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","189"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Radiology"],["dc.bibliographiccitation.lastpage","197"],["dc.bibliographiccitation.volume","242"],["dc.contributor.author","Christiansen, Hans"],["dc.contributor.author","Sheikh, Nadeem"],["dc.contributor.author","Saile, Bernhard"],["dc.contributor.author","Reuter, Felix"],["dc.contributor.author","Rave-Frank, Margret"],["dc.contributor.author","Hermann, Robert Michael"],["dc.contributor.author","Dudas, Jozsef"],["dc.contributor.author","Hille, Andrea"],["dc.contributor.author","Hess, Clemens Friedrich"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T11:07:32Z"],["dc.date.available","2018-11-07T11:07:32Z"],["dc.date.issued","2007"],["dc.description.abstract","Purpose: To prospectively analyze hepcidin, hemojuvelin and ferro-portin-1 expression after x-irradiation or rat liver and isolated rat hepacocytes. Materials and Methods: The treatment of the rats and this study were improved by the local committee and the public authority on animal welfare. Rat livers in vivo and isolated rat hepatocytes in vitro were irradiated. The total number of rats in this study was 43. RNA extracted from livers (1, 3, 6, 12, 24, and 48 hours after irradiation) and from hepatocytes (1, 3, 6, 12, and 24 hours after irradiation) was analyzed with real-time polymerase chain reaction and Northern blot. Cytokines and prohepcidin in serum of irradiated rats were quantitatively detected with enzyme-linked immunosorbent assay. Sham-irradiated animals served as controls in all experiments. Differences between sham-irradiated and irradiated data groups were tested with anaylsis of variance and Dunnett post hoc test. Results: In vivo, a significant radiation-induced increase of hepcidin (P = .034), interleukin (IL) 1 beta (P = .008), IL-6 (P < .011), and tumor necrosis factor alpha (TNF-alpha) (P = .047) expression could be detected within the first 48 hours after irradiation. Expression of hemojuvelin (P = .008) and ferro-portin-1 (P = .002) was significantly decreased. Serum iron levels were decreased because of irradiation (P < .058); prohepcidin serum levels were increased (P = .05). In rat hepatocytes in vitro, hepcidin RNA levels were significantly downregulated after irradiation (P < .001). Incubation of irradiated hepatocytes with IL-1 beta, IL-6, or TNNF-alpha led to upregulation of hepcidin expression in vitro up to 6 hours after irradiation, with subsequent significant down-regulation for incubation with IL-1 beta (P < .001). Hemojuvelin expression behaved in a way opposite to that of hepcidin. Conclusion: x-Irradiation of the liver, induced changes of hepcidin gene expression that are probably induced by acute phase mediators produced within the liver, itself."],["dc.identifier.doi","10.1148/radiol.2421060083"],["dc.identifier.isi","243842500024"],["dc.identifier.pmid","17090718"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52584"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Radiological Soc North America"],["dc.relation.issn","0033-8419"],["dc.title","x-irradiation in rat liver: Consequent upregulation of hepcidin and downregulation of hemojuvelin and ferroportin-1 gene expression"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","321"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Radiation and Environmental Biophysics"],["dc.bibliographiccitation.lastpage","338"],["dc.bibliographiccitation.volume","52"],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Malik, Ihtzaz Ahmed"],["dc.contributor.author","Christiansen, Hans"],["dc.contributor.author","Naz, Naila"],["dc.contributor.author","Sultan, Sadaf"],["dc.contributor.author","Amanzada, Ahmad"],["dc.contributor.author","Blaschke, Martina"],["dc.contributor.author","Cameron, Silke"],["dc.contributor.author","Ahmad, Shakil"],["dc.contributor.author","Hess, Clemens Friedrich"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Moriconi, Federico"],["dc.date.accessioned","2018-11-07T09:22:03Z"],["dc.date.available","2018-11-07T09:22:03Z"],["dc.date.issued","2013"],["dc.description.abstract","The liver is considered a radiosensitive organ. However, in rats, high single-dose irradiation (HDI) showed only mild effects. Consequences of fractionated irradiation (FI) in such an animal model have not been studied so far. Rats