Schulz, Matthias

[["dc.bibliographiccitation.firstpage","3259"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","3273"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Draeger, Julia"],["dc.contributor.author","Simon-Keller, Katja"],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Klemm, Florian"],["dc.contributor.author","Wilting, Joerg"],["dc.contributor.author","Sticht, Carsten"],["dc.contributor.author","Dittmann, Kai"],["dc.contributor.author","Schulz, Matthias"],["dc.contributor.author","Leuschner, Ivo"],["dc.contributor.author","Marx, Alexander"],["dc.contributor.author","Hahn, Heidi"],["dc.date.accessioned","2018-11-07T10:28:26Z"],["dc.date.available","2018-11-07T10:28:26Z"],["dc.date.issued","2017"],["dc.description.abstract","Rhabdomyosarcoma (RMS) is the most common soft tissue sarcoma in children and show characteristics of skeletal muscle differentiation. The two major RMS subtypes in children are alveolar (ARMS) and embryonal RMS (ERMS). We demonstrate that approximately 50% of ARMS and ERMS overexpress the LEF1/TCF transcription factor LEF1 when compared to normal skeletal muscle and that LEF1 can restrain aggressiveness especially of ARMS cells. LEF1 knockdown experiments in cell lines reveal that depending on the cellular context, LEF1 can induce pro-apoptotic signals. LEF1 can also suppress proliferation, migration and invasiveness of RMS cells both in vitro and in vivo. Furthermore, LEF1 can induce myodifferentiation of the tumor cells. This may involve regulation of other LEF1/TCF factors i.e. TCF1, whereas beta-catenin activity plays a subordinate role. Together these data suggest that LEF1 rather has tumor suppressive functions and attenuates aggressiveness in a subset of RMS."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2016"],["dc.identifier.doi","10.18632/oncotarget.13887"],["dc.identifier.isi","000391506300114"],["dc.identifier.pmid","27965462"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14022"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43418"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Impact Journals Llc"],["dc.relation.issn","1949-2553"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.title","LEF1 reduces tumor progression and induces myodifferentiation in a subset of rhabdomyosarcoma"],["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","1331"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","1346"],["dc.bibliographiccitation.volume","61"],["dc.contributor.author","Chuang, Han-Ning"],["dc.contributor.author","van Rossum, Denise"],["dc.contributor.author","Sieger, Dirk"],["dc.contributor.author","Siam, Laila"],["dc.contributor.author","Klemm, Florian"],["dc.contributor.author","Bleckmann, Annalen"],["dc.contributor.author","Bayerlova, Michaela"],["dc.contributor.author","Farhat, Katja"],["dc.contributor.author","Scheffel, Joerg"],["dc.contributor.author","Schulz, Matthias"],["dc.contributor.author","Dehghani, Faramarz"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Binder, Claudia"],["dc.contributor.author","Pukrop, Tobias"],["dc.date.accessioned","2018-11-07T09:21:57Z"],["dc.date.available","2018-11-07T09:21:57Z"],["dc.date.issued","2013"],["dc.description.abstract","The metastatic colonization of the brain by carcinoma cells is still barely understood, in particular when considering interactions with the host tissue. The colonization comes with a substantial destruction of the surrounding host tissue. This leads to activation of damage responses by resident innate immune cells to protect, repair, and organize the wound healing, but may distract from tumoricidal actions. We recently demonstrated that microglia, innate immune cells of the CNS, assist carcinoma cell invasion. Here we report that this is a fatal side effect of a physiological damage response of the brain tissue. In a brain slice coculture model, contact with both benign and malignant epithelial cells induced a response by microglia and astrocytes comparable to that seen at the interface of human cerebral metastases. While the glial damage response intended to protect the brain from intrusion of benign epithelial cells by inducing apoptosis, it proved ineffective against various malignant cell types. They did not undergo apoptosis and actually exploited the local tissue reaction to invade instead. Gene expression and functional analyses revealed that the C-X-C chemokine receptor type 4 (CXCR4) and WNT signaling were involved in this process. Furthermore, CXCR4-regulated microglia were recruited to sites of brain injury in a zebrafish model and CXCR4 was expressed in human stroke patients, suggesting a conserved role in damage responses to various types of brain injuries. Together, our findings point to a detrimental