi, Federico"],["dc.contributor.author","Sheikh, Nadeem"],["dc.contributor.author","Naz, Naila"],["dc.contributor.author","Khan, Sajjad"],["dc.contributor.author","Dudas, Jozsef"],["dc.contributor.author","Mansuroglu, Tuemen"],["dc.contributor.author","Hess, Clemens Friedrich"],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Christiansen, Hans"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T08:44:15Z"],["dc.date.available","2018-11-07T08:44:15Z"],["dc.date.issued","2010"],["dc.description.abstract","Liver damage is a serious clinical complication of gamma-irradiation. We therefore exposed rats to single-dose gamma-irradiation (25 Gy) that was focused on the liver. Three to six hours after irradiation, an increased number of neutrophils (but not mononuclear phagocytes) was observed by immunohistochemistry to be attached to portal vessels between and around the portal (myo)fibroblasts (smooth muscle actin and Thy-1(+) cells). MCP-1/CCL2 staining was also detected in the portal vessel walls, including some cells of the portal area. CC-chemokine (MCP-1/CCL2 and MCP-3/CCL7) and CXC-chemokine (KC/CXCL1, MIP-2/CXCL2, and LIX/CXCL5) gene expression was significantly induced in total RNA from irradiated livers. In laser capture microdissected samples, an early (1 to 3 hours) up-regulation of CCL2, CXCL1, CXCL8, and CXCR2 gene expression was detected in the portal area but not in the parenchyma; with the exception of CXCL1 gene expression. In addition, treatment with an antibody against MCP-1/CCL2 before irradiation led to an increase in gene expression of interferon-gamma and IP-10/CXCL10 in liver tissue without influencing the recruitment of granulocytes. Indeed, the CCL2, CXCL1, CXCL2, and CXCL5 genes were strongly expressed and further up-regulated in liver (myo)fibroblasts after irradiation (8 Gy). Taken together, these results suggest that gamma-irradiation of the liver induces a transient accumulation of granulocytes within the portal area and that (myo)fibroblasts of the portal vessels may be one of the major sources of the chemokines involved in neutrophil recruitment. Moreover, inhibition of more than one chemokine (eg, CXCL1 and CXCL8) may be necessary to reduce leukocytes recruitment. (Am J Pathol 2010, 176:1801-1815; DOI. 10.2353/ajpath.2010.090505)"],["dc.description.sponsorship","Deutsche Krebshilfe [108774]; Bundesamt fur Strahlenschutz [StSch4546]"],["dc.identifier.doi","10.2353/ajpath.2010.090505"],["dc.identifier.isi","000276471500027"],["dc.identifier.pmid","20185578"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6274"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20155"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Investigative Pathology, Inc"],["dc.relation.issn","0002-9440"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Single-Dose Gamma-Irradiation Induces Up-Regulation of Chemokine Gene Expression and Recruitment of Granulocytes into the Portal Area but Not into Other Regions of Rat Hepatic Tissue"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","5379"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY"],["dc.bibliographiccitation.lastpage","5392"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Martius, Gesa"],["dc.contributor.author","Alwahsh, Salamah Mohammad"],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Hess, Clemens Friedrich"],["dc.contributor.author","Christiansen, Hans"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Malik, Ihtzaz Ahmed"],["dc.date.accessioned","2018-11-07T09:45:42Z"],["dc.date.available","2018-11-07T09:45:42Z"],["dc.date.issued","2014"],["dc.description.abstract","Irradiation is known to induce inflammation and affect fat metabolic pathways. The current study investigates hepatic fat accumulation and fatty acid transportation in a rat model of single dose liver irradiation (25-Gy). Rat livers were selectively irradiated in-vivo (25-Gy), sham-irradiated rats served as controls. Hepatic lipids were studied by colorimetric assays in liver and serum. Intracellular lipids, protein and mRNA were studied by Nile red staining, immunohistology, Western Blot analysis and RT-PCR in liver, respectively. Changes in FAT/CD36 expression were studied in-vitro in a human monocyte cell line U937 after irradiation in presence or absence of infliximab (IFX). Nile Red staining of liver cryosections showed a quick (12-48 h) increase in fat droplets. Accordingly, hepatic triglycerides (TG) and free fatty acids (FFA) were elevated. An early increase (3-6 h) in the