Wegwitz, Florian

[["dc.bibliographiccitation.firstpage","8959"],["dc.bibliographiccitation.issue","16"],["dc.bibliographiccitation.journal","Nucleic Acids Research"],["dc.bibliographiccitation.lastpage","8976"],["dc.bibliographiccitation.volume","48"],["dc.contributor.author","Wüst, Hannah M"],["dc.contributor.author","Wegener, Amélie"],["dc.contributor.author","Fröb, Franziska"],["dc.contributor.author","Hartwig, Anna C"],["dc.contributor.author","Wegwitz, Florian"],["dc.contributor.author","Kari, Vijayalakshmi"],["dc.contributor.author","Schimmel, Margit"],["dc.contributor.author","Tamm, Ernst R"],["dc.contributor.author","Johnsen, Steven A"],["dc.contributor.author","Wegner, Michael"],["dc.contributor.author","Sock, Elisabeth"],["dc.date.accessioned","2021-04-14T08:22:59Z"],["dc.date.available","2021-04-14T08:22:59Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1093/nar/gkaa606"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/80763"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1362-4962"],["dc.relation.issn","0305-1048"],["dc.title","Egr2-guided histone H2B monoubiquitination is required for peripheral nervous system myelination"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Cancer Research"],["dc.bibliographiccitation.volume","76"],["dc.contributor.author","Mishra, Vivek Kumar"],["dc.contributor.author","Kari, Vijayalakshmi"],["dc.contributor.author","Subramaniam, Malayannan"],["dc.contributor.author","Baumgart, Simon J."],["dc.contributor.author","Nagarajan, Sankari"],["dc.contributor.author","Wegwitz, Florian"],["dc.contributor.author","Spelsberg, Thomas C."],["dc.contributor.author","Hawse, John R."],["dc.contributor.author","Johnsen, Steven A."],["dc.date.accessioned","2018-11-07T10:19:22Z"],["dc.date.available","2018-11-07T10:19:22Z"],["dc.date.issued","2016"],["dc.identifier.doi","10.1158/1538-7445.CHROMEPI15-A03"],["dc.identifier.isi","000368930800003"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41642"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Cancer Research"],["dc.publisher.place","Philadelphia"],["dc.relation.conference","American-Association-for-Cancer-Research (AACR) Special Conference on Chromatin and Epigenetics in Cancer"],["dc.relation.eventlocation","Atlanta, GA"],["dc.relation.issn","1538-7445"],["dc.relation.issn","0008-5472"],["dc.title","Kruppel-like Transcription Factor-10 (KLF10) suppresses the TGF beta-induced epithelial-to-mesenchymal transition"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","E521"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","International Journal of Cancer"],["dc.bibliographiccitation.lastpage","E533"],["dc.bibliographiccitation.volume","136"],["dc.contributor.author","Lenfert, Eva"],["dc.contributor.author","Maenz, Claudia"],["dc.contributor.author","Heinlein, Christina"],["dc.contributor.author","Jannasch, Katharina"],["dc.contributor.author","Schumacher, Udo"],["dc.contributor.author","Pantel, Klaus"],["dc.contributor.author","Tolstonog, Genrich V."],["dc.contributor.author","Deppert, Wolfgang R."],["dc.contributor.author","Wegwitz, Florian"],["dc.date.accessioned","2018-11-07T09:59:40Z"],["dc.date.available","2018-11-07T09:59:40Z"],["dc.date.issued","2015"],["dc.description.abstract","To study the postulated mutant p53 (mutp53) gain of function effects in mammary tumor development, progression and metastasis, we crossed SV40 transgenic WAP-T mice with mutant p53 transgenic WAP-mutp53 mice. Compared to tumors in monotransgenic WAP-T mice, tumors in bitransgenic WAP-T x WAP-mutp53 mice showed higher tumor grading, enhanced vascularization, and significantly increased metastasis. Bitransgenic tumors revealed a gene signature associated with the oncogenic epithelial-mesenchymal transition pathway (EMT gene signature). In cultures of WAP-T tumor-derived G-2 cancer cells, which are comprised of subpopulations displaying mesenchymal and epithelial phenotypes, this EMT gene signature was associated with the mesenchymal compartment. Furthermore, ectopic expression of mutp53 in G-2 cells sufficed to induce a strong EMT phenotype. In contrast to these in vitro effects, monotransgenic and bitransgenic tumors were phenotypically similar suggesting that in vivo the tumor cell phenotype might be under control of the tumor microenvironment. In support, orthotopic transplantation of G-2 cells as well as of G-2 cells expressing ectopic mutp53 into syngeneic mice resulted in tumors with a predominantly epithelial phenotype, closely similar to that of endogenous