misuse of the glial damage response program by carcinoma cells resistant to glia-induced apoptosis. GLIA 2013;61:1331-1346"],["dc.identifier.doi","10.1002/glia.22518"],["dc.identifier.isi","000321983400011"],["dc.identifier.pmid","23832647"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10955"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29226"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","0894-1491"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.title","Carcinoma cells misuse the host tissue damage response to invade the brain"],["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","227"],["dc.bibliographiccitation.issue","No. 2"],["dc.bibliographiccitation.journal","Library Hi Tech"],["dc.bibliographiccitation.lastpage","230"],["dc.bibliographiccitation.volume","Vol. 22"],["dc.contributor.author","Mittler, Elmar"],["dc.contributor.author","Schulz, Matthias"],["dc.date.accessioned","2020-04-15T08:40:26Z"],["dc.date.available","2020-04-15T08:40:26Z"],["dc.date.issued","2004"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17266"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/64119"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.issn","0737-8831"],["dc.rights.access","openAccess"],["dc.title","ProPrint world-wide print-on-demand services for study and research"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","57"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Clinical & Experimental Metastasis"],["dc.bibliographiccitation.lastpage","65"],["dc.bibliographiccitation.volume","31"],["dc.contributor.author","Binder, Claudia"],["dc.contributor.author","Chuang, Eugenia"],["dc.contributor.author","Habla, Christina"],["dc.contributor.author","Bleckmann, Annalen"],["dc.contributor.author","Schulz, Matthias"],["dc.contributor.author","Bathgate, Ross A. D."],["dc.contributor.author","Einspanier, Almuth"],["dc.date.accessioned","2018-11-07T09:46:51Z"],["dc.date.available","2018-11-07T09:46:51Z"],["dc.date.issued","2014"],["dc.description.abstract","Relaxins are known for their tissue remodeling capacity which is also a hallmark of cancer progression. However, their role in the latter context is still unclear, particularly in breast cancer. In a mouse model with spontaneously arising breast cancer due to erbB2-overexpression we show that exposure to porcine relaxin results in significantly enhanced tumour growth as compared to control animals. This is accompanied by increased serum concentrations of progesterone and estradiol as well as elevated expression of the respective receptors and the relaxin receptor RXFP1 in the tumour tissue. It is also associated with enhanced infiltration by tumour-associated macrophages which are known to promote tumour progression. Additionally, we show in an ex vivo model of metastatic brain colonization that porcine relaxin as well as human brain-specific relaxin-3 promotes invasion into the brain tissue and enhance interaction of breast cancer cells with the resident brain macrophages, the microglia. Relaxin signaling is mediated via RXFP1, since R 3/I5, a specific agonist of the relaxin-3 receptor RXFP3 in the brain, does not significantly enhance invasion. Taken together, these findings strongly support a role of relaxins in the progression of breast cancer where they foster primary tumour growth as well as metastatic colonization by direct and indirect means."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft [Ei 333/11-2, BI 703/3-1]"],["dc.identifier.doi","10.1007/s10585-013-9609-2"],["dc.identifier.isi","000329633500006"],["dc.identifier.pmid","23963762"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11663"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34981"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","1573-7276"],["dc.relation.issn","0262-0898"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Relaxins enhance growth of spontaneous murine breast cancers as well as metastatic colonization of the brain"],["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","3170"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","International Journal of