were exposed to selective liver FI (total dose 60 Gy, 2 Gy/day) or HDI (25 Gy) and were killed three months after the end of irradiation. To study acute effects, HDI-treated rats were additionally killed at several time points between 1 and 48 h. Three months after irradiation, no differences between FI and HDI treatment were found for macroscopically detectable small \"scars\" on the liver surface and for an increased number of neutrophil granulocytes distributed in the portal fields and through the liver parenchyma. As well, no changes in HE-stained tissues or clear signs of fibrosis were found around the portal vessels. Differences were seen for the number of bile ducts being increased in FI- but not in HDI-treated livers. Serum levels indicative of liver damage were determined for alkaline phosphatase (AP), aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyltransferase (gamma GT) and lactate dehydrogenase (LDH). A significant increase of AP was detected only after FI while HDI led to the significant increases of AST and LDH serum levels. By performing RT-PCR, we detected up-regulation of matrix metalloproteinases, MMP-2, MMP-9, MMP-14, and of their inhibitors, TIMP-1, TIMP-2 and TIMP-3, shortly after HDI, but not at 3 month after FI or HDI. Overall, we saw punctual differences after FI and HDI, and a diffuse formation of small scars at the liver surface. Lack of \"provisional clot\"-formation and absence of recruitment of mononuclear phagocytes could be one explanation for scar formation as incomplete repair response to irradiation."],["dc.identifier.doi","10.1007/s00411-013-0468-7"],["dc.identifier.isi","000322033000004"],["dc.identifier.pmid","23595725"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29250"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0301-634X"],["dc.title","Rat model of fractionated (2 Gy/day) 60 Gy irradiation of the liver: long-term effects"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","41"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","International Journal of Radiation Biology"],["dc.bibliographiccitation.lastpage","47"],["dc.bibliographiccitation.volume","83"],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Schmidberger, Heinz"],["dc.contributor.author","Christiansen, Hans"],["dc.contributor.author","Boll, Christine"],["dc.contributor.author","Lehmann, Joerg"],["dc.contributor.author","Weiss, Elisabeth"],["dc.date.accessioned","2018-11-07T11:06:44Z"],["dc.date.available","2018-11-07T11:06:44Z"],["dc.date.issued","2007"],["dc.description.abstract","Background and purpose: To test the combined effects of oxaliplatin and radiation versus cisplatin and radiation using human cervical and lung cancer cell lines. Material and Methods: CaSki cervical cancer cells, and A549 lung cancer cells were cultured under standard conditions. Cells were treated with escalating doses of gamma-irradiation (0 - 6 Gy), and with oxali- and cisplatin for 2 h or 24 h, or a combination of both. Cell survival was measured by a colony-forming assay. Survival curves were fitted to the data using the linear quadratic model. Sensitizer enhancement ratios (SER) were calculated at the 37% survival level, and isobologram analysis was applied to test for the drug-radiation interactions. Results: Oxaliplatin as well as cisplatin alone were cytotoxic in both cell lines. In CaSki cells, oxaliplatin and cisplatin significantly increased radiation toxicity. In A549 cells no increase of radiation toxicity was observed after treatment with cisplatin, however, isobologram analysis revealed supra-additive interaction between oxaliplatin and radiation in A549 cells. Conclusion: Oxaliplatin had the same effectiveness on tumor cells as cisplatin and induced enhanced radiation toxicity in lung cancer cells, where cisplatin was not able to achieve radiosensitization."],["dc.identifier.doi","10.1080/09553000601121108"],["dc.identifier.isi","000244144600004"],["dc.identifier.pmid","17357438"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52386"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Taylor & Francis Ltd"],["dc.relation.issn","0955-3002"],["dc.title","Comparison of the combined action of oxaliplatin or cisplatin and radiation in cervical and lung cancer cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","29"],["dc.bibliographiccitation.lastpage","39"],["dc.bibliographiccitation.seriesnr","1213"],["dc.contributor.author","Krause, Petra"],["dc.contributor.author","Rave-Frank, Margret"],["dc.contributor.author","Christiansen, Hans"],["dc.contributor.author","Koenig, Sarah"],["dc.contributor.editor","Christ, Bruno"],["dc.contributor.editor","Oerlecke, Jana"],["dc.contributor.editor","Stock, Peggy"],["dc.date.accessioned","2021-06-02T10:44:23Z"],["dc.date.available","2021-06-02T10:44:23Z"],["dc.date.issued","2014"],["dc.identifier.doi","10.1007/978-1-4939-1453-1_3"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/87018"],["dc.notes.intern","DOI-Import GROB-425"],["dc.publisher","Springer New York"],["dc.publisher.place","New York, NY"],["dc.relation.crisseries","Methods in Molecular Biology"],["dc.relation.eisbn","978-1-4939-1453-1"],["dc.relation.isbn","978-1-4939-1452-4"],["dc.relation.ispartof","Methods in Molecular Biology"],["dc.relation.ispartof","Animal Models for Stem Cell Therapy"],["dc.relation.ispartofseries","Methods in Molecular Biology; 1213"],["dc.title","Preconditioning of the Liver for Efficient Repopulation by Primary Hepatocyte Transplants"],["dc.type","book_chapter"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","621"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","The Oncologist"],["dc.bibliographiccitation.lastpage","631"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Wolff, Hendrik Andreas"],["dc.contributor.author","Conradi, Lena-Christin"],["dc.contributor.author","Schirmer, Markus Anton"],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Sprenger, Thilo"],["dc.contributor.author","Rave-Fränk, Margret"],["dc.contributor.author","Hennies, Steffen"],["dc.contributor.author","Hess, Clemens Friedrich"],["dc.contributor.author","Becker, Heinz"],["dc.contributor.author","Christiansen, Hans"],["dc.contributor.author","Liersch, Torsten"],["dc.date.accessioned","2018-11-07T09:01:50Z"],["dc.date.available","2018-11-07T09:01:50Z"],["dc.date.issued","2011"],["dc.description.abstract","Patients with locally advanced rectal cancer (cUICC stages II/III) are typically treated with preoperative 5-fluorouracil-based (5-FU-based) radiochemotherapy (RCT). However, trials are currently being conducted to improve the complete remission rates and the systemic control by combining 5-FU with oxaliplatin. The primary objective was to identify the subgroups of rectal cancer patients who were at risk for high-grade toxicity. All 196 patients who were included in the present study were treated with 50.4 Gy and chemotherapy that included either 5-FU (n = 115) or 5-FU + oxaliplatin (n + 81). The preoperative RCT was followed by a total mesorectal excision and adjuvant chemotherapy. Acute toxicity was monitored weekly and a toxicity grade >= 3 (Common Toxicity Criteria) for a skin reaction, cystitis, proctitis, or enteritis was defined as high-grade acute organ toxicity. After RCT with 5-FU + oxaliplatin, complete tumor remission was achieved in 13.6% of the patients and in 11.3% after RCT with 5-FU alone. Complete irradiation dosages of 50.4 Gy were given to 99% (5-FU) and 95% (5-FU + oxaliplatin) of the patients. Concomitant chemotherapy was fully administered in 95% of the patients treated with 5-FU compared with the 84% of patients treated with 5-FU + oxaliplatin. A significantly higher proportion of acute organ toxicity was found in the patients who were treated with 5-FU + oxaliplatin compared with those who were treated with 5-FU. Additionally, women with a low body mass index were at the highest risk for acute organ toxicity. These results suggest that there are basic clinical parameters, such as gender and body mass index, that may be potential markers for generating individual risk profiles of RCT-induced toxicity. The Oncologist 2011;16:621-631"],["dc.identifier.doi","10.1634/theoncologist.2010-0414"],["dc.identifier.isi","000290661900012"],["dc.identifier.pmid","21558132"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24528"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Alphamed Press"],["dc.relation.issn","1083-7159"],["dc.title","Gender-Specific Acute Organ Toxicity during Intensified Preoperative Radiochemotherapy for Rectal Cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","285"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","International Journal of Radiation