Schulz, Matthias

[["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","434"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Carcinogenesis"],["dc.bibliographiccitation.lastpage","442"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Klemm, Florian"],["dc.contributor.author","Bleckmann, Annalen"],["dc.contributor.author","Siam, Laila"],["dc.contributor.author","Chuang, Han-Ning"],["dc.contributor.author","Rietkoetter, Eva"],["dc.contributor.author","Behme, Daniel"],["dc.contributor.author","Schulz, M."],["dc.contributor.author","Schaffrinski, Meike"],["dc.contributor.author","Schindler, Stefanie"],["dc.contributor.author","Trümper, Lorenz H."],["dc.contributor.author","Kramer, Franz-Josef"],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Stadelmann, C."],["dc.contributor.author","Binder, Claudia"],["dc.contributor.author","Pukrop, Tobias"],["dc.date.accessioned","2018-11-07T08:59:01Z"],["dc.date.available","2018-11-07T08:59:01Z"],["dc.date.issued","2011"],["dc.description.abstract","A role of WNT signaling for primary breast cancers of the basal-like subtype and as a predictor of brain metastasis has been described. However, a responsible WNT ligand has not been identified. To further clarify this question, we comparatively investigated 22 human breast cancer brain metastases as well as the highly invasive human breast cancer cell line MDA-MB-231 and the weakly motile MCF-7 as models for the basal-like and the luminal A subtype. WNT5A and B were found overexpressed in MDA-MB-231 cells as compared with MCF-7. This corresponded to reduction of MDA-MB-231 invasiveness by WNT inhibitors, whereas MCF-7 invasion was enhanced by recombinant WNT5B and abolished by WNT and Jun-N-terminal kinase antagonists. Expression and subcellular distribution of beta-catenin remained uninfluenced. Consistently, beta-catenin was not localized in the nuclei of brain metastases while there was strong nuclear c-Jun staining. Similar to MDA-MB-231, metastases showed expression of WNT5A/B and the alternative WNT receptors ROR1 and 2. These findings were validated using external gene expression datasets (Gene Expression Omnibus) of different breast cancer subtypes and brain metastases. Hierarchical cluster analysis yielded a close relation between basal-like cancers and brain metastases. Gene set enrichment analyses confirmed WNT pathway enrichment not only in basal-like primaries but also in cerebral metastases of all subtypes. In conclusion, WNT signaling seems highly relevant for basal-like and other subtypes of breast cancers metastasizing into the brain. beta-catenin-independent WNT signaling, presumably via ROR1-2, plays a major role in this context."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft [FOR 942]"],["dc.identifier.doi","10.1093/carcin/bgq269"],["dc.identifier.isi","000288027800025"],["dc.identifier.pmid","21173432"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23785"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0143-3334"],["dc.title","beta-catenin-independent WNT signaling in basal-like breast cancer and brain metastasis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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.artnumber","e55057"],["dc.bibliographiccitation.issue","119"],["dc.bibliographiccitation.journal","Journal of Visualized Experiments"],["dc.contributor.author","Menck, Kerstin"],["dc.contributor.author","Bleckmann, Annalen"],["dc.contributor.author","Schulz, Matthias"],["dc.contributor.author","Ries, Lena"],["dc.contributor.author","Binder, Claudia"],["dc.date.accessioned","2018-11-07T10:28:42Z"],["dc.date.available","2018-11-07T10:28:42Z"],["dc.date.issued","2017"],["dc.description.abstract","The release of extracellular vesicles (EVs) including small endosomal-derived exosomes (Exos, diameter < 100 nm) and large plasma membrane-derived microvesicles (MVs, diameter > 100 nm) is a fundamental cellular process that occurs in all living cells. These vesicles transport proteins, lipids and nucleic acids specific for their cell of origin and in vitro studies have highlighted their importance as mediators of intercellular communication. EVs have been successfully isolated from various body fluids and especially EVs in blood have been identified as promising biomarkers for cancer or infectious diseases. In order to allow the study of MV subpopulations in blood, we present a protocol for the standardized isolation and characterization of MVs from peripheral blood samples. MVs are pelleted from EDTA-anticoagulated plasma samples by differential centrifugation and typically possess a diameter of 100 - 600 nm. Due to their larger size, they can easily be studied by flow cytometry, a technique that is routinely used in clinical diagnostics and available in most laboratories. Several examples for quality control assays of the isolated MVs will be given and markers that can be used for the discrimination of different MV subpopulations in blood will be presented."],["dc.identifier.doi","10.3791/55057"],["dc.identifier.isi","000397847200045"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43486"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Journal Of Visualized Experiments"],["dc.relation.issn","1940-087X"],["dc.title","Isolation and Characterization of Microvesicles from Peripheral Blood"],["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"]]