Cancer"],["dc.bibliographiccitation.lastpage","3183"],["dc.bibliographiccitation.volume","146"],["dc.contributor.author","Blazquez, Raquel"],["dc.contributor.author","Rietkötter, Eva"],["dc.contributor.author","Wenske, Britta"],["dc.contributor.author","Wlochowitz, Darius"],["dc.contributor.author","Sparrer, Daniela"],["dc.contributor.author","Vollmer, Elena"],["dc.contributor.author","Müller, Gunnar"],["dc.contributor.author","Seegerer, Julia"],["dc.contributor.author","Sun, Xueni"],["dc.contributor.author","Dettmer, Katja"],["dc.contributor.author","Barrantes‐Freer, Alonso"],["dc.contributor.author","Stange, Lena"],["dc.contributor.author","Utpatel, Kirsten"],["dc.contributor.author","Bleckmann, Annalen"],["dc.contributor.author","Treiber, Hannes"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Lenz, Christof"],["dc.contributor.author","Schulz, Matthias"],["dc.contributor.author","Reimelt, Christian"],["dc.contributor.author","Hackl, Christina"],["dc.contributor.author","Grade, Marian"],["dc.contributor.author","Büyüktas, Deram"],["dc.contributor.author","Siam, Laila"],["dc.contributor.author","Balkenhol, Marko"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Kube, Dieter"],["dc.contributor.author","Krahn, Michael P."],["dc.contributor.author","Proescholdt, Martin A."],["dc.contributor.author","Riemenschneider, Markus J."],["dc.contributor.author","Evert, Matthias"],["dc.contributor.author","Oefner, Peter J."],["dc.contributor.author","Klein, Chistoph A."],["dc.contributor.author","Hanisch, Uwe K."],["dc.contributor.author","Binder, Claudia"],["dc.contributor.author","Pukrop, Tobias"],["dc.date.accessioned","2019-12-09T11:26:05Z"],["dc.date.accessioned","2021-10-27T13:21:49Z"],["dc.date.available","2019-12-09T11:26:05Z"],["dc.date.available","2021-10-27T13:21:49Z"],["dc.date.issued","2020"],["dc.description.abstract","More than half of all brain metastases show infiltrating rather than displacing growth at the macro-metastasis/organ parenchyma interface (MMPI), a finding associated with shorter survival. The lymphoid enhancer-binding factor-1 (LEF1) is an epithelial-mesenchymal transition (EMT) transcription factor that is commonly overexpressed in brain-colonizing cancer cells. Here, we overexpressed LEF1 in an in vivo breast cancer brain colonization model. It shortened survival, albeit without engaging EMT at the MMPI. By differential proteome analysis, we identified a novel function of LEF1 as a regulator of the glutathione (GSH) system, the principal cellular redox buffer. LEF1 overexpression also conferred resistance against therapeutic GSH depletion during brain colonization and improved management of intracellular ROS. We conclude that besides EMT, LEF1 facilitates metastasis by improving the antioxidative capacity of epithelial breast cancer cells, in particular during colonization of the brain parenchyma."],["dc.identifier.doi","10.1002/ijc.32742"],["dc.identifier.eissn","1097-0215"],["dc.identifier.issn","0020-7136"],["dc.identifier.pmid","31626715"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16874"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/92047"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.eissn","1097-0215"],["dc.relation.issn","1097-0215"],["dc.relation.issn","0020-7136"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","LEF1 supports metastatic brain colonization by regulating glutathione metabolism and increasing ROS resistance in breast cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1477"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","1489"],["dc.bibliographiccitation.volume","58"],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Dehghani, Faramarz"],["dc.contributor.author","Chuang, Han-Ning"],["dc.contributor.author","Lohaus, Raphaela"],["dc.contributor.author","Bayanga, Kathrin"],["dc.contributor.author","Heermann, Stephan"],["dc.contributor.author","Regen, Tommy"],["dc.contributor.author","van Rossum, Denise"],["dc.contributor.author","Klemm, Florian"],["dc.contributor.author","Schulz, Matthias"],["dc.contributor.author","Siam, Laila"],["dc.contributor.author","Hoffmann, Anja"],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Bechmann, Ingo"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Binder, Claudia"],["dc.date.accessioned","2018-11-07T08:39:43Z"],["dc.date.available","2018-11-07T08:39:43Z"],["dc.date.issued","2010"],["dc.description.abstract","Although there is increasing evidence that blood-derived macrophages support tumor progression, it is still unclear whether specialized resident macrophages, such as brain microglia, also play a prominent role in metastasis formation. Here, we show that microglia enhance invasion and colonization of brain tissue by breast cancer cells, serving both as active transporters and guiding rails. This is antagonized by inactivation of microglia as well as by the Wnt inhibitor Dickkopf-2. Proinvasive microglia demonstrate altered morphology, but neither upregulation of M2-like cytokines nor differential gene expression. Bacterial lipopolysacharide shifts tumor-educated microglia into a classical M1 phenotype, reduces their proinvasive function, and unmasks inflammatory and Wnt signaling as the most strongly regulated pathways. Histological findings in human brain metastases underline the significance of these results. In conclusion, microglia are