@article{LapaLueckerathKleinleinetal.2016,
  author    = {Lapa, Constantin and L{\"u}ckerath, Katharina and Kleinlein, Irene and Monoranu, Camelia Maria and Linsenmann, Thomas and Kessler, Almuth F. and Rudelius, Martina and Kropf, Saskia and Buck, Andreas K. and Ernestus, Ralf-Ingo and Wester, Hans-J{\"u}rgen and L{\"o}hr, Mario and Herrmann, Ken},
  title     = {\(^{68}\)Ga-Pentixafor-PET/CT for Imaging of Chemokine Receptor 4 Expression in Glioblastoma},
  series = {Theranostics},
  volume    = {6},
  journal   = {Theranostics},
  number    = {3},
  doi       = {10.7150/thno.13986},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-168174},
  pages     = {428-434},
  year      = {2016},
  abstract  = {Chemokine receptor-4 (CXCR4) has been reported to be overexpressed in glioblastoma (GBM) and to be associated with poor survival. This study investigated the feasibility of non-invasive CXCR4-directed imaging with positron emission tomography/computed tomography (PET/CT) using the radiolabelled chemokine receptor ligand \(^{68}\)Ga-Pentixafor. 15 patients with clinical suspicion on primary or recurrent glioblastoma (13 primary, 2 recurrent tumors) underwent \(^{68}\)Ga-Pentixafor-PET/CT for assessment of CXCR4 expression prior to surgery. O-(2-\(^{18}\)F-fluoroethyl)-L-tyrosine (\(^{18}\)F-FET) PET/CT images were available in 11/15 cases and were compared visually and semi-quantitatively (SUV\(_{max}\), SUV\(_{mean}\)). Tumor-to-background ratios (TBR) were calculated for both PET probes. \(^{68}\)Ga-Pentixafor-PET/CT results were also compared to histological CXCR4 expression on neuronavigated surgical samples. \(^{68}\)Ga-Pentixafor-PET/CT was visually positive in 13/15 cases with SUV\(_{mean}\) and SUV\(_{max}\) of 3.0±1.5 and 3.9±2.0 respectively. Respective values for \(^{18}\)F-FET were 4.4±2.0 (SUV\(_{mean}\)) and 5.3±2.3 (SUV\(_{max}\)). TBR for SUV\(_{mean}\) and SUV\(_{max}\) were higher for \(^{68}\)Ga-Pentixafor than for \(^{18}\)F-FET (SUV\(_{mean}\) 154.0±90.7 vs. 4.1±1.3; SUV\(_{max}\) 70.3±44.0 and 3.8±1.2, p<0.01), respectively. Histological analysis confirmed CXCR4 expression in tumor areas with high \(^{68}\)Ga-Pentixafor uptake; regions of the same tumor without apparent \(^{68}\)Ga-Pentixafor uptake showed no or low receptor expression. In this pilot study, \(^{68}\)Ga-Pentixafor retention has been observed in the vast majority of glioblastoma lesions and served as readout for non-invasive determination of CXCR4 expression. Given the paramount importance of the CXCR4/SDF-1 axis in tumor biology, \(^{68}\)Ga-Pentixafor-PET/CT might prove a useful tool for sensitive, non-invasive in-vivo quantification of CXCR4 as well as selection of patients who might benefit from CXCR4-directed therapy.},
  language  = {en}
}
@article{FeldheimKesslerFeldheimetal.2023,
  author    = {Feldheim, Jonas and Kessler, Almuth F. and Feldheim, Julia J. and Schmitt, Dominik and Oster, Christoph and Lazaridis, Lazaros and Glas, Martin and Ernestus, Ralf-Ingo and Monoranu, Camelia M. and L{\"o}hr, Mario and Hagemann, Carsten},
  title     = {BRMS1 in gliomas — an expression analysis},
  series = {Cancers},
  volume    = {15},
  journal   = {Cancers},
  number    = {11},
  issn      = {2072-6694},
  doi       = {10.3390/cancers15112907},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-319225},
  year      = {2023},