serum level of HDL-C, TG and cholesterol was measured after single dose irradiation followed by a decrease thereafter. Furthermore, expression of the fat transporter protein FAT/CD36 was increased, immunohistochemistry revealed basolateral and cytoplasmic expression in hepatocytes. Moreover, apolipoprotein-B100, -C3 and enzymes (acetyl-CoA carboxylase, lipoprotein-lipase, carnitine-palmitoyltransferase, malonyl-CoA-decarboxylase) involved in fat metabolism were induced at 12-24 h. Early activation of the NFk beta pathway (I kappa B alpha) by TNF-alpha was seen, followed by a significant elevation of serum markers for liver damage (AST and GLDH). TNF-alpha blockage by anti-TNF-alpha in cell culture (U937) prevented the increase of FAT/CD36 caused by irradiation. Selective liver irradiation is a model for rapid induction of steatosis hepatis and fat accumulation could be triggered by irradiation-induced inflammatory mediators (e g. TNF-alpha)."],["dc.description.sponsorship","Open-Access Publikationsfonds 2014"],["dc.identifier.isi","000345120900098"],["dc.identifier.pmid","25197426"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10890"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34684"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","E-century Publishing Corp"],["dc.relation.issn","1936-2625"],["dc.rights","CC BY-NC 3.0"],["dc.rights","Goescholar"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/3.0"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Hepatic fat accumulation and regulation of FAT/CD36: an effect of hepatic irradiation"],["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","261"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Radiation and Environmental Biophysics"],["dc.bibliographiccitation.lastpage","270"],["dc.bibliographiccitation.volume","49"],["dc.contributor.author","Hille, Andrea"],["dc.contributor.author","Grueger, Susanne"],["dc.contributor.author","Christiansen, Hans"],["dc.contributor.author","Wolff, Hendrik Andreas"],["dc.contributor.author","Volkmer, Beate"],["dc.contributor.author","Lehmann, Joerg"],["dc.contributor.author","Doerr, Wolfgang"],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.date.accessioned","2018-11-07T08:43:51Z"],["dc.date.available","2018-11-07T08:43:51Z"],["dc.date.issued","2010"],["dc.description.abstract","Purpose of this work was to test the effect of tumour-cell-derived keratinocyte growth factor (KGF) or recombinant KGF (palifermin) on cell proliferation and radiation response of human HNSCC cells and normal keratinocytes in vitro. Four tumour cell cultures derived from head and neck squamous cell carcinomas, primary keratinocytes, and immortalized keratinocytes were analysed. Fibroblasts, the natural source of KGF protein, served as controls. KGF expression was observed in primary and immortalized keratinocytes, fibroblasts, and in tumour cells, while significant KGF receptor expression was only found in keratinocytes. Recombinant KGF as well as tumour-cell-derived KGF caused a significant growth stimulation and radioprotection in keratinocytes, which was abolished by a neutralizing anti-KGF antibody. This indicates that tumour-cell-derived KGF is biologically active. In the tumour cell lines, no significant growth stimulation was induced by recombinant KGF, and the neutralizing antibody did not influence tumour cell growth or radiation response. Our results indicate that the normal, paracrine KGF regulatory mechanisms, which are based on KGF receptor expression, are lost in malignant cells, with the consequence of irresponsiveness of the tumour cells to exogenous KGF. In face of the amelioration of the radiation response of normal epithelia, demonstrated in various clinical and various preclinical animal studies, recombinant KGF represents a candidate for the selective protection of normal epithelia during radio(chemo) therapy of squamous cell carcinoma."],["dc.identifier.doi","10.1007/s00411-010-0271-7"],["dc.identifier.isi","000276745900016"],["dc.identifier.pmid","20213138"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/4243"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20068"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0301-634X"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Effect of tumour-cell-derived or recombinant keratinocyte growth factor (KGF) on proliferation and radioresponse of human epithelial tumour cells (HNSCC) and normal keratinocytes in vitro"],["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"]]