critical for the successful colonization of the brain by epithelial cancer cells, suggesting inhibition of proinvasive microglia as a promising antimetastatic strategy. (C) 2010 Wiley-Liss, Inc."],["dc.description.sponsorship","German Research Council (DFG) [For942 BI 703/3-1]"],["dc.identifier.doi","10.1002/glia.21022"],["dc.identifier.isi","000280349900008"],["dc.identifier.pmid","20549749"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6326"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19065"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0894-1491"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Microglia Promote Colonization of Brain Tissue by Breast Cancer Cells in a Wnt-Dependent Way"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1449"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","1460"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Rietkötter, Eva"],["dc.contributor.author","Menck, Kerstin"],["dc.contributor.author","Bleckmann, Annalen"],["dc.contributor.author","Farhat, Katja"],["dc.contributor.author","Schaffrinski, Meike"],["dc.contributor.author","Schulz, Matthias"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Binder, Claudia"],["dc.contributor.author","Pukrop, Tobias"],["dc.date.accessioned","2019-07-10T08:11:45Z"],["dc.date.available","2019-07-10T08:11:45Z"],["dc.date.issued","2013-09-01"],["dc.description.abstract","The bisphosphonate zoledronic acid (ZA) significantly reduces complications of bone metastasis by inhibiting resident macrophages, the osteoclasts. Recent clinical trials indicate additional anti-metastatic effects of ZA outside the bone. However, which step of metastasis is influenced and whether thisis due to directtoxicity on cancer cells or inhibition of the tumor promoting microenvironment, is unknown. In particular, tumor-associated and resident macrophages support each step of organ metastasis and could be a crucial target of ZA. Thus, we comparatively investigate the ZA effects on: i) different types of macrophages, ii) on breast cancer cells but also iii) on macrophage-induced invasion. We demonstrate that ZA concentrations reflecting the plasma level affected viability of human macrophages, murine bone marrow-derived macrophages as well as their resident brain equivalents, the microglia, while it did not influence the tested cancer cells. However, the effects on the macrophages subsequently reduced the macrophage/microglia-induced invasiveness of the cancer cells. In line with this, manipulation of microglia by ZA in organotypic brain slice cocultures reduced the tissue invasion by carcinoma cells. The characterization of human macrophages after ZA treatment revealed a phenotype/response shift, in particular after external stimulation. In conclusion, we show that therapeutic concentrations of ZA affect all types of macrophages but not the cancer cells. Thus, anti-metastatic effects of ZA are predominantly caused by modulating the microenvironment. Most importantly, our findings demonstrate that ZA reduced microglia-assisted invasion of cancer cells to the brain tissue, indicating a potential therapeutic role in the prevention of cerebral metastasis."],["dc.identifier.fs","599082"],["dc.identifier.pmid","24036536"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10758"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60792"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1949-2553"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY 3.0"],["dc.rights.uri","http://creativecommons.org/licenses/by/3.0"],["dc.subject.mesh","Animals"],["dc.subject.mesh","Breast Neoplasms"],["dc.subject.mesh","Cell Communication"],["dc.subject.mesh","Cell Line, Tumor"],["dc.subject.mesh","Cell Proliferation"],["dc.subject.mesh","Coculture Techniques"],["dc.subject.mesh","Diphosphonates"],["dc.subject.mesh","Female"],["dc.subject.mesh","Humans"],["dc.subject.mesh","Imidazoles"],["dc.subject.mesh","MCF-7 Cells"],["dc.subject.mesh","Macrophages"],["dc.subject.mesh","Matrix Metalloproteinases"],["dc.subject.mesh","Mice"],["dc.subject.mesh","Microglia"],["dc.subject.mesh","Tumor Microenvironment"],["dc.title","Zoledronic acid inhibits macrophage/microglia-assisted breast cancer cell invasion."