Bauerschmitz, Gerd Johannes

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Hellinger, Johanna W."],["dc.contributor.author","Schömel, Franziska"],["dc.contributor.author","Buse, Judith V."],["dc.contributor.author","Lenz, Christof"],["dc.contributor.author","Bauerschmitz, Gerd"],["dc.contributor.author","Emons, Günter"],["dc.contributor.author","Gründker, Carsten"],["dc.date.accessioned","2021-04-14T08:31:47Z"],["dc.date.available","2021-04-14T08:31:47Z"],["dc.date.issued","2020"],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.doi","10.1038/s41598-020-74838-8"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17824"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83712"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","2045-2322"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Identification of drivers of breast cancer invasion by secretome analysis: insight into CTGF signaling"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","418"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Cancers"],["dc.bibliographiccitation.volume","14"],["dc.contributor.affiliation","Woelber, Linn; 1Department of Gynecology and Gynecologic Oncology, University Medical Center Hamburg—Eppendorf, 20246 Hamburg, Germany; k.prieske@uke.de (K.P.); j.hambrecht@uke.de (J.H.); a.jaeger@uke.de (A.J.)"],["dc.contributor.affiliation","Hampl, Monika; 3Department of Gynecology, University Medical Center Duesseldorf, 40225 Duesseldorf, Germany; hampl@med.uni-duesseldorf.de"],["dc.contributor.affiliation","Eulenburg, Christine zu; 4Department of Epidemiology, UMCG, Universität Groningen, 9713 Groningen, The Netherlands; christine.eulenburg@googlemail.com"],["dc.contributor.affiliation","Prieske, Katharina; 1Department of Gynecology and Gynecologic Oncology, University Medical Center Hamburg—Eppendorf, 20246 Hamburg, Germany; k.prieske@uke.de (K.P.); j.hambrecht@uke.de (J.H.); a.jaeger@uke.de (A.J.)"],["dc.contributor.affiliation","Hambrecht, Johanna; 1Department of Gynecology and Gynecologic Oncology, University Medical Center Hamburg—Eppendorf, 20246 Hamburg, Germany; k.prieske@uke.de (K.P.); j.hambrecht@uke.de (J.H.); a.jaeger@uke.de (A.J.)"],["dc.contributor.affiliation","Fuerst, Sophie; 6Department of Obstetrics and Gynecology, University Hospital, LMU—University of Munich, 80377 Munich, Germany; sophie.fuerst@med.uni-muenchen.de (S.F.); sven.mahner@med.uni-muenchen.de (S.M.)"],["dc.contributor.affiliation","Klapdor, Ruediger; 7Department of Obstetrics and Gynecology, Hannover Medical School, 30625 Hannover, Germany; klapdor.ruediger@mh-hannover.de"],["dc.contributor.affiliation","Heublein, Sabine; 8Department of Obstetrics and Gynecology, University Hospital Heidelberg, 69120 Heidelberg, Germany; sabine.heublein@med.uni-heidelberg.de"],["dc.contributor.affiliation","Gass, Paul; 9Department of Gynecology and Obstetrics, University Hospital Erlangen, Comprehensive Cancer Center Erlangen-EMN, Friedrich-Alexander University Erlangen-Nuremberg, 91054 Erlangen, Germany; paul.gass@uk-erlangen.de"],["dc.contributor.affiliation","Rohner, Annika; 10Department of Gynecology, University Medical Center Tuebingen, 72076 Tuebingen, Germany; Annika.Rohner@med.uni-tuebingen.de"],["dc.contributor.affiliation","Canzler, Ulrich; 11Department of Gynecology and Obstetrics, University Hospital Dresden, Technische Universität Dresden, Dresden, Germany & National Center for Tumor Diseases (NCT), Partner Site Dresden, 01307 Dresden, Germany; ulrich.canzler@uniklinikum-dresden.de"],["dc.contributor.affiliation","Becker, Sven; 12Department of Gynecology and Obstetrics, University Medical Center Frankfurt, 60590 Frankfurt, Germany; sven.becker@kgu.de"],["dc.contributor.affiliation","Bommert, Mareike; 13Department of Gynecology and Gynecologic Oncology, Evang. Kliniken Essen-Mitte, 45136 Essen, Germany; m.bommert@kem-med.com"],["dc.contributor.affiliation","Bauerschlag, Dirk; 14Department of Gynecology, University Medical Center Kiel, 24105 Kiel, Germany; dirk.bauerschlag@uksh.de"],["dc.contributor.affiliation","Denecke, Agnieszka; 15Department of Gynecology, Medical Center Wolfsburg, 38440 Wolfsburg, Germany; agnieszka.denecke@klinikum.wolfsburg.de"],["dc.contributor.affiliation","Hanker, Lars; 16Department of Gynecology and Gynecologic Oncology, University Medical Center Luebeck, 23562 Luebeck, Germany; lars.hanker@uksh.de"],["dc.contributor.affiliation","Runnebaumn, Ingo; 17Department