primary tumors. We conclude that induction of an EMT gene signature by mutp53 in bitransgenic tumors primarily promotes tumor cell plasticity, that is, the probability of tumor cells to undergo EMT processes under appropriate stimuli, thereby possibly increasing their potential to disseminate and metastasize. What's new? Despite the loss of transcriptional activity, mutant p53 (mutp53) proteins display gain of function properties, such as the ability to contribute to tumor progression. To elucidate functional gains, the present study explored the effects of mutp53 expression in monotransgenic WAP-T mice and bitransgenic WAP-T x WAP-mutp53 mice. Mammary tumors from both models were phenotypically similar and possessed an epithelial-mesenchymal transition (EMT) gene signature associated with tumor cell plasticity. However, mammary tumors in bitransgenic mice showed enhanced metastatic potential. Additional findings from in vitro experiments indicate that the tumor microenvironment plays a key role in regulating tumor cell phenotype and invasiveness."],["dc.identifier.doi","10.1002/ijc.29186"],["dc.identifier.isi","000347705200005"],["dc.identifier.pmid","25195563"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37647"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1097-0215"],["dc.relation.issn","0020-7136"],["dc.title","Mutant p53 promotes epithelial-mesenchymal plasticity and enhances metastasis in mammary carcinomas of WAP-T mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","5885"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Anticancer Research"],["dc.bibliographiccitation.lastpage","5886"],["dc.bibliographiccitation.volume","34"],["dc.contributor.author","Wegwitz, Florian"],["dc.contributor.author","Lenfert, Eva"],["dc.contributor.author","Maenz, Claudia"],["dc.contributor.author","Tolstonog, Genrich V."],["dc.contributor.author","Deppert, Wolfgang R."],["dc.date.accessioned","2018-11-07T09:34:27Z"],["dc.date.available","2018-11-07T09:34:27Z"],["dc.date.issued","2014"],["dc.identifier.isi","000343139500220"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32173"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Int Inst Anticancer Research"],["dc.publisher.place","Athens"],["dc.relation.issn","1791-7530"],["dc.relation.issn","0250-7005"],["dc.title","WAP-T MICE: A PRECLINICAL MOUSE MODEL TO STUDY MAMMARY CARCINOGENESIS, PROGRESSION, AND METASTASIS"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","959"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Cells"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Hoen, Laura"],["dc.contributor.author","Rudisch, Christoph"],["dc.contributor.author","Wick, Michael"],["dc.contributor.author","Indenbirken, Daniela"],["dc.contributor.author","Grundhoff, Adam"],["dc.contributor.author","Wegwitz, Florian"],["dc.contributor.author","Kalkhof, Stefan"],["dc.contributor.author","Hildebrand, Janosch"],["dc.date.accessioned","2022-04-01T10:02:05Z"],["dc.date.available","2022-04-01T10:02:05Z"],["dc.date.issued","2022"],["dc.description.abstract","The human skin and in particular its outermost layer, the epidermis, protects the body from potentially harmful substances, radiation as well as excessive water loss. However, the interference between the various stress responses of the epidermal keratinocytes, which often occur simultaneously, is largely unknown. The focus of this study was to investigate the interference between osmotic stress and DNA damage response. In addition to revealing the already well-described regulation of diverse gene sets, for example, cellular processes such as transcription, translation, and metabolic pathways (e.g., the KEGG citrate cycle and Reactome G2/M checkpoints), gene expression analysis of osmotically stressed keratinocytes revealed an influence on the transcription of genes also related to UV-induced DNA damage response. A gene network regulating the H2AX phosphorylation was identified to be regulated by osmotic stress. To analyze and test the interference between osmotic stress and DNA damage response, which can be triggered by UV stress on the one hand and oxidative stress on the other, in more detail, primary human keratinocytes were cultured under osmotic stress conditions and subsequently exposed to UV light and H2O2, respectively. γH2AX measurements revealed lower γH2AX levels in cells previously cultured under osmotic stress