  abstract  = {The metastatic suppressor BRMS1 interacts with critical steps of the metastatic cascade in many cancer entities. As gliomas rarely metastasize, BRMS1 has mainly been neglected in glioma research. However, its interaction partners, such as NFκB, VEGF, or MMPs, are old acquaintances in neurooncology. The steps regulated by BRMS1, such as invasion, migration, and apoptosis, are commonly dysregulated in gliomas. Therefore, BRMS1 shows potential as a regulator of glioma behavior. By bioinformatic analysis, in addition to our cohort of 118 specimens, we determined BRMS1 mRNA and protein expression as well as its correlation with the clinical course in astrocytomas IDH mutant, CNS WHO grade 2/3, and glioblastoma IDH wild-type, CNS WHO grade 4. Interestingly, we found BRMS1 protein expression to be significantly decreased in the aforementioned gliomas, while BRMS1 mRNA appeared to be overexpressed throughout. This dysregulation was independent of patients' characteristics or survival. The protein and mRNA expression differences cannot be finally explained at this stage. However, they suggest a post-transcriptional dysregulation that has been previously described in other cancer entities. Our analyses present the first data on BRMS1 expression in gliomas that can provide a starting point for further investigations.},
  language  = {en}
}
@article{NicklEckGoedertetal.2023,
  author    = {Nickl, Vera and Eck, Juliana and Goedert, Nicolas and H{\"u}bner, Julian and Nerreter, Thomas and Hagemann, Carsten and Ernestus, Ralf-Ingo and Schulz, Tim and Nickl, Robert Carl and Keßler, Almuth Friederike and L{\"o}hr, Mario and Rosenwald, Andreas and Breun, Maria and Monoranu, Camelia Maria},
  title     = {Characterization and optimization of the tumor microenvironment in patient-derived organotypic slices and organoid models of glioblastoma},
  series = {Cancers},
  volume    = {15},
  journal   = {Cancers},
  number    = {10},
  issn      = {2072-6694},
  doi       = {10.3390/cancers15102698},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-319249},
  year      = {2023},
  abstract  = {While glioblastoma (GBM) is still challenging to treat, novel immunotherapeutic approaches have shown promising effects in preclinical settings. However, their clinical breakthrough is hampered by complex interactions of GBM with the tumor microenvironment (TME). Here, we present an analysis of TME composition in a patient-derived organoid model (PDO) as well as in organotypic slice cultures (OSC). To obtain a more realistic model for immunotherapeutic testing, we introduce an enhanced PDO model. We manufactured PDOs and OSCs from fresh tissue of GBM patients and analyzed the TME. Enhanced PDOs (ePDOs) were obtained via co-culture with PBMCs (peripheral blood mononuclear cells) and compared to normal PDOs (nPDOs) and PT (primary tissue). At first, we showed that TME was not sustained in PDOs after a short time of culture. In contrast, TME was largely maintained in OSCs. Unfortunately, OSCs can only be cultured for up to 9 days. Thus, we enhanced the TME in PDOs by co-culturing PDOs and PBMCs from healthy donors. These cellular TME patterns could be preserved until day 21. The ePDO approach could mirror the interaction of GBM, TME and immunotherapeutic agents and may consequently represent a realistic model for individual immunotherapeutic drug testing in the future.},
  language  = {en}
}
@phdthesis{Kessler2009,
  author    = {Keßler, Almuth Friederike},
  title     = {Der Proteasomenaktivator PA28gamma bei der Tumorentstehung und seine Verbindung zur Stresssignalgebung und zur Zellzyklusregulation},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-74469},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2009},