of Gynecology, Jena University Hospital, 07743 Jena, Germany; Ingo.Runnebaum@med.uni-jena.de"],["dc.contributor.affiliation","Forner, Dirk M.; 18Department of Gynecology, Evangelisches Krankenhaus Kalk, 51103 Cologne, Germany; dirk.forner@evkk.de"],["dc.contributor.affiliation","Schochter, Fabienne; 19Department of Obstetrics and Gynecology, University of Ulm Medical Center, 89081 Ulm, Germany; fabienne.schochter@uniklinik-ulm.de"],["dc.contributor.affiliation","Klar, Maximilian; 20Department of Gynecology, University Medical Center Freiburg, 79106 Freiburg, Germany; maximilian.klar@uniklinik-freiburg.de"],["dc.contributor.affiliation","Schwab, Roxana; 21Department of Gynecology, University Medical Center Mainz, 55131 Mainz, Germany; Roxana.Schwab@unimedizin-mainz.de"],["dc.contributor.affiliation","Koepke, Melitta; 22Department of Obstetrics and Gynaecology, University Hospital Augsburg, 86156 Augsburg, Germany; melitta.koepke@uk-augsburg.de (M.K.); christian.dannecker@med.uni-augsburg.de (C.D.)"],["dc.contributor.affiliation","Kalder, Matthias; 23Department of Gynecology and Obstetrics, University Hospital Marburg, 35043 Marburg, Germany; kalder@med.uni-marburg.de"],["dc.contributor.affiliation","Hantschmann, Peer; 24Department of Gynecology and Obstetrics, Medical Center Altoetting, 84503 Altoetting, Germany; p.hantschmann@innklinikum.de"],["dc.contributor.affiliation","Ratiu, Dominik; 25Department of Gynecology, University Medical Center Koeln, 50937 Koeln, Germany; dominik.ratiu@uk-koeln.de"],["dc.contributor.affiliation","Denschlag, Dominik; 26Department of Gynecology, Hochtaunuskliniken, 61352 Bad Homburg, Germany; dominik.denschlag@hochtaunus-kliniken.de"],["dc.contributor.affiliation","Schroeder, Willibald; 27Department of Gynecology, Medical Center Gynaecologicum Bremen, 28209 Bremen, Germany; prof.schroeder@gynaekologikum-bremen.de"],["dc.contributor.affiliation","Tuschy, Benjamin; 28Department of Gynecology, University Medical Center Mannheim, 68167 Mannheim, Germany; benjamin.tuschy@umm.de"],["dc.contributor.affiliation","Baumann, Klaus; 29Department of Gynecology, Medical Center Ludwigshafen, 67063 Ludwigshafen, Germany; baumann@klilu.de"],["dc.contributor.affiliation","Mustea, Alexander; 30Department of Gynecology and Gynecologic Oncology, University Medical Center Bonn, 53127 Bonn, Germany; alexander.mustea@ukbonn.de"],["dc.contributor.affiliation","Soergel, Philipp; 31Department of Gynecology, University Medical Center Minden, 32429 Minden, Germany; philipp.soergel@muehlenkreiskliniken.de"],["dc.contributor.affiliation","Bronger, Holger; 32Department of Gynecology and Obstetrics, Technical University of Munich, 81675 Munich, Germany; holger.bronger@tum.de"],["dc.contributor.affiliation","Bauerschmitz, Gerd; 33Department of Gynecology, University Medical Center Goettingen, 37075 Goettingen, Germany; gerd.bauerschmitz@med.uni-goettingen.de"],["dc.contributor.affiliation","Kosse, Jens; 34Department of Gynecology, Sana Klinikum Offenbach, 63069 Offenbach am Main, Germany; jens.kosse@sana.de"],["dc.contributor.affiliation","Koch, Martin C.; 35Department of Gynecology, Medical Center Ansbach, 91522 Ansbach, Germany; martin.koch@anregiomed.de"],["dc.contributor.affiliation","Ignatov, Atanas; 36Department of Obstetrics and Gynecology, University Hospital Magdeburg, 39120 Magdeburg, Germany; atanas.ignatov@med.ovgu.de"],["dc.contributor.affiliation","Sehouli, Jalid; 37Department of Gynecology with Center for Oncological SurgeryNOGGO e.V., Charite Universitatsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Virchow Campus Clinic, Charité Medical University, 13353 Berlin, Germany; jalid.sehouli@charite.de"],["dc.contributor.affiliation","Dannecker, Christian; 22Department of Obstetrics and Gynaecology, University Hospital Augsburg, 86156 Augsburg, Germany; melitta.koepke@uk-augsburg.de (M.K.); christian.dannecker@med.uni-augsburg.de (C.D.)"],["dc.contributor.affiliation","Mahner, Sven; 6Department of Obstetrics and Gynecology, University Hospital, LMU—University of Munich, 80377 Munich, Germany; sophie.fuerst@med.uni-muenchen.de (S.F.); sven.mahner@med.uni-muenchen.de (S.M.)"],["dc.contributor.affiliation","Jaeger, Anna; 1Department of Gynecology and Gynecologic Oncology, University Medical Center Hamburg—Eppendorf, 20246 Hamburg, Germany; k.prieske@uke.de (K.P.); j.hambrecht@uke.de (J.H.); a.jaeger@uke.de (A.J.)"],["dc.contributor.author","Woelber, Linn"],["dc.contributor.author","Hampl, Monika"],["dc.contributor.author","Eulenburg, Christine zu"],["dc.contributor.author","Prieske, Katharina"],["dc.contributor.author","Hambrecht, Johanna"],["dc.contributor.author","Fuerst, Sophie"],["dc.contributor.author","Klapdor, Ruediger"],["dc.contributor.author","Heublein, Sabine"],["dc.contributor.author","Gass, Paul"],["dc.contributor.author","Rohner, Annika"],["dc.contributor.author","Jaeger, Anna"],["dc.contributor.author","Bauerschmitz, Gerd"],["dc.contributor.editor","Preti, Mario"],["dc.contributor.editor","Querleu, Denis"],["dc.date.accessioned","2022-02-01T10:31:45Z"],["dc.date.available","2022-02-01T10:31:45Z"],["dc.date.issued","2022"],["dc.date.updated","2022-02-09T13:18:26Z"],["dc.description.abstract","The need for pelvic treatment in patients with node-positive vulvar cancer (VSCC) and the value of pelvic lymphadenectomy (LAE) as a staging procedure to plan adjuvant radiotherapy (RT) is controversial. In this retrospective, multicenter analysis, 306 patients with primary node-positive VSCC treated at 33 gynecologic oncology centers in Germany between 2017 and 2019 were analyzed. All patients received surgical staging of the groins; nodal status was as follows: 23.9% (73/306) pN1a, 23.5% (72/306) pN1b, 20.4% (62/306) pN2a/b, and 31.9% (97/306) pN2c/pN3. A total of 35.6% (109/306) received pelvic LAE; pelvic nodal involvement was observed in 18.5%. None of the patients with nodal status pN1a or pN1b and pelvic LAE showed pelvic nodal involvement. Taking only patients with nodal status ≥pN2a into account, the rate of pelvic involvement was 25%. In total, adjuvant RT was applied in 64.4% (197/306). Only half of the pelvic node-positive (N+) patients received adjuvant RT to the pelvis (50%, 10/20 patients); 41.9% (122/291 patients) experienced recurrent disease or died. In patients with histologically-confirmed pelvic metastases after LAE, distant recurrences were most frequently observed (7/20 recurrences). Conclusions: A relevant risk regarding pelvic nodal involvement was observed from nodal status pN2a and higher. Our data support the omission of pelvic treatment in patients with nodal status pN1a and pN1b."],["dc.description.abstract","The need for pelvic treatment in patients with node-positive vulvar cancer (VSCC) and the value of pelvic lymphadenectomy (LAE) as a staging procedure to plan adjuvant radiotherapy (RT) is controversial. In this retrospective, multicenter analysis, 306 patients with primary node-positive VSCC treated at 33 gynecologic oncology centers in Germany between 2017 and 2019 were analyzed. All patients received surgical staging of the groins; nodal status was as follows: 23.9% (73/306) pN1a, 23.5% (72/306) pN1b, 20.4% (62/306) pN2a/b, and 31.9% (97/306) pN2c/pN3. A total of 35.6% (109/306) received pelvic LAE; pelvic nodal involvement was observed in 18.5%. None of the patients with nodal status pN1a or pN1b and pelvic LAE showed pelvic nodal involvement. Taking only patients with nodal status ≥pN2a into account, the rate of pelvic involvement was 25%. In total, adjuvant RT was applied in 64.4% (197/306). Only half of the pelvic node-positive (N+) patients received adjuvant RT to the pelvis (50%, 10/20 patients); 41.9% (122/291 patients) experienced recurrent disease or died. In patients with histologically-confirmed pelvic metastases after LAE, distant recurrences were most frequently observed (7/20 recurrences). Conclusions: A relevant risk regarding pelvic nodal involvement was observed from nodal status pN2a and higher. Our data support the omission of pelvic treatment in patients with nodal status pN1a and pN1b."],["dc.identifier.doi","10.3390/cancers14020418"],["dc.identifier.eissn","2072-6694"],["dc.identifier.pii","cancers14020418"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/98940"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-517"],["dc.publisher","MDPI"],["dc.relation.eissn","2072-6694"],["dc.rights","Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/)."],["dc.title","Risk for Pelvic Metastasis and Role of Pelvic Lymphadenectomy in Node-Positive Vulvar Cancer-Results from the AGO-VOP.2 QS Vulva