conditions."],["dc.identifier.doi","10.3390/cells11060959"],["dc.identifier.pii","cells11060959"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/105819"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-530"],["dc.relation.eissn","2073-4409"],["dc.title","Osmotic Stress Interferes with DNA Damage Response and H2AX Phosphorylation in Human Keratinocytes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","4275"],["dc.bibliographiccitation.issue","41"],["dc.bibliographiccitation.journal","Oncogene"],["dc.bibliographiccitation.lastpage","4288"],["dc.bibliographiccitation.volume","30"],["dc.contributor.author","Gerstel, Daniela"],["dc.contributor.author","Wegwitz, Florian"],["dc.contributor.author","Jannasch, Katharina"],["dc.contributor.author","Ludewig, P."],["dc.contributor.author","Scheike, K."],["dc.contributor.author","Alves, Frauke"],["dc.contributor.author","Beauchemin, Nicole"],["dc.contributor.author","Deppert, Wolfgang R."],["dc.contributor.author","Wagener, Christoph"],["dc.contributor.author","Horst, Andrea Kristina"],["dc.date.accessioned","2018-11-07T08:51:04Z"],["dc.date.available","2018-11-07T08:51:04Z"],["dc.date.issued","2011"],["dc.description.abstract","We have studied the effects of carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) on tumor angiogenesis in murine ductal mammary adenocarcinomas. We crossed transgenic mice with whey acidic protein promoter-driven large T-antigen expression (WAP-T mice) with oncogene-induced mammary carcinogenesis with CEA-CAM1null mice, and with Tie2-Ceacam1 transgenics, in which the Tie2 promoter drives endothelial overexpression of CEACAM1 (WAP-T x CEACAM1(endo+) mice), and analyzed tumor vascularization, angiogenesis and vessel maturation in these mice. Using flat-panel volume computed tomography (fpVCT) and histology, we found that WAP-T x CEACAM1(endo+) mice exhibited enhanced tumoral vascularization owing to CEACAM1(+) vessels in the tumor periphery, and increased intratumoral angiogenesis compared with controls. In contrast, vascularization of CEACAM1null/WAP-T-derived tumors was poor, and tumor vessels were dilated, leaky and showed poor pericyte coverage. Consequently, the tumoral vasculature could not be visualized in CEACAM1null/WAP-T mice by fpVCT, and we observed poor organization of the perivascular extracellular matrix (ECM), accompanied by the accumulation of collagen IV-degrading matrix metalloproteinase 9(+) (MMP9(+)) leukocytes and stromal cells. Vascular instability and alterations in ECM structure were accompanied by a significant increase in pulmonary metastases in CEACAM1null/WAP-T mice, whereas only occasional metastases were observed in CEACAM1(+) hosts. In CEACAM1(+) hosts, intratumoral vessels did not express CEACAM1, but they were intact, extensively covered with pericytes and framed by a well-organized perivascular ECM. MMP9(+) accessory cells were largely absent. Orthotopic transplantation of primary WAP-T- and CEACAM1null/WAP-T tumors into all three mouse lines confirmed that a CEACAM1(+) host environment is a prerequisite for productive angiogenic remodeling of the tumor microenvironment. Hence, CEACAM1 expression in the tumor periphery determines the vascular phenotype in a tumor, whereas systemic absence of CEACAM1 interferes with the formation of an organized tumor matrix and intratumoral vessel maturation. Oncogene (2011) 30, 4275-4288; doi: 10.1038/onc.2011.146; published online 2 May 2011"],["dc.description.sponsorship","German Research Foundation [SPP1190]"],["dc.identifier.doi","10.1038/onc.2011.146"],["dc.identifier.isi","000296356300005"],["dc.identifier.pmid","21532628"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21845"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","0950-9232"],["dc.title","CEACAM1 creates a pro-angiogenic tumor microenvironment that supports tumor vessel maturation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1369"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Stem Cells"],["dc.bibliographiccitation.lastpage","1376"],["dc.bibliographiccitation.volume","34"],["dc.contributor.author","Hossan, Tareq"],["dc.contributor.author","Nagarajan, Sankari"],["dc.contributor.author","Baumgart, Simon J."],["dc.contributor.author","Xie, Wanhua"],["dc.contributor.author","Magallanes, Roberto Tirado"],["dc.contributor.author","Hernandez, Celine"],["dc.contributor.author","Chiaroni, Pierre-Marie"],["dc.contributor.author","Indenbirken, Daniela"],["dc.contributor.author","Spitzner, Melanie"],["dc.contributor.author","Thomas-Chollier, Morgane"],["dc.contributor.author","Grade, Marian"],["dc.contributor.author","Thieffry, Denis"],["dc.contributor.author","Grundhoff, Adam"],["dc.contributor.author","Wegwitz, Florian"],["dc.contributor.author","Johnsen, Steven