Nitsche, Mirko

[["dc.bibliographiccitation.firstpage","819"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Journal of Rehabilitation Medicine"],["dc.bibliographiccitation.lastpage","823"],["dc.bibliographiccitation.volume","48"],["dc.contributor.author","Costa-Ribeiro, A"],["dc.contributor.author","Maux, A"],["dc.contributor.author","Bosford, T"],["dc.contributor.author","Tenório, Y"],["dc.contributor.author","Marques, D"],["dc.contributor.author","Carneiro, M"],["dc.contributor.author","Nitsche, M"],["dc.contributor.author","Filho, A"],["dc.contributor.author","Monte-Silva, K"],["dc.date.accessioned","2020-12-10T18:43:47Z"],["dc.date.available","2020-12-10T18:43:47Z"],["dc.date.issued","2016"],["dc.identifier.doi","10.2340/16501977-2134"],["dc.identifier.issn","1650-1977"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78227"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Dopamine-independent effects of combining transcranial direct current stimulation with cued gait training on cortical excitability and functional mobility in Parkinson’s disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1254"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Arteriosclerosis, Thrombosis, and Vascular Biology"],["dc.bibliographiccitation.lastpage","1259"],["dc.bibliographiccitation.volume","26"],["dc.contributor.author","Schäfer, Katrin"],["dc.contributor.author","Schroeter, Marco R."],["dc.contributor.author","Dellas, Claudia"],["dc.contributor.author","Puls, Miriam"],["dc.contributor.author","Nitsche, Mirko"],["dc.contributor.author","Weiss, Elisabeth"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Konstantinides, Stavros V."],["dc.date.accessioned","2017-09-07T11:52:41Z"],["dc.date.available","2017-09-07T11:52:41Z"],["dc.date.issued","2006"],["dc.description.abstract","Objective - To investigate the ability of bone marrow ( BM) - derived cells to modulate neointimal growth after injury by expressing plasminogen activator inhibitor-1 ( PAI-1). Methods and Results - We performed BM transplantation ( BMT) in lethally irradiated wild- type ( WT) and PAI-1-/- mice. Three weeks after carotid injury with ferric chloride, analysis of Y-chromosome DNA expression in the vessel wall of female hosts revealed that 20.8 +/- 6.0% of the cells in the neointima and 37.6 +/- 5.7% of those in the media were of BM origin. Lack of PAI-1 in either the host or the donor cells did not affect recruitment of BM-derived cells into sites of vascular injury. The neointima consisted predominantly of smooth muscle cells, and a proportion of these cells expressed PAI-1. Overall, lack of PAI-1 was associated with enhanced neointimal formation. However, importantly, BMTWT -> PAI-1-/- mice exhibited reduced neointimal area ( P = 0.05) and luminal stenosis ( P = 0.04) compared with BMTPAI-1-/--> PAI-1-/- mice. Although PAI-1-expressing cells were shown to be present in BMTWT -> PAI-1-/- lesions, these mice did not exhibit detectable levels of the inhibitor in the circulation, suggesting that local production of PAI-1 by cells in the neointima and media was sufficient to reduce luminal stenosis. Conclusions - PAI-1 from BM-derived cells appears capable of suppressing neointimal growth after vascular injury."],["dc.identifier.doi","10.1161/01.ATV.0000215982.14003.b7"],["dc.identifier.gro","3143681"],["dc.identifier.isi","000237644000012"],["dc.identifier.pmid","16514083"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1221"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1079-5642"],["dc.title","Plasminogen Activator Inhibitor-1 From Bone Marrow–Derived Cells Suppresses Neointimal Formation After Vascular Injury in Mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","699"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Medizinische Klinik - Intensivmedizin und