Study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2616"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Cells"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Kolb, Katharina"],["dc.contributor.author","Hellinger, Johanna"],["dc.contributor.author","Kansy, Maike"],["dc.contributor.author","Wegwitz, Florian"],["dc.contributor.author","Bauerschmitz, Gerd"],["dc.contributor.author","Emons, Günter"],["dc.contributor.author","Gründker, Carsten"],["dc.date.accessioned","2021-04-14T08:26:32Z"],["dc.date.available","2021-04-14T08:26:32Z"],["dc.date.issued","2020"],["dc.description.sponsorship","Deutsche Krebshilfe"],["dc.identifier.doi","10.3390/cells9122616"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81981"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.publisher","MDPI"],["dc.relation.eissn","2073-4409"],["dc.rights","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Influence of ARHGAP29 on the Invasion of Mesenchymal-Transformed Breast Cancer Cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2398"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Cells"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Steifensand, Friederike"],["dc.contributor.author","Gallwas, Julia"],["dc.contributor.author","Bauerschmitz, Gerd"],["dc.contributor.author","Gründker, Carsten"],["dc.date.accessioned","2021-10-01T09:58:24Z"],["dc.date.available","2021-10-01T09:58:24Z"],["dc.date.issued","2021"],["dc.description.abstract","Cancer cells have an increased need for glucose and, despite aerobic conditions, obtain their energy through aerobic oxidation and lactate fermentation, instead of aerobic oxidation alone. Glutamine is an essential amino acid in the human body. Glutaminolysis and glycolysis are crucial for cancer cell survival. In the therapy of estrogen receptor α (ERα)-positive breast cancer (BC), the focus lies on hormone sensitivity targeting therapy with selective estrogen receptor modulators (SERMs) such as 4-hydroxytamoxifen (4-OHT), although this therapy is partially limited by the development of resistance. Therefore, further targets for therapy improvement of ERα-positive BC with secondary 4-OHT resistance are needed. Hence, increased glucose requirement and upregulated glutaminolysis in BC cells could be used. We have established sublines of ERα-positive MCF7 and T47D BC cells, which were developed to be resistant to 4-OHT. Further, glycolysis inhibitor 2-Deoxy-D-Glucose (2-DG) and glutaminase inhibitor CB-839 were analyzed. Co-treatments using 4-OHT and CB-839, 2-DG and CB-839, or 4-OHT, 2-DG and CB-839, respectively, showed significantly stronger inhibitory effects on viability compared to single treatments. It could be shown that tamoxifen-resistant BC cell lines, compared to the non-resistant cell lines, exhibited a stronger reducing effect on cell viability under co-treatments. In addition, the tamoxifen-resistant BC cell lines showed increased expression of proto-oncogene c-Myc compared to the parental cell lines. This could be reduced depending on the treatment. Suppression of c-Myc expression using specific siRNA completely abolished resistance to 4OH-tamoxifen. In summary, our data suggest that combined treatments affecting the metabolism of BC are suitable depending on the cellularity and resistance status. In addition, the anti-metabolic treatments affected the expression of the proto-oncogene c-Myc, a key player in the regulation of cancer cell metabolism."],["dc.description.abstract","Cancer cells have an increased need for glucose and, despite aerobic conditions, obtain their energy through aerobic oxidation and lactate fermentation, instead of aerobic oxidation alone. Glutamine is an essential amino acid in the human body. Glutaminolysis and glycolysis are crucial for cancer cell survival. In the therapy of estrogen receptor α (ERα)-positive breast cancer (BC), the focus lies on hormone sensitivity targeting therapy with selective estrogen receptor modulators (SERMs) such as 4-hydroxytamoxifen (4-OHT), although this therapy is partially limited by the development of resistance. Therefore, further targets for therapy improvement of ERα-positive BC with secondary 4-OHT resistance are needed. Hence, increased glucose requirement and upregulated glutaminolysis in BC cells could be used. We have established sublines of ERα-positive MCF7 and T47D BC cells, which were developed to be resistant to 4-OHT. Further, glycolysis inhibitor 2-Deoxy-D-Glucose (2-DG) and glutaminase inhibitor CB-839 were analyzed. Co-treatments using 4-OHT and CB-839, 2-DG and CB-839, or 4-OHT, 2-DG and CB-839, respectively, showed significantly stronger inhibitory effects on viability