  abstract  = {Das Glioblastom ist der h{\"a}ufigste hirneigene Tumor des Erwachsenen. Es ist hoch invasiv, stark proliferierend und mit einer schlechten Prognose assoziiert. Heutige Therapiean-s{\"a}tze zielen, neben der m{\"o}glichst vollst{\"a}ndigen Resektion des Tumorgewebes, vor allem auf Apoptoseinduktion durch DNA-Sch{\"a}den in Tumorzellen. Daher ist die Aufkl{\"a}rung der molekularen Grundlagen dieser Prozesse essentiell, um Verbesserungen bei den Behandlungsm{\"o}glichkeiten erzielen zu k{\"o}nnen. Der Proteasomenaktivator PA28γ wird im Hirngewebe stark exprimiert, {\"u}ber seine Funktion ist jedoch nur wenig bekannt. Er wurde als Interaktionspartner des Zellzyklus- und DNA-Schadensregulators Mad2b in einem Hefe Two-Hybrid Screen identifiziert. Im Rahmen dieser Arbeit wurde diese Wechselwirkung mittels eines GST-Pulldown Experimentes be-st{\"a}tigt. Obwohl PA28γ in Verbindung mit der Zellproliferation gebracht wird, konnte in GBM-Zelllinien keine signifikante {\"A}nderung der Zellteilungsraten beobachtet werden. Allerdings unterst{\"u}tzte die vermehrte Expression von PA28γ die Apoptose. Um durch neue Interaktionspartner von PA28γ Hinweise auf dessen Funktion zu erhalten, wurde ein Hefe Two-Hybrid Screen durchgef{\"u}hrt: PA28gamma steuert den Abbau von p53 und verweist {\"u}ber die hier neu beschriebene Interaktion mit HIPK1 ebenfalls auf den programmierten Zelltod. Dieser pro-apoptotische Zusammen-hang wird unterst{\"u}tzt durch die Interaktion mit 1A6/DRIM-interacting protein. Die Inter-aktion der Sumo E2 Ligase Ubc9 mit PA28gamma war ein erster Hinweis f{\"u}r eine Sumoylierung des Proteasomenaktivators, die die PA28gamma Aktivit{\"a}t regulieren k{\"o}nnte. Gleichzeitig ist Ubc9, wie auch die E3-Ligase PIAS, im Zusammenhang mit Apoptose beschrieben worden. Diese Fragestellungen wurden in weiterf{\"u}hrenden Arbeiten erforscht. Einen anderen Aspekt beleuchtet die Interaktion von PA28gammamit Catenin alpha. Durch diese Wechselwirkung k{\"o}nnte PA28gamma Einfluß auf Interzellul{\"a}rkontakte nehmen. Gerade im Hin-blick auf das GBM, charakterisiert durch ausgepr{\"a}gtes Migrations- und Invasionsverhal-ten, k{\"o}nnte die Regulation von Interzellul{\"a}rkontakten von besonderer Bedeutung sein. Aufgrund der oben beschriebenen Eigenschaften von PA28gammasollte dieses Protein f{\"u}r eine Therapie mittels DNA-Sch{\"a}den induzierter Apoptose erforscht werden. PA28gamma k{\"o}nnte bei diesen Vorg{\"a}ngen ein zentraler Faktor sein, dessen Manipulation die etablierten Therapieformen unterst{\"u}tzen und deren Wirkung verbessern.},
  subject      = {Proteasomenaktivator},
  language  = {de}
}
@article{FeldheimKesslerFeldheimetal.2022,
  author    = {Feldheim, Jonas and Kessler, Almuth F. and Feldheim, Julia J. and Schulz, Ellina and Wend, David and Lazaridis, Lazaros and Kleinschnitz, Christoph and Glas, Martin and Ernestus, Ralf-Ingo and Brandner, Sebastian and Monoranu, Camelia M. and L{\"o}hr, Mario and Hagemann, Carsten},
  title     = {Effects of long-term temozolomide treatment on glioblastoma and astrocytoma WHO grade 4 stem-like cells},
  series = {International Journal of Molecular Sciences},
  volume    = {23},
  journal   = {International Journal of Molecular Sciences},
  number    = {9},
  issn      = {1422-0067},
  doi       = {10.3390/ijms23095238},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-284417},
  year      = {2022},