Notfallmedizin"],["dc.bibliographiccitation.lastpage","707"],["dc.bibliographiccitation.volume","114"],["dc.contributor.author","Friesecke, S."],["dc.contributor.author","Träger, K."],["dc.contributor.author","Schittek, G. A."],["dc.contributor.author","Molnar, Z."],["dc.contributor.author","Bach, F."],["dc.contributor.author","Kogelmann, K."],["dc.contributor.author","Bogdanski, R."],["dc.contributor.author","Weyland, A."],["dc.contributor.author","Nierhaus, A."],["dc.contributor.author","Nestler, F."],["dc.contributor.author","Olboeter, D."],["dc.contributor.author","Tomescu, D."],["dc.contributor.author","Jacob, D."],["dc.contributor.author","Haake, H."],["dc.contributor.author","Grigoryev, E."],["dc.contributor.author","Nitsch, M."],["dc.contributor.author","Baumann, A."],["dc.contributor.author","Quintel, M."],["dc.contributor.author","Schott, M."],["dc.contributor.author","Kielstein, J. T."],["dc.contributor.author","Meier-Hellmann, A."],["dc.contributor.author","Born, F."],["dc.contributor.author","Schumacher, U."],["dc.contributor.author","Singer, M."],["dc.contributor.author","Kellum, J."],["dc.contributor.author","Brunkhorst, F. M."],["dc.date.accessioned","2020-12-10T14:07:57Z"],["dc.date.available","2020-12-10T14:07:57Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1007/s00063-017-0342-5"],["dc.identifier.eissn","2193-6226"],["dc.identifier.issn","2193-6218"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70342"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Internationales Register zur Nutzung des Adsorbers CytoSorb® bei Intensivpatienten"],["dc.title.alternative","International registry on the use of the CytoSorb® adsorber in ICU patients. Study protocol and preliminary results"],["dc.title.subtitle","Studienprotokoll und erste Ergebnisse"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","195"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Strahlentherapie und Onkologie"],["dc.bibliographiccitation.lastpage","202"],["dc.bibliographiccitation.volume","183"],["dc.contributor.author","Hermann, Robert Michael"],["dc.contributor.author","Fest, Jan"],["dc.contributor.author","Christiansen, Hans"],["dc.contributor.author","Hille, Andrea"],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Nitsche, Mirko"],["dc.contributor.author","Gruendker, Carsten"],["dc.contributor.author","Viereck, Volker"],["dc.contributor.author","Jarry, Hubertus"],["dc.contributor.author","Schmidberger, Heinz"],["dc.date.accessioned","2018-11-07T11:03:57Z"],["dc.date.available","2018-11-07T11:03:57Z"],["dc.date.issued","2007"],["dc.description.abstract","Background and Purpose: Simultaneous radiotherapy with chemotherapy is a standard treatment for inoperable non-small cell lung cancer (NSCLC), but the clinical outcome still remains poor. To further intensify treatment, substances need to be identified, which increase the effect of radiation on tumor cells without further enhancing toxicity to normal tissue. Hormones have a different toxicity profile than radiation or cytostatic drugs. As NSCLC often express estrogen receptors (ERs), the combination of genistein or estradiol and radiation in vitro was investigated. Material and Methods: A549 NSCLC cells with an inducible expression of a mutated TP53 and fibroblasts of a male donor (DF-18) were examined. ER expression was immunocytologically confirmed in all studied cell lines. Clonogenic survival was measured after incubation of the cells with genistein or estradiol (0.01 mu M and 10 mu M as maximum clinically applicable dose) and irradiation with different doses (0-4 Gy). The differentiation state of fibroblasts after combined therapy was analyzed. Results: A549 cells expressing mutated TP53 were more radioresistant than TP53 wild-type cells. Incubation of nonfunctional TP53 cells with genistein or estradiol increased radiosensitivity in both tested concentrations. By contrast, radiosensitivity of A549 with wild-type TP53 and DF-18 was not altered by hormonal incubation. In DF-18 radiation induced growth arrest that was not increased by additional hormonal incubation. Conclusion: NSCLC cells with nonfunctional TP53 might be sensitized against radiation by genistein or estradiol. As genistein is better tolerable than estradiol in patients, additional studies are warranted to assess potential gains of this combination therapy."],["dc.identifier.doi","10.1007/s00066-007-1561-0"],["dc.identifier.isi","000245452600006"],["dc.identifier.pmid","17406801"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51725"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Urban & Vogel"],["dc.relation.issn","0179-7158"],["dc.title","Radiosensitization dependent on p53 function in bronchial carcinoma cells by the isoflavone genistein and estradiol in vitro"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1544"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Nature