Biology"],["dc.bibliographiccitation.lastpage","298"],["dc.bibliographiccitation.volume","84"],["dc.contributor.author","Koenig, Sarah"],["dc.contributor.author","Krause, Petra"],["dc.contributor.author","Schmidt, Thordis-Karen"],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Rothe, Hilka"],["dc.contributor.author","Hermann, Robert Michael"],["dc.contributor.author","Becker, Heinz"],["dc.contributor.author","Hess, Clemens Friedrich"],["dc.contributor.author","Christiansen, Hans"],["dc.date.accessioned","2018-11-07T11:20:07Z"],["dc.date.available","2018-11-07T11:20:07Z"],["dc.date.issued","2008"],["dc.description.abstract","Purpose: Hepatocyte transplantation following liver irradiation (IR) and partial hepatectomy (PH) leads to extensive liver repopulation. We investigated the changes in the liver induced by IR explaining the loss of reproductive integrity in endogenous hepatocytes. Materials and methods: Right lobules of rat liver underwent external beam IR (25 Gy). A second group was subjected to additional 33% PH of the untreated left liver lobule. Liver specimens and controls were analyzed for DNA damage, apoptosis, proliferation and cell cycle related genes (1 hour to up to 12 weeks). Results: Double strand breaks (phosphorylated histone H2AX) induced by IR rapidly declined within hours and were no longer detectable after 4 days. No significant apoptosis was noted and steady mRNA levels (B-cell lymphoma 2-associated X protein (BAX), caspase 3 and 9) were in line with the lack of DNA fragmentation. However, gene expression of p53 and p21 in irradiated liver tissue increased. Transcripts of cyclin D1, proliferating cell nuclear antigen (PCNA), and cyclin B augmented progressively, whereas cyclin E was only affected moderately. Following PH, irradiated livers displayed persistently high protein levels of p21 and cyclin D1. However, cell divisions were infrequent, as reflected by low PCNA levels up to four weeks. Conclusion: IR leads to a major arrest in the G1/S phase and to a lesser extent in the G2/M transition of the cell cycle, resulting in reduced regenerative response following PH. The persistent block of at least four weeks may promote preferential proliferation of transplanted hepatocytes in this milieu."],["dc.identifier.doi","10.1080/09553000801953359"],["dc.identifier.isi","000254631200004"],["dc.identifier.pmid","18386194"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55458"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Taylor & Francis Ltd"],["dc.relation.issn","1362-3095"],["dc.relation.issn","0955-3002"],["dc.title","Irradiation as preparative regimen for hepatocyte transplantation causes prolonged cell cycle block"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","30"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Strahlentherapie und Onkologie"],["dc.bibliographiccitation.lastpage","35"],["dc.bibliographiccitation.volume","186"],["dc.contributor.author","Wolff, Hendrik Andreas"],["dc.contributor.author","Gaedcke, Jochen"],["dc.contributor.author","Jung, Klaus"],["dc.contributor.author","Hermann, Robert Michael"],["dc.contributor.author","Rothe, Hilka"],["dc.contributor.author","Schirmer, Markus"],["dc.contributor.author","Liersch, Torsten"],["dc.contributor.author","Herrmann, Markus Karl Alfred"],["dc.contributor.author","Hennies, Steffen"],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Hess, Clemens Friedrich"],["dc.contributor.author","Christiansen, Hans"],["dc.date.accessioned","2018-11-07T08:48:37Z"],["dc.date.available","2018-11-07T08:48:37Z"],["dc.date.issued","2010"],["dc.description.abstract","Purpose: To test for a possible correlation between high-grade acute organ toxicity during preoperative radiochemotherapy and complete tumor regression after total mesorectal excision in multimodal treatment of Locally advanced rectal cancer. Patients and Methods: From 2001 to 2008, 120 patients were treated. Preoperative treatment consisted of normofractionated radiotherapy at a total dose of 50.4 Gy, and either two cycles of 5-fluorouracil (5-FU) or two cycles of 5-FU and oxaliplatin. Toxicity during treatment was monitored weekly, and any toxicity CTC (Common Toxicity Criteria) grade 2 of enteritis, proctitis or cystitis was assessed as high-grade organ toxicity for later analysis. Complete histopathologic tumor regression (TRG4) was defined as the