  abstract  = {Glioblastoma leads to a fatal course within two years in more than two thirds of patients. An essential cornerstone of therapy is chemotherapy with temozolomide (TMZ). The effect of TMZ is counteracted by the cellular repair enzyme O\(^6\)-methylguanine-DNA methyltransferase (MGMT). The MGMT promoter methylation, the main regulator of MGMT expression, can change from primary tumor to recurrence, and TMZ may play a significant role in this process. To identify the potential mechanisms involved, three primary stem-like cell lines (one astrocytoma with the mutation of the isocitrate dehydrogenase (IDH), CNS WHO grade 4 (HGA)), and two glioblastoma (IDH-wildtype, CNS WHO grade 4) were treated with TMZ. The MGMT promoter methylation, migration, proliferation, and TMZ-response of the tumor cells were examined at different time points. The strong effects of TMZ treatment on the MGMT methylated cells were observed. Furthermore, TMZ led to a loss of the MGMT promoter hypermethylation and induced migratory rather than proliferative behavior. Cells with the unmethylated MGMT promoter showed more aggressive behavior after treatment, while HGA cells reacted heterogenously. Our study provides further evidence to consider the potential adverse effects of TMZ chemotherapy and a rationale for investigating potential relationships between TMZ treatment and change in the MGMT promoter methylation during relapse.},
  language  = {en}
}
@article{NicklSchulzSalvadoretal.2022,
  author    = {Nickl, Vera and Schulz, Ellina and Salvador, Ellaine and Trautmann, Laureen and Diener, Leopold and Kessler, Almuth F. and Monoranu, Camelia M. and Dehghani, Faramarz and Ernestus, Ralf-Ingo and L{\"o}hr, Mario and Hagemann, Carsten},
  title     = {Glioblastoma-derived three-dimensional ex vivo models to evaluate effects and efficacy of Tumor Treating Fields (TTFields)},
  series = {Cancers},
  volume    = {14},
  journal   = {Cancers},
  number    = {21},
  issn      = {2072-6694},
  doi       = {10.3390/cancers14215177},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-290340},
  year      = {2022},
  abstract  = {Simple Summary In glioblastoma, tumor recurrence is inevitable and the prognosis of patients is poor, despite multidisciplinary treatment approaches involving surgical resection, radiotherapy and chemotherapy. Recently, Tumor Treating Fields (TTFields) have been added to the therapeutic set-up. These alternating electric fields are applied to glioblastoma at 200 kHz frequency via arrays placed on the shaved scalp of patients. Patients show varying response to this therapy. Molecular effects of TTFields have been investigated largely in cell cultures and animal models, but not in patient tissue samples. Acquisition of matched treatment-na{\"i}ve and recurrent patient tissues is a challenge. Therefore, we suggest three reliable patient-derived three-dimensional ex vivo models (primary cells grown as microtumors on murine organotypic hippocampal slices, organoids and tumor slice cultures) which may facilitate prediction of patients' treatment responses and provide important insights into clinically relevant cellular and molecular alterations under TTFields. Abstract Glioblastoma (GBM) displays a wide range of inter- and intra-tumoral heterogeneity contributing to therapeutic resistance and relapse. Although Tumor Treating Fields (TTFields) are effective for the treatment of GBM, there is a lack of ex vivo models to evaluate effects on patients' tumor biology or to screen patients for treatment efficacy. Thus, we adapted patient-derived three-dimensional tissue culture models to be compatible with TTFields application to tissue culture. Patient-derived primary cells (PDPC) were seeded onto murine organotypic hippocampal slice cultures (OHSC), and microtumor development with and without TTFields at 200 kHz was observed. In