Neuroscience"],["dc.bibliographiccitation.lastpage","1553"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Mildner, Alexander"],["dc.contributor.author","Schmidt, Hauke"],["dc.contributor.author","Nitsche, Mirko"],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Mack, Matthias"],["dc.contributor.author","Heikenwalder, Mathias"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Priller, Josef"],["dc.contributor.author","Prinz, Marco R."],["dc.date.accessioned","2018-11-07T10:49:48Z"],["dc.date.available","2018-11-07T10:49:48Z"],["dc.date.issued","2007"],["dc.description.abstract","Microglia are crucially important myeloid cells in the CNS and constitute the first immunological barrier against pathogens and environmental insults. The factors controlling microglia recruitment from the blood remain elusive and the direct circulating microglia precursor has not yet been identified in vivo. Using a panel of bone marrow chimeric and adoptive transfer experiments, we found that circulating Ly-6C(hi)CCR2(+) monocytes were preferentially recruited to the lesioned brain and differentiated into microglia. Notably, microglia engraftment in CNS pathologies, which are not associated with overt blood-brain barrier disruption, required previous conditioning of brain (for example, by direct tissue irradiation). Our results identify Ly-6C(hi)CCR2(+) monocytes as direct precursors of microglia in the adult brain and establish the importance of local factors in the adult CNS for microglia engraftment."],["dc.identifier.doi","10.1038/nn2015"],["dc.identifier.isi","000251172900011"],["dc.identifier.pmid","18026096"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48513"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1097-6256"],["dc.title","Microglia in the adult brain arise from Ly-6C(hi)CCR2(+) monocytes only under defined host conditions"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1814"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Blood"],["dc.bibliographiccitation.lastpage","1823"],["dc.bibliographiccitation.volume","110"],["dc.contributor.author","Uhmann, Anja"],["dc.contributor.author","Dittmann, Kai"],["dc.contributor.author","Nitzki, Frauke"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Koleva, Milena"],["dc.contributor.author","Frommhold, Anke"],["dc.contributor.author","Zibat, Arne"],["dc.contributor.author","Binder, Claudia"],["dc.contributor.author","Adham, Ibrahim M."],["dc.contributor.author","Nitsche, Mirko"],["dc.contributor.author","Heller, Tanja"],["dc.contributor.author","Armstrong, Victor"],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Wienands, Juergen"],["dc.contributor.author","Hahn, Heidi"],["dc.date.accessioned","2018-11-07T10:58:34Z"],["dc.date.available","2018-11-07T10:58:34Z"],["dc.date.issued","2007"],["dc.description.abstract","A first step in hematopoiesis is the specification of the lymphoid and myeloid lineages from multipotent progenitor cells in the bone marrow. Using a conditional ablation strategy in adult mice, we show that this differentiation step requires Patched (Ptch), the cell surface-bound receptor for Hedgehog (Hh). In the absence of Ptch, the development of T- and B-lymphoid lineages is blocked at the level of the common lymphoid progenitor in the bone marrow. Consequently, the generation of peripheral T and B cells is abrogated. Cells of the myeloid lineage develop normally in Ptch mutant mice. Finally, adoptive transfer experiments identified the stromal cell compartment as a critical Ptch-dependent inducer of lymphoid versus myeloid lineage commitment. Our data show that Ptch acts as a master switch for proper diversification of hematopoietic stem cells in the adult organism."],["dc.identifier.doi","10.1182/blood-2007-02-075648"],["dc.identifier.isi","000249671700022"],["dc.identifier.pmid","17536012"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50494"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Hematology"],["dc.relation.issn","0006-4971"],["dc.title","The Hedgehog receptor Patched controls lymphoid lineage commitment"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","447"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","International Journal of Clinical Oncology"],["dc.bibliographiccitation.lastpage","452"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Nitsche, Mirko"],["dc.contributor.author","Prinz, Marco"],["dc.contributor.author","Hermann, Robert