A."],["dc.date.accessioned","2018-11-07T10:15:04Z"],["dc.date.available","2018-11-07T10:15:04Z"],["dc.date.issued","2016"],["dc.description.abstract","Cellular differentiation is accompanied by dramatic changes in chromatin structure which direct the activation of lineage-specific transcriptional programs. Structure-specific recognition protein-1 (SSRP1) is a histone chaperone which is important for chromatin-associated processes such as transcription, DNA replication and repair. Since the function of SSRP1 during cell differentiation remains unclear, we investigated its potential role in controlling lineage determination. Depletion of SSRP1 in human mesenchymal stem cells elicited lineage-specific effects by increasing expression of adipocyte-specific genes and decreasing the expression of osteoblast-specific genes. Consistent with a role in controlling lineage specification, transcriptome-wide RNA-sequencing following SSRP1 depletion and the induction of osteoblast differentiation revealed a specific decrease in the expression of genes involved in biological processes related to osteoblast differentiation. Importantly, we observed a specific downregulation of target genes of the canonical Wnt signaling pathway, which was accompanied by decreased nuclear localization of active beta-catenin. Together our data uncover a previously unknown role for SSRP1 in promoting the activation of the Wnt signaling pathway activity during cellular differentiation."],["dc.identifier.doi","10.1002/stem.2287"],["dc.identifier.isi","000375896900021"],["dc.identifier.pmid","27146025"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40740"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1549-4918"],["dc.relation.issn","1066-5099"],["dc.title","Histone Chaperone SSRP1 is Essential for Wnt Signaling Pathway Activity During Osteoblast Differentiation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","88"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Neurochemistry"],["dc.bibliographiccitation.lastpage","100"],["dc.bibliographiccitation.volume","137"],["dc.contributor.author","Falker, Clemens"],["dc.contributor.author","Hartmann, Alexander K."],["dc.contributor.author","Guett, Inga"],["dc.contributor.author","Dohler, Frank"],["dc.contributor.author","Altmeppen, Hermann"],["dc.contributor.author","Betzel, Christian"],["dc.contributor.author","Schubert, Robin"],["dc.contributor.author","Thurm, Dana"],["dc.contributor.author","Wegwitz, Florian"],["dc.contributor.author","Joshi, Pooja"],["dc.contributor.author","Verderio, Claudia"],["dc.contributor.author","Krasemann, Susanne"],["dc.contributor.author","Glatzel, Markus"],["dc.date.accessioned","2018-11-07T10:16:26Z"],["dc.date.available","2018-11-07T10:16:26Z"],["dc.date.issued","2016"],["dc.description.abstract","Alzheimer's disease is a common neurodegenerative, progressive, and fatal disorder. Generation and deposition of amyloid beta (A) peptides associate with its pathogenesis and small soluble A oligomers show the most pronounced neurotoxic effects and correlate with disease initiation and progression. Recent findings showed that A oligomers bind to the cellular prion protein (PrPC) eliciting neurotoxic effects. The role of exosomes, small extracellular vesicles of endosomal origin, in Alzheimer's disease is only poorly understood. Besides serving as disease biomarkers they may promote A plaque formation, decrease A-mediated synaptotoxicity, and enhance A clearance. Here, we explore how exosomal PrPC connects to protective functions attributed to exosomes in Alzheimer's disease. To achieve this, we generated a mouse neuroblastoma PrPC knockout cell line using transcription activator-like effector nucleases. Using these, as well as SH-SY5Y human neuroblastoma cells, we show that PrPC is highly enriched on exosomes and that exosomes bind amyloid beta via PrPC. Exosomes showed highest binding affinity for dimeric, pentameric, and oligomeric A species. Thioflavin T assays revealed that exosomal PrPC accelerates fibrillization of amyloid beta, thereby reducing neurotoxic effects imparted by oligomeric A. Our study provides further evidence for a protective role of exosomes in A-mediated neurodegeneration and highlights the importance of exosomal PrPC in molecular mechanisms of Alzheimer's