compared to single treatments. It could be shown that tamoxifen-resistant BC cell lines, compared to the non-resistant cell lines, exhibited a stronger reducing effect on cell viability under co-treatments. In addition, the tamoxifen-resistant BC cell lines showed increased expression of proto-oncogene c-Myc compared to the parental cell lines. This could be reduced depending on the treatment. Suppression of c-Myc expression using specific siRNA completely abolished resistance to 4OH-tamoxifen. In summary, our data suggest that combined treatments affecting the metabolism of BC are suitable depending on the cellularity and resistance status. In addition, the anti-metabolic treatments affected the expression of the proto-oncogene c-Myc, a key player in the regulation of cancer cell metabolism."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.doi","10.3390/cells10092398"],["dc.identifier.pii","cells10092398"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/90055"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-469"],["dc.relation.eissn","2073-4409"],["dc.relation.orgunit","Klinik für Gynäkologie und Geburtshilfe"],["dc.rights","CC BY 4.0"],["dc.title","Inhibition of Metabolism as a Therapeutic Option for Tamoxifen-Resistant Breast Cancer Cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Oncology"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Hellinger, Johanna W."],["dc.contributor.author","Hüchel, Silke"],["dc.contributor.author","Goetz, Lena"],["dc.contributor.author","Bauerschmitz, Gerd"],["dc.contributor.author","Emons, Günter"],["dc.contributor.author","Gründker, Carsten"],["dc.date.accessioned","2020-12-10T18:44:36Z"],["dc.date.available","2020-12-10T18:44:36Z"],["dc.date.issued","2019"],["dc.description.abstract","Background and Objective: Matricellular proteins modulate the micro environment of tumors and are recognized to contribute to tumor cell invasion and dissemination. The cysteine-rich angiogenic inducer 61 (CYR61) is upregulated in mesenchymal transformed and invasive breast cancer cells. CYR61 correlates with poor prognosis of breast cancer patients. The signaling mechanism that causes invasive properties of cancer cells regarding to epithelial-mesenchymal transition (EMT) needs further research. In this study, we investigated the signaling mechanism, which is responsible for reduced cell invasion after suppression of CYR61 in mesenchymal transformed breast cancer cells and in triple negative breast cancer cells. Methods: We addressed this issue by generating a mesenchymal transformed breast cancer cell line using prolonged mammosphere cultivation. Western blotting and quantitative PCR were used to analyze gene expression alterations. Transient gene silencing was conducted using RNA interference. Proliferation was assessed using AlamarBlue assay. Invasiveness was analyzed using 2D and 3D invasion assays. Immune-histochemical analysis of patient tissue samples was performed to examine the prognostic value of CYR61 expression. Results: In this study, we investigated whether CYR61 could be used as therapeutic target and prognostic marker for invasive breast cancer. We discovered an interaction of CYR61 with metastasis-associated protein S100A4. Suppression of CYR61 by RNA interference reduced the expression of S100A4 dependent on ERK1/2 activity regulation. Non-invasive breast cancer cells became invasive due to extracellular CYR61 supplement. Immune-histochemical analysis of 239 patient tissue samples revealed a correlation of higher CYR61 and S100A4 expression with invasive breast cancer and metastasis. Conclusion: Our data suggest that suppression of CYR61 impedes the formation of an invasive cancer cell phenotype by reducing ERK1/2 phosphorylation thereby suppressing S100A4. These findings identify mechanisms by which CYR61 suppresses cell invasion and suggest it to be a potential therapeutic target and prognostic marker for invasive breast cancer and metastasis."],["dc.identifier.doi","10.3389/fonc.2019.01074"],["dc.identifier.eissn","2234-943X"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16551"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78520"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","2234-943X"],["dc.rights","http://creativecommons.org/licenses/by/4.0/"],["dc.title","Inhibition of CYR61-S100A4 Axis Limits Breast Cancer Invasion"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]