Michael"],["dc.contributor.author","Christiansen, Hans"],["dc.contributor.author","Weiss, Elisabeth"],["dc.date.accessioned","2021-06-01T10:49:17Z"],["dc.date.available","2021-06-01T10:49:17Z"],["dc.date.issued","2005"],["dc.identifier.doi","10.1007/s10147-005-0529-2"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86233"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","1437-7772"],["dc.relation.issn","1341-9625"],["dc.title","Paraganglioma of the cerebellum: case report and review of the literature"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","643"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","International Journal of Radiation Biology"],["dc.bibliographiccitation.lastpage","657"],["dc.bibliographiccitation.volume","84"],["dc.contributor.author","Nitsche, Mirko"],["dc.contributor.author","Christiansen, Hans"],["dc.contributor.author","Hermann, Robert Michael"],["dc.contributor.author","Luecke, Eva-Maria"],["dc.contributor.author","Peters, Kerstin"],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Schmidberger, Heinz"],["dc.contributor.author","Pradier, Olivier"],["dc.date.accessioned","2018-11-07T11:20:07Z"],["dc.date.available","2018-11-07T11:20:07Z"],["dc.date.issued","2008"],["dc.description.abstract","Purpose: Despite proven antitumor activity of gemcitabine in chemoradiotherapy of advanced head and neck cancer, many authors refer to severe acute and late local and haematological toxicity. Fludarabine does imply nearly the same mechanisms of action as gemcitabine, inhibiting various enzymes involved in DNA replication. This investigation focuses on the combined effect of either fludarabine or gemcitabine and radiation on human squamous carcinoma cell lines in vitro, providing data for future decisions on head and neck chemoradiotherapy regimen. Materials and methods: ZMK-1, A549, BW-225, GR-145, OH-65 and CaSki cell lines were incubated with either drug at defined schedules and irradiated at a single fraction dose of 2 Gy every 24 hours up to 8 Gy. Cytotoxic effects were measured by colony-forming assays, quantitative determination of apoptosis and isobologram analysis. Results: Incubation of fludarabine led to a radiosensitizing effect in the A549, CaSki and ZMK-1 cell lines and an additive effect in the BW-225, GR-145 and OH-65 cell lines. Treatment with gemcitabine only indicated significant radiosensitization in the CaSki cell line in combination with augmented resistance against gemcitabine application alone. Conclusions: Our results reveal a potential radiosensitizing effect of fludarabine and its possible application in chemoradiotherapy of advanced head and neck carcinoma and possibly other tumor entities."],["dc.identifier.doi","10.1080/09553000802241754"],["dc.identifier.isi","000258002000003"],["dc.identifier.pmid","18661380"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55460"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Informa Healthcare"],["dc.relation.issn","0955-3002"],["dc.title","The combined effect of fludarabine monophosphate and radiation as well as gemcitabine and radiation on squamous carcinoma tumor cell lines in vitro"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","483"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Oncology Reports"],["dc.bibliographiccitation.lastpage","488"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Strik, H. M."],["dc.contributor.author","Schmidt, K."],["dc.contributor.author","Lingor, P."],["dc.contributor.author","Tönges, L."],["dc.contributor.author","Kugler, W."],["dc.contributor.author","Nitsche, M."],["dc.contributor.author","Rabinovich, G. A."],["dc.contributor.author","Bähr, M."],["dc.date.accessioned","2017-09-07T11:49:27Z"],["dc.date.available","2017-09-07T11:49:27Z"],["dc.date.issued","2007"],["dc.description.abstract","Galectins are evolutionarily conserved beta-galactoside-binding lectins which recognize specific glycoconjugates on the cell surface and the extracellular matrix. Accumulating evidence indicates that these proteins are involved in a variety of physiological and pathological processes including tumor growth and metastasis. Up-regulated expression of galectin-1 is a hallmark of a variety of malignant tumors. Here, we examined the expression of galectin-1 in glioma cell lines, the influence of ionizing irradiation and the intracellular and extracellular effects of this protein on tumor cell proliferation and migration. Galectin-1 was detected in both A172 and U118 glioma cells by immunoblot