disease."],["dc.identifier.doi","10.1111/jnc.13514"],["dc.identifier.isi","000372980100008"],["dc.identifier.pmid","26710111"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41039"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1471-4159"],["dc.relation.issn","0022-3042"],["dc.title","Exosomal cellular prion protein drives fibrillization of amyloid beta and counteracts amyloid beta-mediated neurotoxicity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","25"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","International Journal of Cancer"],["dc.bibliographiccitation.lastpage","36"],["dc.bibliographiccitation.volume","137"],["dc.contributor.author","Jannasch, Katharina"],["dc.contributor.author","Wegwitz, Florian"],["dc.contributor.author","Lenfert, Eva"],["dc.contributor.author","Maenz, Claudia"],["dc.contributor.author","Deppert, Wolfgang R."],["dc.contributor.author","Alves, Frauke"],["dc.date.accessioned","2018-11-07T09:55:37Z"],["dc.date.available","2018-11-07T09:55:37Z"],["dc.date.issued","2015"],["dc.description.abstract","In this study, the effects of the standard chemotherapy, cyclophosphamide/adriamycin/5-fluorouracil (CAF) on tumor growth, dissemination and recurrence after orthotopic implantation of murine G-2 cells were analyzed in the syngeneic immunocompetent whey acidic protein-T mouse model (Wegwitz et al., PLoS One 2010; 5:e12103; Schulze-Garg et al., Oncogene 2000; 19:1028-37). Single-dose CAF treatment reduced tumor size significantly, but was not able to eradicate all tumor cells, as recurrent tumor growth was observed 4 weeks after CAF treatment. Nine days after CAF treatment, residual tumors showed features of regressive alterations and were composed of mesenchymal-like tumor cells, infiltrating immune cells and some tumor-associated fibroblasts with an intense deposition of collagen. Recurrent tumors were characterized by coagulative necrosis and less tumor cell differentiation compared with untreated tumors, suggesting a more aggressive tumor phenotype. In support, tumor cell dissemination was strongly enhanced in mice that had developed recurrent tumors in comparison with untreated controls, although only few disseminated tumor cells could be detected in various organs 9 days after CAF application. In vitro experiments revealed that CAF treatment of G-2 cells eliminates the vast majority of epithelial tumor cells, whereas tumor cells with a mesenchymal phenotype survive. These results together with the in vivo findings suggest that tumor cells that underwent epithelial-mesenchymal transition and/or exhibit stem-cell-like properties are difficult to eliminate using one round of CAF chemotherapy. The model system described here provides a valuable tool for the characterization of the effects of chemotherapeutic regimens on recurrent tumor growth and on tumor cell dissemination, thereby enabling the development and preclinical evaluation of novel therapeutic strategies to target mammary carcinomas."],["dc.identifier.doi","10.1002/ijc.29369"],["dc.identifier.isi","000353297600003"],["dc.identifier.pmid","25449528"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36792"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1097-0215"],["dc.relation.issn","0020-7136"],["dc.title","Chemotherapy of WAP-T mouse mammary carcinomas aggravates tumor phenotype and enhances tumor cell dissemination"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1185"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Nature Cancer"],["dc.bibliographiccitation.lastpage","1203"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Tu, Mengyu"],["dc.contributor.author","Klein, Lukas"],["dc.contributor.author","Espinet, Elisa"],["dc.contributor.author","Georgomanolis, Theodoros"],["dc.contributor.author","Wegwitz, Florian"],["dc.contributor.author","Li, Xiaojuan"],["dc.contributor.author","Urbach, Laura"],["dc.contributor.author","Danieli-Mackay, Adi"],["dc.contributor.author","Küffer, Stefan"],["dc.contributor.author","Bojarczuk, Kamil"],["dc.contributor.author","Singh, Shiv K."],["dc.date.accessioned","2022-04-01T10:02:40Z"],["dc.date.available","2022-04-01T10:02:40Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1038/s43018-021-00258-w"],["dc.identifier.pii","258"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/105977"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-530"],["dc.relation.eissn","2662-1347"],["dc.rights.uri","https://www.springer.com/tdm"],["dc.title","TNF-α-producing macrophages determine subtype identity and prognosis via AP1 enhancer reprogramming in pancreatic cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]