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","13540"],["dc.bibliographiccitation.issue","24"],["dc.bibliographiccitation.journal","International Journal of Molecular Sciences"],["dc.bibliographiccitation.volume","22"],["dc.contributor.affiliation","Buentzel, Judith; 1Department of Hematology and Medical Oncology, University Medical Center Goettingen, 37075 Goettingen, Germany; mschulz@gdwg.de (M.S.); annalen.bleckmann@ukmuenster.de (A.B.); claudia.binder@med.uni-goettingen.de (C.B.)"],["dc.contributor.affiliation","Klemp, Henry Gerd; 2Department of Pediatrics and Adolescent Medicine, University Medical Center Goettingen, 37075 Goettingen, Germany; henrygerd.klemp@stud.uni-goettingen.de (H.G.K.); rkraetzner@gwdg.de (R.K.)"],["dc.contributor.affiliation","Kraetzner, Ralph; 2Department of Pediatrics and Adolescent Medicine, University Medical Center Goettingen, 37075 Goettingen, Germany; henrygerd.klemp@stud.uni-goettingen.de (H.G.K.); rkraetzner@gwdg.de (R.K.)"],["dc.contributor.affiliation","Schulz, Matthias; 1Department of Hematology and Medical Oncology, University Medical Center Goettingen, 37075 Goettingen, Germany; mschulz@gdwg.de (M.S.); annalen.bleckmann@ukmuenster.de (A.B.); claudia.binder@med.uni-goettingen.de (C.B.)"],["dc.contributor.affiliation","Dihazi, Gry Helene; 3Metabolomics Platform, Department of Clinical Chemistry, University Medical Center Goettingen, 37075 Goettingen, Germany; gryhelene.dihazi@med.uni-goettingen.de (G.H.D.); frank.streit@med.uni-goettingen.de (F.S.)"],["dc.contributor.affiliation","Streit, Frank; 3Metabolomics Platform, Department of Clinical Chemistry, University Medical Center Goettingen, 37075 Goettingen, Germany; gryhelene.dihazi@med.uni-goettingen.de (G.H.D.); frank.streit@med.uni-goettingen.de (F.S.)"],["dc.contributor.affiliation","Bleckmann, Annalen; 1Department of Hematology and Medical Oncology, University Medical Center Goettingen, 37075 Goettingen, Germany; mschulz@gdwg.de (M.S.); annalen.bleckmann@ukmuenster.de (A.B.); claudia.binder@med.uni-goettingen.de (C.B.)"],["dc.contributor.affiliation","Menck, Kerstin; 4Department of Medicine A (Hematology, Oncology, Hemostaseology and Pulmonology), University Hospital Muenster, 48149 Muenster, Germany; kerstin.menck@ukmuenster.de"],["dc.contributor.affiliation","Wlochowitz, Darius; 5Medical Bioinformatics, University Medical Center Goettingen, 37075 Goettingen, Germany; dwl@bioinf.med.uni-goettingen.de"],["dc.contributor.affiliation","Binder, Claudia; 1Department of Hematology and Medical Oncology, University Medical Center Goettingen, 37075 Goettingen, Germany; mschulz@gdwg.de (M.S.); annalen.bleckmann@ukmuenster.de (A.B.); claudia.binder@med.uni-goettingen.de (C.B.)"],["dc.contributor.author","Buentzel, Judith"],["dc.contributor.author","Klemp, Henry Gerd"],["dc.contributor.author","Kraetzner, Ralph"],["dc.contributor.author","Schulz, Matthias"],["dc.contributor.author","Dihazi, Gry Helene"],["dc.contributor.author","Streit, Frank"],["dc.contributor.author","Bleckmann, Annalen"],["dc.contributor.author","Menck, Kerstin"],["dc.contributor.author","Wlochowitz, Darius"],["dc.contributor.author","Binder, Claudia"],["dc.date.accessioned","2022-01-11T14:05:29Z"],["dc.date.available","2022-01-11T14:05:29Z"],["dc.date.issued","2021"],["dc.date.updated","2022-09-03T19:53:04Z"],["dc.description.abstract","Malignant cells differ from benign ones in their metabolome and it is largely unknown whether this difference is reflected in the metabolic profile of their microvesicles (MV), which are secreted into the blood of cancer patients. Here, they are present together with MV from the various blood and endothelial cells. Harvesting MV from 78 breast cancer patients (BC) and 30 controls, we characterized the whole blood MV metabolome using targeted and untargeted mass spectrometry. Especially (lyso)-phosphatidylcholines and sphingomyelins were detected in a relevant abundance. Eight metabolites showed a significant discriminatory power between BC and controls. High concentrations of lysoPCaC26:0 and PCaaC38:5 were associated with shorter overall survival. Comparing BC subtype-specific metabolome profiles, 24 metabolites were differentially expressed between luminal A and luminal B. Pathway analysis revealed alterations in the glycerophospholipid metabolism for the whole cancer cohort and in the ether lipid metabolism for the molecular subtype luminal B. Although this mixture of blood-derived MV contains only a minor number of tumor MV, a combination of metabolites was identified that distinguished between BC and controls as well as between molecular subtypes, and was predictive for overall survival. This suggests that these metabolites represent promising biomarkers and, moreover, that they may be functionally relevant for tumor progression."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.doi","10.3390/ijms222413540"],["dc.identifier.pii","ijms222413540"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/97673"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-507"],["dc.relation.eissn","1422-0067"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Metabolomic Profiling of Blood-Derived Microvesicles in Breast Cancer Patients"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]