absence of any viable tumor cells. Results: A significant coherency between high-grade acute organ toxicity and complete histopathologic tumor regression was found, which was independent of other factors Like the preoperative chemotherapy schedule. The probability of patients with acute organ toxicity >= grade 2 to achieve TRG4 after neoadjuvant treatment was more than three times higher than for patients without toxicity (odds ratio: 3.29, 95% confidence interval: [1.01, 10.96]). Conclusion: Acute organ toxicity during preoperative radiochemotherapy in rectal cancer could be an early predictor of treatment response in terms of complete tumor regression. Its possible impact on local control and survival is under further prospective evaluation by the authors' working group."],["dc.description.sponsorship","German Research Foundation (DFG) [KFO 179]"],["dc.identifier.doi","10.1007/s00066-009-2037-1"],["dc.identifier.isi","000273623400005"],["dc.identifier.pmid","20082185"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21259"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Urban & Vogel"],["dc.relation.issn","0179-7158"],["dc.title","High-Grade Acute Organ Toxicity During Preoperative Radiochemotherapy as Positive Predictor for Complete Histopathologic Tumor Regression in Multimodal Treatment of Locally Advanced Rectal Cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","149"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","International Journal of Radiation Oncology*Biology*Physics"],["dc.bibliographiccitation.lastpage","157"],["dc.bibliographiccitation.volume","83"],["dc.contributor.author","Schirmer, Markus Anton"],["dc.contributor.author","Mergler, Caroline Patricia Nadine"],["dc.contributor.author","Rave-Fränk, Margret"],["dc.contributor.author","Herrmann, Markus Karl Alfred"],["dc.contributor.author","Hennies, Steffen"],["dc.contributor.author","Gaedcke, Jochen"],["dc.contributor.author","Conradi, Lena-Christin"],["dc.contributor.author","Jo, Peter"],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Hess, Clemens Friedrich"],["dc.contributor.author","Becker, Heinz"],["dc.contributor.author","Ghadimi, Michael B."],["dc.contributor.author","Brockmöller, Jürgen"],["dc.contributor.author","Christiansen, Hans"],["dc.contributor.author","Wolff, Hendrik Andreas"],["dc.date.accessioned","2018-11-07T09:10:56Z"],["dc.date.available","2018-11-07T09:10:56Z"],["dc.date.issued","2012"],["dc.description.abstract","Purpose: Transforming growth factor-beta1 is related to adverse events in radiochemotherapy. We investigated TGFB1 genetic variability in relation to quality of life-impairing acute organ toxicity (QAOT) of neoadjuvant radiochemotherapy under clinical trial conditions. Methods and Materials: Two independent patient cohorts (n = 88 and n = 75) diagnosed with International Union Against Cancer stage II/III rectal cancer received neoadjuvant radiation doses of 50.4 Gy combined with 5-fluorouracil-based chemotherapy. Toxicity was monitored according to Common Terminology Criteria for Adverse Events. QAOT was defined as a CTCAE grade >= 2 for at least one case of enteritis, proctitis, cystitis, or dermatitis. Nine germline polymorphisms covering the common genetic diversity in the TGFB1 gene were genotyped. Results: In both cohorts, all patients carrying the TGFB1 Pro25 variant experienced QAOT (positive predictive value of 100%, adjusted p = 0.0006). In a multivariate logistic regression model, gender, age, body mass index, type of chemotherapy, or disease state had no significant impact on QAOT. Conclusion: The TGFB1 Pro25 variant could be a relevant marker for individual treatment stratification and carriers may benefit from adaptive clinical care or specific radiation techniques. (C) 2012 Elsevier Inc."],["dc.description.sponsorship","German Research Foundation (DFG) [KFO 179]"],["dc.identifier.doi","10.1016/j.ijrobp.2011.05.063"],["dc.identifier.isi","000302993900044"],["dc.identifier.pmid","22000747"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26603"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","0360-3016"],["dc.title","Acute Toxicity of Radiochemotherapy in Rectal Cancer Patients: A Risk Particularly for Carriers of the TGFB1 Pro25 variant"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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"]]