addition, organoids were generated from acute material cultured on OHSC and treated with TTFields. Lastly, the effect of TTFields on expression of the Ki67 proliferation marker was evaluated on cultured GBM slices. Microtumors exhibited increased sensitivity towards TTFields compared to monolayer cell cultures. TTFields affected tumor growth and viability, as the size of microtumors and the percentage of Ki67-positive cells decreased after treatment. Nevertheless, variability in the extent of the response was preserved between different patient samples. Therefore, these pre-clinical GBM models could provide snapshots of the tumor to simulate patient treatment response and to investigate molecular mechanisms of response and resistance.},
  language  = {en}
}
@phdthesis{Schuler2005,
  author    = {Schuler, Patrick},
  title     = {Lokalisation und Blockade der Serinprotease uPA im C6-Glioblastom-Modell der Ratte},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-18967},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2005},
  abstract  = {Gegenstand dieser Doktorarbeit war die Beschreibung des Urokinaseplaminaktivators uPA im C6-Sph{\"a}roidmodell der Ratte und dessen Lokalisation in Bezug auf den Prim{\"a}rtumor. Das hierbei verwendete Tiermodell basiert auf der C6-Tumorzellreihe, welche durch Transfektion von Rattengliomzellen mit dem Vaskularisierungsfaktor VEGF entwickelt wurde. Die gesteigerte Expression von VEGF resultiert in einer st{\"a}rkeren Vaskularisierung und einer erh{\"o}hten Wachstumsrate des Tumors. Im Vorfeld der Tumorimplantation konnte die Expression von uPA durch die C6-Tumorzellen mittels reverser RNA-Transkription und Polymerasekettenreaktion nachgewiesen werden. In vitro gelang der Nachweis von uPA im C6-Sph{\"a}roiden mittels Fluoreszenz-F{\"a}rbung. Im Rahmen des Tierversuches wurden aus den Tumorzellen ca. 300µm große Sph{\"a}roide hergestellt, welche den Ratten in den Kortex des linken Frontallappens implantiert wurden und dort solide Hirntumoren bildeten. Die Versuchstiere wurden anschließend in zwei Gruppen aufgeteilt. Der Positivgruppe wurde t{\"a}glich {\"u}ber einen Zeitraum von 19 bzw. 21 Tagen der Proteasehemmer WX-UK1 in die Bauchh{\"o}hle injiziert, die Kontrollgruppe erhielt ein Placebo. Nach Ablauf des Behandlungszeitraumes konnte an den explantierten Gehirnen mittels histochemischer Peroxidasef{\"a}rbung die Protease uPA im Tumorgewebe nachgewiesen werden. Die Konzentration von uPA war besonders im invasionsaktiven Bereich des Tumors erh{\"o}ht. Dieser entspricht der Randzone des soliden Tumors, sowie den distanzierten Zellnestern im gesunden Hirngewebe, welche als so genannte Invasionszone zusammengefasst werden. Die tragende Rolle von uPA bei der Invasion der Tumorzellen in das gesunde Hirngewebe konnte somit best{\"a}tigt werden. Die Messung von erh{\"o}hten uPA-Konzentrationen an der Basalmembran von Hirngef{\"a}ßen korreliert mit Beobachtungen, dass die Tumorzellen entlang von Gef{\"a}ßen und Plexus migrieren, aber nicht in der Lage sind, in das Gef{\"a}ßlumen einzudringen. Der Nachweis der erfolgreichen orthotopen Sph{\"a}roidimplantation mittels MRT-Bildgebung der Hirntumoren unterstreicht den Vorteil der offenen Implantationstechnik gegen{\"u}ber der Zellinjektion. Die peritoneale Verabreichung des Proteasehemmers WX-UK1 f{\"u}hrte im Rahmen dieser Untersuchungen zu keiner signifikanten Reduktion des Tumorwachstums, welches mittels Volumenmessung im MRT dokumentiert wurde. Des Weiteren konnte keine Minderung der uPA-Konzentration in den Tumoren der Positivgruppe gegen{\"u}ber der Kontrollgruppe gemessen werden. Neben der fehlenden Biodistribution des Wirkstoffes kommt hierf{\"u}r auch eine mangelnde Spezifit{\"a}t von WX-UK1 f{\"u}r uPA oder ein alternativer Aktivierungsweg der Proteolyse innerhalb der Tumorzellen in Betracht. Diese Arbeit f{\"u}hrt zur Weiterentwicklung des C6-Sph{\"a}roidmodells und unterst{\"u}tzt die zuk{\"u}nftige Entwicklung von Wirkstoffen gegen das Tumorwachstum auf Basis der anti-invasiven Therapie.},