analysis. Ionizing irradiation induced a statistically significant up-regulation in glioma cell lines. RNA-interference-mediated silencing resulted in a significant suppression of the proliferation of the A172 cells, while the addition of recombinant galectin-1 had no effect. On the other hand, the migratory capacity of both cell lines was reduced after galectin-1 down-regulation, and up-regulated by the addition of exogenous galectin-1. Our results provide evidence of a role for galectin-1 in the regulation of glioma cell proliferation and migration. While an intracellular mechanism seemed to prevail in galectin-1-mediated regulation of tumor cell proliferation, the control of cell migration was exerted by both intracellular and extracellular mechanisms. In addition, this protein was up-regulated by ionizing radiation, indicating that the blockade of this protein should be performed before radiotherapy to avoid any undesired stimulating effects. Given the multifactorial role of galectin-1 in the regulation of tumor escape and metastasis, we conclude that targeting galectin-1 may have therapeutic benefits in the treatment of malignant glioma."],["dc.identifier.doi","10.3892/or.18.2.483"],["dc.identifier.gro","3143463"],["dc.identifier.isi","000248298300027"],["dc.identifier.pmid","17611674"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/980"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1021-335X"],["dc.relation.issn","1021-335X"],["dc.title","Galectin-1 expression in human glioma cells: Modulation by ionizing radiation and effects on tumor cell proliferation and migration"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1067"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","International Journal of Radiation Oncology*Biology*Physics"],["dc.bibliographiccitation.lastpage","1074"],["dc.bibliographiccitation.volume","65"],["dc.contributor.author","Christiansen, Hans"],["dc.contributor.author","Hermann, Robert Michael"],["dc.contributor.author","Martin, Alexios"],["dc.contributor.author","Florez, Rodrigo"],["dc.contributor.author","Kahler, Elke"],["dc.contributor.author","Nitsche, Mirko"],["dc.contributor.author","Hille, Andrea"],["dc.contributor.author","Steiner, Wolfgang"],["dc.contributor.author","Hess, Clemens Friedrich"],["dc.contributor.author","Pradier, Olivier"],["dc.date.accessioned","2018-11-07T09:32:05Z"],["dc.date.available","2018-11-07T09:32:05Z"],["dc.date.issued","2006"],["dc.description.abstract","Purpose: The aim of this study was to evaluate the efficacy of adjuvant radiotherapy after transoral laser microsurgery for advanced recurrent head-and-neck squamous cell carcinoma (HNSCC). Patients and Methods: Between 1988 and 2000, 37 patients with advanced local recurrences (23 local and 14 locoregional recurrences) of HNSCC without distant metastases were treated in curative intent with organ-preserving transoral laser microsurgery and adjuvant radiotherapy (before 1994 split-course radiotherapy with carboplatinum, after 1994 conventional radiotherapy). Initial therapy of the primary (8.1% oral cavity, 35.1% oropharynx, 13.5% hypopharynx, and 43.3% larynx) before relapse was organ-preserving transoral laser microsurgery without any adjuvant therapy. Results: After a median follow-up of 124 months, the 5-year overall survival rate was 21.3%, the loco-regional control rate 48.3%, respectively. In multivariate analysis, stage of original primary tumor (Stage I/II vs. Stage III/IV), and patient age (< 58 years vs. >= 58 years) showed statistically significant impact on prognosis. In laryngeal cancer, larynx preservation rate after treatment for recurrent tumor was 50% during follow-up. Conclusion: Our data show that organ-preserving transoral laser microsurgery followed by adjuvant radiotherapy is a curative option for patients who have advanced recurrence after transoral laser surgery and is an alternative to radical treatment. (c) 2006 Elsevier Inc."],["dc.identifier.doi","10.1016/j.ijrobp.2006.03.007"],["dc.identifier.isi","000238878800015"],["dc.identifier.pmid","16750331"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31668"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","0360-3016"],["dc.title","Long-term follow-up after transoral laser microsurgery and adjuvant radiotherapy for advanced recurrent squamous cell carcinoma of the head and neck"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]