  language  = {de}
}
@article{LoehrHaertigSchulzeetal.2022,
  author    = {L{\"o}hr, Mario and H{\"a}rtig, Wolfgang and Schulze, Almut and Kroiß, Matthias and Sbiera, Silviu and Lapa, Constantin and Mages, Bianca and Strobel, Sabrina and Hundt, Jennifer Elisabeth and Bohnert, Simone and Kircher, Stefan and Janaki-Raman, Sudha and Monoranu, Camelia-Maria},
  title     = {SOAT1: A suitable target for therapy in high-grade astrocytic glioma?},
  series = {International Journal of Molecular Sciences},
  volume    = {23},
  journal   = {International Journal of Molecular Sciences},
  number    = {7},
  issn      = {1422-0067},
  doi       = {10.3390/ijms23073726},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-284178},
  year      = {2022},
  abstract  = {Targeting molecular alterations as an effective treatment for isocitrate dehydrogenase-wildtype glioblastoma (GBM) patients has not yet been established. Sterol-O-Acyl Transferase 1 (SOAT1), a key enzyme in the conversion of endoplasmic reticulum cholesterol to esters for storage in lipid droplets (LD), serves as a target for the orphan drug mitotane to treat adrenocortical carcinoma. Inhibition of SOAT1 also suppresses GBM growth. Here, we refined SOAT1-expression in GBM and IDH-mutant astrocytoma, CNS WHO grade 4 (HGA), and assessed the distribution of LD in these tumors. Twenty-seven GBM and three HGA specimens were evaluated by multiple GFAP, Iba1, IDH1 R132H, and SOAT1 immunofluorescence labeling as well as Oil Red O staining. To a small extent SOAT1 was expressed by tumor cells in both tumor entities. In contrast, strong expression was observed in glioma-associated macrophages. Triple immunofluorescence labeling revealed, for the first time, evidence for SOAT1 colocalization with Iba1 and IDH1 R132H, respectively. Furthermore, a notable difference in the amount of LD between GBM and HGA was observed. Therefore, SOAT1 suppression might be a therapeutic option to target GBM and HGA growth and invasiveness. In addition, the high expression in cells related to neuroinflammation could be beneficial for a concomitant suppression of protumoral microglia/macrophages.},
  language  = {en}
}
@article{SchulzMawambaLoehretal.2022,
  author    = {Schulz, Ellina and Mawamba, Viviane and L{\"o}hr, Mario and Hagemann, Carsten and Friedrich, Alexandra and Schatzschneider, Ulrich},
  title     = {Structure-activity relations of Pd(II) and Pt(II) thiosemicarbazone complexes on different human glioblastoma cell lines},
  series = {Zeitschrift f{\"u}r Anorganische und Allgemeine Chemie},
  volume    = {648},
  journal   = {Zeitschrift f{\"u}r Anorganische und Allgemeine Chemie},
  number    = {12},
  issn      = {0044-2313},
  doi       = {10.1002/zaac.202200073},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-318281},
  year      = {2022},
  abstract  = {Ten thiosemicarbazone ligands obtained by condensation of pyridine-2-carbaldehyde, quinoline-2-carbaldehyde, 2-acetylpyridine, 2-acetylquinoline, or corresponding 2-pyridyl ketones with thiosemicarbazides RNHC(S)NHNH\(_{2}\) and R=CH\(_{3}\), C\(_{6}\)H\(_{5}\) were prepared in good yield. The reaction of [PdCl\(_{2}\)(cod)] with cod=1,5-cyclooctadiene or K\(_{2}\)[PtCl\(_{4}\)] resulted in a total of 17 Pd(II) and Pt(II) complexes isolated in excellent purity, as demonstrated by \(^{1}\)H, \(^{13}\)C, and, where applicable, \(^{195\)Pt NMR spectroscopy combined with CHNS analysis. The cytotoxicity of the title compounds was studied on four human glioblastoma cell lines (GaMG, U87, U138, and U343). The most active compound, with a Pd(II) metal centre, a 2-quinolinyl ring, and methyl groups on both the proximal C and distal N atoms exhibited an EC\(_{50}\) value of 2.1 μM on the GaMG cell lines, thus being slightly more active than cisplatin (EC\(_{50}\) 3.4 μM) and significantly more potent than temozolomide (EC\(_{50}\) 67.1 μM). Surprisingly, the EC\(_{50}\) values were inversely correlated with the lipophilicity, as determined with the "shake-flask method", and decreased with the length of the alkyl substituents (C\(_{1}\)>C\(_{8}\)>C\(_{10}\)). Correlation with the different structural motifs showed that for the most promising anticancer activity, a maximum of two aromatic rings (either quinolinyl or pyridyl plus phenyl) combined with one methyl group are favoured and the Pd(II) complexes are slightly more potent than their Pt(II) analogues.},
  language  = {en}
}
@article{DufnerKesslerJustetal.2022,
  author    = {Dufner, Vera and Kessler, Almuth Friederike and Just, Larissa and Hau, Peter and Bumes, Elisabeth and Pels, Hendrik Johannes and Grauer, Oliver Martin and Wiese, Bettina and L{\"o}hr, Mario and Jordan, Karin and Strik, Herwig},
  title     = {The emesis trial: depressive glioma patients are more affected by chemotherapy-induced nausea and vomiting},
  series = {Frontiers in Neurology},
  volume    = {13},
  journal   = {Frontiers in Neurology},
  issn      = {1664-2295},
  doi       = {10.3389/fneur.2022.773265},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-262859},
  year      = {2022},
  abstract  = {Purpose Glioma patients face a limited life expectancy and at the same time, they suffer from afflicting symptoms and undesired effects of tumor treatment. Apart from bone marrow suppression, standard chemotherapy with temozolomide causes nausea, emesis and loss of appetite. In this pilot study, we investigated how chemotherapy-induced nausea and vomiting (CINV) affects the patients' levels of depression and their quality of life. Methods In this prospective observational multicentre study (n = 87), nausea, emesis and loss of appetite were evaluated with an expanded MASCC questionnaire, covering 10 days during the first and the second cycle of chemotherapy. Quality of life was assessed with the EORTC QLQ-C30 and BN 20 questionnaire and levels of depression with the PHQ-9 inventory before and after the first and second cycle of chemotherapy. Results CINV affected a minor part of patients. If present, it reached its maximum at day 3 and decreased to baseline level not before day 8. Levels of depression increased significantly after the first cycle of chemotherapy, but decreased during the further course of treatment. Patients with higher levels of depression were more severely affected by CINV and showed a lower quality of life through all time-points. Conclusion We conclude that symptoms of depression should be perceived in advance and treated in order to avoid more severe side effects of tumor treatment. Additionally, in affected patients, delayed nausea was most prominent, pointing toward an activation of the NK1 receptor. We conclude that long acting antiemetics are necessary totreat temozolomide-induced nausea.},
  language  = {en}
}